Tabata Training The Science and History of HIIT 9780323913027, 0323913024

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Tabata Training

The Science and History of HIIT

First Edition

Izumi Tabata

Graduate School of Sport and Health Science, Kusatsu, Shiga, Japan

Table of Contents

Cover image

Title page

Copyright

Preface

Reference

Chapter 1: Introduction

Abstract

Introduction

References

Chapter 2: Scientific bases for the superiority of the Tabata training

Abstract

Quantification of aerobic energy-releasing system

Quantification of anaerobic energy-releasing system

Nomenclature

References

Chapter 3: History of Tabata training

Abstract

History of oxygen deficit

Fitness tests at the laboratory for exercise physiology and biomechanics, University of Tokyo

Visit to Oslo, 1983

Training camp for top skaters, 1989

Analysis of the two training protocols introduced by Mr. Irisawa

Recommended practical procedures for Tabata training

References

Chapter 4: Later scientific evidence

Abstract

Evolution of IE1 into Tabata training!

Effects of training combining Tabata training and resistance training on MAOD and V̇o2max

Different protocols for high-intensity intermittent training

Effects of running Tabata training on V̇o2max

Effects of biweekly Tabata bike training on V̇o2max and MAOD

Effects of Tabata bike training on the V̇o2max of college swimmers

Effects of Tabata sprint bike training on the V̇o2max of college skiers

Hints for Tabata training

Effects of Tabata training on excess postexercise oxygen uptake (EPOC)

Effects of Tabata training on colon cancer prevention

Gene expression profile of adaptation of muscle to Tabata training

Effects of Tabata training on circulation

Effects of Tabata training on bone metabolism

Effects of Tabata training on small intestine

Tabata-style training using bodyweight for athletes

Tabata-style training using bodyweight for health-oriented people

Effects of nonexhaustive Tabata-style training on V̇o2max

Effects of nonexhaustive weight-bearing Tabata-style training on V̇o2max

Hints for Tabata-style nonexhaustive weight-bearing training

Blood lactate and sport performance

References

Chapter 5: Epilogue and acknowledgments

Abstract

Acknowledgments

Other interesting features of Tabata training

Future research

References

Index

Copyright

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Preface

Young animals practice hunting on their own or with their parents’ guidance. They do not expect that such hunting activities and vigorous play with peers improve their physical fitness, resulting in more fruitful hunting. In this context, hominids also might have practiced hunting 1.5 million years ago, for example, by throwing spears (Umminger, 2000). It may not have been the intention of either animals or ancient hominids to improve their fitness. Ancient Egyptian soldiers organized systematic wrestling training in ~ 3400 BC (Umminger, 2000). It is thought that the aim of this training was to win wrestling matches and not to improve fitness. Most animals avoid demanding exercises other than hunting practice. It is well known, however, that ancient Greeks were inspired by Plato to train with strenuous exercise to improve their fitness and physiques. Therefore, exercise training for the purpose of improving physical fitness may be specific to humans. From this perspective, the Tabata training explored in this book could be thought of as quintessentially human, because it is one of the most demanding forms of exercise training. Given this context, it might appear natural that Tabata training emerged and has gained appreciation by people in the past 20 years, although it may be that the primary reason why people prefer Tabata training is that it is not time-consuming. The training was unexpectedly named after me by an unknown person, and I have been recognized as one of its representatives. Because the training has been taken up not only by a small number of elite athletes but also by an extremely large number of exercise lovers, I have felt a sense of responsibility to provide scientific evidence as to whether this training is beneficial or hazardous. This book is a compilation of evidence that I have collected to date. That includes evidence not only of the effects of Tabata training on the performance of athletes ranging from elite to school level but also of the possible effects of health promotion among the general public by preventing lifestyle-related diseases. Further, I recognize that in addition to such applied physiological research, Tabata-style training conducted with rats can be used as a tool for finding cellular signals induced by exercise and elucidating molecular mechanism(s) regarding their effects on cell metabolism and expression of proteins with physiological functions. I think there will always be a need for more data on the effects of Tabata training on various aspects of the human body. It is my great pleasure to share such data, in addition to the history of Tabata training, which I love to present to young scientist and coaches. I hope they invent even better trainings in collaboration with researchers and coaches with scientific backgrounds at the field (rink) side, just like my own experience with the coach of Olympic medal-winning speed skaters, Mr. Kouichi Irisawa. May they win medals at many future games!

Reference

Umminger, 2000 Umminger W. Überarbeitete und ergänzte Ausgabe der Chronik des Sports, 5000 Jahre Sportgeschichte. München, Germany: Alinea Verlag; 2000.

Chapter 1: Introduction

Abstract

In recent years, in addition to moderate-intensity prolonged exercise training, highly motivated athletes and people who enjoy exercise for health promotion have been using high-intensity intermittent/interval training (HIIT). Kenney et al. (2019) attributed this revival of interest in HIIT between the 1970s and 2000s to appearance of Tabata training articles published in 1996 and 1997 (Tabata et al., 1996, 1997). This is the first scientific book written exclusively on Tabata training by an author who has been studying the training named after him. This chapter introduces the book’s contents, including chapters on the scientific basis for the superiority of the Tabata training (Chapter 2), history of Tabata training (Chapter 3), later scientific evidence (Chapter 4), and an epilogue that looks to the future (Chapter 5).

Keywords

Tabata training; High-intensity intermittent/interval training (HIIT)

Introduction

Maximal aerobic power, measured as maximal oxygen uptake (V̇o2max), is closely related to both sports performance and prevention of lifestyle-related diseases. Moderate-intensity prolonged exercise training has been used to improve athletic performance and promote health. In recent years, in addition to this conventional training, so-called “aerobic training,” high-intensity intermittent/interval training (HIIT) has been utilized by highly motivated athletes and people who enjoy exercise for health promotion. HIIT itself is not new. In the 1930s, Dr. Gösta Holmér introduced HIIT as the Fartlek training. A bit later, Dr. Woldemar Gershler trained Rudolf Harbig, who set the world record for the 800-m race in 1939 in Milan, using HIITs. HIIT, also known as “interval training,” was made more popular in that era by the late Czech runner Emil Zátopek, who won gold medals in the 5000 and 10,000-m races, as well as the marathon at the Summer Olympics in Helsinki in 1952. More recently, Lord Sebastian Coe, who medaled in the 1980 and 1984 Olympics, was trained by his father using HIIT (Coe, 2013). I believe that the revival of interest in HIIT was triggered by our publications (Kenney et al., 2019). If you Google the Tabata protocol, Tabata method, or Tabata training, you will get more than 600,000 hits. These were all named after me by an unknown person who read our scientific papers published in 1996 and 1997 (Tabata et al., 1996, 1997). The number of entries reflects the increasing public interest in Tabata training, a form of HIIT. In terms of protocol, the original or authentic Tabata training is defined as an exhausting, short, intermittent bicycle exercise training consisting of 6 to 7 sets of 20-s cycling at an intensity of 170% V̇o2max with a 10-s rest between bouts. In terms of metabolic profile, Tabata training was found to stress both the aerobic and anaerobic energy-releasing systems maximally, resulting in maximal effects on the two systems as shown by a robust increase in both V̇o2max and maximal accumulated oxygen deficit (MAOD). In addition to the evidence of the success of Japanese speed skaters who routinely used the Tabata training, the scientifically proven unique features of the training allow athletes who adopt it to feel the improvement themselves, resulting in further use of Tabata training in their routines. I consider that this trend might extend to exercise enthusiasts and, finally, to all health-oriented people. It was not my idea to name this training the Tabata training. Some unknown people who read our papers and introduced the training decided to call it the Tabata protocol or Tabata training. Since this training was originally designed by Mr. Koichi Irisawa, it might have been more appropriate to call it the Irisawa protocol. Experimental data for the two papers were collected in 1988–89 at the National Institute of Fitness and Sports in Kanoya (NIFSK, Kanoya, Kagoshima, Japan). The reason that I started to study Tabata training is explained here in Chapter 3. After a sabbatical a St. Louis in 1990–91, I moved to the National Institute of Health and Nutrition (Tokyo, Japan). Their mission is to provide nonmedical tools, such as exercise, physical activity, and nutrition (Ishikawa-Takata and Tabata, 2007; Tabata, 2006a,b), to prevent noncommunicable diseases. I

therefore did not have a chance to study exercise as a tool to improve sports performance. Thus, the Tabata training/protocol was disseminated by scientists who read my papers and wrote articles on Tabata, or perhaps by journalists and others who read the articles and passed the general idea on to friends without a true grasp of the original concept of Tabata training. Recently, some concerns about Tabata training have been raised in Medicine and Science in Sports and Exercise (Gentil et al., 2016), a leading peer-reviewed journal of our community. In response, using unpublished data I collected at Ritsumeikan University (2000–2021), I decided to write this book in order to return to the original concept. Hopefully, readers will find this book useful should they decide to attempt their own Tabata training in future. In 2019, I wrote a review paper (Tabata, 2019) that attracted the attention of many readers in this field. I guess one reason for this global attention might be that the review, “Tabata training: One of the most energetically effective high-intensity intermittent training methods,” was written by the scientist who first studied the specific training named after him after a long period of silence. Before publishing this book, I published three books for exercisers in Japanese in 2015, 2019, and 2020. The first book was translated into Taiwanese, Korean, and Chinese. The second was being translated into Russian. More than 40,000 copies of the first Japanese version of the Tabata training were sold. One day in August 2015, the book was ranked seventh in Amazon Japan among all categories! This represents the first book for scientists. The contents provide more evidence than the previously mentioned review. I hope this book, written in English for researchers and instructors, will be welcomed in the English reading world, including not only academic but also athletic and sports enthusiast communities. This book contains chapters on the scientific basis for the superiority of the Tabata training (Chapter 2), history of Tabata training (Chapter 3), later scientific evidence (Chapter 4), and an epilogue (Chapter 5). Chapter 2 describes the theory of basic human metabolism consisting of aerobic and anaerobic energyreleasing systems with a detailed introduction of the concepts of V̇o2max and MAOD, and the historical development of the two measures. I highlight the science behind MAOD, which Fox, who studied HIIT extensively in terms of V̇o2max in the 1970s (Fox, 1984), did not consider. Chapter 3 describes the historical events leading up to the publication of the two original Tabata papers (Tabata et al., 1996, 1997). It may interest readers to learn how the Tabata training, originally designed by a coach, was broadcast to the public after communication with and help from many other researchers around the world. Chapter 4 is a summary of studies related to Tabata training, collected at the National Institute of Fitness and Sports (Kanoya), National Institute of Health and Nutrition (NIHN), and Ritsumeikan University Japan. The findings collected from animal experiments at NIHN highlighted HIIT as a tool to study exercise-induced cellular signals that enhance transcription-regulated expression of proteins that have physiological function. These include glucose transporter 4 (GLUT4), which is a rate-limiting step of glucose metabolism in skeletal muscle, and peroxisome proliferator-activated receptor γ coactivator-1 (PGC1α), which stimulates many of the exercise-induced proteins. In 2000 (Goto et al., 2000), we first reported an increase in the mRNA of PGC1α, which is regarded as a master key of exercise-induced adaptations in skeletal muscle for several cellular functions. In a latter

section of this chapter, I introduce unpublished material collected at Ritsumeikan University. Since they involve descriptive and practical studies, they have not been published in journals. However, they contain specific evidence strictly related to the authentic Tabata training and Tabata-style trainings derived from the original. Over the past 20 years, many types of training have been developed from the authentic Tabata training, and as I considered various effects claimed for them might or might not be true, I felt that I should study and collect evidence on trainings that bore my name. Chapter 5 was written to suggest future research approaches to further improve the Tabata training and invent better training based on scientific evidence. I believe that once readers learn about and understand the theory of Tabata training practices, they will feel confident in designing their own original Tabata or Tabata-style trainings and using them in their exercise routines.

References

Coe, 2013 Coe S. DEB COE, Running my Style, the Autobiography. London, UK: Hoddder & Stoughton Ltd; 2013. Fox, 1984 Fox E.L. Sports Physiology. second ed. New York, USA: Saunders College Publishing; 1984. Gentil et al., 2016 Gentil P., Naves J.P.A., Viana R.B., Coswig V., Dos Santos Vaz M., Bartel C., Del Vecchio F.B. Revisiting Tabata’s protocol. Med. Sci. Sports Exerc. 2016;48(10):2070–2071. Goto et al., 2000 Goto M., Terada S., Kato M., Katoh M., Yokozeki T., Tabata I., Shimokawa T. cDNA cloning and mRNA analysis of PGC-1 in epitrochlearis muscle in swimming-exercised rats. Biochem. Biophys. Res. Commun. 2000;274:350–354. Ishikawa-Takata and Tabata, 2007 Ishikawa-Takata K., Tabata I. Exercise and physical activity reference for health promotion 2006 (EPAR2006). J. Epidemiol. 2007;17(5):177. Kenney et al., 2019 Kenney W.L., Wilmore J.H., Costill D.L. Research Perspective 9.2 Tabata training: The Original HIIT. Physiology of Sport and Exercise. seventh ed. Champaign, Illinoi, USA: Human Kinetics; 2019.241. Tabata, 2006a Tabata I. Exercise and Physical Activity Reference for Health Promotion (EPAR2006).https://nibiohn.go.jp/eiken/programs/pdf/epar2006.pdf0. 2006a. Tabata, 2006b Tabata I. Exercise and Physical Activity Guide for Health Promotion.https://nibiohn.go.jp/eiken/programs/pdf/exercise_guide.pdf. 2006b. Tabata, 2019 Tabata I. Tabata training: one of the most energetically effective high-intensity intermittent training methods. J. Physiol. Sci. 2019;69(4):559–572. Tabata et al., 1996 Tabata I., Nishimura K., Kouzaki M., Hirai Y., Ogita F., Miyachi M., Yamamoto K. Effects of moderate-intensity endurance and high-intensity intermittent training on anaerobic capacity and V̇o2max. Med. Sci. Sports Exerc. 1996;28(10):1327–1330. Tabata et al., 1997 Tabata I., Irisawa K., Kouzaki M., Nishimura K., Ogita F., Miyachi M. Metabolic profile of high intensity intermittent exercises. Med. Sci. Sports Exerc. 1997;29(3):390–395.

Chapter 2: Scientific bases for the superiority of the Tabata training

Abstract

This chapter describes the biochemical and physiological bases of aerobic and anaerobic energyreleasing systems that provide energy for ATP resynthesis consumed during various types of exercises/physical activities. Specifically, it reviews basic knowledge regarding maximal oxygen uptake (V̇o2max) and maximal accumulated oxygen deficit (MAOD), which represent the typical and most important fitness measures of aerobic and anaerobic energy-releasing systems, respectively. These bases provide scientific evidence demonstrating that, in terms of metabolic profiles, Tabata training is superior to other training methods. Further, nomenclature regarding high-intensity intermittent/interval training (HIIT) is provided so that readers can clearly understand Tabata training.

Keywords

Adenosine triphosphate (ATP); Creatine phosphate; Lactate; Aerobic energy-releasing system; V̇o2max; Anaerobic energy-releasing system; Maximal accumulated oxygen deficit (MAOD); Excess postexercise oxygen consumption (EPOC); Interval training; Intermittent training

High-intensity exercise protocols for improving sport performance are not new. So-called “interval training” was first popularized by the Czech runner Emil Zátopek, who won gold medals in the 5000 and 10,000 m, as well as the marathon, at the Helsinki Olympic games in 1952 (Thoma, 1982). The training appears to have evolved out of Fartlek training, which was invented by Swedish coach Gösta Holmér in the 1930s (https://en.wikipedia.org/wiki/Fartlek). Interval training consists of several short bouts of high-intensity exercise with low-intensity exercise in between. Since Zátopek won all the medals for long-distance events, it proved such training is absolutely effective for the aerobic energyreleasing system, which is fundamental for endurance. Furthermore, also in the 1930s, Dr. Woldemar Gerschler coached Mr. Rudolf Harbig, who set new world records for 400 m and 800 m in 1939. Mr. Harbig trained using high-intensity interval training prescribed by Dr. Gerschler (Kenny et al., 2012). He finished with a new world record of 1:46.6. In August 1955 (16 years later), his time was finally broken by the Belgian runner Roger Moens (1:45.7). As first, Mr. Zátopek called his training, which consisted of alternating high-intensity running and slow jogging, interval training. Since we used bicycle ergometers and allowed subjects to just rest between bouts of high-intensity exercise, we called our protocol intermittent training. However, I asked several scientists whether they call the Tabata protocol interval training or intermittent training. Most of them said that “verbally, we would call yours an intermittent exercise (training). However, you can call the

Tabata protocol either interval or intermittent. Especially, when talking to laymen or normal people rather than to scientists, it may be better to use interval training, as that is the more common term.” Research on interval training was initiated by extensive research conducted by Fox and his colleagues in the 1970s (Fox and Mathews, 1974; Fox et al., 1975). Fox reported the scientific bases of the effects of interval training at various intensities, with different numbers of sets and durations of training at maximal aerobic power. He proved that exercise intensity is a key factor for improving maximal oxygen uptake by interval training (Fox, 1979). Recently, Dr. Gibala highlighted high-intensity exercise as a useful tool for improving metabolic function in skeletal muscle (Gibala and McGee, 2008). Consequently, high-intensity exercise has received broad attention in terms of discovering the most effective training methods. Because readers need to learn about metabolism to understand the advantage of Tabata training, I now present basic information regarding muscle metabolism during exercise. Physical activity requires body movement, which is facilitated by the bones, on which contraction of skeletal muscle exerts force. Contraction of skeletal muscle, meanwhile, demands ATP (adenosine triphosphate), which acts like currency between skeletal muscle contractive machinery and energyproducing factories. When ATP is converted to ADP (adenosine diphosphate) and Pi (inorganic phosphate), energy for muscle contraction is delivered simultaneously. As the ATP stored in skeletal muscle is limited, muscle cannot continue to contract if ATP is not being resynthesized from ADP and Pi and using energy through the inverse direction of the formula. For this process, energy-releasing systems deliver energy. Human skeletal muscle has two energy-releasing systems. One is an aerobic system that produces energy by oxidating carbohydrate and lipids using oxygen delivered by the cardiorespiratory system. For specific intensities of exercise, both aerobic and anaerobic energyreleasing systems supply energy for ATP resynthesis. The contribution ratio of aerobic to anaerobic energy released during a specific exercise depends on the relative intensity of that exercise. Generally, during low-intensity exercise/physical activity, the aerobic energy system supplies more energy than the anaerobic, while during high-intensity exercise, the anaerobic system dominates.

Quantification of aerobic energy-releasing system

The amount of aerobic energy released is quantified by measuring oxygen uptake during a specific exercise (see Fig. 2.1). Approximately 5.0 kcal of energy is released when 1 L of oxygen is consumed. Therefore, if a subject’s oxygen uptake is 2 L of oxygen per min during 3 min of exercise, energy consumption for the exercise is calculated as 30 kcal (2 L/min × 3 min × 5 kcal/L).

Fig. 2.1 Measurement of oxygen uptake using Douglas Bag method.

During low-intensity exercise, oxygen uptake (L/min) increases gradually from the resting level and reaches a steady state (meaning it does not change) in 2–3 min. This value is regarded as the oxygen uptake for that specific exercise. It is thought that oxygen consumption for ATP resynthesis for an exercise is equal to the oxygen supply from the cardiorespiratory system. Fig. 2.2 shows that oxygen uptake is less than the steady-state level during the first min of exercise, suggesting that oxygen uptake does not cover energy demand for resynthesizing ATPs during this exercise period, since ATP consumption should not differ between the first min of exercise and the tenth. How then it is possible that the subject can continue to exercise? It is because system(s) other than the aerobic energy-releasing system resynthesize(s) ATP to compensate for that consumed during the exercise. Because humans have only two ATP-resynthesizing systems, when ATP cannot be resynthesized by the aerobic energyreleasing system (shown as a shadowed area in Fig. 2.2), it must be delivered by the anaerobic system. The shadowed area is called “oxygen deficit”; theoretically, it is the O2 equivalent to ATP resynthesized by the anaerobic energy-releasing system. It is interesting that the unit of oxygen deficit, which represents anaerobic energy release (“anaerobic means not oxygen (aerobic)”), is a liter of oxygen, which is also the measure for quantifying aerobic energy release. This is because oxygen deficit is calculated as the difference between accumulated oxygen demand (liter [L] of O2) and accumulated oxygen uptake (L of O2). In Fig. 2.2, oxygen deficit is calculated to be 1.0 L of oxygen, since oxygen demand is 30 L (3 L/min [steady-state oxygen uptake of the exercise]) × 10 min, and measured oxygen uptake during the 10-min exercise is 29.0 L). During low intensity exercise/physical activity, oxygen deficit never appears after steady state of oxygen uptake is established. The contribution of the aerobic energy-releasing system is calculated to be 97% (29 L/30 L × 100%). If you were to continue this exercise longer than 30 min, the contribution of the aerobic energy-releasing system would increase up to 100%. Therefore, such exercises are called “aerobic exercise.”

Fig. 2.2 Oxygen uptake during submaximal steady-state exercise.

Maximal oxygen uptake (V̇o2max: parameter for aerobic energy release)

As shown in Fig. 2.3, oxygen uptake increases linearly by exercise intensity. The intensity of running and bicycling is described by running speed (m/min) and watt (J/s), respectively. The linearity of the relationship (r > 0.99) is surprisingly high, suggesting that oxygen delivery to muscles is tightly regulated by sophisticated mechanisms! In biological events, such a close relationship is not often found for such complicated organ involvement. This relation indicates that the oxygen delivery system accurately delivers the amount of oxygen that exercising muscles need to resynthesize the ATP used for a given intensity of exercise.

Fig. 2.3 Relationship between exercise intensity of cycle ergometer and oxygen uptake ( ).

This linearity makes it possible to estimate “oxygen demand” at a given intensity exercise during which oxygen uptake is not “measured.” Oxygen demand is a value (L/min or mL/kg/min) for whatever oxygen is needed for a specific exercise at a specific intensity. For example, in Fig. 2.3, oxygen uptake of the exercise at 170 W is not measured. However, oxygen demand during exercise at this intensity can be estimated by interpolating the values using the measured plots or linear regression line formula (i.e., 0.30 + 0.013 × 170 = 2.51 L/min). As shown in the Fig. 2.4, however, at higher intensities, oxygen uptake (red dots) does not plot on the regression line established using low- to middle-intensity exercise. This phenomenon is called the “leveling off” between exercise intensity and oxygen uptake, suggesting that the oxygen delivery system cannot deliver enough oxygen to resynthesize ATP for that intensity of exercise. The highest value (red dots) measured during the exercise that normally lasts 2–3 min is called the “maximal oxygen uptake,” maximal aerobic power, (means per unit of time [min]; power also means per unit of time). Confirming the leveling-off phenomena is a condition that shows has been correctly measured (Taylor et al., 1955). The regression line established from measured oxygen uptake at an intensity that is lower than the intensity that corresponds to represents intensity called “submaximal,” while exercise intensity higher than that of measured is called “supramaximal.”

Fig. 2.4 Criterion of determination V̇o 2max (leveling off).

This relationship was established by measuring the oxygen uptake at 6 to 9 different intensities of 10min exercises. This time-consuming procedure, which need at least 3 days of testing, has been also used to measure the in Scandinavian countries. Without establishing a linear relationship (r > 0.99) between the oxygen uptake and the exercise intensity at a submaximal range, the leveling off of the oxygen uptake in response to increased exercise intensity, which is the only criterion for measuring the maximal oxygen uptake (Taylor et al., 1955; Medbø et al., 1988), cannot be confirmed. Without this leveling off, the measurement is regarded not as , but as peak or (Poole and Jones, 2017). It should be noted that, for estimating oxygen demand at even submaximal intensity, the relationship between exercise intensity (the work rate) and the oxygen uptake measured by an incremental test should not be used. The oxygen uptake at a specific exercise intensity measured by an incremental test procedure, which normally allots an identical time (1–2 min) for each exercise intensity, does not necessarily represents the oxygen uptake (i.e., steady-state oxygen uptake) and oxygen demand, which is balanced with energy for resynthesizing the ATP consumed during exercise at the specific intensity. This is because the time necessary for the oxygen uptake to reach the steady state (which is defined as the oxygen uptake/demand balance of the specific exercise) differs based on the exercise intensity. The time necessary for the oxygen uptake to reach the steady state of oxygen consumption at a higher exercise intensity is longer than that at a lower exercise intensity (Åstrand and Rodahl, 1977). Since the work rate during swimming is theoretically related to (swimming speed (m/s))³, a linear relationship between exercise intensity and oxygen uptake is established by the relationship between the exercise intensity (swimming speed (m/s))³ and the oxygen uptake (Ogita et al., 1996). Since energy requirements for resynthesizing ATP for supramaximal intensity exercise is assumed to increase linearly with exercise intensity (the hypothesis is that economy of mechanical energy production to energy consumption is equal), the energy requirement expressed as a unit of oxygen uptake (oxygen demand) should increase as plotted on the regression line established by measured oxygen uptake at submaximal intensity exercises. Since humans have only one energy-releasing system other than the aerobic system, the anaerobic energy-releasing system provides energy as depicted by the blue arrow in Fig. 2.5.

Fig. 2.5 Aerobic and anaerobic energy release during different intensity exercise.

V̇o2max as athletics-related fitness

The of the endurance athlete is higher than that of sedentary people. Furthermore, improvement of by training enhances athletic performance in sporting events. As shown in Fig. 2.6, running performance in a 5000-m event is highly related to , suggesting that determines about 51% of 5000-m running performance (Fig. 2.6). Therefore, has been regarded as an indicator of athletic-related fitness.

Fig. 2.6 Relationship between and 5000-m running performance ( Yamaji et al., 1990).

Individual can vary from 40 (sedentary) to 85 mL/kg/min among young men. (Since not the absolute value [L/min], but the relative value to body weight is more related to endurance, especially for running, mL/kg/min is often used.) Marathon runners have a high of around 85 mL/kg/min. Such a high allows them to run full marathons very fast (average running speed is 14.5 s/100 m—can you believe this? Could you run 400 m in 68 s?).

decreases as people age (Cao et al., 2010a,b). Since absolute intensity (oxygen uptake (oxygen demand) [mL/kg/min]) does not differ between elderly and young persons, one of the reasons why it takes greater effort (perceived exertion) for the older person to do the same work as a younger counterpart is the relatively higher intensity (% ) of the specific activity due to age-related decline of . Therefore, maintaining V̇o2max into middle and old age, and/or raising in youth and middle age by training (Tabata training) is recommended for those wishing to maintain an active life style into their middle and later years.

V̇o2max as health-related fitness

Numerous epidemiological studies have demonstrated people with higher are at less risk of suffering from noncommunicative diseases (NCDs) such as diabetes mellitus, ischemic heart diseases, and stroke. Sawada et al. (2003) showed that people whose is within the 50–75 percentile have 37% less risk compared to those with the lowest (0–25 percentile) (Sawada et al., 2003). Epidemiological studies do not clarify mechanism(s) for the induction of NCDs. However, Sato et al. (1986) showed that glucose disposal rate was linearly related to the of subjects, suggesting that people whose is higher have less risk of diabetes mellitus. This may be one explanation for the preventive effects of higher on diabetes mellitus.

The limiting factors for V̇o2max

V̇o2max is the maximal oxygen uptake of an individual during a unit of time. There are three possible rate-limiting factors for . The first is lung function, which is measured as maximal respiratory volume (L of ventilated air/min). The second is the ability of the heart to deliver blood with oxygen to the working muscles, which is measured as maximal cardiac output (L of blood/min). Finally, the third is the capability of the exercising muscles to utilize the oxygen (L of oxygen/min). Therefore, as shown

Fig. 2.7, that factor which is the least able limits the flow of oxygen uptake as a whole (i.e., maximal oxygen uptake). You might image that, as in this figure, the total number of cars able to pass through a specific road system is limited by the part of the road with the fewest driving lanes (Fig. 2.7).

Fig. 2.7 Plausible model of limiting step of .

Physiology tells us that the lungs, whose surface amounts to the area of half a tennis court, afford sufficient time and area to exchange the oxygen inspired air to the blood (approximately 200 mL/beat). Therefore, one cannot increase the by deliberately increasing ventilation. To experimentally determine the rate-limiting step of , we performed a one-leg bicycle test. We compared maximal oxygen uptake using two legs ( ) to the peak oxygen uptake observed during one-leg bicycling (Fig. 2.8).

Fig. 2.8 One-leg and conventional two-leg bicycle exercise [(right) I. Tabata; 33 years old; and (left) F. Ogita pedal using their right and left legs, respectively].

The peak oxygen uptake during one-leg bicycling was approximately 80% of using two legs (Fig. 2.9).

Fig. 2.9 for conventional two-leg bicycle exercise and peak oxygen uptake measured during one leg bicycle exercise (Ogita and Tabata, unpublished).

This result reveals the rate-limiting step of maximal oxygen uptake. During one-leg bicycling, the heart can deliver virtually most of the blood (maximal cardiac output) to the one exercising leg, which can consume the oxygen delivered; meanwhile, two-legged cycling means that only half of maximal cardiac output is available to each leg. This amount is far less than the amount that a leg muscle can take up if enough oxygen is available (as in one-leg cycling) (Fig. 2.10).

Fig. 2.10 Postulated blood flow to exercising legs during one- and two-leg bicycle ergometer exercise.

Therefore, in general, is rate-limited by the heart pumping function of blood (i.e., cardiac output). Referring to the question addressed in relation to the discussion above the Fig. 2.7, the right answer is number 3. Maximal oxygen uptake is reported to be linearly related to the maximal cardiac output (Åstrand et al., 1964). Since maximal cardiac output as a measure of the pumping function of the heart is a product of heart rate (beats per minute) and stroke volume (the quantity of blood pumped from the heart during one heartbeat), both parameters may contribute to maximal cardiac output. However, it is known that the maximal heart rate of the endurance-trained athlete, whose cardiac output is high, is less than that of a sedentary person. Therefore, it is assumed that people with high maximal cardiac output and have high stroke volume. This large stroke volume is a result of a larger left ventricle volume known as sport heart.

Effects of training on V̇o2max

For submaximal intensity exercise (exercise intensity < ), intensity is measured and quantified as % . Therefore, exercise intensity for increasing was described as 50%–85% (American College of Sports Medicine, 1978) and 50%–85% of maximum oxygen uptake reserve (V̇o2R) (American College of Sports Medicine, 1998); moderate [e.g., 40%–59% heart rate reserve (HRR) or R] to vigorous (e.g., 60%–89% HRR or V̇o2R) (Garber et al., 2011) exercise was recommended by the American College of Sports Medicine, depending on fitness levels (sedentary to moderately trained). The last version of their guide stated that highly trained athletes may need to exercise at “near maximal” (i.e., 95%–100% ) to improve , whereas 70%–80% may provide a sufficient stimulus to moderately trained athletes. As described above, for submaximal intensity exercise, quantitative measures (% , % R) are available in terms of increasing . However, in terms of elevating for athletic performance, intensity of HIIT as oxygen demand, especially supramaximal intensity HIIT, was not described except in our study (Medbø et al., 1988) and others (Foster et al., 2015; Ogita et al., 2014; Ramsbottom et al., 2001; Ravier et al., 2009) that utilized the time-consuming method of estimating oxygen demands for bicycling and running exercise. As already mentioned, this might have simply been because the oxygen demands of the supramaximal level are difficult to quantitate. Recommendations for exercise prescriptions of HIIT at supramaximal intensity were lacking in quantitative expression and rather descriptive; for example, “maximal effort,” “sprinting,” “exhaustive.” Although (Fox, 1979) reported in the 1970s that twice a week interval training increased , further research is needed to clarify how much improvement can be expected by specific HIIT, and such studies should be systemically integrated for scientists and instructors to

approximately/appropriately predict their effects on . For this purpose, we are collecting data (see Chapters 4 and 5).

Quantification of anaerobic energy-releasing system

Performance in most exercise sports depends on the amount of energy release per unit of time. Since the energy release (ATP consumption) is equal to the energy supply from the aerobic and anaerobic energysupply systems, it well known that increasing the ability of the two energy-supply systems by physical training is the best way to enhance sport performance. As for most physical properties, the more demanding the training the greater the improvement of the property, it is necessary to measure energy supply from the two systems during exercise in order to evaluate that exercise’s efficacy as a form of training. The aerobic energy released is determined by measuring oxygen uptake during exercise. By comparing the oxygen uptake value with the subject’s maximal oxygen uptake (%V̇o2max), the stress on the aerobic energy release can be evaluated during exercise and training. The anaerobic energy-releasing system releases ATP directly by two biochemical reactions. Through reaction 1, ATP is produced from creatine phosphate (CrP). In reaction 2, ATP is produced by a sequence of reactions, called glycolysis (glycogenolysis), which produces lactate from glycogen in working muscle and glucose transported from circulating blood. Neither of the anaerobic energyreleasing systems require oxygen, hence the name anaerobic (“an” means “not”). Since reaction 2 produces lactate, this system is called “lactic energy-releasing system,” while reaction 2 is named as alactic energy-releasing system, because reaction 2 does not produce lactate.

1.CrP + ADP → ATP + Pi. 2.Glycogen → Lactate + ATPs.

Biochemical parameters of anaerobic energy are changes in the amount of decreased creatine phosphate and increased lactate in working muscle. During the first minutes of low intensity exercise, most ATP is resynthesized by the reaction 1 described above, resulting in decreased CrP in muscle without accumulation of lactate neither in muscle nor circulating blood. When exercise intensity increases, reaction 2 emerges. To detect changes in the biochemical substrate, the biopsy technique (see Fig. 2.11) was developed in the 1960s in Scandinavia. An analysis of only 3–4 mg of tissue from a human muscle allows measurement of the changes in concentration of most muscle metabolites, including ATP, CrP, and lactate.

Fig. 2.11 Biopsy needle for muscle tissue sampling.

I have 20 holes in my thigh muscle; 16 were made in Norway, and 4 were made in the USA. For the biopsy technique, only the first needle inserted to introduce anesthesia may cause a little pain. The rest of the procedure is painless. As described above, aerobic energy release can be quantified by measuring oxygen uptake. Using the biopsy method with biochemical analyses, it is also possible to evaluate qualitative changes in the anaerobic energy-releasing system for any kind of exercise. However, since the biopsy method can only measure changes in concentration, it is not possible to quantitate the energy supply from the anaerobic energy-releasing system. For this purpose, one must know the mass of muscle that has been recruited during a specific exercise. It was, however, not feasible to estimate muscle volume recruited by a specific exercise.

What is oxygen deficit?

Krogh and Lindhard in 1920 (Krogh and Lindhard, 1920) introduced a method to evaluate the anaerobic energy supply as oxygen deficit during exercise. Oxygen deficit is anaerobic energy release expressed as amount of oxygen (thus conventionally expressed in L). It may be confusing that the amount of energy released by the anaerobic system is expressed in the same units as, aerobic energy release (i.e., liters of O2). It is because anaerobic energy release is calculated as the difference between accumulated oxygen demand and accumulated oxygen uptake during exercise (dashed area of Fig. 2.12).

Fig. 2.12 Oxygen uptake and oxygen deficit during 4-min submaximal intensity exercise.

As shown in Fig. 2.13, at submaximal (low) intensity exercise, measured oxygen uptake gradually increases and reaches a steady-state level within 1 to 2 min. This value is called the “oxygen uptake (L/min)” of the specific exercise. This rate of oxygen uptake is thought to be balanced with energy consumption for ATP resynthesis per unit of time for the exercise, thus equaling the oxygen demand. One thing that confuses people is that oxygen uptake is not the absolute amount of oxygen but rather the rate of oxygen uptake. Now I regret to say that our pioneers should have called it “oxygen uptake rate” or “rate of oxygen uptake.”

Fig. 2.13 Calculation of oxygen deficit measured during 4-min submaximal intensity exercise.

If one needs to estimate energy consumption during a 10-min exercise in which the steady-state oxygen consumption level (oxygen demand [L/min]) is 2.0 L/min, one can calculate that 2.0 L/min × 10 min × 5.0 kcal/L to get 100 kcal. For this purpose, we need to know the oxygen demand (L/min) of the specific exercise. Therefore, for calculating the energy consumption of physical activity that we do not normally do for more than 2 min—for example, cutting vegetables on a chopping board—we need to ask subjects to do the physical activity/exercise and measure oxygen uptake from 2 to 3 min after the start of the physical activity/exercise, because oxygen uptake (L/min) during the first minute does not correspond to the rate of energy release of the activity/exercise and cannot be used for calculating its energy consumption. Because, depending on time during the first minutes, oxygen uptake at specific time points does not necessary reach the real oxygen uptake of the physical activity/exercise even at submaximal intensity, we call oxygen uptake only measured at the steady state the “oxygen demand.” Since it is a rate, it is conventionally expressed in L/min. As shown in Fig. 2.12, oxygen demand for a specific exercise is equal to measured oxygen uptake (L/min) during the exercise measured at least 2 min after the start of the exercise. Since the subjects execute the same intensity exercise, energy consumption for resynthesizing ATP during the initial part of the exercise should be the same. But as stated above, oxygen uptake does not reach the oxygen demand immediately. This phenomenon should be explained by the dashed area of the figure, which represents energy supplied from nonaerobic energy-releasing systems, i.e., the anaerobic system. We call this part oxygen deficit (L O2), which can be calculated as the difference between accumulated oxygen demand and accumulated oxygen uptake from the start until the steady state of oxygen consumption is attained. During low-intensity exercise, oxygen deficit is not observed once the steady state is attained. The next figure (Fig. 2.13) shows oxygen uptake during a 4-min exercise where the oxygen demand (steady-state oxygen uptake) is 2.0 L/min. Calculated accumulated oxygen demand is 8.0 L. Measured accumulated oxygen uptake during the exercise is 7.0 L. Oxygen deficit, calculated as the difference between accumulated oxygen demand (8.0 L) and accumulated oxygen uptake (7.0 L), is 1.0 L. Therefore, the contribution of the aerobic energy-releasing system to the total energy supply for the exercise is 87.5% (7.0 L/8.0 L × 100). Since, as described, oxygen deficit is not observed after the steady-state uptake level is attained at this intensity of exercise, if the subject continued the exercise for 30 min, the contribution of the aerobic energy-releasing system would be 98.3% (59.0 L/(2.0 L/min × 30 min) × 100). Because this value (98.3%) is very close to 100%, we call this an “aerobic exercise.” During the first minutes of physical activity/exercise at low intensity, the alactic energy-releasing system functions to resynthesize ATP, compensating for the gap between ATP breakdown by muscle contraction and ATP resynthesis by the aerobic energy-releasing system. Therefore, no lactate is produced and no increase in blood lactate is observed. When oxygen uptake reaches steady a state 2– 3 min after the start of the exercise, this system stops resynthesizing ATP. As exercise intensity increases, the lactic acid energy-releasing system contributes ATP resynthesis and lactic acid

accumulates in the blood. When oxygen uptake reaches the steady state, the anaerobic energy-releasing system, including both the lactic and alactic systems, ceases to resynthesize ATP with some spilling of lactate, which is inevitably produced due to the equilibrium of lactate/pyruvate. Lactate concentration in the blood during low (50% ) to moderate (70% ) intensity exercise decreases as exercise time is prolonged (Tabata, 1994). As mentioned above, we can now evaluate anaerobic energy release without using the invasive biopsy technique, but by just measuring oxygen deficit. This is a technical advantage.

What is maximal accumulated oxygen deficit (MAOD)?

By comparing accumulated oxygen deficit during the exercise to maximal accumulated oxygen deficit (MAOD), stress on the anaerobic energy system can be evaluated. What is MAOD? MAOD represents an individual’s highest amount of anaerobic energy release, and is gauged as the highest accumulated oxygen deficit measured during high-intensity exhaustive exercise lasting 2– 10 min (L or mL/kg). As described above, the accumulated oxygen deficit represents the accumulated oxygen demand minus the accumulated oxygen uptake (Fig. 2.14).

Fig. 2.14 Calculation for determining oxygen deficit for 2.5-min exhausting exercise.

For estimating the oxygen demand of exhausting bouts of longer duration exercise, an assumption must be addressed. This is because the intensity of the exercise is supramaximal (Fig. 2.15); thus, oxygen demand at the intensity is not the same as steady-state oxygen uptake during the exercise, as was the case for submaximal intensities. However, we hypothesize that, even when exercise intensity is supramaximal, the relationship between intensity and oxygen demand does not change, allowing us to use the same formula to predict oxygen demand, not by interpolating but by extrapolating the linear relationship between the power and the oxygen demand established in the pretests to calculate oxygen demand for supramaximal intensities. Let us present an example of the calculation of accumulated oxygen deficit. First, a subject biked to exhaustion in 2.5 min. As the exercise intensity was 250 W, the extrapolated oxygen demand was 3.55 L/min. Therefore, accumulated oxygen demand was 3.55 L/min × 2.5 min (8.88 L). Since the measured total oxygen uptake using the Douglas bag method was 5.77 L, accumulated oxygen deficit was calculated to be 8.88–5.77 = 3.11 L.

Fig. 2.15 Estimation of oxygen demand for supramaximal intensity exercise.

To estimate oxygen demand at supramaximal intensity by extrapolation from the established relationship between exercise intensity and oxygen demand (uptake) at submaximal intensity, the original investigation of maximal accumulated oxygen deficit (MAOD) measured oxygen uptake during 6 to 9 bouts of 10-min constant-intensity exercise with intensity ranging from approximately 30% to 85% of the (Medbø et al., 1988). As described for oxygen uptake, it should be noted that, for estimating oxygen demand at supramaximal intensity, the relationship between exercise intensity (the work rate) and the submaximal level oxygen uptake measured by an incremental test (e.g., a graded exertion test [GXT]) (Viana et al., 2018) should not be used. This is because oxygen uptake measured by GXT does not necessarily represent the real oxygen uptake at the intensity (measured as steady-state oxygen uptake). Therefore, the supramaximal intensity oxygen demand estimated using oxygen uptake measured by GXT would differ significantly from that using the constant intensity multiple 10-min exercises.

Oxygen deficit for 30-s to 10-min exhausting exercise

As shown in Fig. 2.16, oxygen deficit increases from 30 s and plateaus at 2–10 min of exhaustive exercise, suggesting that anaerobic energy, measured as accumulated oxygen deficit, has maximal values for individuals (Medbø et al., 1988). Dr. Hermansen named this value MAOD, which is a quantitative measure of the maximal value of anaerobically released energy.

Fig. 2.16 Accumulated oxygen deficit for exhaustive exercise lasting 30 s to 9 min ( Medbø et al., 1988 ).

As shown in Fig. 2.16, MAOD differs significantly among subjects. The MAOD of MKS is approximately 60% higher than that of KTS. The MAOD of middle-distance runners and speed skaters are higher, while in contrast, the MAOD of endurance runners is not much different from that of nonathletes. Fig. 2.17 shows a different way of explaining exercise intensity and accumulated oxygen deficit during bicycle exercises. Oxygen deficit is lowest for 30-s exhaustive exercise, where exercise intensity is 186% . Oxygen deficit for 2-min and 4-min exhaustive exercise, where exercise intensity is 119% and 110% , respectively, does not differ. As already described, oxygen deficit measured for 2- and 4-min exhaustive exercise is regarded as maximal oxygen deficit.

Fig. 2.17 Oxygen deficit estimated for 30-s to 4-min exhaustive exercise ( Medbø and Tabata, 1993).

In terms of competitive sports, this figure may give us important information regarding how to win races of variable exercise time. Since MAOD limits performance of sports with exercise duration longer than 2 min, athletes who have higher MAOD may win such sports. On the other hand, as oxygen deficit of exhaustive exercise lasting less than 2 min does not reach MAOD, MAOD does not limit the performance of athletes with the ability to accumulate oxygen deficit as fast as possible (rate of oxygen deficit accumulation corresponding to rate of ATP resynthesis by anaerobic energy-releasing system). For skating, this might be made possible by a skating technique that recruits as many muscles as extensively as possible during the race. Two female Japanese speed skaters competed in the last Olympic games in Pyeongchang, Korea (2018). Nao Kodaira won the gold medal in the 500-m race (record: 36.94 s), which might correspond to the 30s exhaustive exercise depicted on the left column of Fig. 2.18. The accumulated oxygen deficit of this exercise does not reach MAOD. Miho Takagi got the silver medal and placed fifth in the 1500-m race (1:54.55) and 3000-m race (4:01.35), respectively, which could correspond to the 2 min and 4 min exhaustive exercise depicted the center-right and right columns of Fig. 2.18, respectively. Accumulated oxygen deficit in this exercise reached MAOD. These results indicate that Kodaira excelled at competition that does not reach MAOD, while Takagi was superior at races during which MAOD is reached. In another way, Kodaira shines at consuming oxygen deficit as fast as possible with her technique of skating on both straight and curved courses. Takagi might stand out in races lasting longer than 2 min because she has higher MAOD.

Fig. 2.18 MAOD and performance of speed skate.

Our interest was in “which of these two super skaters would perform better in a 1000-m race?” Since 1min exhaustive exercise is relatively similar to 30-s exhaustive exercise that does not reach MAOD, we expected, from Fig. 2.18, that Kodaira would finish the 1000-m race faster than Takagi. As we predicted, Kodaira received the silver medal and Takagi the bronze medal (1:13:98), even though the difference was small (0.16 s). In addition, Kodaira was sixth in the 1500-m race at 1:56.11, which was not much slower than Takagi’s time (1:54.55), suggesting that these two athletes have extraordinary fitness and technique in terms of anaerobic metabolism and skating, respectively.

Biochemical basis of MAOD

Fig. 2.19 shows the changes in the CrP of the exercising muscle (alactic energy-releasing system) during 30-s to 4-min exhaustive exercise. Rate decrease in CrP observed during 30-s exhaustive exercise is higher than that of 2 and 4 min. However, after 30 s of exhaustive exercise, CrP remained at a relatively higher level, while after both 2- and 4-min exhaustive exercise, CrP decreased, demonstrating that energy delivered from the alactic energy-releasing system for resynthesizing ATP for such exercise seemed to be exhausted.

Fig. 2.19 Changes in muscle CrP content during 30-s to 4-min exhaustive exercise.

Fig. 2.20 shows the changes in muscle lactate concentration (lactate production) in exhausting exercise of different durations. Lactate concentration rises to the highest level after both 2- and 4-min exhaustive exercise, while lactate concentration does not reach this level after 0.5 to 1 min exhausting exercise, suggesting that lactate is not related to fatigue in such durations of exhaustive exercise.

Fig. 2.20 Changes in muscle lactate concentration content during 30-s to 4-min exhaustive exercise.

Fig. 2.21 shows changes in pH during 30-s to 4-min exhaustive exercise. Muscle pH might induce fatigue if it decreased to a critical level (6.6). After both 2- and 4-min exhaustive exercise, pH was reduced to the critical level, while shorter durations of exhaustive exercise did not reach that level. These changes in biochemical parameters suggest that fatigue during 2- and 4-min (maybe up to 10min) exhaustive exercise is caused by critical pH level that disables muscle from contracting, and CrP depletion.

Fig. 2.21 Changes in muscle pH during 30-s to 4-min exhaustive exercise.

After calculating ATP production using CrP and lactate values observed before and after the exercises, ATP production from the anaerobic energy-releasing system during 30-s to 4-min exhaustive exercise is shown in Fig. 2.22. This figure is just same as Figs. 2.16 and 2.17 showing oxygen deficit estimated during the same duration exhaustive exercise, suggesting that the oxygen deficit and MAOD correctly reflect anaerobic energy release evaluated by changes in biochemical parameters by the biopsy technique! These experimental qualifications of oxygen deficit and MAOD allowed us to further evaluate metabolic profiles of high-intensity, intermittent exercises and develop the Tabata protocol.

Fig. 2.22 Estimated ATP resynthesized by anaerobic energy-releasing system.

As shown in Fig. 2.23, anaerobic energy release calculated using maximal oxygen deficit is linearly related to ATP turnover rate estimated using data observed in biopsy samples before and after the exhaustive exercise (Medbø and Tabata, 1993).

Fig. 2.23 Relationship between ATP turnover rate in muscle and whole body oxygen deficit ( Medbø and Tabata, 1993).

Anaerobic exercise?

For exercise that humans can continue for more than an hour (e.g., walking or jogging), the aerobic energy-releasing system provides almost 100%. Therefore, those activities are called “aerobic exercise.” As shown in Fig. 2.24, the relative contribution of the aerobic energy-releasing system decreases as exercise intensity increases. Exhaustive exercise lasting only 2–3 min depends 60%–70% on the aerobic energy-releasing system (Medbø and Tabata, 1993). Short-lasting high-intensity exercise is often called “anaerobic exercise.” However, as shown in Fig. 2.24, the aerobic energy-releasing system supplies at least 10% for the exercise lasting 10 s (Kouzaki and Tabata, unpublished). One-hundred-meter running is not solely an “anaerobic” exercise. This is why researchers hesitate to use the term “anaerobic exercise” as frequently as laymen.

Fig. 2.24 Relative contribution of aerobic energy-releasing system on energy supply for 10-s to 3min exhausting bicycle exercises ( Medbø and Tabata, 1993; Tabata and Kouzaki, unpublished).

Training for elevating MOAD

MAOD is reported to be elevated by ~ 10% after 6-week HIIT consisting of eight 20-s exercise bouts at an intensity that causes exhaustion in 35 to 40 s when subjects work continuously at this speed (Medbø and Burgers, 1990). Eight-week HIIT consisting of three 2-min constant intensity bicycling bursts at 120% increased MAOD of both male and female untrained young subjects by ~ 12%. Ogita et al. (2014) reported that a higher-intensity (approximately 250% ) and shorter-duration (five 5-s exercise bouts with a 10-s rest between bouts) intermittent swimming training protocol performed for 4 weeks improved the swimmers’ MAOD and by 22% and 5%, respectively. Ramsbottom et al. (2001) observed increases of 18.6% and 20.9% in men and women, respectively, after 6-week combined training with 1min maximal shuttle run, interval track run (200, 400, and 600 m), and shuttle run sprints (5 and 10 m). Ravier et al. (2009) reported that a running training protocol modified from Tabata training elevated the (4.6%) and MAOD (10.3%) of karate athletes who also performed other types of repetitive exercise. However, due to lack of systematic studies and/or systematic reviews in terms of effects on MAOD, it has not been feasible thus far to recommend appropriate exercise intensity, duration (set), frequency, and time period (weeks) of training that definitively improve MAOD.

Nomenclature

Before starting to describe Tabata training, I would like to define nomenclature related to HIIT. Tabata training is defined as training at the intensity that exhausts subjects after completing the sixth or during the seventh/eighth sets of 20-s bicycle exercise bouts with a 10-s rest between the exercise bouts. This exercise/training was originally developed for bicycling exercise (Tabata et al., 1996, 1997). At more than 20 years after the publication of the original studies (Tabata et al., 1996, 1997), the exercise intensity has not been emphasized; only the procedure of the training has been featured, especially among general exercisers. For example, following such a protocol (8 sets of a 20-s exercise with a 10-s rest between the exercise bouts) using walking as the exercise can be expected to result in no improvement of the . Only training adopting the protocol with an exercise intensity that exhausts the subject after the sixth or during the seventh/eighth sets of the 20-s exercise bout with a 10-s rest between the exercise bouts (i.e., Tabata training) elevates both the and the MAOD to the extent that was reported by the original investigation. Such increases in the two energy-releasing systems (i.e., the aerobic and anaerobic energy-releasing systems) cannot be obtained by walking, the exercise intensity of which is estimated as < 30% in Tabata protocol. Therefore, the term “Tabata training” emphasizing not only the procedure but also the exercise intensity that exhausts the subject after 6th or during 7th/ 8th sets of the exercise should be used for the name of the training, and this term will be used hereafter in this book (Tabata et al., 1996, 1997).

Interval or intermittent?

In a popular method of interval training, an individual exercise at low intensity between bouts of highintensity exercise (Fox and Mathews, 1974). In contrast, intermittent training (including Tabata training (Tabata et al., 1996, 1997), exercisers completely stop the exercise and rest for a while. Training that involves such a “complete stop” period is thus called “intermittent” training (Tabata et al., 1996, 1997). Intermittent training and interval training thus differ significantly, and it is important to keep in mind that Tabata training is an intermittent-exercise training method.

HIIT, SIT, or?

Tabata training has been considered one of the high-intensity “interval or intermittent” training (HIIT) methods, which have varied considerably in terms of the characteristics of the training exercise, i.e., the exercise mode, intensity, and durations of exercise and rest. Weston et al. (2014) defined HIIT as “near

maximal” (in other words, “submaximal”) effort generally performed at an intensity that elicits > 80% (often 85%–95%) of the maximal heart rate. Thompson (2017) suggested a broader definition of HIIT in which HIIT typically involves short bursts of high-intensity exercise followed by a short period of rest or recovery and typically takes < 30 min to perform. In contrast, sprint interval training (SIT) is characterized by efforts performed at intensities equal to or greater than the pace that would elicit a , including “all-out” or “supramaximal” efforts (Weston et al., 2014). The word “sprint” implies moving as fast as possible from the start of an exercise (https://www.merriam-webster.com/dictionary/interval), with an eventual decline in speed and/or a discontinuation of the exercise. In contrast, in the original and authentic Tabata training protocol, the exercise intensity is constant (i.e., 170% ) from the first to the last session of the exercise. Using the word “sprint” to describe Tabata training exercise is therefore not accurate. In exercise physiology, the intensity of a specific exercise has been defined relative to the as “submaximal,” “maximal,” and “supramaximal” when the oxygen demand is less than, equal to, and greater than the , respectively. Since the oxygen demand for Tabata training is higher than the (i.e., 170% ), the original Tabata training is “supramaximal intensity intermittent training.” In terms of the exercise:recovery ratio, Tabata training is different from other SITs, as Sloth et al. (2013) defined SIT as a protocol that includes duration of bouts: 10 to 60 s, intensity: maximal, “all-out,” volume: ≥ 12 repetitions, recovery:≥5 times the duration of work, and Gist et al. (2014) defined it as intensity: “allout,” “supramaximal,” “maximal,” or “≥ ,” SIT work:rest ratio of 30-s:4-min (rest interval of 3–5 min). Tabata training is thus not SIT in terms of the classical terminology of SIT. Tabata training is an original and unique training method that can be described by either the classic but familiar term “interval training” or the modern and “cool” term “HIIT,” which includes a variety of training methods using intermittent/interval high-intensity exercise.

Tabata or Tabata-style training

Since measuring oxygen deficit during body-bearing exercise has not been possible thus far, and, as discussed later, oxygen uptake during such exercises does not necessarily amount to measured for running, it is not feasible to ensure that a specific body-bearing exercise stresses both the aerobic and anaerobic energy-releasing systems maximally, which is the key character of the authentic Tabata training. Furthermore, “Tabata trainings” do not seem to induce fatigue in people (not elite sportsmen/women), which is a necessary condition (requirement) for eliciting and MAOD during specific exercise. Therefore, such exercises, including body-bearing exercise, should not be called “Tabata training.” I propose that they instead be called “Tabata-style trainings,” which, irrespective of exercise intensity, consist of 8 sets of 20-s exercise with 10-s rest between bouts. In this respect, the initially popularized title of “Tabata protocol” could be an alternative.

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Chapter 3: History of Tabata training

Abstract

I first present a history of the concept of oxygen deficit, which is a key measure of the anaerobic energy system. Oxygen deficit was introduced ~ 100 years ago by Krogh and Lindhard (1920). This is followed by an account of the personal commitment of legendary scientists to anaerobic energy-releasing systems in the period from the 1960s to 1980s. I describe how I (Tabata) personally came to study high-intensity intermittent exercise training (HIIT), including Tabata training, which Kouichi Irisawa developed and introduced to speed skaters in the 1980s. This chapter further features experimental evidence showing that Tabata training maximally stresses both the aerobic and anaerobic energy-releasing systems (Tabata et al., 1996) and therefore elevates both V̇o2max and maximal accumulated oxygen deficit (MAOD) (Tabata et al., 1997). As a result, Tabata training is superior to other conventional training methods in terms of improving both aerobic and anaerobic energy-releasing systems.

Keywords

Tabata training; High-intensity intermittent training (HIIT); Oxygen deficit; Maximal accumulated oxygen deficit (MAOD); V̇o2max; Excess postexercise oxygen consumption (EPOC)

History of oxygen deficit

Before embarking on the history of Tabata training, I would like to briefly outline the concept of oxygen deficit, which is a key measure for the anaerobic energy-releasing system. Oxygen deficit is defined as the difference between accumulated oxygen demand (liter O2) and measured accumulated oxygen uptake during exercise. Accumulated oxygen demand is calculated as oxygen demand (L/min) multiplied by exercise time (min). At submaximal intensity exercise, oxygen demand is equal to measured oxygen uptake at the steady state observed 2–3 min after the start of the exercise. The oxygen deficit principle was first introduced by August Krogh and Johannes Lindhard in 1920, but the idea of “oxygen deficit of the alveolar expired air” had already appeared in 1913 (Krogh and Lindhard, 1913). They suggested that oxygen deficit must represent the anoxybiotic (anaerobic) reactions that take place during the first phase of the contraction process. Lactate formation after relatively high-intensity exercise was already recognized in the 18th century (Asmussen, 1971). Fletcher and Hopkins (1907) demonstrated that when excised frog muscle was stimulated to contract, lactic acid was produced, and when the fatigued muscle was placed in oxygen, the lactate disappeared. Since ATP, creatine phosphate, and their role in muscle contraction were not discovered until 1927 (Eggleton and Eggleton, 1927; Fiske and Subbarow, 1927; Fiske and SubbaRow, 1929; Lohmann, 1929) and 1930 (Lungsgaad, 1930), respectively, Fletcher and Hopkins hypothesized that lactate produced from unknown precursor(s) directly stimulated the muscle to contract, and that oxygen was necessary to convert the lactate back to the precursor(s) for recovery. In 1920, Meyerhof identified glycogen as a precursor of lactate (Meyerhof, 1920). Extensive studies later revealed that oxygen deficit could be explained by: (1) changes in the oxygen stores in the body, comprised of oxygen bound to hemoglobin and myoglobin, dissolved in the body fluids, and present in the lungs; (2) breakdown of phosphocreatine and ATP in the exercising muscles; and (3) breakdown of glycogen to lactic acid, which is partly distributed in the blood and extracellular fluid (Medbø et al., 1988). In terms of anaerobic metabolism, the classic notion of “oxygen debt” (Hill and Lupton, 1923) is another important principle defined as “the total amount of oxygen used, after cessation of exercise in recovery therefrom.” Hill and Lupton hypothesized that elevated V̇o2 after exercise was necessary for the repayment of the deficit in O2 consumption incurred during exercise (Gaesser and Brooks, 1984). A simpler, more practical explanation is: “if oxygen consumption during exercise was inadequate to meet energy demand—that is, if there was a “deficit” in oxygen consumption—then the body borrowed on its energy reserve (or credit). After exercise, then, the body has to pay back those credits, plus some interest” (Brooks et al., 2005). The oxygen debt principle may reflect the observation of the Krogh and Lindhard (1920) that “their experiments clearly show that oxygen deficit is not at all recovered during work and is not finally made up by oxidation until after the work has ceased,” suggesting that excess oxygen consumption after exercise (oxygen debt) could quantitatively represent anaerobic metabolism during exercise (oxygen deficit). The effects of six-month training on oxygen debt were reported in 1942 with maximal oxygen uptake (Knehr et al., 1942). Again, since neither ATP nor creatine phosphate was known at that time, it was believed that oxygen debt was used to remove lactate. After creatine phosphate was discovered in 1927,

Margaria et al. (1933) modified the oxygen debt principle, partitioning the debt into separate fast, initial (“alactacid”) and slow, second (“lactacid”) components, indicating oxygen that provides energy for resynthesizing creatine phosphate and for resynthesizing glycogen, respectively. However, later studies showed that oxygen debt could not be explained simply by replenishing the substrate consumed during exercise. Several factors are responsible for the delayed return of oxygen uptake to the resting value after exercise cessation. Increased ventilation, elevated heart rate, elevated body (Claremont et al., 1975) and muscle temperature (Q10 effect; Brooks et al., 1971), enhanced respiratory uncoupling (Brand et al., 1994), increased blood catecholamine (Gladden et al., 1982), etc. can all contribute to elevated resting oxygen consumption (Gaesser and Brooks, 1984; Moniz et al., 2020). An “ultra slow” component of postexercise oxygen consumption may persist for several hours after prolonged exercise. Professor Eric Newsholme (Department of Physiology, University of Oxford), who was a friend of Lars Hermansen, suggested that this was attributable to substrate cycling (Newsholm, 1978). I cooked Japanese dishes for Dr. Newsholme and Lars’ family at Lars’ home when Dr. Newsholme visited Oslo in 1983. Later, he invited us to visit his laboratory in 1984. During a tour of Merton College at Oxford University where he served as a mentor, I happened to pass close by the Prince of Japan, who studied at the college, and his bodyguards in the corridors, much closer than would have ever happened in Japan. Since neither qualitative nor quantitative explanations of “oxygen debt” were feasible until recently, Gaesser and Brooks (1984) proposed that such word “debt,” including “lactic oxygen debt” and “alactic oxygen debt” should not be used, but should be replaced by excess postexercise oxygen consumption (EPOC), which does not imply causality. As pioneering scientists studied exercise intensities that were high enough to produce lactate, but presumably at submaximal intensity lower than that which elicits maximal oxygen uptake, oxygen deficit appeared to be equal to oxygen debt. Later studies, however, showed that oxygen debt (EPOC) is higher than oxygen deficit, especially at supramaximal intensity, suggesting that oxygen debt (EPOC) does not quantitatively reflect anaerobic metabolism “during supramaximal intensity exercises.” Therefore, in terms of quantitative comparison/evaluation, only oxygen deficit has been used, including in our studies, to compare the metabolic contribution of aerobic and anaerobic metabolism for resynthesizing ATP consumed during exercise. The late Dr. Lars Hermansen, who was my supervisor in Oslo, reintroduced the oxygen deficit principle first introduced by Krogh and Lindhard in 1920. During his time in Stockholm in the Department of Physiology III at the Karolinska Institute (1964–67), he appears to have become interested in anaerobic metabolism. He inspired other physiologists, including Karlsson (1971), Karlsson and Saltin (1971), Knuttgen and Saltin (1973), and Linnarsson et al. (1974) while completing his PhD thesis on aerobic energy release (“Oxygen transport during exercise in human subjects”; Hermansen, 1974). Lars had a paper (Title: Anaerobic energy release) published on anaerobic metabolism during exercise in the first issue of Medicine and Science in Sports (Hermansen, 1969), suggesting that even then he was recognized as a leading scientist of anaerobic metabolism during physical exercise in males. Since we lost Per-Olof Åstrand and Bengt Saltin, supervisors and friends of Lars, I cannot ask them about this. It is pity that I did not have the chance to discuss how Lars became interested in anaerobic metabolism when I was in Oslo (1983–85) before he died at the early age of 50 years (March 8, 1994). I recently asked Drs. Björn Ekblom and David Costill, who worked with Lars at that time, about this.

Neither, however, knew how Lars became involved in the study of anaerobic metabolism. To reach Dr. Costill, I e-mailed Dr. John Kirwan of the Pennington Biomedical Research Center, who earned his PhD under Dr. Costill. We have been friends since studying together in at Holloszy’s lab at the Washington University School of Medicine, in St. Louis, MO, in 1990–91. In addition, Dr. Wendy Kohrt (Professor of Medicine in the Division of Geriatric Medicine at the University of Colorado Anschutz Medical Campus, University of Colorado Medical School) was my good friend at that time. These two researchers conducted human studies, while I concentrated on animal studies (Tabata et al., 1994). They were quite kind to short-stay foreign researchers, and we developed strong friendships. Ms. May Chen, a chief technician, and Dr. Eric Gulve, who took care of me during my animal research at Holloszy’s lab, introduced me to these two friends. We would often run together in Forest Park near the lab on Friday evenings. I served as a subject in Kirwan’s study investigating the effects of muscle damage caused by eccentric exercise on glucose metabolism (Kirwan et al., 1992). I remember that I had difficulty climbing up and down stairs for three days after the downhill running for that experiment. John and I took a trip in his Volvo (his license plate read “V̇o2max”) to Muncie, Indiana, for a symposium celebrating the 25th anniversary of Professor Costill’s lab at Ball State University. On the wall of the laboratory, I spied his picture among the PhD graduates from Costill’s lab. At that symposium, I met Dr. Phil Gollnick (University of Washington), who looked happy when I told him that Professor Katsuta (Professor Emeritus of University of Tsukuba), whom he had accepted as a visiting scientist, led histochemical and biochemical research on exercise and muscles in Japan. I guess Dr. Gollnick’s interactions with Lars during a stay in Stockholm were an important factor in his choosing to study anaerobic metabolism. Later, he wrote a review with Lars in the first issue of the prestigious journal, Exercise and Sport Science Review (Gollnick and Hermansen, 1973). It is interesting that my American boss, the late Dr. John Holloszy, contributed an article on “aerobic metabolism” in the same issue of the journal (Holloszy, 1973). In retrospect, I feel happy and lucky to have been supervised by these two legendary scientists in human metabolism, both aerobic and anaerobic. At that time, biochemistry was becoming a primary research tool for analyzing human metabolism during exercise (Asmussen, 1971). In addition, the biopsy technique developed by Bergström (1962), Bergström and Hultman (1966), and Lowry and Passoneau, 1972’s fluorometry measurement (1972) enabled exercise physiologists to directly study anaerobic metabolism by measuring metabolites in human skeletal muscle. Even though Lars included a figure with changes in phosphocreatine concentration in human skeletal muscle after maximal work lasting 2.5 min without reference in the review paper, he cited articles about the metabolic aspect revealed by biochemical analyses of animal muscles. Interestingly, he did not use “oxygen deficit,” referring only to “oxygen debt” in his first review (Hermansen, 1969). Meanwhile, when I was at Holloszy’s lab at Washington University School of Medicine in St Louis in 1990, I would often pass Dr. Lowry in the halls. He was still active at that time. Lars had given me his book, A Flexible System of Enzymatic Analysis (Lowry and Passoneau, 1972) when I was in Oslo. From the Stockholm group, probably inspired by Lars Hermansen, Karlsson and Saltin published the first paper on oxygen deficit determined as the difference between total oxygen demand and total oxygen uptake (Karlsson and Saltin, 1970). To calculate oxygen demand, they assumed that the mechanical work efficiency of bicycling was 22.5%, irrespective of individual subjects. In the 1980s, in addition to Hermansen’s laboratory, two independent groups in the USA developed the

idea of accumulated O2 deficit as the difference between accumulated oxygen uptake and oxygen demand estimated by linear extrapolation using the relation between oxygen uptake and exercise intensity at the submaximal level (Pate et al., 1983; Foster et al., 1989). All three groups independently proposed establishing the individual relation between exercise intensity and steady state O2 uptake at submaximal intensities, and to extrapolate these relations linearly to supramaximal intensities during high-intensity short-duration exercise. All three determined the accumulated O2 deficit for several exercises carried out to complete exhaustion, but at different intensities, and thus, different durations. All groups identified a maximum value for exercises lasting ~ 2 min or more, and took that value as the subject’s anaerobic capacity. After Lars died in 1984, the Norwegian group finally proposed the principles outlined above (Medbø et al., 1988) and validated their results against measured muscle metabolites (Medbø and Tabata, 1993). Later, Dr. Jon Medbø, my friend and collaborator in Oslo, told me that when Lars had found the Pate et al., 1983 abstract in the issue of the journal of Medicine and Science in Sports and Exercise 15(2) that I hand delivered from Montreal after attending the American College of Sport and Medicine annual meeting in 1983, he appeared frustrated and anxious, and speeded up studies on MAOD using three predoctoral students (myself, Drs. Jon Medbø, A.-C Mohn) with the help of Dr. R. Bahr, who took biopsies.

Fitness tests at the laboratory for exercise physiology and biomechanics, University of Tokyo

In 1980, Mr. Kouichi Irisawa, a coach of the Tsumagoi High School Speed Skating Team, asked the late Dr. Isamu Nemoto, a member of the scientific committee for the Japanese Speed Skating team of the Japan Skate Federation and a PhD student at the Laboratory for Exercise Physiology and Biomechanics, led by professor Mitsumasa Miyashita of the Faculty of Education of University of Tokyo, Japan for help. Professor Miyashita accepted Irisawa’s proposal, and asked all laboratory members, including me, then an undergraduate student, to measure the fitness of speed skaters at Tsumagoi High School under Nemoto’s directions. I likely measured the lean body mass of subjects using underwater weighing methods. At that time, Tsumagoi was known as the largest village and largest cabbage-producing area in Japan; the village was also famous for its skating farm. This was why many world-class speed skaters trained in this village. Interestingly, these included several Olympic speed skaters with the name Kuroiwa, such as Akira Kuroiwa (bronze medal in the 500-m race at the 1988 Calgary Olympic Games), and Toshiyuki Kuroiwa (silver medal in the 500-m race at the 1992 Albertville Olympic Games). This was because many residents in the village had the name Kuroiwa, although they were not related. Mr. Irisawa started his career as a physical education teacher at one of the village’s junior high schools. He spotted a promising skater (Akira Kuroiwa) and followed him to the Tsumagoi high school when he moved there. Together with Mr. Kumagawa, he coached many good speed skaters at the school. With the help of Irisawa and Kumagawa, Dr. Nemoto’s group further developed their research regarding the effects of sex and age (10–18 years) on isokinetic muscle power in a total of 553 subjects from Tsumagoi village (Kanehisa et al., 1984).

Visit to Oslo, 1983

As a visiting scientist, I studied at the Institute of Muscle Physiology (Oslo, Norway) from January 1983 through March 1985. It was during my PhD course year at the University of Tokyo, and was made possible by my mentor, Dr. Miyashita at the University of Tokyo. In response to my stated desire to study the biochemistry of exercise abroad, he contacted his US friend Dr. Phil Gollnick at Washington State University. However, Dr. Gollnick was then moving from the Department of Physical Education to the College of Veterinary Medicine. He recommended that Professor Miyashita send me to Oslo where his friend Lars Hermansen could supervise my work on biochemical research. For my first overseas travel (January 1983), I flew from Tokyo to Oslo via Moscow and Copenhagen on a Russian airline. Since there were few passengers, my flight from Moscow to Copenhagen was canceled, and I arrived about 12 h later than scheduled. I sent a telegram from Narita New Tokyo Airport, but it was Sunday, and there was no one to receive the telegram at the institute. Mr. Odd Vaage, who worked at the institute with Lars Hermansen, waited a very long time for me, picked me up and took me to the dormitory. I was very grateful for this Norwegian hospitality. Fig. 3.1 shows my first experiments in Oslo, where I was a subject in a study of submaximal and maximal oxygen uptake. The figure shows the relation between work intensity (number of watts in bicycle exercise) and oxygen uptake (L/min) for me (Fig. 3.1). These data were obtained 9–10 days after I arrived in Oslo.

Fig. 3.1 Relationship between work rate (watts) and oxygen uptake during the last 1 or 2 min of submaximal exercise, and during the last 30–60 s of supramaximal intensity exercise. These measurements were conducted 9–10 days after I Tabata arrived in Oslo in 1983.

While I knew that these two parameters should be correlated, I was extremely excited and surprised that the relation was so linear (almost a straight line), even though the values were calculated by measuring sampling time (sec), expired gas volume (L), oxygen and carbon dioxide concentrations (%), temperature (°C), and atmospheric pressure (hPa), which have their own measurement errors. I think that these accurate measurements were enabled by the apparatus at the institute and the enthusiasm of the researchers there (led by the late Dr. Lars Hermansen). For example, they measured oxygen uptake not by fixed time, switching the Douglas bag every 30 s, but by the time from the start to the end of several respirations during ~ 30 s periods using special systems (Fig. 3.2).

Fig. 3.2 A special switching apparatus was used to collect respiratory gas from exercising subjects with a mouthpiece attached to a Douglas bag (connected to the two transparent blue tubes (light gray in print version)). The mouthpiece (not shown) was connected by a hose (not shown) to the blue valve.

When inspiration was observed to begin, we moved the lever so that expired air would be collected in a Douglass bag through a three-way cock. The lever simultaneously started an analog stopwatch by pushing the switch. The start of inspiration was defined as the respiration valve sinking. After ~ 30 s, we again moved the lever when we visually confirmed the start of inspiration. This time, the lever pushed the switch of the stopwatch to off, and we recorded the duration (time) measured by the watch. The switch of the stopwatch was then reset. This method was intended to minimize the effects of changing gas concentrations in the measured and calculated values of oxygen uptake; since oxygen and carbon dioxide concentrations change during the course of respiration, it is better to collect the expired gas of the entire breath (i.e., from start to end of respiration). Furthermore, the difference of two measures of oxygen uptake as candidates of maximal oxygen uptake obtained at the supramaximal exercise intensities were very small, less than 0.05 L/min, which was within the range that Ekblom estimated for the measurement error of maximal oxygen uptake, 2.1% (Ekblom, 1968). Actually, recognizing the accuracy of oxygen uptake and maximal oxygen uptake measurements, and being convinced of the accuracy of estimated oxygen demands at supramaximal intensity exercise from the relation between work rate and oxygen uptake at submaximal intensity exercises was my first step toward my MAOD research, which later led to Tabata training research. The bicycle shown in Fig. 3.3 was used for experiments. This bike was donated by the August Krogh Institute in Copenhagen, and maintained by the workshop at the institute. At first I could not participate because the saddle of the bike was too high for me. A technician from the workshop came and made a new lower hole to adjust the saddle. This hole was only used for experiments where I was the subject. I recognized that it is good to have such personnel at a research institute (Figs. 3.4 and 3.5).

Fig. 3.3 Krogh bike donated by the August Krogh Institute in Copenhagen Denmark.

Fig. 3.4 Seminar schedule for national-level junior speed skaters in 1989 in Takasaki, Gunma.

Fig. 3.5 Principles for developing training.

In 1984, Mr. Irisawa Koichi was also visiting as a coach to the Norwegian Skating Federation. He had come to Oslo just after the Sarajevo Winter Olympic Games (1984). We stayed in the same dormitory in a suburban area of Oslo and became friends. We often discussed the metabolic characteristics of speed skating. He was one of the subjects of our study. We measured maximal oxygen uptake of Mr. Akira Kuroiwa who got a bronze medal at 500 m speed skating, 1988 Calgary Winter Olympic Game. After one-year stay in Oslo, Mr. Irisawa returned to Japan, where he was appointed as a head coach of the Japanese Speed Skating Team. He recommended that I be appointed a fitness coach for the National Speed Skating Team.

Training camp for top skaters, 1989

Mr. Irisawa Koichi asked me to give a lecture to junior speed skaters during a training seminar camp held in 1989. The camp was a little bit different compared to those of other sports. During the 5 days program (Fig. 3.5), there was no class where former elite skaters and/or famous coaches gave their opinions or impressions on how to skate. Most were lectures to junior high and senior high school students. The lectures involved exercise physiology, sports biomechanics, nutrition, biomechanics, and sport sociology! Ms. Maki Tabata, who would win the silver medal (team pursuit) at the Vancouver Winter Olympic Games (2010), was a junior high school student when she attended the training seminar camp. I can remember the hotel telephone operator misconnected a call from her mother to my room because we have same name (Tabata). The junior skaters, including Ms. Tabata, learned several aspects of exercise science at their young age. I believe that the knowledge she gained enabled her to continue her athletic activity and finally win her first Olympic medal when she was 35 years old. By the way, during the five days, there were only two or three classes in which the skaters used their bodies. One was a training class held on the afternoon of May 6. To be honest, before I joined the camp there was no name on the program for that training. But after I arrived at the camp venue, I found my name in the program. I was born in the southern part of Japan where there is no ice outside even in the winter. I learned to skate by myself at age 14, but did not have any experience in training. I am still not sure why Mr. Irisawa appointed me to teach the training practice. Afterward, although I was confused, I decided to introduce the training, which Mr. Irisawa adopted. Because he had coached many Olympian skaters, and his training was deemed worthy of being introduced to junior skaters who aimed to participate in the Olympics. I asked Mr. Irisawa what kind of exercise training he used, and showed junior skaters and their coaches his two training protocols without belief based on the science of the training.

Analysis of the two training protocols introduced by Mr. Irisawa

A month and a half later, another camp was planned for senior speed skaters. I was afraid that Mr. Irisawa would again appoint me to that training class. Since senior skaters, who were very motivated to win gold medals at the Olympics, and their coaches, who were supposed to have much more knowledge about training and lived on the speed skaters’ performance, might ask why I was introducing the training method invented by Mr. Irisawa, a rival coach, I decided to analyze the two training protocols at my laboratory, the National Institute of Fitness and Sport in Kanoya, located more than 1400 km away from the camp. Both of protocols (IE1 and IE2) involved high-intensity, intermittent exercises (Tabata et al., 1997). IE1 was an exhausting intermittent exercise (exercise intensity: 170% V̇o2max, 20-s exercise, 10-s pause). After the 6th or during the 7th sets, subjects became exhausted. IE2 was an intermittent exercise (intensity: 200% V̇o2max, 30-s exercise, 2-min pause), which exhausted skaters after 4th or during the 5th sets of the 30-s exercise bouts. Performance of most exercise sports depends on the amount of energy output per unit of time. Since energy output (ATP consumption) is equal to total energy supply from aerobic and anaerobic energysupply systems, it is well known that increasing the ability of the two energy supplying systems by physical training is a way to enhance sports performance. Since, for most physical properties, the more demanding the training the greater the improvement of the property, it was necessary to measure energy supply from the two systems during exercise to evaluate their efficacy (Fig. 3.6).

Fig. 3.6 Oxygen uptake during high-intensity intermittent exercise (Tabata training) ( Tabata et al., 1997 ).

The aerobic energy released is determined by measuring oxygen uptake during exercise. By measuring oxygen uptake (Fig. 3.7) and comparing that value with subjects’ V̇o2max, it was possible to evaluate the stress on the aerobic energy release system during training/exercise. As shown in Fig. 3.7, the oxygen uptake measured during the last part of IE1 was not different from the V̇o2max, suggesting that it recruited the oxygen delivery system maximally (Tabata et al., 1997).

Fig. 3.7 Peak oxygen uptake deficit during the last 10 s of the two protocols for intermittent exercises and the maximal oxygen uptake ** indicates a significant difference from the maximal oxygen uptake ( P < 0.01). #Indicates a significant difference from the peak oxygen uptake during the last 10 s of the IE1 exercise ( P < 0.05) ( Tabata et al., 1997 ).

During the first bouts of exercise, oxygen uptake does not increase rapidly. As a result, anaerobic energy release contributes 70% to 80% of the total energy requirement, suggesting that such exercise is “anaerobic,” which most of us can feel. However, as stated above, oxygen uptake increases during exercise and finally reaches subjects’ V̇o2max during the last bouts, indicating that this is the best “aerobic exercise” in terms of relative stress (100% of V̇o2max) on the aerobic energy-releasing system (Tabata et al., 1997). This allowed us to hope that a training using this protocol might improve V̇o2max maximally. IE2 did not elevate oxygen uptake to the level of V̇o2max during any exercise bouts, suggesting that this protocol did not stress the aerobic energy-releasing system maximally (Fig. 3.8).

Fig. 3.8 Oxygen deficit and EPOC (excess postexercise oxygen consumption) during high-intensity intermittent exercise (Tabata training) ( Tabata et al., 1997 ).

Next, we estimated accumulated oxygen deficit for intermittent exercise, as shown in Fig. 3.9 (Tabata et al., 1997). To estimate oxygen deficit for intermittent exercise, we also used the oxygen deficit principle. First, we estimated the oxygen demand by extrapolating the linear relationship between oxygen uptake and exercise intensity, and quantified total accumulated oxygen demand for each intermittent exercise. Then, we summed up the oxygen deficit during each exercise by subtracting measured oxygen uptake from oxygen demand for each set of exercises. During rest periods, energy requirement (i.e., oxygen demand) should have been the same as resting oxygen uptake; in reality, however, oxygen uptake during the rests between exercise bouts was higher than the resting value, suggesting that during rest periods, oxygen was used to supply energy for resynthesizing creatine phosphate, which is a major component of anaerobic metabolism. So the oxygen uptake over resting value after exercise was called EPOC (excess postexercise oxygen consumption). To put it simply, during the rest periods between exercise bouts, oxygen deficit from the exercise is partially paid back. Therefore, we subtracted total EPOC from total oxygen deficit during exercise to calculate overall oxygen deficit for the intermittent exercise program.

Fig. 3.9 Accumulated oxygen deficit of two high-intensity intermittent exhaustive exercise regimen (IE1 and IE2). Maximal oxygen deficit (MAOD) and accumulated oxygen deficits of the two intermittent exercise protocols. **Indicates a significant difference from the maximal oxygen uptake ( P < 0.01). ##Indicates a significant difference from the MAOD and accumulated oxygen deficit of the IE1 exercise ( P < 0.01) ( Tabata et al., 1997 ).

These calculations revealed that accumulated oxygen deficit of the IE1 equaled the MAOD, and thus appeared to stress the anaerobic energy system maximally (Fig. 3.10). Since humans have only two energy supply systems, namely aerobic and anaerobic, I found that IE1 was one of the most effective exercise training protocols for improving both aerobic and anaerobic energy supply systems almost maximally and simultaneously. On the other hand, the anaerobic energy-releasing system seemed not to be fully stressed during exhaustive IE2. Based on these data, we suggested IE1 is superior to IE2 for the purpose of improving both the anaerobic and aerobic energy-releasing systems.

Fig. 3.10 Effects of endurance training (ET) and high-intensity intermittent training (Tabata training) on V̇o 2max . There was a significant increase from the pretraining value at * P < 0.05 and ** P < 0.01 ( Tabata et al., 1996 ).

On the first day of the training camp for senior skaters, I reported this result to Mr. Irisawa. He said he would use only IE1 for their training. Both IE1 and IE2 are exhaustive, meaning athletes cannot do more training later in the day. Therefore, if Mr. Irisawa had been using IE1 for two days and IE2 for two other days, he could now use IE1 for two days and try another new training for two days. Or he could have adopted IE1 for three days, leaving more time for other kinds of training, such as training in technique. It is likely that these results have contributed to the medal count in recent Olympic games. Since I now had this empirical scientific evidence, on this occasion, I taught only IE1 with enormous confidence, like a real coach. Since I also may have believed that IE1 (high-intensity intermittent exercise) was anaerobic exercise and could be used as training for the anaerobic energy-releasing system, I might have planned to measure anaerobic energy release to evaluate its effects on the anaerobic energy-releasing system. In terms of specificity of training and training effects, it is not, however, scientifically rational to measure aerobic energy release (i.e., oxygen uptake) to evaluate “anaerobic exercise” as a training for the anaerobic energy-releasing system. The reason I measured oxygen uptake during IE1 was to quantify anaerobic energy release by measuring accumulated oxygen deficit to evaluate its efficacy for improving the anaerobic energy-releasing system. Since oxygen deficit is quantified as the difference between total oxygen demand and accumulated oxygen uptake, the measurement of oxygen uptake during high-intensity intermittent exercise was inevitable. Therefore, I measured aerobic metabolism (oxygen uptake) of “anaerobic exercise.” When Mr. Kouji Nishimura, an undergraduate student, came up and showed me the results of oxygen uptake and accumulated oxygen deficit, I was first excited that accumulated oxygen deficit with IE1 was not different from the MAOD of subjects, suggesting that IE1 could be one of the best anaerobic training programs. Second, I was surprised by the high values of oxygen uptake during the last phase of the IE1. I checked the raw data again and again with Futoshi Ogita and Motohiko Miyachi, who were master course students and helped conduct Mr. Nishimura’s experiment for their graduate thesis. We found no error regarding the oxygen uptake data, however. After statistical analysis of the data, we found that oxygen uptake during the last phase of IE1 was not significantly different from V̇o2max, suggesting that IE1 stresses the aerobic energy-releasing system maximally and, therefore, could be one of the best forms of aerobic training (Figs. 3.5 and 3.6). To quantify accumulated oxygen deficit during supramaximal intensity intermittent exercise using measured oxygen uptake and EPOC, together with estimated oxygen demand was my idea. However, this idea would not have occurred to me without my experiences in Oslo where I learned the principles of MAOD from Lars Hermansen and took part in numerous experiments and discussions with his colleagues. Later, we conducted a training study to verify the hypothesis (Tabata et al., 1997). The study included two training experiments. For the first experiment, seven subjects exercised using a mechanically braked cycle ergometer (Monark, Stockholm, Sweden), five days a week for six weeks. For four days a week, subjects biked following the IE1 protocol [Tabata et al., 1996; 10-min bicycle ergometer exercise

(pedaling frequency: 90 repetition per minute [RPM] at an intensity of 50% V̇o2max as a warm up 10 min prior to start of IE1)]. Since the high intensity intermittent exercise consisting of 20 s exercise at 170% V̇o2max with 10 s rest between the bouts exhausted those specific subjects during the 7th or during the 8th sets of exercise bout, we asked those subjects to bike for 7–8 sets until exhaustion for the first training days. Exercise was terminated when the pedaling frequency dropped below 85 rpm. One day per week, usually on Wednesday, the subjects exercised for 30 min at an intensity of 70% V̇o2max before carrying out four sets of the 20-s intermittent exercise at 170% V̇o2max with a 10-s rest between bouts. This session was not exhaustive (like a relaxing day). The MAOD was determined before the experiment, at two and four weeks into the training, and after the training. V̇o2max was determined before, at weeks three and five, and after the training. When the subjects became fit enough to complete the high-intensity exercise for nine sets, exercise intensity was elevated by 11 watts the next training day. After three weeks of training, mean V̇o2max had increased significantly by 5 mL/kg/min (Fig. 3.11). While it also tended to increase in the last part of the training period, the changes observed did not reach the level of significance. The final V̇o2max after six weeks of training was 55 ± 6 mL/kg/min, a value 7 ± 1 mL/kg/min above the pretraining value. Increase in V̇o2max observed after the high-intensity intermittent exercise training using IE1 was comparable to that observed after typical endurance training. The MAOD increased by 23% after four weeks of training (Fig. 3.12). It increased further toward the end of the training period. After the training period, anaerobic capacity reached 77 ± 9 mL/kg, 28% higher than the pretraining value.

Fig. 3.11 Effects of endurance training (ET) and high-intensity intermittent training (Tabata training) on anaerobic capacity (maximal oxygen deficit). Significant increase from the pretraining value at * P < 0.05 and ** P < 0.01. Significant increase from the 2-week value at # P < 0.05 ( Tabata et al., 1996 ).

In addition to MAOD, intermittent training increased V̇o2max significantly. This was the first study to demonstrate an increase in both MAOD and V̇o2max. High-intensity intermittent training was already known to be a very potent means of increasing maximal oxygen uptake (Fox, 1979). In terms of the frequency of high-intensity interval training to improve V̇o2max, Fox (1979) showed that the magnitude of V̇o2max increase did not vary between two and four times a week. Therefore, the four times a week training with the easy day adopted in the study might have been too demanding. As shown in a later chapter, training twice a week appears to be sufficient to increase V̇o2max in sedentary-to-active people, while more frequent training might be necessary to improve the aerobic power of elite athletes. In terms of training frequency for speed skaters, Professor Irisawa told me that he prescribes the full Tabata training (i.e., 7–8 × 20-s exercises) three days per week until two weeks prior to races. He also instructs skaters to use the short version of Tabata exercise (3 × 20-s exercises) on race days in order to activate their body before races. For the second experiment of the study, which was done as a positive control, seven male subjects started training after their V̇o2max and MAOD were measured. They exercised five days a week for six weeks at an intensity that elicited 70% of each subject’s V̇o2max. The pedaling rate was 70 rpm, and the duration of the training was 60 min. As each subject’s V̇o2max increased during the training period, exercise intensity was increased from week to week as necessary to elicit 70% of the actual V̇o2max. During the training, the MAOD was measured before the training, at four weeks, and after the training. V̇o2max was determined before and after the training, and every week during the training period. When subjects’ V̇o2max increased, exercise intensity (watts) was increased so that the oxygen demand of the training exercise was maintained at 70% V̇o2max. As shown in Fig. 3.11, V̇o2max was increased by this endurance training. However, no change in MAOD was found after the training. This result supports the idea that the accumulated oxygen deficit is a specific measure of the maximal anaerobic energy release. Due to the increased V̇o2max after the training, subjects could exercise for more than six min at the power used for the pretraining 2- to 3-min MAOD test. Therefore, the exercise power for the posttraining MAOD test was increased by 6% ± 3% to exhaust each subject in 2–3 min. However, the MAOD appeared unaffected by the higher power used at the posttraining test, suggesting that this value is able to distinguish between aerobic and anaerobic energy release at different exercise intensities. After the training study, we submitted a manuscript including the hypothesis based on the metabolic profile of IE1 and IE2 that Irisawa developed for speed skaters, and the training study in Medicine and Science in Sports and Exercise. Associate Editor Dr. Carl Foster recommended that we split the paper in two, because there was too much content in the original manuscript for one paper. I rewrote two manuscripts and resubmitted them to the same journal. Simply due to the different handling time of the two submitted manuscripts, the hypothesis paper (Tabata et al., 1997) was published later than the training study for verifying the hypothesis (Tabata et al., 1996). For me, a young researcher needing publications for promotion, Dr. Foster’s recommendation was much appreciated.

I moved to the National Institute of Health and Nutrition in Tokyo in 1991 after one year at Dr. Holloszy’s laboratory in St Louis, and did not perform further studies on MAOD, but conducted animal experiments on the effects of exercise training on glucose transport activity and glucose transporter 4 (GLUT4) from the viewpoint of exercise intensity (Kawanaka et al., 1997; Terada et al., 2004, 2005; Yamaguchi et al., 2010; Fujimoto et al., 2010). Since, presumably, exercise-related signal(s) induce training responses in recruited skeletal muscle, it was natural to assume that the higher the exercise signal(s), the higher the training response. The reason that high-intensity training has not been studied in terms of aerobic metabolism and health outcomes might be because medical communities are not familiar with high-intensity training. Moreover, it was an accepted notion that exercise intensity to prevent and treat diseases should be light to moderate. Rat models of Tabata training described in the following chapter (Terada et al., 2001) are a good tool for studying exercise (intensity-related) signals to induce changes in skeletal muscle function, including protein expressions. There is specificity between training and training effects. For example, the fact that muscle hypertrophy is observed only in muscles undergoing resistance training is cited as specificity of training. In line with this, metabolic specificity means that aerobic training improves the aerobic energy-releasing system, while anaerobic training enhances the anaerobic energy-releasing system. From the viewpoint of metabolic specificity, it is easy to believe that the typical aerobic training improved V̇o2max, which is a parameter for the aerobic energy-releasing system. We found that the high-intensity intermittent training (HIIT) (IE1), which appears to be an anaerobic exercise, increased V̇o2max because HIIT is, in term of stressing the aerobic energy-releasing system, the ultimate aerobic training (Tabata et al., 1996). Thus, the metabolic profile of HIIT and its effects relates to the principle of metabolic specificity. A unique aspect of our studies is that we measured oxygen uptake (aerobic energy release) during an exercise that other people considered anaerobic. It is another example of metabolic specificity that HIIT elevated MAOD dramatically, because it is one of the best forms of anaerobic training that stresses the anaerobic energy-releasing system maximally, while typical aerobic training does not affect MAOD at all. These studies suggested that high-intensity intermittent exercise is a very effective tool for improving both aerobic and anaerobic energy-releasing systems simultaneously in a short period of time. Since, as already mentioned, both aerobic and anaerobic energy release are important for most types of sport, HIIT is therefore one of the best training methods for improving sports-related physical fitness. Before we published our first two papers, it was believed that aerobic training only improved the aerobic energy-releasing system (V̇o2max), while anaerobic training affected only the anaerobic energyreleasing system (MAOD). However, HIIT was found to be one of the best forms of both aerobic and anaerobic training, elevating both V̇o2max and MAOD. In addition, the short duration of HIIT, as compared with that of typical aerobic training (> 20 min), may be attractive to highly motivated athletes with limited time. One of the most important changes explaining the improvement of the MAOD after HIIT - probably including Tabata training- is the enhanced buffer capacity of muscles recruited during the HIIT (Sharp et al., 1986). This enhanced capacity allows more muscle lactate formation, which results in proportional glycolytic ATP production for high-intensity exercises. Sharp et al. (1986) reported that, after 8-week sprint training, their subjects’ muscle buffer capacity was increased by ~ 37%. This robust increase in buffering capacity may explain the majority of the elevation of the MAOD after HIIT including Tabata training.

In addition, carnosine is regarded as a minor contributing factor (5%–10%) to muscle buffer capacity (Sahlin, 2014). In this context, it is interesting that the levels of the mRNA and protein of carnosine synthase 1 were increased by Tabata training (Miyamoto-Mikami et al., 2018), suggesting that the body’s carnosine content might be elevated by Tabata training as demonstrated after a HIIT (De Salles Painelli et al., 2018). In terms of the increase in V̇o2max after HIIT, there has been some disagreement regarding whether the main location of the adaptation is central (cardiorespiratory: cardiac output) or peripheral (skeletal muscle: metabolic enzymes). The improvement in V̇o2max after specific training may be due to both central and peripheral factors, which correspond to increased cardiac output and oxygen extraction and/or oxygen consumption in working skeletal muscle, respectively. These factors can be further explained by increased maximal cardiac output/stroke volume of heart and increased oxidative enzyme activity in skeletal muscle, respectively. Since the increase in V̇o2max after HIIT, including Tabata training, is very rapid (e.g., 2–3 weeks; Tabata et al., 1996; Weston et al., 2014), and changes in the morphology of the heart cannot be expected within such a short time period, the increase in the V̇o2max during the early phase of Tabata training is most likely due to peripheral factors. However, Burgomaster et al. (2005) reported that after two weeks of SIT training, subjects’ V̇o2 peak did not increase, although the activity of citrate synthase (CS) was enhanced by 38%, suggesting that changes in peripheral factors do not necessarily induce increase in V̇o2 peak. Daussin et al. (2008) suggested that adaptation after interval training occurs both centrally and peripherally. Macpherson et al. (2011) reported that six-week run-sprint interval training improved subjects’ aerobic performance but not maximal cardiac output, whereas another research group reported that six-week high-intensity interval training did increase subjects’ cardiac output and V̇o2max (Astorino et al., 2017). The authors of the latter study attributed the initial increase in cardiac output after the early phase of high-intensity interval training to plasma volume expansion (Astorino et al., 2017), which was apt to occur in sedentary subjects with lower V̇o2max values compared to the recreationally active subjects of the Macpherson et al. study. Further research is necessary to address the discrepancy of these findings. There were no changes in the body weight of training subjects, suggesting that this training is not particularly effective in reducing body weight (Tabata et al., 1996). These results were reproduced by our following experiments (Hirai and Tabata, 1996; Kouzaki and Tabata, 1998). The reason for this was clarified by our recent investigation regarding the effects of Tabata training on energy consumption at rest after training (Tsuji et al., 2017). After the publication of these two papers (Tabata et al., 1996, 1997), training using the IE1 protocol began to be referred to as the “Tabata protocol,” “Tabata interval training,” or “Tabata-style training,” and these terms began to be used by many people, including both sport-oriented athletes and healthoriented nonathletes. Further research on “Tabata” or “Tabata-style” exercise training was then conducted. For example, Foster et al. elegantly reproduced the effect of 8 weeks of Tabata training on aerobic energy-releasing system (18% increase in the V̇o2max) (Foster et al., 2015). Tabata training spread very fast in nonathlete communities, inspired by scientists who had read our original papers and written articles on Tabata; for example, Koch, 2004. Meanwhile, in athletic circles, many athletes, including Yasuhiro Shimizu, who won gold and bronze medals in the 500 and 1000-m speed skating races, respectively, at Nagano 2002, and the silver medal in the 500-m at the 2002 Salt Lake City Olympics, used Tabata training.

On the first day of class ~ 5 years ago, I asked the freshmen at my university whether they had heard of Tabata training. Ten percent of them answered yes. This year, more than 60% reported knowing Tabata training, suggesting that a high percentage of high school students know Tabata training and have experience using the training.

Recommended practical procedures for Tabata training

The first article regarding Tabata training was published over 30 years ago, and no further paper was published by the authors of the original article until recently. There has thus been some confusion about Tabata training, especially concerning the methodology. The following practical tips for executing authentic Tabata training are presented in order to prevent the misunderstanding of Tabata training. First, before an individual engages in Tabata training, warming up for 10 min at approximately 50% V̇o2max is recommended (Tabata et al., 1996, 1997). Authentic Tabata training consists of 6–8 exhaustive sets of 20-s high-intensity bicycle exercise (intensity: 170% V̇o2max) with a 10-s rest between the exercise bouts (Tabata et al., 1996, 1997). For determining the optimal exercise intensity of the training, the exercise intensity equivalent to the subject’s 170% V̇o2max is first determined. The 170% V̇o2max is an intensity that exhausts the subject by approximately 50 s of bicycling (if the subject continues to bicycle at that time). The exercise intensity should be determined individually. The subject should then be instructed to continue bicycling until exhaustion (described below) after a 20-s cycling bout with a 10-s rest interval. If the subject can continue to bicycle for more than eight sets, the exercise intensity should be increased. If the subject cannot bike for less than six sets, the exercise intensity is reduced. Therefore, the intensity of Tabata training does not have to be 170% V̇o2max; the intensity that exhausts the subject after the sixth or during the seventh set should be used for the first days of training. Exhaustion during bicycle exercise is determined as follows. During the bicycling, when the pedaling frequency tends to less than the fixed rate (normally 90 repetitions per minute [rpm]), we encourage the subject verbally with phrases such as “Come on, come on!” With this verbal encouragement, a subject can often increase the pedaling frequency to 90 rpm. When encouragement has been given but the subject’s pedaling frequency gradually declines to 85 rpm, we define it as exhaustion and let the subject stop bicycling. For bicycling exercise, it is important to raise the pedaling frequency to the fixed rate as soon as possible to set the correct load for the subject. A pedaling frequency of 100 rpm might be good for cyclists. In the original Tabata study, 90 rpm was used. The reason why we use a higher pedaling frequency than that used for normal bicycle exercise (50–70 rpm) is that without such a high pedaling frequency, a high-enough load cannot be set for heavy-weight top athletes. In the original Tabata training experiments, Monark bicycles (whose highest load is 7 kP) were used, but even with such a heavy weight, the load is not high enough to exhaust elite athletes within 6–8 sets of Tabata training if 50–70 rpm is used. By using 90 rpm, an adequate work rate, which is a function of weight (kP) and rpm, is assured for highly trained athletes.

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Chapter 4: Later scientific evidence

Abstract

This chapter provides scientific evidence regarding the effects of Tabata training, Tabata-style training, and Tabata-style nonexhaustive training on the V̇o2max and MAOD of various athletic and healthoriented individuals. In addition, we present the molecular adaptation of skeletal muscle to Tabata-style training in experimental animals. Most of the data were collected in my laboratory by colleagues, postdocs, and students at the National Institute of Fitness and Sport (Kanoya, Kagoshima, Japan), National Institute of Health and Nutrition (Tokyo, Japan), and Ritsumeikan University (Kusatsu, Shiga, Japan). I include most of my research history and career. These data can help us to develop future Tabata and Tabata-style training based on the definition in Chapter 2, and contribute to enhance sport performance and health.

Keywords

Tabata training; Tabata-style training; V̇o2max; MAOD; GLUT4; Mitochondria; AMPK; Colon cancer; Bone; EPOC

Evolution of IE1 into Tabata training!

Today, the HIIT protocol of IE1 (Tabata et al., 1997) called the Tabata training, Tabata interval training, Tabata-style training, or Tabata protocol is used by a huge number of people, including both sportsoriented athletes and ordinary health-oriented individuals. Since the original protocol was quite demanding, we supposed that only highly motivated elite athletes would use the protocol to elevate both the aerobic and anaerobic energy-releasing system. However—unexpectedly—many health-oriented, fun-oriented, or accomplishment-oriented people utilize the training method. The rumor is that on the east coast of the USA, busy people were first fascinated by the method because it revealed that it takes only 3–4 min to increase fitness, whereas before it had been thought that at least 20 min were necessary to improve maximal oxygen uptake. In particular, young clinical doctors, who found the scientific evidence published in journals, spread the method by word of mouth. Meanwhile, on US west coast, the Tabata protocol was first introduced by people who loved resistance training, since they found the training similar to those they were using, i.e., high-intensity resistance training is effective for improving not only muscular strength but also the aerobic energy-releasing system. In the academic community, it was nice to hear that several professors used our papers (Tabata et al., 1996, 1997) in their seminars for master course students. These events were to be expected, since our publications were cited in the famous textbook of exercise physiology (Kenney et al., 2020). On YouTube, many videos showing different kinds of modified Tabata training and Tabata-style training can be found. It is interesting to observe people developing their own Tabata training to match their favorite exercise and their abilities. These developments were not expected. Since these articles were published in 1996 and 1997, and no more have been published specifically on this training protocol, the Tabata protocol has more or less been developed by the lay public. In these terms, it is one of the most successful examples of exercise training. However, in terms of scientific evidence, there are many claims for “effects” of the training that have not been proven scientifically. For example, I believe that the effect of the training on fat burning, which was first mentioned on web sites, has not been proved. Energy consumption during the short-term training exercise is negligible. After the exercise, oxygen uptake is known to be higher than the resting metabolic rate. However, excess postexercise oxygen consumption (EPOC) has not yet been quantified. Therefore, further research on effect of the Tabata Protocol on fat combustion and subsequent fat reduction in the body should be conducted. Recently, high-intensity interval training was found to be more enjoyable than moderate-intensity continuous exercise (Bartlett et al., 2011). Achieving a strong sense of accomplishment after such highintensity exercise was proposed to be related to enjoyment of HIIT. This enjoyment of HIIT may explain worldwide prevalence of HIIT, including Tabata training, and efficacy of HIIT for specific populations (Jung et al., 2015). You may think strange, but as a scientist, I have been trying to find side or adverse effects of highintensity exercise training in addition to frequently referred risk of injury associated to participating high-intensity exercise. It is well known that high-intensity exercise elevates blood pressure which may be lethal. Therefore, I have been not recommending such Tabata training to elderly. However, even I am

65 years old, I do some Tabata training myself so far safely. Many clients asked me to develop new Tabata training for elderly. So we are now studying effects of different exercise intensity (from 100% to 160% V̇o2max) of Tabata training on blood pressure of professors ages 50–60 year old. We may start 100% V̇o2max exercise first, because it is better check blood pressure at the safer level. Even though these procedures are not common in such scientific studies (most studies adopt random order procedure for designing order of different intensity exercises). If we cannot adopt lower intensity than 170% V̇o2max which is used for our original investigation, magnitude of effects on the training on aerobic and anaerobic energy-releasing system would be less than that expected to be got after the original investigation. However, it might give us not maximal but proportional effect in terms of exercise intensity. Therefore, we are designing and conducting new research on elderly people. The reason that I started studying effect of high-intensity exercise on colon cancer development is that, since, generally, one of the mechanism explaining cancer development is reduced immune function and high-intensity exercise was known to reduce immune function, while low to moderate-intensity exercise improves immune function (Nieman, 1994), we were afraid that high-intensity exercise may enhance cancer development. But we found that Tabata training may reduce risk of colon cancer by decreasing chemically induced ACF which is the precancer cell and present the first step of colon cancer development. The mechanism was described in this book. However, one more thing that I wanted to remark is that it is due to our comprehensive treatment of the experimental animals as we do for human so that their immune function is not blunted by the Tabata training. In the following section, I describe experimental results obtained in my laboratory at the National Institute of Fitness and Sports in Kanoya, the National Institute of Health and Nutrition, Tokyo, and Ritsumeikan University, Kusatsu, Japan.

Effects of training combining Tabata training and resistance training on MAOD and V̇o2max

Principally, MAOD is a combined quantity multiplied by the volume of muscle (specifically, plasma volume of muscle) and concentration of creatine phosphate and maximal lactate concentration that an individual can tolerate. Therefore, we further investigated change of MAOD after resistance training that enlarges muscle volume. This training consisted of HIIT for 6 weeks and HIIT + RT for 6 weeks (Hirai and Tabata, 1996), which models training adopted at team led by Mr. Irisawa. During HIIT, subjects (age: 23 ± 1 year; height: 172 ± 5 cm; weight: 71 ± 8 kg, V̇o2max: 52.0 ± 7.2 mL/kg/min) trained using the Tabata training 5 days a week. During HIIT + RT, they used the Tabata training for 3 days and then performed resistance training three days a week. Resistance training consisted of: (1) 4 sets of squat and leg curl exercises at 12-repetition max (RM) with 30-s rest between sets; (2) 2 sets of maximal bouts of the same exercise with a load of 90%, 80%, and 70% of 1 RM. After the IT and RT period, the subject lifted a barbell mass 12 times (12 RM) for squat was increased by 108 ± 8%. HIIT training increased MAOD by 18 ± 9% (pre: 69.4 ± 6.4 mL/kg; fifth week: 82.1 ± 11.6 mL/kg). HIIT and RT training further increased MAOD by 38 ± 19% (post: 95.8 ± 16.4 mL/kg), suggesting that increase in muscle volume by resistance training is effective for MAOD expansion (Fig. 4.1). However, Minahan and Wood reported that resistance training did not affect the MAOD (Minahan and Wood, 2008). It is thus not known whether the increase in the MAOD obtained with an IT + RT regimen is attributable to combined effects of resistance training and HIIT or just to HIIT. Further research can be expected to elucidate this issue.

Fig. 4.1 Effects of combined Tabata (IT) and resistance training (RT) on maximal accumulated oxygen deficit. * and ** indicate significant difference from the pretraining value at P < 0.05 and 0.01, respectively. + and ++ indicate significant differences from the 3-week value at P < 0.05 and 0.01, respectively. # and ## indicate significant differences from the 6-week value at P < 0.05 and 0.01, respectively. § and §§ indicate significant differences from the 9-week value at P < 0.05 and 0.01, respectively ( Hirai and Tabata, 1996).

V̇o2max increased during the 6-week HIIT by 11 ± 2%, while no significant change was observed during the HIIT and RT training period (Fig. 4.2). This result may indicate that, in terms of highintensity intermittent training, a different strategy is necessary for further improvement in the aerobic energy-releasing system. Hickson demonstrated that simultaneous training for strength and endurance will result in a reduced capacity to develop strength, but will not affect the magnitude of the increase in the V̇o2max (Hickson, 1980). Studies that eliminate the interference of one type of fitness over another type should be devised to address this issue.

Fig. 4.2 Effects of combined Tabata (IT) and resistance training (RT) on V̇o 2max . * and ** indicate significant differences from the pretraining value at P < 0.05 and 0.01, respectively. + and ++ indicate significant differences from the 3-week value at P < 0.05 and 0.01, respectively. ( Hirai and Tabata, 1996).

During the IT-alone period, both the maximal power during the Wingate test, and the circumference (cm) of thigh muscle were not changed. However, after the IT and RT period, the maximal power was significantly increased by 10 ± 3% (P < 0.05) with a significant increase in the thigh muscle circumference (3 ± 1%, P < 0.01). These results may indicate that (1) Tabata training itself does not affect maximal anaerobic power, and (2) an increase in muscle mass is necessary to induce an increase in the maximal anaerobic power. After 12 weeks of HIIT and RT training, no changes were observed in the body weight of the training subjects, suggesting again that this training does not seem to be effective in reducing weight. During the HIIT-only period, the thigh circumference (cm) of subjects did not change; it was, however, significantly enlarged after HIIT and RT. These results may suggest that HIIT does not affect muscle volume for young active men and that only RT can induce hypertrophy of the recruited muscles. Actually, most of the subjects complained that their jeans pants no longer fit. I bought new jeans for them.

Different protocols for high-intensity intermittent training

“Tabata training” was originally developed by an experienced coach, Irisawa Koichi, who examined athletes’ condition during different training protocols. I have been thinking that the training should really be called the Irisawa training. I wanted to develop my “Tabata training” according to a hypothesis based on physiology, which is my specialty. To develop new HIIT exercises, we compared several high intensity intermittent exercise (HIIE) protocols in terms of recruitment of aerobic and anaerobic energyreleasing systems (Kouzaki and Tabata, 1998) (Fig. 4.3).

Fig. 4.3 Different protocols of high-intensity intermittent exercise (black bars depict exercise time at intensity of % V̇o 2max (vertical axis: Exercise intensity %, horizontal axis: exercise time (s)) ( Kouzaki and Tabata, 1998 ).

The exercise protocol resembled Tabata training, but there were several hypotheses to test these specific regimens. The hypothesis was based on the experimental data (Kouzaki and Tabata, unpublished). To identify a better exercise intensity for a new Tabata training protocol than the authentic Tabata training (170% V̇o2max), we wanted to incorporate higher exercise intensity, because we hypothesized that the higher the intensity, the higher the oxygen uptake, even for extremely high intensity (i.e., supramaximal and short [20-s] duration). However, if the exercise intensity of the first 20-s bout were higher than 170% V̇o2max, subjects could not perform six or seven 20-s bouts with only 10-s rest between sets, exercise intensity during later sets of 20-s exercise would be reduced gradually. To design the new training, we measured oxygen uptake during supramaximal intensity exercises. Nine male students (age: 22 ± 2 years; height: 171 ± 5 cm; weight: 66.2 ± 6.7 kg; V̇o2max: 53.8 ± 2.6 mL/kg/min; MAOD: 72.6 ± 4.1 mL/kg) exercised on a bicycle ergometer to exhaustion for a fixed time: 10 s (12 ± 2 s), 20 s (20 ± 1 s), 30 s (29 ± 1 s), 40 s (39 ± 1 s), 60 s (68 ± 6 s), and 120 s (131 ± 13 s). The exercise intensity corresponded to 284 ± 16, 256 ± 18, 223 ± 11, 187 ± 7, 148 ± 8, and 130 ± 6% V̇o2max, respectively. As shown in Fig. 4.4, oxygen uptake during the exercises increased from the onset to the end (Kouzaki and Tabata, unpublished). Oxygen uptake up to 20 s of exercise at 40–20 s to exhaustion (180%–250% V̇o2max) did not differ, but was higher than that observed during the 60 s and 120 s to exhaustion (150% and 130% V̇o2max). More specifically, oxygen uptake during the first 10 s of exercise depends on exercise intensity up to 30 s (220% V̇o2max), then plateaus at higher intensities with shorter duration to exhaustion (Fig. 4.5). Although there have been arguments as to whether or not pulmonary oxygen uptake at exercise onset represents metabolism in exercising muscles (Krogh and Lindhard, 1913; Casaburi et al., 1989), these data may suggest that exercise intensity over 220% V̇o2max stimulates the aerobic energy-releasing system maximally.

Fig. 4.4 Time course of oxygen uptake during exercises of various durations to exhaustion at various intensities (Kouzaki and Tabata, unpublished).

Fig. 4.5 Relationship between oxygen demand and oxygen uptake during 10-s period after the start of various exhaustive exercises, ** P < 0.01 (Kouzaki and Tabata, unpublished).

Therefore, we first designed a protocol of first and second sets at 220% V̇o2max, third and fourth sets at 200% V̇o2max, and fifth and sixth sets at 180% V̇o2max. However, oxygen deficit accumulated during extremely high intensities (> 180% V̇o2max) does not amount to MAOD, suggesting that such exercise does not maximally stimulate the anaerobic energy-releasing system. Since the intensity of the last set of the described protocol is 180% V̇o2max, oxygen deficit during such intermittent exercise might not reach MAOD. Therefore, we designed a second protocol as first and second sets at 200% V̇o2max, third and fourth sets at 180% V̇o2max, and fifth and sixth sets at 160% V̇o2max. We found that oxygen uptake during the first to fourth exercise sets of one of the proposed HIIT protocols, IDE200 (Intensity: 200% V̇o2max [first and second sets]; 180% V̇o2max [third and fourth sets]; 160% V̇o2max [fifth and sixth sets]; exercise time: 20 s; rest time: 10 s) (Fig. 4.3) was significantly higher than that observed for Tabata training (Fig. 4.6). This suggested that IDE200 may stimulate aerobic energy-releasing systems more and faster than the original Tabata training (Kouzaki and Tabata, 1998).

Fig. 4.6 Oxygen uptake during IE170 (Tabata training) and IDE200. *Indicates a significant difference in oxygen uptake between IE170 and IDE200 at P < 0.05 ( Kouzaki and Tabata, 1998).

Peak oxygen uptake during the four intermittent exercise protocols was not different among the intermittent exercises (IE170 [Tabata training]: 47.6 ± 4.5 mL/kg/min; IE200: 49.1 ± 3.7 mL/kg/min; IE190 48.8 ± 3.9 mL/kg/min; IDE200: 49.1 ± 4.5 mL/kg/min). In addition to the aerobic energy-releasing system, IDE200 was found to be the most demanding on the anaerobic energy-releasing systems. This was because the oxygen deficit during IDE200 was not significantly different from that observed during IE170 (Tabata training). Furthermore, peak lactate concentration after IDE200 was significantly higher than that observed for IE170 (Fig. 4.7).

Fig. 4.7 Oxygen deficit accumulated during a constant intensity exercise and four intermittent exercises, and peak blood lactate concentration after the exercises (130CE: constant intensity exercise at 130% V̇o 2max ). ** indicates a significant difference compared to CE130 at P < 0.01. ¶ indicates a significant difference compared to IE170 (Tabata training exercise) at P < 0.05. † and †† indicate a significant difference compared to IE200 at P < 0.05 and 0.01, respectively ( Kouzaki and Tabata, 1998).

To test the effects of IDE200 on aerobic and anaerobic energy-releasing systems, we did an 8-week training study using IDE200 five days per week. The subjects (age: 22 ± 1 years; height: 169 ± 3 cm; weight: 69.0 ± 6.7 kg; V̇o2max: 52.6 ± 5.4 mL/kg/min; MAOD: 68.2 ± 8.7 mL/kg) were encouraged to complete 6 sets. When they could complete sixth sets of exercise at an intensity of 160% V̇o2max, the intensity of all sets was increased by 11 watts. As shown in Fig. 4.8, MAOD increased significantly, by 32%, while V̇o2max was also elevated significantly by 14%. These effects on aerobic and anaerobic energy-releasing systems were comparable to those observed in the original Tabata studies (Tabata et al., 1996).

Fig. 4.8 Effects of 8-week high-intensity intermittent training on maximal accumulated oxygen deficit (upper panel) and V̇o 2max (lower panel) (horizontal axis: training duration (w)). * and ** indicate a significant difference at p 70% V̇o2max) exercise on health promotion was sufficient, even though he, himself, loved stationary rowing machine exercise at a rather high intensity, and loved watching high-intensity sports like boxing. He also used interval exercises for animal experiments to deplete muscle glycogen in rats (Holloszy, 1967). When I met Dr. Holloszy at the National Institute of Fitness and Sport in Kanoya, Japan, in 1991, I showed him rough drafts of the results of the two Tabata training papers. After my presentation, he quickly said “I have no idea about exercise where the intensity is more than V̇o2max.” I speculate that there were two reasons for this: (1) he was not interested in supramaximal exercise the intensity of which could not be quantified; and (2) he was skeptical of possible health-related outcomes, especially on longevity, from even vigorousintensity exercises. In this context, epidemiological research on the effects of HIIT on longevity will be challenging. Several epidemiological studies have reported that people who engaged in strenuous physical activities had a lower risk of colon cancer (Kono et al., 1991). Whether for or against, however, it is important to collect evidence without preconceptions as to whether HIIT may be beneficial for longevity. I am not a religious leader who recommends only one way of thinking. As a scientist, I would like to increase the variety of exercises for people with various interests. I am not recommending only Tabata training to all people. I am simply presenting the scientific evidence for Tabata training and encouraging people to choose the exercises that interest them the most. Any exercise is effective and beneficial for health promotion. So, if one finds, in one’s life, an exercise program that is interesting and enjoyable, it will benefit both your life and health. Tabata training is one option! The important thing is that people should not be sedentary with no exercise habits! The late Hiroaki Tanaka recommended very lowintensity exercise training (Tanaka and Jackowska, 2016). Everybody should try aerobics exercise, resistance training, and so on. Furthermore, we know that nonexercise physical activity including sweeping, playing with kids, and gardening are also effective in preventing lifestyle-related diseases, including diabetes, stroke, cardiovascular disease, and cancer (Tabata, 2006a,b).

Determining the side/adverse effects of Tabata training

As noted above, it also is necessary to investigate the possible detrimental side effects of Tabata training and other types of HIIT and to find solutions to prevent such side effects by diet/supplements, other physical conditioning, and/or other methods. In terms of Selye’s general adaptation hypothesis (Selye, 1951), we observed serum cortisol concentration in the morning during a different kind of HIIT period (Tabata et al., 1989). The HIIT consisted of bicycle ergometer exercise at an intensity of 90% V̇o2max. Duration was calculated by (lean body mass [LBM:kg] × 10 kcal)/(oxygen uptake of the training exercise [L/min] × 5 kcal) (~ 25– 30 min). If subjects became exhausted during the exercise, they were told to rest for 5 min and then restart the exercise. They trained five days per week for seven weeks. At 09:00 am every Tuesday, blood was drawn. After a week of training, serum cortisol concentration had increased in the early morning (p < 0.05). It continued rising until the fourth week, and then fell. There was no significant difference in the concentration of this hormone between the pre- and posttraining levels. Commonly, the term “adaptation” has been used to refer to the stage that is characterized by a return to prestress level of circulating cortisol concentration during continuous or repeated exposure to a stressful stimulus. From this perspective, Fig. 5.1 suggests that adrenocortical adaptation began the fifth week and was completed by the sixth week of the training period. At the same time, we observed a significant decrease of serum lactate dehydrogenase and creatine kinase activity, which were increased during the first week (unpublished data). This result suggests that, in human beings, adaptation in the hypothalamus–pituitary–adrenal axis occurred relatively later, even after high blood cortisol concentration was observed.

Fig. 5.1 Effects of HIIT on morning serum cortisol ( Tabata et al., 1989 ).

Previous studies suggested that it was not the total amount of exercise but exercise intensity that was the dominant factor inducing high resting blood cortisol concentration during a period of physical training. Since the intensity of Tabata training (170% V̇o2max) is higher than that of this study (90% V̇o2max), serum cortisol concentration in the morning might have been even higher with Tabata training. If so, Tabata training would be regarded as more stressful in terms of resting serum concentration of cortisol in the morning. The effects of Tabata training on morning serum cortisol concentration should be assessed to determine whether Tabata training is in fact more stressful than other forms of endurance training. Ambroży et al. (2021) reported that strength and endurance training based on HIIT (circuit training) increased morning testosterone levels in men aged 35 to 40 years, while mean cortisol concentrations did not change significantly after the training experiment. Since this study did not measure serum cortisol concentration in the morning during the training period, it is not known whether morning cortisol concentration changed at all, or if it increased before returning to pretraining values at the end of the investigation, as was observed in our study. Further experiments are needed to determine this. As high-intensity exercise may reduce immunological functions (Nieman, 1994), we can speculated that in terms of any cancer prevention that can be initiated by low immunological function, high-intensity exercise training may have no or adverse effects. However, as shown in the previous chapter, Tabata training may help to prevent colon cancer by enhancing the production and elevating the blood concentration of secreted protein acidic and rich in cysteine (SPARC), a myokine that decreases the number of aberrant crypt foci (ACF), which are the first step of colon cancer induction. It does this by inducing the apoptosis of ACF in the colon (Aoi et al., 2013). These biological results may explain the epidemiological finding that vigorous exercise may help prevent, not worsen colon cancer (Matsuo et al., 2017). Another recent investigation suggested that this result is evidence that Tabata training does not reduce immunological function (Harnish and Sabo, 2016). High-intensity exercise may deteriorate quality of sleep if is done in the late evening due to elevated sympathetic activity. To ensure good sleep, strategies for reducing sympathetic activities without drugs are needed. Some studies have suggested that HIIT can improve sleep (Jahrami et al., 2021). A school teacher told me that they taught elementary school kids to do Tabata-style body-weight training, and afterwards the kids found that they could get to sleep earlier, suggesting that Tabata training may be helpful in establishing a healthy lifestyle, especially “get up early and eat breakfast, and sleep early.”

Study of basic research on Tabata and Tabata-style training

In order to prescribe science-based training, more basic research on HIIT involving Tabata training is needed to further delineate the mechanisms underlying the beneficial effects on sport-oriented and

health-oriented outcomes, both of which contribute to improved quality of life. Since Tabata training induces the expression of proteins related not only to sports performance but also to health promotion (Miyamoto-Mikami et al., 2018), more research on the possible effects of Tabata training and other training that uses a Tabata protocol on health outcomes is expected. Again, I want to emphasize the research on Tabata-style training conducted with rats, which elevated cellular signals to the highest level, as a tool for finding cellular signals induced by exercise and elucidating their effects on cell metabolism and function after exercise training in the future.

Study on motivation for Tabata training

Tabata training is very demanding (Foster et al., 2015), and thus participation in Tabata training might be limited to highly motivated athletes who are familiar with the scientific evidence regarding Tabata training or are persuaded to engage in the training by coaches who know the Tabata training research findings. In a study of women who were simply recreationally active, their perceived enjoyment of a weight-bearing HIIT increased from pre- to posttraining, suggesting that chronic exposure to such training may elevate people’s enjoyment of the training (Funch et al., 2017). In addition, the dropout rate in the Chuiesiri et al. (2018) study of obese preadolescent boys was quite low (6.3%), and Logan et al. (2016) reported a high adherence rate among inactive volunteer adolescents to an all-out-type HIIT using various types of weight-bearing exercise; 90% of their subjects completed the regimen. These rates may indicate that the HIIT was tolerable and positively accepted. However, the results of another investigation suggested that training at high intensities would be rated as not enjoyable (Ekkekakis et al., 2008). A psychological inquiry regarding study subjects’ enjoyment of Tabata training is required. The development of low-intensity training using a Tabata protocol and training at the same intensity as that used in Tabata training but with a smaller number (3–4 sets) of exercise bouts (Fujimoto et al., 2010) is expected; with a lower-intensity or a smaller number protocol, subjects would more easily enjoy the training. To avoid a mismatch of Tabata training and potential participants, it might be interesting to find gene(s) that enhance or diminish enjoyment of Tabata training. Further, genes that maximize the effects of Tabata training on participants should be identified.

Importance of delivering the science of Tabata training to athletes

On the first day of my freshmen class every year, I ask the students, “Have you heard of Tabata training?” before introducing myself. Since I was a dean until March 2016, I was introduced to freshmen at the entrance ceremony. My term as dean ended in April 2017, however, so I now introduce myself on the first day of class. In 2017, less than 10% of students answered “Yes.” This April, it was

40%–60%. I think this number might be higher in the USA and other countries. My wife Meiko worked as a tour guide for foreign guests before the COVD19 pandemic. When she asked such people “Do you know Tabata training,” she estimates that one in 20 guests answered “Yes.” Tabata training is quite popular these days. This year, I have no freshmen class. Instead, I provided freshman with an online video introducing myself and Tabata training. Several students wrote that they had had a hard time before Tabata training in high school. They may well hate Tabata training. Other students confessed that if they had known the superiority of Tabata training, they would have concentrated and performed the training as hard as possible. My video was only 15 min long, but they understood what I wanted them to. Therefore, for the best training effects, I would like to ask coaches to explain the mechanisms described in this book to their players/students or to ask them to learn them themselves. One student confessed that when he felt the exercise was desperately hard, he screamed “Who introduced such crazy hard training?” According to a student survey, I might be hated by millions of young athletes. So, for my sake, please inform your players/students about the theory of Tabata training so that they will be convinced and motivated by scientific knowledge. As mentioned in the previous chapter, nonexhaustive Tabata-style trainings have effects on the aerobic energy-releasing system. However, to increase MAOD, maximal effort appear requisite. One student suggested that mutual verbal encouragement allows them to tolerate Tabata training. I think that it is necessary to teach the science of hard training, including Tabata training, not only to adults but also to kids for in order to achieve the best training results.

More rink-side study

As described in Chapter 3, the IE1 training protocol (Tabata training) emerged during discussions between a top coach with an exceptional instinct for developing new training methods based on interactions with athletes and an exercise physiologist who was good at scientifically analyzing the characteristics of exercise. Tabata training was thus initiated both as a clinical (practical) and bedside (rink-side or gym-side) training. After the results described above were reported to Mr. Irisawa, he stopped using the other training (IE2) for his skaters and concentrated on the IE1 protocol (i.e., Tabata training). To develop better training methods, we need to continue to confer with good coaches in the future. This is especially important and recommended to young researchers. In conclusion, I have summarized the evidence for Tabata and Tabata-style training in this book. I plan to collect more data that will be useful to for prescribing Tabata and Tabata-style training appropriately for people with various fitness levels. Other researchers have also been conducting studies of Tabata and Tabata-style training that may help people maintain or improve their fitness during COVID19 (Schwendinger and Pocecco, 2020). If possible, I would like to write a second edition of this book in the future that will include this data. I am sure that I and other researchers will continue to find meaningful new evidence, which will, I hope, motivate sport- and health-oriented people to take part in new Tabata and Tabata-style training in the future.

References

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Index

Note: Page numbers followed by f indicate figures and t indicate tables.

A

Aberrant crypt foci (ACF) 87, 134

Adenosine diphosphate (ADP) 6

Aerobic energy releasing system, Vo2max 6–15, 7f, 61

athletics-related fitness 11, 11f

health-related fitness 12

limiting factors 12–14, 12–14f

maximal oxygen uptake 8–10, 8–10f

training effects 14–15

Aerobic

exercise 80–81

training (AT) 94–95

AMPK (5′AMP-activated protein kinase) 79

Anaerobic energy-releasing system, MAOD 15–27, 16f

biochemical basis 23–25, 23–26f

exercise 25–27, 26f

maximal accumulated oxygen deficit 19–21, 19–20f

oxygen deficit, 30-s to 10-min exhausting exercise 16–19, 17f, 21–23, 21–23f

training 27

B

Burpee jumps (BJ) 107–108

C

Ca²+ 79

CaMK activation 81

Cortisol 133

COVID19 pandemic 100–101, 106

Creatine phosphate 15–16

Cyclic AMP response element (CRE) 82

E

Epilogue, tabata training

athletes 135–136

determining side/adverse effects 133–134, 133f

endurance effect 129

future research 129–137

HIIT longevity 131–132

interesting features 129

motivation 135

muscle fiber recruitment 129

rink-side study 136–137

tabata-style training, research 135

Epitrochlearis muscle 78, 78–79f, 85f

Excess post exercise oxygen consumption (EPOC) 34–35, 59–60

Exercise intensity 5–6

F

Fitness tests, exercise physiology, biomechanics 37–38

G

General adaptation hypothesis 131

GLUT4 (glucose transporter 4) 3, 50, 79, 81, 85–87

Graded exertion test (GXT) 20–21

H

Hermansen, L. 21, 34–36, 38, 47–48

High-intensity intermittent/interval training (HIIT) 1, 48–49

Holloszy, J.O. 36, 76–77, 77f, 131–132

I

Institute of Muscle Physiology (Oslo, Norway), 1983 38–42, 39–42f

Irisawa’s training protocols, analysis 43–52, 44–47f, 49f, 63

J

Jumping jacks (JJ) 107–108

L

Lactate 15–16

Low-intensity exercise (LIE) 81

M

Maximal accumulated oxygen deficit (MAOD) 1–2, 130

Mitochondrial DNAs 81

Moderate-intensity exercise (MIE) 75–76

Mountain climber (MC) 107–108

N

National Institute of Fitness and Sports in Kanoya (NIFSK) 2, 60

National Institute of Health and Nutrition (NIHN) 3, 60

Nomenclature 27–29

HIIT, SIT 28–29

interval, intermittent 28

tabata/tabata-style training 29

O

Oxygen deficit 33–37

P

Parathyroid hormone (PTH) 96–97

PGC-1α (Peroxisome proliferator-gamma coactivator-1α) 81

Phosphofructokinase (PFK) 91–92

Proteomic technique 85

Pulse wave velocity (PWV) 94–95

Pushups (PU) 107–108

R

Resistance training 50–51, 59, 61, 79–80

Ritsumeikan University 60

S

Secreted protein acidic and rich in cysteine (SPARC) 88

Sprint interval training (SIT) 28

Squat jumps (SJ) 107–108

T

Tabata training 1, 59

athletes, bodyweight 100–106

baseball players 105–106

female badminton players 104–105

female football players 104, 104f

kendo players 103–104

lacrosse players 102–103, 102f

rugby players 103

track 101

bike training, Vo2max

college swimmers 70

MAOD 69–70

sprint bike, college skiers 71

blood lactate, sport performance 118–120, 119–120f

bone metabolism 96–99, 97–99f

circulation 93–96, 95–96f

colon cancer prevention 87–91, 87–92f

excess postexercise oxygen uptake (EPOC) 73–87, 74–75f

glucose metabolism 76–78, 77–79f

nonexhaustive HIIE, GLUT4 85–87, 86f

protein expression 79

skeletal muscle metabolism 79–85, 80f, 82–85f

gene expression profile, muscle adaptation 91–93, 94f

health-oriented people, bodyweight 106–110

exercise intensity 106–109, 107f, 108–109t

Vo2max 109–110

high-intensity intermittent, protocols 63–67, 64–68f

hints 71–73

IE1, evolution 59–61

nonexhaustive weight-bearing, Vo2max 110–116

bicycling 110–111, 111t, 112f

burpee jump 113–114

cardiorespiratory fitness, breast cancer survivors 115–116

hints 116–118, 116–117t

running 111–112, 113f

Sawai 114–115

practical procedures 53

resistance training, MAOD, Vo2max 61–63, 62f

running, Vo2max 68–69

active young males 68–69

runners 69

small intestine 99–100

style training

Kendo 103

lacrosse 102

Rugby 103

Training camp, top skaters 1989 42–43

U

Universal Studios International 108

V

Vascular endothelial growth factors (VEGF) 93–94

Vastus lateralis (VL) muscle 89

W

Wingate test 61–63

Z

Zátopek, E. 5