The relationships between absolute peak muscle power (Wpeak), muscle cross sectional area (CSAtot, i.e. the sum of both thigh and calf CSA) and muscle high energy phosphate concentration (adenosine 5'-triphosphate [ATP] and phosphocreatine concentrations [PC]) were studied in 47 subjects classified into five groups: A, 10 sedentary (S) subjects aged 20-35 years; B, 9 S aged 35-50 years; C, 9 S aged more than 50 years; D, 13 children aged 8-13 years; and E, 6 athletes (top level volleyball players) aged 24 (SD 3) years. The Wpeak was measured during a maximal vertical high jump off both feet on a force platform. The CSAtot was measured anthropometrically. The [ATP] and [PC] were determined by 31Phosphorus nuclear magnetic resonance spectroscopy. The Wpeak decreased with age, was 65% lower in D than in A, and 43% higher in E than in A. The CSAtot did not vary with age, was 45% smaller in D than in A, and 15% greater in E than in A. The [ATP] and [PC] were essentially the same in all groups. The changes observed in Wpeak were only partially accounted for by changes in CSAtot. Therefore, in addition to the variables investigated, other factors appear to have been involved in the determination of Wpeak with increasing age and training. An important role may be played by hormonal, particularly at puberty, and neural factors.

The effects of supplemental oxygen (O2) versus air on working calf muscle metabolism were studied in seven patients with stable chronic obstructive pulmonary disease (COPD) and chronic hypoxemia (PaO2 = 57 +/- 3 SE mm Hg) and seven age-matched control subjects. Oxygen and air were randomly administrated at 24-h intervals, and O2 flow rate was adjusted to correct hypoxemia (PaO2 = 87 +/- 4 mm Hg) in the COPD group. The relative concentrations of ATP, phosphocreatine (PCr), inorganic phosphate (Pi), phosphomonoesters (PME), and the intracellular pH (pHi) were determined with 31P magnetic resonance spectroscopy at rest, during a graded standardized and localized exercise protocol (360 active plantar flexions), and during recovery. In resting muscle no significant effect of added O2 was demonstrable in each group with regard to pHi, Pi/PCr, and ATP/(PCr+Pi+PME) ratios. Mechanical data were similar between the two groups and between the two tests during the whole exercise. The indices of muscular oxidative metabolism (Pi/PCr and pHi at the end of exercise and recovering PCr resynthesis rate) were impaired in the COPD group compared with that in the control group during air (all p < 0.05). All these parameters were significantly improved with added O2 in the COPD group (p < 0.05), whereas no similar effects were observed in the control group. However, these beneficial effects were incomplete since the exercising Pi/PCr ratio remained higher in the COPD group than in the control group during added O2. This energetic muscular impairment could correspond to tissular damage related to chronic hypoxemia.

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These findings imply that hypoxic hypoxia significantly raises CBV in different brain areas, in proportion to the severity of the insult. These results support the notion that the vasodilatory effect of hypoxia is deleterious in patients with reduced intracranial compliance.