Initial aerobic power does not alter muscle metabolic adaptations to short-term training

Abstract

To investigate the hypothesis that training-induced increases in muscle mitochondrial potential are not obligatory to metabolic adaptations observed during submaximal exercise, regardless of peak aerobic power (V˙o 2 peak) of the subjects, a short-term training study was utilized. Two groups of untrained male subjects ( n = 7/group), one with a high (HI) and the other with a low (LO)V˙o 2 peak(means ± SE; 51.4 ± 0.90 vs. 41.0 ± 1.3 ml ⋅ kg−1 ⋅ min−1; P< 0.05), cycled for 2 h/day at 66–69% ofV˙o 2 peak for 6 days. Muscle tissue was extracted from vastus lateralis at 0, 3, and 30 min of standardized cycle exercise before training (0 days) and after 3 and 6 days of training and analyzed for metabolic and enzymatic changes. During exercise after 3 days of training in the combined HI + LO group, higher ( P < 0.05) concentrations (mmol/kg dry wt) of phosphocreatine (40.5 ± 3.4 vs. 52.2 ± 4.2) and lower ( P < 0.05) concentrations of Pi (61.5 ± 4.4 vs. 53.3 ± 4.4), inosine monophosphate (0.520 ± 0.19 vs. 0.151 ± 0.05), and lactate (37.9 ± 5.5 vs. 22.8 ± 4.8) were observed. These changes were also accompanied by reduced levels of calculated free ADP, AMP, and Pi. All adaptations were fully expressed by 3 min of exercise and by 3 days of training and were independent of initialV˙o 2 peak levels. Moreover, maximal activity of citrate synthase, a measure of mitochondrial capacity, was only increased with 6 days of training (5.71 ± 0.29 vs. 7.18 ± 0.37 mol ⋅ kg protein−1 ⋅ h−1; P < 0.05). These results demonstrate that metabolic adaptations to prolonged exercise occur within the first 3 days of training and during the non-steady-state period. Moreover, neither time course nor magnitude of metabolic adaptations appears to depend on increases in mitochondrial potential or on initial aerobic power.

Metabolic, enzymatic, and transporter responses in human muscle during three consecutive days of exercise and recovery

“…Given the acute reductions observed for some enzymes, such as COX and hexokinase during exercise, it is clear that the reductions are transitory, recovering between exercise days (hexokinase) or by the 2nd day of inactivity. The failure to find increases in the maximal activities of the CAC and the rate-limiting enzymes of glycogenolysis and glycolysis during the recovery days was not surprising, given the results of several previous experiments that have reported no change in response to several sessions of exercise (21,61). To our knowledge, decreases in COX have not been reported with either exercise or short-term training.…”

“…It is clear from these results that 2 days of exercise, prior to measurement on the 3rd day, did not protect muscle phosphorylation potential as we have previously reported with shortterm training. In our previous studies, the shortest period of training employed using prolonged submaximal exercise was 3 days with the metabolic adaptations measured on the 4th day (21). It would appear that an additional day of prolonged exercise is needed to observe clear improvements in phosphorylation potential.…”

“…These studies indicate that training-like adaptations can be observed within the first few sessions of regular exercise in the absence of increases in V max of a range of mitochondrial enzymes (21,28,61). Current evidence indicates that the metabolic adaptations are mediated by events outside of the muscle, namely, increased V O 2 kinetics during the nonsteady rate (60), which occurs secondary to a more rapid adjustment in blood flow (71).…”

Comparative effects of a low-carbohydrate diet and exercise plus a low-carbohydrate diet on muscle sarcoplasmic reticulum responses in males

“…For these tests, respiratory gas exchange was measured before exercise and for 4-to 5-min periods at selected times during the exercise. All respiratory gas exchange measurements (both progressive and prolonged protocols) were made using an open-circuit gas collection system, standardized by Hughson et al (28), as commonly employed in our laboratory (19). The gas collection system was calibrated daily, 30 min before each test session, by using standardized gas samples of known concentrations.…”

Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

“…Although, we could find no evidence for a greater impairment in neuromuscular function during submaximal exercise in hypoxia, such may not be the case with progressive exercise. In contrast to submaximal exercise where force levels and motor unit firing rates are relatively low and V O 2 and muscle energy homeostasis are well protected (24,50), the generation of increased forces needed to perform progressive exercise exaggerates the demands on membrane excitability and V O 2 requirements and, in the process, greatly elevates metabolic by-product accumulation in muscle (6,49).…”