Time-dependent effects of short-term training on muscle metabolism during the early phase of exercise.

In this study, we investigated the hypothesis that the metabolic adaptations observed during steady-state exercise soon after the onset of training would be displayed during the nonsteady period of moderate exercise and would occur in the absence of increases in peak aerobic power (Vo2peak) and in muscle oxidative potential. Nine untrained males [age = 20.8 +/- 0.70 (SE) yr] performed a cycle task at 62% Vo2peak before (Pre-T) and after (Post-T) training for 2 h/day for 5 days at task intensity. Tissue samples extracted from the vastus lateralis at 0 min (before exercise) and at 10, 60, and 180 s of exercise, indicated that at Pre-T, reductions (P < 0.05) in phosphocreatine and increases (P < 0.05) in creatine, inorganic phosphate, calculated free ADP, and free AMP occurred at 60 and 180 s but not at 10 s. At Post-T, the concentrations of all metabolites were blunted (P < 0.05) at 60 s. Training also reduced (P < 0.05) the increase in lactate and the lactate-to-pyruvate ratio observed during exercise at Pre-T. These adaptations occurred in the absence of change in Vo2peak (47.8 +/- 1.7 vs. 49.2 +/- 1.7 mlxkg(-1)xmin(-1)) and in the activities (molxkg protein(-1)xh(-1)) of succinic dehydrogenase (3.48 +/- 0.21 vs. 3.77 +/- 0.35) and citrate synthase (7.48 +/- 0.61 vs. 8.52 +/- 0.65) but not cytochrome oxidase (70.8 +/- 5.1 vs. 79.6 +/- 6.6 U/g protein; P < 0.05). It is concluded that the tighter metabolic control observed following short-term training is initially expressed during the nonsteady state, probably as a result of increases in oxidative phosphorylation that is not dependent on changes in Vo2peak while the role of oxidative potential remains uncertain.

Failure of hypoxia to exaggerate the metabolic stress in working muscle following short-term training.

This study investigated the effects of hypoxia (experiment 1) and the effects of hypoxia following short-term training (experiment 2) on metabolism in working muscle. In experiment 1, eight males with a peak aerobic power (VO2peak) of 45 +/- 1.7 ml x kg(-1) x min(-1) (x +/- SE) cycled for 15 min at 66.1 +/- 2.1% VO2peak while breathing room air [normoxia (N)] or 14% O(2) [hypoxia (H)]. In experiment 2, nine males with a VO2peak of 43.3 +/- 1.6 ml x kg(-1) x min(-1) performed a similar protocol at 60.7 +/- 1.4% VO2peak during N and during H following 5 days of submaximal exercise training (H + T). Tissue samples extracted from the vastus lateralis before exercise and at 1, 3, and 15 min of exercise indicated that compared with N, H resulted in lower (P < 0.05) concentrations (mmol/kg dry wt) of creatine phosphate and higher (P < 0.05) concentrations of creatine, inorganic phosphate, and lactate, regardless of exercise time. When the exercise was performed at H + T and compared with N, no differences were observed in creatine phosphate, creatine, inorganic phosphate, and lactate, regardless of duration. Given the well-documented effects of the short-term training model on elevating VO2 kinetics and attenuating the alterations in high-energy phosphate metabolism and lactate accumulation, it would appear that the mechanism underlying the reversal of these adaptations during H is linked to a more rapid increase in oxidative phosphorylation, mediated by increased oxygen delivery and/or mitochondrial activation.