ENERGY SUPPLY AND MUSCLE FATIGUE IN HUMANS

Limitations in energy supply is a classical hypothesis of muscle fatig ue. The present paper reviews the evidence available from human studie s that energy deficiency is an important factor in fatigue. The maxima l rate of energy expenditure determined in skinned fibres is close to the rate of adenosine triphosphate (ATP) utilisation observed in vivo and data suggest that performance during short bursts of exercise (<5 s duration) primarily is limited by other factors than energy supply ( e.g. V-max of myosine adenosine triphosphatase (ATPase), motor unit re cruitment, engaged muscle mass). Within 10 s of exercise maximal power output decreases considerably and coincides with depletion of phospho creatine. During recovery, maximal force and power output is restored with a similar time course as the resynthesis of phosphocreatine. Incr eases in muscle store of phosphocreatine through dietary supplementati on with creatine increases performance during high-intensity exercise. These findings support the hypothesis that energy supply limits perfo rmance during high-intensity exercise. It is well documented that pre- exercise muscle glycogen content is related to performance during mode rate intensity exercise. Recent date indicates that the interfibre var iation in phosphocreatine is large after prolonged exercise to fatigue and that some fibres are depleted to the same extent as after high-in tensity exercise. Despite relatively small decreases in ATP, the produ cts of ATP hydrolysis (Pi and free ADP) may increase considerably. Fre eADP calculated from the creatine kinase reaction increases 10-fold bo th after high-intensity exercise and after prolonged exercise to fatig ue. It is suggested that local increases in ADP may reach inhibitory l evels for the contraction process.