ADAPTATIONS IN MUSCLE METABOLISM TO PROLONGED VOLUNTARY EXERCISE AND TRAINING

In previous research we established using a short-term (5-7 days) trai ning model that increases in muscle oxidative potential are not a prer equisite for the characteristic energy metabolic adaptations (lower la ctate, glycogen depletion, and phosphocreatine hydrolysis) observed du ring prolonged exercise. To investigate whether increased muscle aerob ic potential further potentiates the metabolic adaptive response, seve n healthy male volunteers [maximal O-2 uptake (Vo(2max)) = 45.1 +/- 1. 1 (SE) ml.kg(-1).min(-1)] engaged in an 8-wk training program consisti ng of 2 h of cycle exercise at 62% of pretraining Vo(2max), 5-6 times/ wk. Analysis of tissue samples obtained from the vastus lateralis aft er 60 min of exercise revealed that by 4 wk of training muscle lactate concentration, phosphocreatine hydrolysis, and glycogen depletion wer e depressed (all P < 0.05). Further training for 4 wk had no additiona l effect (P > 0.05). The ratio of fructose B-phosphate to fructose 1,6 -phosphate, an index of phosphofructokinase activity, was not altered with training. Muscle oxidative potential as estimated from the maxima l activity of succinic dehydrogenase increased by 31% by 4 wk of train ing (P < 0.05) before plateauing during the final 4 wk of training. Th e increase in Vo(2max) of 15.6% (P < 0.05) noted with training was als o primarily expressed during the initial 4 wk. O-2 uptake during subma ximal exercise was unchanged. Because the metabolic response was simil ar in magnitude to that previously observed with short-term training, we concluded that, at least for the conditions of this study, the deve lopment of increased muscle aerobic potential is of minimal consequenc e on the magnitude of the energy metabolic adaptations examined.