
Physiology News Magazine
Physiological determinants of success in track athletics
In the first of a series of articles on exercise physiology, Andrew Jones considers what makes an Olympic champion as athletes prepare to compete in the Athens Games
Features
Physiological determinants of success in track athletics
In the first of a series of articles on exercise physiology, Andrew Jones considers what makes an Olympic champion as athletes prepare to compete in the Athens Games
Features
Andrew M Jones
Reader in Applied Physiology, Manchester Metropolitan University, Alsager, UK and Consultant Exercise Physiologist to UK Athletics
https://doi.org/10.36866/pn.54.8
The track athletics events (100 m, 200 m, 400 m, 800 m, 1,500 m, 3,000 m steeplechase, 5,000 m and 10,000 m), along with the marathon, will undoubtedly be among the ‘showpieces’ at the forthcoming Olympic Games in Athens. The male and female winners of these rather disparate events are rightly acknowledged as possessing extraordinary physical capabilities, which result from a combination of both genetic and training-related factors. The purpose of this short article is to briefly review the physiology of elite level performance in track athletics or, in other words, to consider the physiological factors which predispose Olympic athletes to be ‘citius’(from the Olympic motto ‘citius, altius, fortius’ – faster, higher, stronger) than their non-athletic counterparts.
The limitations to athletic performance and the main causes of fatigue are closely linked to the principal metabolic pathways by which adenosine triphosphate (ATP) is re-synthesised to meet the energy demand of the exercise. At the onset of a race, the ATP stored within the contracting muscles is broken down to release energy to fuel muscle contraction. The average running speed that can be sustained in a race, and therefore the average rate of ATP turnover, is typically highest in the 100 m and falls as the race distance increases. For example, in the 100 m race (which has a duration of < 10 s in elite male sprinters), the average energy expenditure is ~ 4 kJ.s-1 whereas in the marathon (which has a duration of ~ 2 h and 5 min in elite male runners), the average energy expenditure is ~ 1.7 kJ.s-1. Obviously, therefore, it is important that ATP is re-synthesised at a very high rate to enable the attainment of the maximal running speeds required in sprint events, and for ATP to be re-synthesised at a moderately high rate but for long periods of time to enable the maintenance of the high (but sub-maximal) running speeds in long distance events.
The human body has a number of metabolic pathways which are well suited to meeting the demands of both high-intensity short-duration exercise and low-intensity long-duration exercise. What distinguishes an Olympic athlete from his or her sedentary counterpart is the athlete’s extraordinary ability to liberate energy at a rapid rate from the appropriate metabolic pathway(s) and to limit and tolerate the development of fatigue as the race progresses. In the 100 m race, phosphocreatine (PCr) hydrolysis is the principal mechanism by which ATP is re-synthesised. This energy pathway can produce ATP at a very high rate, though only for a short period of time and, as such, it is ideally suited to meet the energy demand of sprinting. The maximal rate at which ATP can be broken down at the myosin ATPase to support muscle contraction and the rate at which ATP can be re-synthesised through PCr hydrolysis (and other metabolic pathways) are therefore the principal determinants of success in sprint events. It is therefore not surprising that elite sprinters generally possess an extremely high proportion (and a large number) of ‘fast-twitch’ fibres (which have a high activity of myosin ATPase and a high maximum power output compared to ‘slow-twitch’ fibres) in their locomotory muscles (Costill et al. 1976).
During maximal-intensity exercise, the finite intra-muscular stores of PCr can only support ATP re-synthesis for a few seconds so that other metabolic pathways become progressively more important as sources of ATP as the race distance increases. For example, during 200 m and 400 m sprinting, the O2-independent breakdown of muscle glycogen is responsible for the majority of the ATP re-synthesised. The high rates of muscle glycogenolysis in these events, however, results in a significant increase in lactic acid production. The consequent reduction in muscle pH has been suggested to be a cause of muscle fatigue in some circumstances (but see Westerblad et al. 2002). ‘Anaerobic glycolysis’ also makes an important contribution to ATP re-synthesis in the middle distance running events and the accumulation of lactate (and the fall in pH) is a possible cause of fatigue in these events too. In the ‘long sprints’ (200 m, 400 m and also, arguably, 800 m), therefore, the capacity to re-synthesise ATP at a rapid rate through ‘substrate-level phosphorylation’ and to tolerate the consequent disturbances to homeostasis are likely to be important determinants of performance.
Anaerobic glycolysis can produce ATP at a high rate, but it is unable to sustain this rate for sufficiently long to be the principal energy supply pathway for events beyond the 400 m. Rather, the energy supplied in middle distance and long distance running events derives principally from oxidative phosphorylation. At the onset of exercise, muscle oxygen consumption increases immediately but, in the elite endurance athlete, it takes approximately 1-2 minutes before the oxygen uptake (VO2) approaches the ‘steady-state’ requirement for the running speed being maintained. This means that some athletic events are over before oxidative metabolism can make an appreciable contribution to energy supply. It should also be noted that, in the middle distance running events, the ATP turnover rate required will exceed the maximal ATP turnover rate that can be supported by oxidative metabolism. Nevertheless, the maximal rate at which an athlete can re-synthesise ATP through oxidative pathways (denoted by his or her ‘VO2 max’) is probably the most important determinant of performance in events from 800 m to 5,000 m (and possibly 10,000 m). This is consistent with the fact that the VO2 max values of elite endurance athletes (70-90 mlO2.kg-1.min-1) are typically twice those of age-matched sedentary people.
The 10,000 m track race and the marathon are run at intensities below the VO2 max (i.e. typically at 80-95 % VO2 max) and other ‘sub-maximal’ physiological factors therefore become progressively more important in these events (Jones & Doust, 2001). One of these factors is ‘running economy’, which represents the steady-state oxygen cost of running a given distance (km) per unit body mass (kg). The energy cost of running at the same speed varies considerably between individuals but it is generally lower (i.e. running economy is better) in athletes. Possessing good running economy is important in long distance races because it means that any absolute VO2, and therefore fraction of the VO2 max, that is sustained equates to a higher running speed. The running speed above which muscle lactate production exceeds lactate clearance also correlates strongly with long distance running performance. Furthermore, the concept of ‘critical velocity’, which is given by the asymptote of the hyperbolic velocity vs. time to fatigue relationship, is useful in modelling performance potential in athletes (Fukuba & Whipp, 1999).
Finally, the ability to utilise fat as substrate for oxidative metabolism is important in sparing the oxidation of the limited endogenous carbohydrate stores. The depletion of muscle glycogen has been linked to the fatigue process, particularly in the marathon (Karlsson & Saltin, 1971). Again, in light of the preceding discussion, it is interesting to note here that endurance athletes generally have a high proportion of ‘slow-twitch’ muscle fibres in their locomotory muscles. Slow-twitch fibres generally have greater mitochondrial and capillary density, a greater capacity for fat metabolism, and may be more efficient at low forces relative to ‘fast-twitch’ fibres (Bottinelli & Reggiani, 2000).
It should be re-emphasised here that the energy pathways discussed above do not operate in isolation; rather, they are all activated at the onset of exercise. However, the relative contribution of the various energy pathways to the total ATP turnover rate will vary with the intensity and duration of exercise (which are themselves co-dependent). One important determinant of performance (at least for events > 400 m), which has perhaps been overlooked previously, is the rapidity with which oxidative phosphorylation can be ‘switched on’ at the start of a race. The rise in VO2 following the onset of exercise is generally much faster in athletes compared to their sedentary counterparts, but this factor may even partially discriminate performance differences between athletes. In the transition from a standing start to, say, 1,500 m race pace, faster ‘VO2 kinetics’ will reduce the depletion of PCr and the accumulation of lactate and hydrogen ions, and reduce fatigue. Furthermore, the energy from substrate-level phosphorylation that is ‘spared’ as a consequence of the fast VO2 response might be used subsequently in a sprint finish.
This article has highlighted the physiological factors (principal energy pathways and possible causes of fatigue) that contribute to the determination of performance in the athletic track events. The physiological characteristics and capabilities of the Olympic athlete derive from a combination of genetic predisposition and arduous physical training. While it is the author’s belief that these physiological factors represent some of the most important determinants of athletic success, it should be acknowledged that biomechanical, psychological, tactical, nutritional and environmental factors also have the potential to impact upon performance to a greater or lesser extent. Knowledge of the physiological demands and limitations to performance enables the exercise physiologist to assist in the construction of appropriate training programmes for athletes specialising in different events and to advise athletes on other (legal) performance enhancing strategies. These strategies include supplementation with creatine to increase the PCr content of muscle (for sprinters), with bicarbonate to increase buffering capacity (for middle distance runners), or with carbohydrate to increase muscle glycogen storage (for long distance runners). With the forthcoming Olympic Games taking place in the heat of Athens, appropriate strategies for acclimatisation and hydration are also very important (this is the topic of the next article in this series). There are clearly a large number of both physiological and non-physiological factors that can determine the outcome of a race such that the relationship between an athlete’s physiological capacities and their likelihood of success is not straightforward. While this can be a little frustrating for the physiologist it is, of course, good news for spectators, broadcasters, and bookmakers.
References
Bottinelli R, Reggiani C (2000). Human skeletal muscle fibres: molecular and functional diversity. Progress in Biophysics and Molecular Biology 73, 195-262
Costill DL, Daniels J, Evans W, Fink W, Krahenbuhl G, Saltin (1976). Skeletal muscle enzymes and fiber composition in male and female track athletes. J Appl Physiol 40, 149-154.
Fukuba Y, Whipp BJ (1999). A metabolic limit on the ability to make up for lost time in endurance events. J Appl Physiol 87, 853-861.
Jones AM, Doust JH (2001). Limitations to submaximal exercise performance. In Eston R & Reilly T. Kinanthropometry and Exercise Physiology Laboratory Manual, Vol 2: Exercise Physiology.. Routledge, London.
Karlsson J, Saltin B (1971). Diet, muscle glycogen and endurance performance. J Appl Physiol 31, 203-206.
Westerblad H. Allen DG, Lannergren J (2002). Muscle fatigue: lactic acid or inorganic phosphate the major cause? News Physiol Sci 17, 17-21.