Acute and chronic responses of skeletal muscle to endurance and sprint exercise. A review.

Review Article

Sports Medicine 10 (6): 365-389, 1990 0112-1642/ 90/ 0012-0365/ $12.50/0 © Adis International Limited

All rights reserved. SPORT2338

Acute and Chronic Responses of Skeletal Muscle to Endurance and Sprint Exercise A Review

Peter J. Abernethy, Robert Thayer and Albert W. Taylor School of Sport and Leisure Studies, University of New South Wales, Sydney, New South Wales, Australia, School of Physical Education and Recreational Studies, Lakehead University, Thunder Bay, Ontario, and Faculty of Physical Education and Department of Physiology, Faculty of Medicine, University of Western Ontario, London, Ontario, Canada

Contents

Summary .... ..... ...... .. .. .. .. .. ............................................................................. ............................. 365 I. Exercise Stress and the Influence on Skeletal Muscle Morphology .............. .......... .. ...... 368 1.1 Contractile Properties and Fibre Proportion .................... ................ ............ .............. 368 1.2 Fibre Areas ............ ...... ... .... .. ........................ ................................... ... ....... ..................... 369 1.3 Ultrastructure ...... .. ........... ........ .. ... .. .................................. ................... .......................... 371 2. Intramuscular Substrate Used in Exercise ............................... ....... ........... ........................ 372 2.1 Glycogen Metabolism ......... ... ........... ........................................................ ................. ... 372 2.2 Lipid Metabolism ......... ... ...... .. ........................ .... ............... .......... .. ... .... ... ................. .... 375 2.2 Amino Acid Metabolism ............ ............................................ .. .................................... 377 3. Enzymatic Response of Skeletal Muscle to Exercise and Training ........ .......... ............... 379 3.1 Glycolytic Enzyme Response .......................................... ......................................... .... 379 3.2 Oxidative Enzyme Response .. ............................................ ...................... .................... 381 4. Phosphagen Response .. ............... ..... .. .... ................ ..................................... ........................ 382 4.1 Phosphagen Response to Endurance Training ............................................. .............. 382 4.2 Phosphagen Response to Sprint Training ...................... ..... ..................... ................... 383 4.3 Acute Phosphagen Response to Endurance Exercise ......................... ........................ 383 4.4 Acute Phosphagen Response to Sprint Exercise ........................... ....... ....................... 383 5. Conclusion ......... .. .. ....... ............. ........................... ......... ................... .. ........ .... ... ...... ... .......... 384

Summary

Skeletal muscle adapts to the stress of endurance and sprint exercise and training. There are 2 main types of skeletal muscle fibre - slow twitch (ST) and fast twitch (FTa, FTb, FTc). Exercise may produce transitions between FT and ST fibres. Sprint training has decreased the proportion of ST fibres and significantly increased the proportion of FTa fibres, while endurance training may convert FTb to FTa fibres, and increase the proportion of ST fibres (i.e. FTb -+ FTa -+ FTc -+ ST). However, the high proportion of ST fibres documented for elite endurance athletes may be simply the result of natural selection. ST fibres function predominantly during submaximal exercise, whereas FT fibres are recruited as exercise intensity approaches V02max and/or glycogen stores are depleted. Long distance runners have greater ST and FT fibre areas than untrained controls. How-

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ever, doubt remains as to whether the ST or FT fibre area is greatest in endurance athletes. Increases in FT fibre area seem to occur during the first 2 months of training, whereas ST fibre areas appear to increase after 2 to 6 months of training. Sprint training leads to the preferential use of FT fibres and male, but not female sprinters have larger FT fibres than untrained controls. Mitochondrial proteins and oxidative enzymes, as opposed to V02max, are important determinants of the duration of endurance exercise. Endurance training increases intramuscular glycogen stores in both FT and ST fibres and produces a 'glycogen-sparing' effect which is characterised by an increased free fatty acid (FFA) metabolism. The activity of glycogen synthase is also increased by endurance training. Sprint training increases glycogen concentrations similarly in all fibre types, reduces the rate of glycogen utilisation at submaximal workloads and allows supramaximal workloads to be maintained for longer periods of time. During endurance exercise the pattern of glycogen depletion varies between muscle fibre types and between muscle groups. Glycogen stores in ST fibres are utilised initially, followed by stores in FTa then FTb fibres. Sprint activities are associated with a much greater rate of glycogen depletion. However, it is unlikely that glycogen depletion causes fatigue during sprinting. Sprint work is associated with a preferential depletion of glycogen from FTb then FTa and ST fibres. Endurance training appears to increase triglyceride stores adjacent to mitochondria and ST fibres have greater triglyceride stores than FT fibres. Endurance exercise is associated with a preferential use of triglycerides from ST fibres and endogenous triglycerides may account for over 50% of the total lipid oxidised during exercise. The oxidation of fat is unlikely to be a significant factor in sprinting tasks. Skeletal muscle has an increased capacity to form alanine from pyruvate after endurance training and leucine oxidation may also be enhanced. The largest increase in amino acid metabolism during exercise occurs from intra- rather than extramuscular sources. The pool of free amino acids is used by the glucose-alanine cycle and during BCAA oxidation. However, prolonged physical activity reduces the amino acids available for these metabolic pathways, suggesting that the use of protein as an energy substrate is limited. In contrast, short term exercise is associated with high plasma alanine levels and thus, it is likely that BCAA oxidation increases during sprinting. Glycolytic and oxidative enzyme responses may be significantly altered by both endurance and sprint training. Endurance training may increase phosphofructokinase (PFK), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) activity, whereas sprint training may increase PFK, phosphorylase, lactate dehydrogenase and glyceraldehyde dehydrogenase activity. Creatine phosphate (CP) activity and ATP levels are higher in FT than ST fibres. Endurance training reduces CP and ATP depletion at submaximal workloads, but also increases CP and ATP concentrations. Superior sprinters are able to utilise phosphagens quickly and more completely than lesser competitors over distances up to 80m, but this may result from genetic predisposition rather than training. Extreme and prolonged training may produce skeletal muscle fibre type conversion. Additionally, acute and chronic exercise alter skeletal muscle substrate, metabolism and phosphagen profiles thus influencing physical performance and sporting success. Obviously, such skeletal muscle changes are important to coaches and athletes wishing to design training programmes to maximise the performance of a specific motor activity.

During the past two decades the application of science to sport has become increasingly prevalent. Various exercise regimens have been developed to elicit specific training adaptations. Many of the

training programmes adhere to either an endurance or sprint format, or in some instances a combination of the two. For many years research results were speculative as to the effects of various

Skeletal Muscle Responses to Exercise

training programmes on the metabolism of human skeletal muscle. The development of the muscle biopsy technique (Bergstrom 1962) has permitted direct investigation of skeletal muscle. It is now possible to determine how muscle adapts to the stress of various training formats. The present review article compiles the available research related to the acute and chronic response of skeletal muscle to endurance and sprint training formats. The ability of humans to perform various forms of exercise resides in the metabolic and contractile properties of the motor unit and its integration by the nervous system. From a physiological and contractile viewpoint fibres belonging to the same motor unit exhibit similar characteristics (Gollnick 1982a; Lexell et al. 1983; Pette & Spamer 1986). However, skeletal muscle is an extremely heterogeneous tissue (Gollnick 1982a; Saltin et al. I 977). The variability in motor units stems from 2 main features: a spectrum of fibres and diversity in their assembly (Pette I 984). Histochemical methods have been developed to qualitatively discriminate between fibre types. The delineation between various fibre types has been made possible by the fact that the multimolecular form of the protein in the myofibrils responsible for the ATPase stain is selectively inactivated by preincubation in an acid or alkaline medium (Brooke & Kaiser 1970). The histochemical analysis of muscle has resulted in several classification schemes being utilised to identify and categorise fibre types. The present paper will adopt the nomenclature of ST, FTa, FTb and FTc as proposed by Saltin et al. (1977). Myosin ATPase activity is greater in FT than ST fibres and is positively correlated with the speed offibre contraction (Barany 1967; Viitasalo & Komi 1978). This has also been shown to be the case for Ca++-activated myosin ATPase and Mg++-simulated ATPase (Essen et al. 1975; Taylor et al. 1974; Thorstensson et al. I 977). These differences may partially explain why the time to peak tension of ST fibres is relatively long in comparison with FT fibres (Buchthal & Schmalbruch 1970; Gollnick 1982a). Differences between FT and ST fibres extend to include nerve terminals, neuromuscular

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junction, morphological and ultrastructural characteristics (Hoppeler 1986; Pickett I 980). Delineation of fibre types into ST and FT can also be accomplished on the basis of metabolic properties (Essen et al. 1975; Pette & Spamer 1986). The ST fibre has been shown to be characterised by a greater content of mitochondrial enzymes for the end terminal oxidation of carbohydrates and fats (Gollnick & Saltin 1982b; Saltin et al. I 977). The FT fibre possesses a greater glycolytic enzyme capacity, but lower oxidative metabolism (Essen et al. 1975; Saltin et al. 1977). FT fibres have historically been histochemically subgrouped into FTa, b or c fibres. The FTb fibres have a lower oxidative potential and a higher glycolytic capacity than the FTa fibres (Essen et al. 1975; Saltin et al. I 977). Pette and Spamer (1986) recently argued that single fibre analysis does not support the FTa and FTb dichotomy, but rather a continuum of metabolic capacities across the FT fibre population. FTc fibres are seldom found in human muscle samples. Thomson et al. (1979) indicated that FTc fibres accounted for less than 1% of all fibres. The oxidative potential of FTc fibres is similar to that of ST fibres, while glycolytic activity is similar to that of Ffa fibres (Essen et al. 1975). However, while small in number the role of FTc fibres may be significant in transformations in fibre type (Janssen et al. 1978). Alternatively, Brooke and Kaiser (1974) consider the FTc fibre to be undifferentiated muscle. Their presence in adult tissue may be indicative of muscle regeneration. Thus, the functional significance of the FTc fibre still remains unclear. Three distinct myosin heavy chains have been identified: slow, fast A and fast B (Billeter et al. 1981). In addition, 5 myosin light chains have been identified (Bileter et al. 1981). The fast B, fast A and slow myosin heavy chains are found exclusively in FTb, FTa and ST fibres, respectively. However, the FTc fibre was described by Jolesz and Streter (1981) as 'promiscuous', because it contains both fast and slow heavy chain myosin. This tends to lend credence to the notion that the FTc fibre is the intermediate state between FT and ST fibres (Baumann et al. 1987).

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The total number of fibres may vary between sites within a given muscle. This was found to be the case for the proximal and distal portions of the vastus lateralis muscle by Lexell et al. (1983). In addition, the distribution of fibre types varies as a function of depth, with a predominance of FT fibre at the surface and ST fibres in the deeper regions of the muscle (Lexell et al. 1983).

1. Exercise Stress and the Influence on Skeletal Muscle Morphology Several stressors have been shown to influence the morphology of skeletal muscle: cross innervation (Buller et al. 1960; Maier & Pette 1987), hormonal regulation (Ianuzzo et al. 1977) and exercise (Costill et al. 1976a). As exercise input represents the primary focus of this paper the other areas will not be discussed. 1.1 Contractile Properties and Fibre Proportion There is some evidence that exercise and inactivity may cause transitions between FT and ST fibres (Green et al. 1983, 1984; Haggmark et al. 1981; Howald et al. 1985; Schantz et al. 1982; Simoneau et al. 1985; Sjostrom et al. 1987). These studies have generally been characterised by high intensity endurance training, for several hours each day over several months (Howald 1982). The promiscuous FTc fibre has been nominated as the intermediate state between FTa and ST fibres (Billeter et al. 1981). FT to ST fibre transition may also be due partially to the replacement ofFT fibre with new ST fibres (Pette 1984). Jacobs et al. (1987) reported that 6 weeks of sprint training produced a decrease in the proportion of ST fibres and a significant increase in the proportion of FTa fibres. The absence of a change in the proportion of various fibre types for the control group suggested that the variation reported for the experimental group was not due to methodological error. There are several lines of evidence which conflict with the hypothesis of fibre type transition arising from training. First, in a cross-sectional


study by Prince et al. (1976) it was concluded that the percentage of ST fibres was determined very early in life and not to be subject to change with exercise. Second, a similar proportion of FT and ST fibres in the trained and untrained muscles of elite athletes does not support the notion of fibre type transitions (Clarkson et al. 1982; Jansson et al. 1978). Third, Komi et al. (1977) found that monozygous twins have essentially identical muscle fibre distribution. Furthermore, Essen-Gustavsson et al. (1986) reported no consistent change in the proportion of FT and ST fibres in individuals between the ages of 20 and 70 years. Finally, it has been reported that elite distance and marathon runners have a greater percentage ofST fibres than the normal population (Costill et al. 1976b; Houston 1978). This observation could be explained by the fact that in a general population a small percentage of individuals would be expected to exhibit an unusually high percentage of either FT or ST fibres in muscle (Gollnick 1982a). The high proportion of ST fibres reported in many elite endurance athletes, on balance, appears to be the result of a process of natural selection (Houston 1978). Several studies have reported a conversion of FTb to FTa as a direct result of endurance training (Andersen & Henriksson 1977a; Green et al. 1979; Houston 1978; Jansson & Kaijser 1977; Katsuta et al. 1988; Prince et al. 1976). The work of Prince et al. (1976) suggested that humans can adapt to endurance activity with changes in the FT fibre subgroups, i.e. FTb/FTa. Houston (1978) suggested that this conversion was indicative of a change in the composition of the light chains in the head of the myosin molecule of fast fibres, i.e. FTb to FTa. This suggestion appears to be erroneous, because light chain myosin composition is identical in FTa and FTb fibres (Billeter et al. 1981). Bauman et al. (1987) revealed an accumulation of slow myosin light chains in FTa fibres following an 8-week endurance training programme. Thus, human skeletal muscle may adapt to the stress of heavy endurance training by increasing the proportion of ST fibres (FTb -+ FTa -+ FTc -+ ST) [Bauman et al. 1987].


1.2 Fibre Areas

1.2. I Endurance Training Response ST fibres are predominantly recruited during submaximal tasks (Gollnick et al. 1974a; Piehl 1974). FT fibre involvement in these activities is increased as the intensity of the task approaches V02max and/or as reserves of glycogen are depleted (Gollnick et al. 1974a). There is some evidence that the relative area of ST fibres is greater than that of FT fibres in endurance athletes (Costill et al. 1976b; Gerard et al. 1986; Gollnick et al. 1972a, 1973a). It is equivocal, however, whether these differences in relative area are evident in absolute terms. Gregor et al. (1981) reported that the area of ST fibres are 28 and 34% greater than that of FT fibres for endurance runners and pentathletes, respectively. In contrast, other studies reported that FT fibres of endurance athletes were greater in area than ST fibres by the order of 13 (Prince et al. 1976) and 15% (Costill et al. 1976a) in endurance athletes. Houston (1978) argued that it is more difficult to size order fibre types of endurance- and sprint-trained athletes than sedentary individuals. In comparison, sedentary males and females between the ages of 20 and 70 years display a mean cross-sectional area of fibre types where FTa > ST > FTb and ST > FTa > FTb, respectively (Essen-Gustavsson et al. 1986). Saltin et al. (1977) reported that males between 20 and 30 years old had a cross-sectional profile of FTa> FTb > ST. Males tended to have larger crosssectional areas than females for all fibre types between 20 and 70 years (Essen-Gustavsson et al. 1986). Endurance trained runners on occasion have demonstrated a larger ST and FT fibre area than untrained controls (Costill et al. 1976a,b; Prince et al. 1976). The ST and FTa fibres of trained runners were 39 and 27%, respectively, greater in area than controls (Prince et al. 1976). This suggested that the chronic overload of training selectively hypertrophied fibres involved in oxidative metabolism. However, this conclusion is equivocal. Fibre areas for both male and female swimmers were very similar to untrained individuals of the same age

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(Houston 1978). Furthermore, in a study examining the rat diaphragm, Tamaki (1987) reported a reduction in fibre area with endurance training in comparison with control animals. The small fibre area in conjunction with the increased capillary supply would facilitate diffusion of gases and enhance oxidative metabolism. As endurance training can span a wide range of relative and absolute intensities, a variety of patterns of fibre hypertrophy have been reported in response to such training. Low intensity endurance activities have resulted in preferential use of ST fibres with no hypertrophy (Schantz et al. 1983). However, cycling for 4 days per week over a period of 4 to 5 months produced selective ST fibre hypertrophy (Gollnick et al. I 973a; Taylor et al. 1978). Single leg cycling over 4 weeks produced an increase in the relative area occupied by ST fibres. In contrast, Fournier et al. (1982) reported that running by adolescent boys produced ST, FTa and FTc hypertrophy. Andersen and Henriksson (1977a) reported significant FTa and FTb fibre hypertrophy following 8 weeks of cycle ergometry. There was a similar absolute increment in ST area, but this was statistically nonsignificant. Selective Ffa and Ffb fibre hypertrophy followed a season of ice hockey (Green et al. 1979). Training for this sport has a large anaerobic component in addition to the aerobic training. Ff fibre hypertrophy may be related not only to the intensity of endurance training, but also to the training history of the individuals involved. Lavoie et al. (1980) introduced a group of novices to an 8-week swimming programme and reported a significant increase in FT fibre area of the triceps brachii. This selective hypertrophy of Ff fibres may have been caused by the greater tension development in previously inactive muscle. A similar phenomenon was reported by Bylund et al. (1977) with an increase in FT fibre area during the first 8 weeks of training, but no further increase between the second and sixth month. The reverse was true for ST fibre area which increased significantly from month 2 to month 6. Swim training for 6.5 weeks by elite swimmers, while increasing relative area of FTa fibres, did not produce absolute changes in area

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(Houston et al. 1981). Thus, there is conflicting evidence as to which fibres and the sequence in which fibres are hypertrophied by endurance training. There still exists conflicting evidence as to the length of time necessary to induce ST hypertrophy. Four days per week over a period of 4 to 5 months has been shown to be sufficient (Gollnick 1973a; Taylor et al. 1978). However, Bylund et al. (1977) suggested the necessity of longer duration programmes. 1.2.2 Sprint Training Response Sprint training is characterised by a high intensity effort sustained for a short period of time. Several studies have demonstrated that sprint training leads to a preferential utilisation ofFT fibres (Gollnick et al. 1973b). Kayakers who utilised a cocktail of continuous, sprint and resistance training exhibited much larger FTa than ST fibres (Clarkson et al. 1982). Clarkson et al. (1982) also found that the FTa and FTb fibre areas were significantly greater in the highly trained biceps brachii of kayakers than the lesser trained vastus lateral is. However, 6 weeks of sprint training on a cycle ergometer by students did not produce FT or ST fibre hypertrophy (Jacobs et al. 1987). Furthermore, swimmers demonstrated no significant differences in fibre area from untrained controls (Houston 1978). Absolute changes may not have occurred due to the elite nature of the swimmers or the short duration of the studies (Houston et al. 1981; Jacobs et al. 1987). Interestingly, increased circumference of muscles has been found to exist following sprint training, although ST and FT fibre hypertrophy was nonsignificant (Thorstensson et al. 1975). The relative FT fibre area was greatest in a group of sprinters when compared with other elite track and field athletes (Costi11 et al. 1976a). Male, but not female, sprinters had FT fibres which were larger in size than their untrained counterparts. This reported difference for the male sprinters may be due to the training regimen or a genetic predisposition toward larger FT fibres. However, while nonsignificant, female sprinters have been reported to

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have ST fibres which are 8% larger than their FT fibres (Gregor et al. 1981). 1.2.3 Acute Response to Endurance Exercise There is a paucity of research related to the influence of acute endurance exercise on muscle fibre area. A unique study (Sjostrom et al. 1987) examined the effects of a prolonged distance run (3529km) lasting 7 weeks. The subject experienced a decrease in the size of both ST and FT fibres and an accompanying increase in the relative proportion of ST fibres following the run. However, it is not clear if these changes were an acute response to the individual exercise bouts or a chronic training effect arising from the 7 weeks of exercise. Exhaustive exercise produced marked mitochondrial swelling in both cardiac and skeletal muscle of guinea pigs (Taylor et al. 1976). Similar results were reported in the mitochondria of rats and thoroughbred horses run to exhaustion by Gollnick and King (1969) and Nimmo and Snow (1982). Gale (1974) attributed the results of Gollnick and King (1969) to an artefact created by the use of osmium during fixation. Osmium was also the fixation medium for Nimmo and Snow (1982) and consequently their results may also reflect an artefact (Hoppeler 1986). The artefact created by osmium fixation may be the result of a decrease in the phospholipid content of trained mitochondria (Dohm et al. 1975). Neither Brooks et al. (1971) nor Kayor et al. (1986) reported disruption of mitochondria in response to extensive endurance exercise, nor is there evidence of mitochondria being redistributed in response to an extensive endurance challenge (Kayor et al. 1986). Fibre shrinkage occurred following a IOOkm run and an 85km crosscountry ski race (Kayor et al. 1986; Lithell et al. 1979a). This reduction was attributed to a reduction in both glycogen and endogenous lipid stores (Hoppeler et al. 1986; Kayor et al. 1986). Water release accompanies the oxidation of glycogen (Lithell et al. 1979a). The greatest shrinkage was evident at the subsarcoplasmic level (Hoppeler et al. 1986). During exhaustive exercise lasting in excess of I hour there is an increase in the uptake of Ca++


into mitochondria which may act to buffer cytoplasmic Ca++ (Tate et al. 1978). However, beyond a certain level, the uptake of Ca++ would inhibit ATP production (Tate et al. 1978). The accumulation ofMg++ in exhaustive activity may diminish the negative effects of excessive Ca++ uptake. Ca++ uptake may also be dependent on the absolute amount of work completed, as hamsters swum to exhaustion did not present any changes in mitochondrial uptake (Tate et al. 1978). Furthermore, exhaustive running for less than 15 minutes reduced mitochondrial Ca++ uptake (Boner et al. 1976), suggesting that Ca++ uptake by the mitochondria may be a function of time. 1.2.4 Acute Response to Sprint Exercise Limited work has been completed on the effects of sprint exercise. The results of Nimmo and Snow (1982) suggest that sprint activity continued until exhaustion disrupts the mitochondria of thoroughbred horses. Elite sprint athletes on completing 20 sprint repetitions presented paracrystalline inclusions into the mitochondria, abnormally shaped mitochondria and increased density of subsarcolemmal mitochondria (Friden et al. 1988). The function of mitochondria is probably compromised by such changes in shape (Friden et al. 1988), but this has yet to be confirmed. Z-Band and focal streaming were reported in this study, most commonly in fibres with few mitochondria. It is not clear whether the reduced Ca++ uptake reported for endurance activities lasting between 10 and 15 minutes (Tate et al. 1978) is also evident in sprint activity. 1.3 Ultrastructure 1.3.1 Endurance Training Response Holloszy (1967) argued that increased oxidative capacity of skeletal muscle from training was linked to an increase in the number of mitochondria, an increase in the size of the mitochondria or a change in composition of the mitochondria. Subsequent investigations have indicated that the composition of mitochondria is not changed by training (Davies et al. 1981; Hoppeler 1986). Thus, increments in

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mitochondrial protein following training (Bylund et al. 1977; Friden et al. 1984; Katsuta et al. 1988) are the result of an increased size and/or number of mitochondria. Younger (22 years) males may have fewer, but larger mitochondria than their older (57 years) peers (Kiessling et al. 1973). Trained individuals tend to have larger (Hoppeler et al. 1973) and more (Kiessling et al. 1974) mitochondria than untrained individuals. Some have argued that differences in the number and shape of interfibrillar and subsarcolemmal mitochondria make it difficult to quantitatively measure mitochondrial function with either parameter (Hoppeler 1986). Kiessling et al. (1973) reported a significant correlation (r = 0.85) between the volume fractions of subsarcolemmal and interfibrillar mitochondria. Mitochondrial factors (protein and oxidative enzymes) rather than V02max appear to play an important role in determining the length of time for which an endurance challenge may be met (Davies et al. 1981; Gollnick & Saltin 1982b). The rationale for this conclusion is that large increments in mitochondrial capacity are only accompanied by modest increases in V02max (Ingier 1979; Davies et al. 1981). This increased oxidative capacity resulted in an enhanced ability to utilise lipid as a substrate following endurance training (Karlsson et al. 1974). Gollnick and SaItin (1982b) proposed that the mitochondrial adaptation to training enhanced ADP translocation into the mitochondria. This would provide ADP for the electron transport system and inhibit phosphofructokinase. Furthermore, the associated increase in pyruvate dehydrogenase activity could help limit pyruvate concentrations to levels less than the Michaelis constant (Km) for lactic dehydrogenase. These adaptations proposed by Gollnick and Sa1tin (l982b) would conceivably enhance lipid oxidation. Mitochondria have been geographically classified as either interfibrillar or subsarcolemmal (Hoppe1er 1986). The interfibrillar mitochondria have a cylindrical shape, while the subsarcolemma1 mitochondria are spherical. Davies (1981) argued that as functional and structural differences between interfibrillar and subsarcolemmal mitochon-

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dria had not been demonstrated and consequently should be considered as a single population. The weakness with this approach is that mitochondria proximal to the sarcolemma may be more prone to disruption (Nimmo & Snow 1982). In addition, the relative proliferation of subsarcolemmal mitochondria is greater than interfibrillar mitochondria in response to endurance training (Hoppeler et al. 1985; Rosier et al. 1985). Furthermore, Hoppeler et al. (1985) hypothesised that subsarcolemmal mitochondria may be preferentially involved in ATP synthesis from blood-borne lipids. Finally, the volume-density of central mitochondria has been found to be significantly and directly correlated with V02max (r = 0.82; Hoppeler et al. 1973). Cross-sectional investigations indicated that athletes had more mitochondria at both the sarcolemmal and interfibrillar sites than untrained men and women (Hoppeler et al. 1973). In the untrained state, mitochondria are most evident in ST fibres and least evident in FTb fibres (ST > FTa > FTb) [Bylund et al. 1977; Hoppeler et al. 1986]. In response to endurance training there is a greater increment in mitochondria for FTa fibres than either ST or FTb fibres (Hoppeler et al. 1986). However, mitochondrial content was still significantly greater in ST than FT fibres following 6 months of training (Bylund et al. 1977). An early study suggested that younger males increased the number of mitochondria in response to endurance training, while older males responded by increasing the size of mitochondria (Kiessling et al. 1973). However, this difference may have been an artefact created by comparing cross-sectional data with longitudinal data. Recently, Katsuta et al. (1988) reported that mitochondrial response in rats trained 2 hours/day 5 times/week was similar to that in rats run to exhaustion twice per week. This suggests that the maximal limit for mitochondrial adaptation may be a function of time or the absolute amount of work completed in training. Finally, the mitochondrial adaptation of females may be less than that of males (Costill et al. 1979). However, this adaptive difference appears not to have any metabolic significance, at least for workloads approximately 70% V02max.


1.3.2 Sprint Training Response There is a paucity of data in this area. Friden et al. (1988) reported tht the morphometry of mitochondria in elite sprinters was not abnormal, although there was some structural deviation in all 5 sprinters investigated.

2. Intramuscular Substrate Use in Exercise 2.1 Glycogen Metabolism 2.1.1 Glycogen Response to Endurance Training Endurance training can increase the intramuscular stores of glycogen (Gollnick et al. I 972a, I 973a; Taylor et al. 1971, 1972a, 1978). It has been suggested that training which increases V02max also increases glycogen concentration. The results of Bylund et al. (1977) do not support this notion. Significant increments in both V02max and glycogen occurred in response to the first 8 weeks of endurance training. However, the significant increment in glycogen may have been due to the proximity of the last bout of exercise and not training. An additional 6 months of training produced a nonsignificant increase in V02max, and a significant reduction in the level of glycogen. Glycogen concentrations in individuals of various activity backgrounds presented similar glycogen concentrations in FT and ST fibres (Essen et al. 1975). Increments in glycogen concentration as a result of training appear to be similar for both FT and ST fibres (Essen et al. 1977a; Gollnick et al. I 972a, 1973a). Essen (1978a), Gollnick et al. (1981) and Bell and Jacobs (1989) have reported higher glycogen levels in FT than ST fibres, but as Essen (1978) noted, there was a large and overlapping range of glycogen concentrations in FT and ST fibres. Furthermore, some glycogen depletion from ST fibres may have occurred prior to measurement because of routine daily activities; many of these activities typically involve ST, but not FT fibres (Essen 1978a). The depletion of glycogen in endurance tasks is a major correlate with fatigue (Bergstrom et al. 1967; Gollnick et al. 1982c; Henriksson 1977; Ter-


jung et al. 1972}. However, endurance training has a 'glycogen sparing' effect (Henriksson 1977). This 'glycogen sparing' is evidenced by increased lipid utilisation for a given absolute workload following training (Baldwin et al. 1975; Davies et al. 1981; Hurley et al. 1986). There is an increased endotheliallipoprotein lipase (LPL) [Nikkila et al. 1978], fj-oxidation (Costill et al. 1979) and carnitine acyltransferase (Gollnick & Saltin 1982b) enzyme activity following training. Increased FFA metabolism and oxidation of FFA produces citrate which inhibits glycogenolysis via phosphofructokinase. In addition, a high [ATP]/([ADP]· [Pi)) ratio in the cytosol has been shown to inhibit PFK (Essen 1977; Mansour 1963, 1965). Though Constable et al. (1987) recently questioned whether the reduction in glycolysis with training was due to PFK inhibition, at least in stimulated rat muscle. Furthermore, glycogen synthetase activity is increased by endurance training (Taylor et al. 1972a). Finally, the activity of the enzymes of the malate-aspartate shuttle were increased by endurance training (Schantz et al. 1986). This increases the supply of NAD+ for glycogen to pyruvate conversion through aerobic metabolism. However, the a-glycerophosphate shuttle was not enhanced by training (Schantz et al. 1986). All these adaptations contribute to the increased lipid metabolism and 'glycogen sparing' reported for a given submaximal workload following training. In apparent contradiction to these adaptations, Taylor et al. (1972b) reported that phosphorylase activity was significantly increased by endurance training. Taylor et al. (1971) also re>,orted that glycogen utilisation was greater following training for a work regimen in which the subjects worked at between 60 and 80% V02max. However, in the post-training challenge subjects were able to work at a higher workload for a longer period of time (120 vs 80 minutes). Furthermore, there is a suggestion that following training, glycogen depletion of FT fibres may be less than prior to training (Henriksson I 977). 2.1.2 Glycogen Response to Sprint Training Boobis et al. (1983a) reported that sprint training significantly increased muscle glycogen concentration. The intensity of staining for the periodic

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acid Schiff reaction (PAS) suggested that glycogen levels were similar in ST, FTa and FTb fibres of elite sprinters (Friden et al. 1988). Sprint training increases glycogen concentrations similarly for all fibre types. Sprint training reduces the rate of glycogen utilisation for a given submaximal (approximately 60% V02max) workload (Karlsson et al. 1974). With the exception of the first 5 minutes of the 90-minute challenge glycogen depletion was significantly less following training in addition, increased glycogen stores permit the maintenance of supramaximal workloads for longer periods of time (Asmussen et al. 1974). Sprint training enhances performance of supramaximal workloads, by enhancing both· elements of what Asmussen et al. (1974) described as the enzyme-substrate (phosphorylase-glycogen) complex (Boobis et al. 1983a; Roberts et al. 1982). These changes enhance the velocity of glycogenolysis. While it would appear that phosphofructokinase does not limit anaerobic performance (Gollnick et al. 1982c), phosphorylase activity may do so (Roberts et al. 1982). Sprint training does not appear to enhance endothelial lipoprotein lipase (LPL) activity (Nikkila et al. 1978). 2.1.3 Acute Glycogen Response to Endurance Exercise The level of glycogen is a major determinant of how long a submaximal challenge may be met (Bergstrom et al. 1967; Gollnick et al. 1981, 1982c; Ivy 1991). The rate of glycogen breakdown is closely linked to the intensity of the endurance exercise (Gollnick et al. 1974a). Furthermore, the rate of glycogenolysis is a direct function of the available glycogen (Gollnick et al. 1981). Many studies have demonstrated a principal depletion of muscle glycogen in ST fibres as a result of submaximal endurance activity (Costill et al. 1973; Essen 1978a; Gollnick et al. 1972b, I 974a; Green 1978; Henriksson 1977; Thomson et al. 1979). The depletion of glycogen from FT fibres increases with the intensity ofthe submaximal activity and as ST fibres become depleted of glycogen (Gollnick et at. 1974a). Furthermore, at 85% V02max glycogen depletion was greater from FTa

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and FTb fibres (Andersen & Sjogaard 1976). This indicates that the depletion of glycogen from fibres is initially from ST fibres, then FTa followed by FTb fibres for submaximal tasks. The pattern of glycogen depletion varies between muscle groups for a given activity (Costill et al. 197 I, 1974; Essen 1977). For example, glycogen depletion is greater in the gastrocnemius than either the soleus or vast us lateralis when running on a flat surface (gastrocnemius> soleus> vastus lateralis) [Costill et al. 1974]. Running uphill however, changes the pattern and extent of glycogen depletion (gastrocnemius> vastus lateralis > soleus) [Costill et al. 1974]. There is also evidence to suggest gender differences in the extent of glycogen depletion. Running at 65% of V02max for 90 minutes led to significantly greater glycogen depletion in men than in women (Tarnopolsky et al. 1990). In this study men and women were matched on relative V02max, training history and diet. Women were also matched on menstrual status. The gender differences did not appear to be related to differences in exogenous lipid metabolism. ST fibres have greater 'glycogen sparing' properties than FT fibres because of their enzymatic and capillarisation profiles (Jacob 1981a). In addition, ST fibre recruitment assists in maintaining lactate at optimal levels, as these fibres (ST) possess the heart specific LDH isoenzyme (Jacobs 1981). The preferential recruitment of ST fibres in submaximal endurance activities is metabolically understandable. As endogenous stores of carbohydrate are depleted, there is an increased uptake of exogenous glucose which extends endurance capacity (Gollnick et al. 198 I). The control of glucose uptake from the blood appears to reside with local factors (Gollnick et at. 1981). Glucose-6-P04 activity changes with muscle glycogen levels (Gollnick et al. 1981). High levels of glucose-6-P04 inhibit hexokinase, which in turn inhibits the uptake of glucose. Low glycogen levels in muscle result in an increased uptake of glucose and lactate from the blood (Gollnick et al. 1981). Glucose-6-P04 activity is greater following moderate intensity aerobic activity (60%


V02max) than higher intensity aerobic activity (80% V02max) [Gollnick et al. 1981]. Finally, phosphorylase a activity is significantly reduced by fatiguing endurance activity in trained and untrained individuals (Taylor et al. 1972b). 2.1.4 Acute Glycogen Response to Sprint Exercise Significant glycogen depletion has been reported in sprint activities lasting as little as 6 seconds (Boobis et al. 1983a). Six seconds of maximal cycle activity reduced muscle glycogen reserves by 14% (Boobis et al. 1983a), while 30 seconds of sprint running and cycling produced a 20 to 25% reduction (Boobis et al. 1983b; Cheetham et al. 1986). Gollnick et al. (l973b) and Thomson (1979) reported a 50% reduction in muscle glycogen reserves following 6 to 10 I-minute repetitions at between 120 and 150% V02max. The rate of glycogen depletion in sprint activities is high, being much greater than that associated with endurance tasks (Cheetham et al. 1986). In spite of this, it remains unlikely that glycogen depletion represents a cause of fatigue. The supramaximal nature of sprint work results in the preferential depletion of glycogen from FT motor units (Gollnick et at. 1973b, 1974a; Green 1978; Thomson et al. 1979). Thomson (1979) and Green (1978) reported that glycogen depletion was greater in Ffb fibres than FTa fibres, which in turn was greater than in ST fibres following 10 I-minute repetitions at 120% V02max (FTb > FTa > ST). This pattern of depletion was not surprising since FTa fibres do not possess the glycogenic capabilities of the FTb fibre (Essen et al. 1975; Thomson et at. 1979). In a recent histochemical study, glycogen depletion was reported in ST and FTb fibres, but not FTa fibres (Friden et al. 1988). The work challenge in this study involved 20 sprint running repetitions lasting 25 seconds each (Friden et at. 1988). Whether the differences between the results of Friden et al. (1988), Green (1978) and Thomson (1979) are indicative of differences related to the duration or intensity of the respective challenges is not yet clear. Glycogen depletion occurs in sprint activities.


However, factors appear to conspire to reduce carbohydrate metabolism in periods following sprint activity. Glycogen synthase activity is greater following exercise producing exhaustion in 3 to 5 minutes than following exercise producing exhaustion in 30 minutes (Taylor et al. 1972a). This increased glycogen synthase activity may explain the rapid glycogen repletion reported by Hermanssen and Vaage (1977). In addition, Chasiotis et al. (1982) reported that glycogen synthase activity (I and D forms) reciprocated that of phosphorylase. While glycogen synthase activity was depressed in the first 30 seconds of an exhaustive cycling bout lasting between 4 and 6 minutes, it had returned to pre-exercise levels after 4 to 6 minutes of exhaustive cycling. 2.2 Lipid Metabolism

2.2.1 Lipid Response to Endurance Training Intramuscular triglyceride stores are greater in ST fibres than FT fibres (Essen 1977; Essen et al. 1975). Training has been shown to significantly increase local lipid stores in some (Hoppeler et al. 1985; Howald et al. 1985), but not all studies (Kiessling et al. 1974). Training appears to increase triglyceride depots directly adjacent to the mitochondria (Hoppeler et al. 1973, 1985). Furthermore, the deposition of triglyceride in response to training is different for FT and ST fibres. Six weeks of cycle training (30 sessions at 70% V02max) produced significant increments in local lipid stores in both FTb (144%) and FTa (90%), but not ST fibres (22%) [Howald et al. 1985]. These increments in intramuscular triglyceride stores may be the result of greater endothelial lipoprotein lipase (LPL) activity in endurance trained muscle (Nikkila et al. 1978). The 'glycogen sparing' effect of endurance training is complemented by increased lipid utilisation for a given submaximalload (Baldwin et al. 1975; Davies et al. 1981; Hurley et al. 1986). Increased capacity to metabolise fats takes place with no change (Gyntelberg et al. 1977; Karlsson et al. 1974) or perhaps even a reduction (Gollnick 1977; Hurley et al. 1986) in the concentration of plasma free

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fatty acids (FFA). These findings do not necessarily mean that lipolysis decreases or is unchanged by endurance training. Exogenous lipolysis possibly increases with training and is matched by equivalent or greater increments in FFA uptake by the muscle (Gollnick 1977). This is supported by the finding that training enhances the uptake of palmitate (Bylund et al. 1977), although Costill et al. (1979) argued that the rate of FFA mobilisation may be a point of limitation. However, a recent report has indicated that blood glycerol concentrations after 90 minutes of exercise were significantly less following training (Hurley 1986). This suggested that exogenous lipolysis may be decreased by training. The reduction was countered by increased endogenous triglyceride utilisation. Thus, training may produce not only a greater reliance on lipid during submaximal tasks but also an increased usage of endogenous lipids. There is preferential enhancement of subsarcolemmal mitochondria with endurance training (Hoppeler et al. 1985). Hoppeler et al. (1985) hypothesised that this adaptation brought the oxidative apparatus closer to the poorly diffusable blood borne FFAs. In addition, mitochondrial protein enhancement produces parallel increments in pyruvate dehydrogenase and carnitine acyltransferase activity (Gollnick & Saltin 1982b). Carnitine acyltransferase assists in the production of acetyl CoA from lipid sources, while pyruvate dehydrogenase helps maintain pyruvate levels at less than the Km oflactic dehydrogenase (Gollnick & Saltin 1982b). Furthermore, an increased mitochondrial concentration assists in the translocation of ADP to the mitochondria. This provides ADP for the electron transport system and in turn inhibits phosphofructokinase activity (Mansour 1965). All these mitochondrial adaptations facilitate lipid utilisation. The citric acid cycle in the trained and untrained states does not differentiate between acetyl subunits derived from carbohydrate or lipid sources (Gollnick & Saltin 1982b). For there to be a 'glycogen sparing' effect more acetyl subunits must be derived from fats following training. Gollnick and Saltin (1982b) proposed that increased mitochon-

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dria, carnitine acyltransferase and /3-oxidation enzymes not only enhanced fatty acid conversion, but also maintained a Km for citrate synthase which was more conducive to lipid utilisation. Endothelial LPL activity of the skeletal muscle was reported to be significantly greater in endurance runners than either sprint runners or normal controls (Nikkila et al. 1978). However, the use of heparin in the incubation procedure of this experiment only measured LPL bound to the endothelium of capillaries (Oscai & Palmer 1988). Thus, the results of Nikkila et al. (1978) suggest that the uptake of triglycerides by muscle tissue is enhanced by chronic endurance training. This may explain the higher endogenous triglyceride concentrations reported by Hoppeler et al. (1985). Endogenous LPL activity is also increased by training (Oscai et al. 1982). Endogenous LPL appears to mobilise endogenous triglycerides (Oscai et al. 1982; for review see Oscai & Palmer 1988). This increased endogenous LPL activity appears to run counter to the increased endogenous triglyceride levels reported following training. 2.2.2 Lipid Response to Sprint Training The metabolism of lipid in exercise is thought to be an inverse function of the performance intensity (Gollnick 1977; Oscai & Palmer 1988). However, research to substantiate this statement is sparse. Sprint training does produce a 'glycogen sparing' effect for submaximal workloads (Karlsson et al. I 974). Sprint training programmes recruit both Ff and ST fibres (Friden et al. 1988; Thomson et al. 1979; Thorstensson et al. 1975) and have been shown to increase V02max (Saltin et al. 1976). The increased oxidative potential of Ff and ST fibres may have resulted in an enhanced metabolism of lipid during the performance of high intensity activity. However, Staudte et al. (1973) failed to find increments in 3-hydroxyacyl-CoA dehydrogenase activity in sprint-trained rats. To our knowledge intramuscular triglyceride concentrations have not been measured in individuals undertaking sprint training. Endothelial LPL activity levels in sprint runners are equivalent to those found in sedentary individuals and sig-


nificantly less than those of endurance runners (Nikkila et al. 1978). This parameter in isolation does not provide an insight into intramuscular triglyceride levels, as endogenous LPL activity may be elevated, depressed or unchanged by sprint training. 2.2.3 Acute Lipid Response to Endurance Exercise Not surprisingly endogenous lipid utilisation involves triglyceride oxidation and not the structural phospholipids (Carlson et al. 1971). Several studies have reported significant intramuscular triglyceride depletion in response to endurance exercise (Carlson et al. 1971; Costill et al. 1973; Essen et al. 1977; Lithell et al. 1979b; Havel et al. 1967; Hoppeler et al. 1986). It is not uncommon for endogenous triglycerides to provide 50% or more of the total lipid oxidised during exercise (Carlson et al. 1971; Hoppeler 1986; Oscai & Palmer 1988). Furthermore, during activity there is a preferential utilisation of triglyceride from ST fibres (Lithell et al. 1979b). Exercise greater than I hour in duration activates the endothelial-bound LPL which facilitates the muscles' ability to metabolise blood-borne triglycerides (Lithell et al. 1979a,b, 1981). Despite this, endogenous triglyceride stores have been shown to be significantly depleted in rats for at least 24 hours following a 2-hour swim (Oscai et al. 1982). This was probably due to the elevated activity of endogenous LPL for the 24 hours following the swim. In the heart LPL activity appears to be proportional to the intensity of the task (Oscai et al. 1982). Women utilised significantly more lipid than matched men when running for 90 minutes at 65% V02max (Taruopolsky et al. 1990). However, the plasma glycerol and FFA levels were similar for men and women, suggesting that there is greater endogenous lipid utilisation by women. The utilisation of intramuscular lipid during endurance exercise appears to be linked to the uptake of plasma FFA (Gollnick et al. 1981). Reducing the available plasma FFA by the administration ofnicotinic acid did not lead to its substitution by endogenous triglyceride (Gollnick et al. 1981). The


mechanism linking the uptake and oxidation of plasma FFA to the utilisation of endogenous triglyceride is not clear. Intramuscular triglyceride may only act to eliminate the energy deficit existing between total lipid and plasma lipid oxidation (Carlson et al. 1971). The uptake of plasma FFAs is limited, and consequently this energy deficit occurs commonly during endurance exercise. Reasons for the poor uptake of plasma FFAs include: capillary obstruction (Rose & Goresky 1977) and poor diffusion characteristics of FFAs (Hoppeler 1986).

2.2.4 Acute Lipid Response to Sprint Exercise Interval of sprint exercise has been thought not to rely on lipid substrate to meet the metabolic demands of this exercise form. This may account for the lack of research in the area. There is no evidence to demonstrate that intracellular triglyceride limits sprint performance (Gollnick 1982c). However, the work of Essen and colleagues (Essen 1977; Essen et al. 1977) suggested that there may be increased fat metabolism during the periods between sprint repetitions. This would spare carbohydrate for the actual sprint repetitions. However, this work was conducted at 100% ~02max and has yet to be verified during supramaximal activity. The research by Lithell et al. (1979a) suggests that a sprint task would not elevate endothelial LPL activity. However, Oscai et al. (1982) reported that the greater the submaximal intensity of a swimming task the greater the endogenous LPL activity in the cardiac tissue. However, sprint training was not shown to increase 3-hydroxyacyl-CoA dehydrogenase activity in the skeletal muscle of rats (Staudte et al. 1973). This suggested that fat oxidation was nonsignificant in sprinting tasks. 2.3 Amino Acid Metabolism

2.3.1 Amino Acid Response to Endurance Training Endurance training increased the capacity of the skeletal muscle to form alanine from pyruvate as there was an 80 and 50% increase in mitochondrial and cytoplasmic alanine aminotransferase activity,

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respectively (Mole et al. 1973). This may counterbalance the decreased pyruvate availability resulting from the 'glycogen sparing' influence of training (Asmussen et al. 1974). Trained guinea pigs had greater levels of alanine in the venous circulation than controls when run to exhaustion over 2 minutes (Weiker et al. 1983). In addition, endurance training appears to enhance leucine oxidation (Henderson et al. 1985; Varasheski & Lemon 1983). Lemon and Nagle (1981) proposed that the enhanced oxidation may in part be the result of increased camitine palmitoyltransferase activity following training reported by Mole et al. (1971). Elevated hydrolase activity has also been reported following training (Pilstrom et al. 1978). More investigation is required to expand our understanding of the effects of endurance training on amino acid metabolism.

2.3.2 Amino Acid Response to Sprint Training To our knowledge no study has investigated the effects of sprint training on amino acid metabolism. 2.3.3 Acute Amino Acid Response to Endurance Exercise Energy may be derived from protein sources via either the glucose-alanine cycle (Eller & Viru 1983; Felig & Wahren 1971; Viru 1987) or the oxidation of branched chain amino acids (BCAA) [Lemon & Nagle 1981; Rennie et al. 1981; White & Brooks 1981; Wolfe et al. 1982]. The estimated contribution of protein towards ATP production in an endurance task has ranged from 1% (Lemon et al. 1983) to 25% (Dohm et al. 1985). The discrepancies in the estimated contribution of protein to metabolism are in part the result of large interindividual differences (Lemon et al. 1983) and methodological variations between studies (Dohm et al. 1985; Wolfe et al. 1982). The pool of free amino acids is used by both the glucose-alanine cycle and during BCAA oxidation. The resting free amino acid pool is insufficient to account for the increased protein metabolism associated with exercise (Dohm et al. 1985). The pool is expanded by increasing protein deg-

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radation and decreasing protein synthesis within the skeletal muscle (Dohm et al. 1985; Viru 1987). However, the pool is not supplemented by contractile protein degradation (Rennie et al. 1981; see review by Viru 1987). In addition, proteins are taken from extramuscular sources including the liver (Felig 1977; Lemon et al. 1984; Millward et al. 1982). These extramuscular sources, for example, may account for 50% of leucine oxidation (Wolfe et al. 1982). However, during exercise the greatest relative increase in amino acid metabolism would appear to be from intramuscular sources (600 vs 150%) [Wolfe et al. 1982]. The amino acids available for oxidation or the glucose-alanine cycle are reduced by prolonged physical activity (Eller & Viru 1983). It was proposed that this reduction would limit protein utilisation as an energy substrate (Eller & Viru 1983). Alanine is formed by the transamination of pyruvate and an amino group (Felig 1977). Pyruvate, while predominantly derived from carbohydrate sources may also arise from amino acid sources (Viru 1987). While amino groups are made available through BCAA oxidation this is not the only source of amino groups (Garber et al. 1976). Felig (1977) proposed that amino groups could also be made available through the purine-nucleotide cycle. The alanine is then transferred to the liver for gluconeogenesis and the elimination of the amino groups (Felig 1977). Viru (1987) in his review indicated that alanine aminotransferase activity is increased with prolonged activity. This would explain the greater alanine concentrations associated with later sampling times for a given workload reported by Felig and Wahren (1971). Alanine concentration appears to be related to the level of available pyruvate (Felig & Wahren 1971). Consequently, endurance activity utilising carbohydrate, particularly via glycolysis will increase pyruvate levels (Felig & Wahren 1971). However, some work by Viru (1987) suggests that the association between pyruvate and alanine may not be causal (see next section). Lemon et al. (1984) argued that BCAA oxidation as evidenced by leucine oxidation provided energy for all stages of a task and that this contri-

Sports Medicine IO (6) 1990

bution was proportional to intensity. Millward et al. (1982) spoke of exercise specifically activating BCAA oxidation. For workloads between 25 and 89% V02max the correlation between leucine oxidation and intensity was very high (r = 0.986) [Millward et al. 1982]. The absolute amount of energy provided via leucine metabolism is small because of its small pool size in comparison with glucose or alanine (glucose> alanine> leucine) [White & Brooks 1981].

2.3.4 Acute Amino Response to Sprint Exercise During short term exercise glycogenolysis and glycolysis lead to an increased rate of pyruvate production. Thus conditions would appear to exist for the provision of carbons and the consequent synthesis of alanine. Weicker et al. (1983) demonstrated a significantly elevated plasma alanine level in response to running, particularly after 200 and 400m efforts (200m = 400m > 1500m > 100m). They proposed that the elevated serum alanine level following short term exercise is derived mainly from carbohydrate sources. However, recently Viru (1987) demonstrated that high blood lactate and presumably high pyruvate levels could be dissociated from one another. It was hypothesised that for there to be significant increments in alanine production there had to BCAA translocation from the liver. To our knowledge there has been no investigation into BCAA oxidation and sprint activities. However, one would expect BCAA oxidation to increase if the strong positive correlation continues to exist for supramaximal workloads, as well as submaximal workloads (Millward et al. 1982).

3. Enzymatic Response of Skeletal Muscle to Exercise and Training 3.1 Glycolytic Enzyme Response

3.1.1 Glycolytic Enzyme Response to Endurance Training Gollnick et al. (1974b) indicated that FT fibres had a greater glycolytic capacity than ST fibres. Single fibre analysis indicated that FT and ST fibres


were distinguishable by their lactic dehydrogenase (LDH) activity (Lowrie et al. 1978). Enzymes of metabolism, because of their short half lives, are very sensitive to the effects of training (Pette & Spamer 1979). Thus, the potential exists for endurance training to rapidly alter the glycolytic potential of skeletal muscle. There is evidence that endurance training decreased total LDH activity and the relative activity of the muscle (m) form of LDH (Sjodin et al. 1976a,b). However, in the glycolytic pathway, phosphorylase and phosphofructokinase (PFK) have been reported to be the rate limiting enzymes (Gollnick 1982c). Thus, changes in LDH activity appear to be of little significance to glycolytic function. Hexokinase responds in direct proportion, at least initially to increments in aerobic power (Holloszy 1975; Green et al. 1983). However, the response of hexokinase is not typical of all glycolytic enzymes. In fact, in Green and coworkers' (1983) classic rat study, 15 weeks of intensive endurance training produced significant reductions in the activity of enzymes involved in glycogen breakdown (phosphorylase 44%), glycolysis (LDH 39%) and gl uconeogenesis (fructose-I, 6-diphosphatase 75%) in the deep portion of the vastus lateralis. Green et al. (1983) suggested that training rearranged the enzyme patterns of Ff fibres to reflect that of ST fibres. Some studies involving humans have reported increments in PFK activity with training. Enhanced PFK activity may be a function of an interaction between duration, intensity and modality of training. Training programmes of 12 weeks or less involving a variety of training formats and modalities have failed to change PFK activity (Fournier et al. 1982; Henriksson & Reitman 1976). However, training for an hour 4 times per week for 5 months on a cycle ergometer at 75 to 90% V02max increased PFK activity by 100% (Gollnick et al. 1973a; Taylor et al. 1978). In contrast, 6 months of running activities and games at an intensity between 80 and 90% maximum heart rate did not increase PFK activity (Bylund et al. 1977). However, a programme similar to that of Bylund et al. (1977) involving adolescent boys and lasting

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16 weeks did increase PFK activity (Eriksson et al. 1973). Cycling for 20 minutes at high heart rates 3 times a week for just 2 weeks produced significant increments in PFK activity in 11- to 13-year-old boys (Eriksson et al. 1973). However, the results of Eriksson et al. (1973) may have been contaminated by the inherently lower PFK actvity in adolescents. A study involving 15- to 17-year-old males running at 70 to 80% maximum heart rate for 3 months did not increase PFK actvity (Taylor et al. 1981). Thus, while endurance training can on occasion increase PFK activity, it is not clear to what degree training duration, intensity, frequency or modality influence this adaptation. Phosphorylase activity was found to be similar in elite distance runners, middle distance runners and untrained individuals (Costi11 et al. I 976a,b). Increments in phosphorylase activity appear to require high intensity sprint training (Costill et al. I 976a). Furthermore, the intracellular levels of inorganic phosphate (Pi), AMP, ADP and ATP may control the rate of glycolysis to a large extent (Holloszy 1975). It was proposed by Ivy et al. (1980) that the reduced cytoplasmic concentrations of Pi, AMP and ADP and increased concentration of ATP could inhibit glycolysis following endurance training for a given submaximal task. However, there is evidence to suggest that increased inhibition of PFK was not the cause of the reduced glycolysis following training (Constable et al. 1987). 3.1.2 Glycolytic Enzyme Response to Sprint Training Considering the important role of glycolysis in sprint tasks, an increased ability to shunt pyruvate to lactate and an enhanced availability of NAD would be beneficial responses to sprint training. LDH and phosphorylase activity levels have been found to be greatly elevated above sedentary levels in elite trained sprinters (Costill et al. 1976a,b). High intensity training appears to be required for glycolytic adaptation to occur. Subjects following an intensive interval training programme of eight 200m sprints (work: rest ratio 1 : 4) demonstrated a significant increase in the activity of PFK, phos-

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phorylase, LDL and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) over 5 weeks (Roberts et al. 1982). Sprint training for four I-hour sessions each week for 12 weeks increased PFK levels significantly in young males (Taylor et al. 1981), while 6 weeks of training involving just 2 x 15 and 2 x 30 seconds of maximal effort also produced significant increment in PFK activity (Jacobs et al. 1987). In contrast, Sjodin et al. (I 976a,b) reported no change in LDH activity or the proportion of M or H forms following 8 weeks of sprint training. This discrepancy between the studies suggests that a threshold amount of anaerobic work may be required before glycolytic enzyme adaptation occurs. Staudte et al. (1973) reported that adaptation of the glycolytic enzymes was greater in the soleus (ST) muscle than the rectus femoris (FT) of the rat following 3 weeks of sprint training. This may have been because the rectus femoris was already better adapted to anaerobic tasks than the soleus. Roberts et al. (1982) suggested that following training phosphorylase levels were less than those of PFK, and consequently may limit sprinting performance. However, the Km of PFK and phosphorylase are greater than any reported metabolic flux, which suggests that neither enzyme would limit sprint performance (Gollnick I 982c). 3.1.3 Acute Glycolytic Enzyme Response to Endurance Exercise Endurance tasks may be classified as either being less than or greater than anaerobic threshold. While there is still much debate about the definition of anaerobic threshold (Keul et al. 1979; Kinderman et al. 1979; Mader et al. 1977; Ritz & Heidland 1977; Skinner & Mclellan 1980; Wasserman & Mcilroy 1964) it is clear that it has more to do with aerobic metabolism than anaerobic metabolism (Ivy et al. 1980; Rusko et al. 1980). However, the role of glycolytic enzymes may change depending on whether the endurance challenge does or does not exceed anaerobic threshold. Gollnick et al. (1973a) suggested that the increased PFK activity in response to endurance training could break down glycogen for both the aerobic and anaerobic pathways, i.e. glycolysis may


provide pyruvate for transport into the citric acid cycle for submaximal workloads. The research conducted by Haller et al. (1981) involving McArdle's disease sufferers tends to support this contention. For workloads in excess of anaerobic threshold varying degrees of glycolytic metabolism occur. However, we are not in a position yet to state if the glycolytic enzymes limit submaximal work exceeding anaerobic threshold. The rate of glycogenolysis may partially depend on shifts between phosphorylase b to phosphorylase a. However, work presented by Chasiotis et al. (1982) indicated that while the phosphorylase b to phosphorylase a shift does provide a link between the breakdown of creatine phosphate and glycogenolysis, it does not limit glycogenolysis. Jacobs (1981) proposed that the rate of glycogenolysis was limited by the availability of glycogen (i.e. the state of the enzyme substrate complex) [Asmussen et al. 1974]. This contention is supported by the work of Gollnick et al. (1981). 3.1.4 Acute Glycolytic Enzyme Response to Sprint Exercise Glycolytic metabolism is used from the initiation of sprint activity (Boobis et al. 1983b; Hirvonen et al. 1987; Jacobs et al. 1983). A significant increase in phosphorylase, PFK, GAPDH and LDH activity has been observed as a result of sprint training (Roberts et al. 1982). Therefore, one would suspect that the activity of all enzymes would be elevated throughout a sprinting challenge. ATP production via glycolysis was similar for running sprints between 40 and 100m (Hirvonen et al. 1987). However, the activity levels of the rate-limiting enzymes (PFK or phosphorylase) do not appear to inhibit sprint performance (Gollnick 1982c). The rapid increase in Pi associated with creatine phosphate splitting may be important in initially activating phosphorylase (Chasiotis et al. 1982).

3.2 Oxidative Enzyme Response 3.2.1 Oxidative Enzyme Response to Endurance Training Enzymes involved in oxidative phosphorylation are sensitive to endurance training (Holloszy 1975). For example, Gollnick et al. (1973a) reported a 95%


increase in succinic dehydrogenase (SOH) activity following 5 months of training. However, the proportionate increase in oxidative enzyme activity varies between the mitochondria, citrate cycle and cytoplasm (Holloszy 1975). Two enzymes, SOH (mitochondria) and maleate dehydrogenase (MOH; cytoplasm) in the oxidative phosphorylation pathway have been extensively assayed to determine if various training regimens have influenced this pathway. Neither of these enzymes are rate limiting (White et al. 1978). SOH represents an enzyme which has been reported to be covalently bound to the mitochondrial membrane and whose activity is generally thought to be indicative of total mitochondrial concentration (Gollnick 1982a,c), although Costill et al. (1979) did question if SOH activity was representative of mitochondrial level. In the untrained fibre SOH activity appears to be greatest in ST fibres and least in FTb fibres (ST > FTc > FTa > FTb) [Essen et al. 1975], although even within ST fibres there is a range of oxidative potentials (Pette & Spamer 1986). Furthermore, SOH activity appears to be even along the entire length of the fibre (Pette et al. 1980). The normal value of SOH activity in the vastus lateralis is approximately 6 to 7 ~mol/g/min (Saltin et al. 1977). Untrained adolescents and adult males presented similar SOH activity levels (Fournier et al. 1982). Three months running by adolescents increased their SOH activity by 42% to 9.1 ~mol/g/min. However, this does not approach the levels associated with middle distance and distance runners (Costill et al. I 976b). Similar results to that of Fournier et al. (1982) were reported by Taylor et al. (1981). Endurance training can enhance SOH activity levels (Bylund et al. 1977; Costill et al. 1973; Jansson et al. 1982; Svedenhag et al. 1983). Thus, it is not surprising that several endurance training studies have reported increments in SOH activity and V02max (Gollnick et al. 1973a; Taylor et al. 1978). The relationship between changes in SOH and V02max is not direct however. During periods of detraining SOH activity drops rapidly, while V02max does not (Gollnick & Saltin 1982b; Hen-

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riksson & Reitman 1977b; Houston et al. 1979). Anaerobic threshold appears to be related to oxidative metabolism more than to glycolytic metabolism (Ivy et al. 1980; Rusko et al. 1980). Rusko et al. (1980) reported that anaerobic threshold was correlated with SOH activity. Several studies have indicated increased mitochondrial enzyme activity with endurance training ranging from 40 to 90% (Andersen & Henriksson I 977b; Hurley et al. 1986; Jansson et al. 1982; Svedenhag et al. 1983). This is consistent with the SOH activity found in muscle of elite distance runners (20 to 25 ~mol/g/min). Similar values have been reported for highly trained orienteers whose gastrocnemius SOH activity levels were the same in both ST and FT fibres (Jansson & Kaijser 1977). It appears that the enzymatically determined increments in oxidative capability following endurance training are not solely confined to the ST fibres, but reflect changes in the FT fibres and indicate a high degree of adaptability in the FTa and FTb (Bylund et al. 1977; Jansson & Kaijser 1977). Chronic nerve stimulation of the FT tibialis anterior muscle of the rabbit resulted in a significant increase in SOH actvity in both FTa and FTb fibres (pette & Tyler 1983). Oxidative enzyme adaptation appears to be related to the amount of training and not fibre composition (Jansson & Kaijser 1977; Costill et al. 1976a). In addition the format of endurance training appears to influence the site of SOH adaptation. Seven weeks of interval training preferentially enhanced the SOH activity of FT fibres (Henriksson & Reitman 1976). In contrast, a continuous training format produced a selective SOH enhancement in ST fibres (Henriksson & Reitman 1976). MOH has been shown to increase activity levels with endurance training (Costill et al. 1979). In contrast to SOH, it appeared that MOH activity increased initially with training and then plateaued (Costill et al. 1979). Costill et al. (1979) reported that moderately and highly trained subjects had similar MOH activity (Costill et al. 1979). Therefore it may simply require a disproportionate amount of time and work to effect further changes in MOH activity.

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Andersen and Henriksson (I 977b), Bylund et al. (1977) and Svedenhag et al. (1983) have demonstrated dramatic increases in citrate synthase and cytochrome C oxidase activities with endurance training. Similar findings have been reported for 3hydroxyacyl-CoA dehydrogenase (HAD), an enzyme involved in fatty acid oxidation (Bylund et al. 1977). Continuous training increased the HAD activity. This may be due to the elevated concentration of arterial FFA and the reliance on FFA oxidation during prolonged heavy exercise (Jansson & Kaijser 1977). However, continuity oftraining may also be of importance in increasing HAD activity (Orlander et al. 1977). Orlander et al. (1977) investigated HAD activity in response to two 7week training periods separated by a week of inactivity. HAD activity was increased after the first, but not the second training period. The magnitude of change in activity levels of mitochondrial enzymes as a result of endurance training is well above the percentage increase in maximal oxygen uptake. However, these increments in enzyme activity are highly correlated with the enhanced capacity to meet a submaximal challenge following training (Gollnick & Saltin 1982b). Furthermore, it appears unlikely that enzymes are exposed to substrate concentrations that surpass the Michaelis constant (Km). Consequently, the disproportionate increase in enzyme activity may result in a greater control over reaction velocity. Following endurance training the Km for citrate synthase is more conducive to lipid oxidation (Gollnick & Saltin 1982b). Thus, more acetyl units are derived from fat than carbohydrate.

3.2.2 Oxidative Enzyme Response to Sprint Training Despite sprinters having SDH activity greater than untrained individuals, their level was less than middle distance and distance runners (Costill et al. 1976a). This difference may be related to the amount of work completed in training, or to differences between sprint and endurance training. No differences were observed in SDH activity between orienteers completing predominantly interval training and extreme distance running (Jansson &


Kaijser 1977). However, it is doubtful if these athletes were completing each interval at a sprint intensity. A training study with swimmers also demonstrated similar increments in HAD and SDH enzyme activity through interval and continuous training (Houston et al 1981). Differences may have been apparent if either or both training regimens altered performance parameters like peak ,,"02 associated with tethered swimming. For this to occur it may have been preferable to train a squad with a less extensive training history, or a longer duration and/or more intensive training regimen. Some early studies reported that sprint training which enhanced ,,"02max also enhanced the activity of some oxidative enzymes (Saltin et al. 1976; Staudte et al. 1973), but not all (Staudte et al. 1973; e.g., HAD). However, adolescent boys who demonstrated a significant increase in absolute ,,"02max from sprint training failed to demonstrate any change in SDH activity (Fournier et al. 1982; Taylor et al. 1981). A sprint training programme which resulted in significant increments in ,,"02max and MDH activity did not increase SDH activity significantly (Roberts et al. 1982). These results suggest that sprint training promotes cytoplasmic adaptation over mitochondrial adaptation. However citrate synthase activity was also increased by 6 weeks of sprint exercise (Jacobs et al. 1987).

4. Phosphagen Response 4.1 Phosphagen Response to Endurance Training ATP levels have been generally reported to be similar for FT and ST fibres (Gollnick et al. 1982a). However, Jansson and coworkers' (1982) findings indicate a greater concentration in FT than ST fibres. Creatine phosphate (CP) activity is greater in FT than ST fibres (Essen, 1978b). The human skeletal muscle phosphagen pool consists of approximately 15 mmol/kg wet muscle ofCP and 4.5 mmol/kg of ATP (Gollnick 1982a). This represents a limited energy reserve capable of supporting maximal exercise for only a few seconds (Gollnick 1982c). The notion of a phosphagen pool has been contested by Bessman and Carpenter (1985). They

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contend that there is a creatine phosphate shuttle and that creatine is the stimulus for enhanced V02 with exercise. In this shuttle CP is broken down at the myofibril and the resultant creatine is resynthesised at the mitochondria, to be reutilised again at the myofibril. However, the benefit of an enhanced phosphagen shuttle in endurance events would appear to be minimal (Gollnick I 982c). Yet Karlsson et al. (1971) reported that phosphagen depletion for submaximal tasks was less in physical education students than army conscripts. The students and conscripts had mean V02max values of 61 and 48 ml/kg/min, respectively. Subsequent studies have demonstrated that training not only reduced ATP and CP depletion for a given submaximal task (Constable et al. 1987; Karlsson et al. 1972), but also increased the concentration of ATP and CP with training (Eriksson et al. 1973; Karlsson et al. 1972). Phosphagen depletion for a given relative submaximal load does not change with training (Karlsson et al. 1972). 4.2 Phosphagen Response to Sprint Training Enhanced phosphagen stores and/or utilisation would potentially enhance sprint performances (Gollnick et al. 1982c). Hirvonen et al. (1987) reported that superior 100m running sprinters were able to utilise phosphagens more rapidly and completely than their lesser competitors over 80m. Whether this ability is due to a genetic predisposition or training has yet to be determined. There is no evidence to indicate that 8 weeks of sprint training enhances ATP or CP levels (Boobis et al. 1983a; Thorstensson et al. 1975). However, with an increase in muscle mass the absolute amount of phosphagen was greater following training in the Thorstensson et al. (1975) study. In the Boobis et al. (1983a) study CP activity was reduced by training. However, the extent of depletion of ATP and CP was not altered in a maximal 30-second cycling task (Boobis et al. 1983a). Thorstensson et al. (1975) did report that myokinase and CP activity was increased with sprint training. The peak muscle and blood lactate concentrations following a sprint task are not changed by training (Boobis et al. 1983a;

Roberts et al. 1982). Roberts et al. (1982) suggested that this may be due to increased ATP, CP, ATPase and myokinase activity following training. However, this proposition is still speculative. 4.3 Acute Phosphagen Response to Endurance Exercise Small decrements in ATP and CP concentrations were associated with workloads less than 60% of V02max while with greater submaximal workloads phosphagen depletion was more extensive (Knuttgen & Saltin 1972). The notion that phosphagen depletion is proportional to endurance work intensity has been borne out in several studies (Hultman et al. 1967; Karlsson et al. 1971). However, ATP and CP depletion has been shown to be similar at fatigue following endurance tasks lasting between 2 and 20 minutes (Karlsson & Saltin 1970). Phosphagen depletion is greater for interval than continuously structured tasks when equated in terms OfV02 (Essen 1977b). Furthermore, CP depletion is greatest in the initial minutes of a submaximal task (Hultman et al. 1967). CP depletion is always greater than ATP depletion in relative terms (Karlsson et al. 1972). Hultman et al. (1967) and Green et al. (1978) suggested that there is a 60% reduction in CP levels prior to reductions in ATP levels. More recent stimulation work involving rat tissue would suggest that CP and ATP depletion may vary between FTa and FTb fibres. This has yet to be verified in humans. 4.4 Acute Phosphagen Response to Sprint Exercise Traditionally it has been thought that phosphagen depletion precedes the initiation of glycolytic metabolism in sprint activities. However, there is now a substantial amount of data indicating that glycolytic metabolism is involved from the initiation of a sprint task (Boobis et al. 1983b; Cheetham et al. 1986; Hirvonen et aI. 1987; Jacobs et al. 1983). Thus, energy derived from glycolytic metabolism and phosphagens occurs for a short duration simultaneously, and represents the period of maxi-

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mal energy availability to the contractile apparatus (Hirvonen et al. 1987). Significant reductions in phosphagen stores have been reported in humans and animals following sprint activity (Jacobs et al. 1982; Snow et al. 1985). In the 30-second sprint running task of the Cheetham et al. (1986) study it was estimated that 63, 31.7 and 5.5% of the total ATP was derived from glycolysis, CP and local ATP depletion, respectively. In this time there were 64 and 37% reductions in CP and ATP stores, respectively. Similar reductions (CP 65%, ATP 42%) were reported by Boobis et al. (1983a,b) following 30 seconds of maximal cycling. This suggests that phosphagen depletion is related to task duration. Boobis et al. (1983b) reported that in a maximal cycling task lasting 6 seconds there were 36 and 8% reductions in CP and ATP, respectively. Thus, in the final 24 seconds of the maximal cycling task, CP and ATP reductions paralleled one another. However, the pattern of phosphagen depletion for activities lasting up to 10 seconds in duration may be a function of task modality and performance level of the participant (Hirvonen et al. 1987). The collective results of Hirvonen's subjects suggested that ATP levels were unaffected and CP levels were decreased following running sprints over distances between 40 and 100m. However, it was clear that the superior sprinters were able to utilise phosphagens more quickly and to a greater extent than lesser sprinters for distances up to 80m. At no time however, have ATP levels been decreased by more than 40 to 45% in humans folowing sprint tasks (Boobis et al. 1983a,b; Hirvonen et al. 1987; Jacobs et al. 1982). Whether this reduction in ATP is sufficient to reduce the number of crossbridges formed and thus cause fatigue is not clear (Cheetham et al. 1986). This scenario becomes more plausible if there is selective depletion of ATP from Ff fibres during sprint tasks. The work of Jansson et al. (1985) suggests this is possible. Hirvonen et al. (1987) argued that work rates were reduced when there was insufficient CP to saturate the available creatine kinase. Their results suggested that this occurred at approximately midpoint in a 100m sprint.

Sports Medicine /0 (6) 1990

5. Conclusion Many athletes endeavour to enhance both sprint and endurance performance. Unfortunately, there has been no research in the area of concurrent sprint and endurance training. It should not be presumed however, that there will be no interaction between sprint and endurance training. It has been shown that there can be both positive and negative interaction between strength and endurance training (Dudley & Djamil 1985; Hickson 1980; Sale et al. 1990). Consequently, research is required into the effects of concurrent endurance and sprint training. On balance, sprint and endurance exercise of either an acute or chronic nature has not been shown to alter the proportion of ST and Ff fibres, although there is some evidence to suggest that with extreme and prolonged training there may be fibre type conversion. Acute and chronic exercise does affect the substrate, metabolic and phosphagen profiles of skeletal muscle tissue and as a result does influence physical performance and success in sport. The utilisation of a particular metabolic pathway or recruitment of a particular fibre type, is dependent on the different physiological demands of the various modes of exercise. These differences are of interest to coaches and athletes as they allow them to utilise training regimens that focus on those parameters required for optimal performance in a specific motor activity. Thus, training programmes must be designed to be highly specific to the exercise demands of the particular activity. In addition, when designing the training programme, the coach must consider both the acute and chronic responses to a specific mode of exercise stress. This will help to ensure a proper emphasis of various training regimens and appropriate recovery periods within and between training sessions.

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Correspondence and reprints: Peter J Abernethy. School of Sport and Leisure Studies. St George Campus. University of New South Wales. P.O. Box 88. Oatley. NSW 2223. Australia.

Acute and Post-Exercise Physiological Responses to High-Intensity Interval Training in Endurance and Sprint Athletes.

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