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

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Abstract
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 V̇O2max and/or glycogen stores are depleted. Long distance runners have greater ST and FT fibre areas than untrained controls. However, 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 V̇O2maxare 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.