In previous studies we have been able to demonstrate tighter metabolic control of muscle metabolism during prolonged steady-state exercise 5 to 6 days after the initiation of training and well before changes in oxidative potential. To examine whether the metabolic adaptations are manifested during the non-steady-state adjustment to submaximal exercise, 11 male subjects (Vo2 peak, 45 +/- 2.4 mL.kg(-1). min(-1), X +/- SE) performed 98 min of cycle exercise at 67% of Vo2 peak prior to and following 3 to 4 days of training for 2 h per day. Analysis of lactate concentration (mmol/kg dry weight) in samples rapidly extracted from vastus lateralis indicated reductions (p < 0.05) of 44% at 3 min ( 42.1 +/- 7.1 vs. 23.6 +/- 7.7), 29% at 15 min (35.4 +/- 6.4 vs. 25.0 +/- 6.0), and 32% at 98 min (22.9 +/- 6.9 vs. 15.6 +/- 3.2) with training. Training also resulted in higher phosphocreatine and lower creatine and P(i) values that were not specific to any exercise time point. In addition, Vo2 was not altered either during the non-steady state or during the steady-state phases of exercise. These results suggest that at least part of the tightening of the metabolic control and the apparent reduction in glycogenolysis and glycolysis in response to short-term training occurs during the adjustment phase to steady-state exercise.

Muscle biopsies were performed on the vastus lateralis muscle prior to and during a high-resistance training (HRT) programme in order to examine the effects of hypertrophy on sarcoplasmic reticulum Ca2+ ATPase activity at rest and during exercise. In six male untrained volunteers (peak aerobic power, Vo2 peak = 3.39 +/- 0.13 L min-1, mean +/- SE), the resting Ca2+ ATPase activity (mumol-min-1 g wet wt-1) at 0 (4.89 +/- 0.20), 4 (5.62 +/- 0.56), 7 (5.15 +/- 0.41) and 12 (4.82 +/- 0.11) weeks was unchanged by HRT. During cycle ergometer exercise, prior to training, Ca(2+)-ATPase was reduced (P < 0.05) by 14% during the initial 30 min at 58% Vo2 peak and (P < 0.05) a further 19% during 30 min at 72% Vo2 peak. Following 7 and 12 weeks of training, the decreases in SR Ca(2+)-ATPase were less pronounced (P < 0.05). These results indicate that muscle hypertrophy, although incapable of altering Ca(2+)-ATPase pump activity at rest, can attenuate the decrease observed in exercise by mechanism(s) as yet unknown.

The purpose of this study was to investigate the significance of fiber type and the effects of the duration of ischemia on metabolic and contractile function of skeletal muscle. Under anesthesia, the distal tendons of the fast twitch extensor digitorum longus (EDL) and slow twitch soleus (SOL) muscles of the right hindlimb of female Wistar rats (250 to 300 gm) were connected to force transducers. Rats were assigned to group 1, 1 hour of ischemia; group 2, 2 hours of ischemia; or group 3, 3 hours of ischemia (n = 10 for each group). After ischemia, muscles were assessed for 2 hours of reperfusion. In both muscles, isometric twitch (Pt) and tetanus (Po) and 11 metabolic parameters were measured and compared with controls. After 1, 2, or 3 hours of ischemia Pt and Po were significantly (p < 0.05) lower than preischemic values. After 2 hours of reperfusion, forces and metabolic parameters of group 1 recovered to preischemic levels. However, contractile function of either muscle failed to recover fully after 2 hours of ischemia and 2 hours of reperfusion (SOL: Pt = 43.7 +/- 12 percent of initial; EDL: Pt = 32.2 +/- 9.2 percent) or after 3 hours of ischemia and 2 hours of reperfusion (SOL: Pt = 26.8 +/- 11 percent of initial; EDL: Pt = 19.3 +/- 6.8 percent). Although ADP and AMP recovered to preischemic levels in both muscles after 2 hours of ischemia and 2 hours of reperfusion, ATP recovered to just 70 percent in the soleus muscles (13.4 +/- 1.7 mmol/kg dry weight) and 60 percent in the extensor digitorum longus muscles (17.93 +/- 4.1 mmol/kg dry weight). After 3 hours of ischemia and 2 hours of reperfusion, ATP was further significantly (p < 0.05) decreased in the soleus muscles (48 percent initial) but not in the extensor digitorum longus muscles. Significant partial correlation coefficients (p < 0.005) were obtained between ATP levels and Pt (SOL: r = 0.757; EDL: r = 0.619) or Po (SOL: r = 0.810; EDL: r = 0.759). For this rat hindlimb model, we conclude that both fiber type and the duration of ischemia significantly affect metabolic and contractile function.

Residence at extreme altitude results in pronounced reductions in muscle mass and the cross-sectional area of the slow and fast twitch fibre types. The reductions in muscle contractile proteins appear not to be accompanied by significant alterations in the proportion of the major fibre types and consequently in the myosin heavy chain isozymes. Acclimatization to extreme altitude is also accompanied by a marked reduction in mitochondrial potential that occurs regardless of activity status. At least during mountaineering expeditions, the maximal activity of cytosolic enzymes involved in anaerobic function appear to be unaffected. In contrast, extreme hypobaric hypoxia with low exercise appears to result in loss of the activities of cytosolic enzymes. The attenuation of glycolysis during exercise accompanying acclimatization does not appear to be due to adaptations in fibre size, capillarization or mitochondrial potential. Rather, evidence from both acclimatization and training at sea level suggests that a depressed blood epinephrine concentration is involved.

We investigated the potential role of selected excitation-contraction coupling processes in females with work-related myalgia (WRM) by comparing WRM with healthy controls (CON) using tissue from extensor carpi radialis brevis (ECRB) and trapezius (TRAP) muscles. For the ECRB, age (mean ± SE) was 29.6 ± 3.5 years for CON (n = 9) and 39.2 ± 2.8 years for WRM (n = 13), while for the TRAP, the values were 26.0 ± 2.1 years for CON (n = 7) and 44.6 ± 2.9 years for WRM (n = 11). For the sarcoplasmic reticulum (SR) of the ECRB, WRM displayed concentrations (nmol·(mg protein)(-1)·min(-1)) that were lower (P < 0.05) for Total (202 ± 4.4 vs 178 ± 7.1), Basal (34 ± 1.6 vs 30.1 ± 1.3), and maximal Ca(2+)-ATPase activity (Vmax, 168 ± 4.9 vs 149 ± 6.3), and Ca(2+)-uptake (5.06 ± 0.31 vs 4.13 ± 0.29), but not SERCA1a and SERCA2a isoforms, by comparison with CON. When age was incorporated as a co-variant, Total, Basal, and Ca(2+)-uptake remained different from CON (P < 0.05), but not Vmax (P = 0.13). For TRAP, none of the ATPase properties differed between groups (P > 0.05) either before or following adjustment for age. No differences (P > 0.05) were observed between the groups for Ca(2+)-release in the SR for either TRAP or ECRB. Similarly, no deficiencies, regardless of muscle, were noted for either the Na(+)-K(+)-ATPase content or the α and β subunit isoform distribution in WRM. This preliminary study provides a basis for further research, with expanded numbers, investigating the hypothesis that abnormalities in SR Ca(2+)-regulation are involved in the cellular etiology of WRM.