Reduced muscle oxidative capacity is independent of O2 availability in elderly people

Impaired O-2 transport to skeletal muscle potentially contributes to the decline in aerobic capacity with aging. Thus, we examined whether (1) skeletal muscle oxidative capacity decreases with age and (2) O-2 availability or mitochondrial capacity limits the maximal rate of mitochondrial ATP synthesis in vivo in sedentary elderly individuals. We used P-31-magnetic resonance spectroscopy (P-31-MRS) to examine the PCr recovery kinetics in six young (26 +/- 10 years) and six older (69 +/- 3 years) sedentary subjects following 4 min of dynamic plantar flexion exercise under different fractions of inspired O-2 (FiO(2), normoxia 0.2; hyperoxia 1.0). End-exercise pH was not significantly different between old (7.04 +/- 0.10) and young (7.05 +/- 0.04) and was not affected by breathing hyperoxia (old 7.08 +/- 0.08, P > 0.05 and young 7.05 +/- 0.03). Likewise, end-exercise PCr was not significantly different between old (19 +/- 4 mM) and young (24 +/- 5 mM) and was not changed in hyperoxia. The PCr recovery time constant was significantly longer in the old (36 +/- 9 s) compared to the young in normoxia (23 +/- 8 s, P < 0.05) and was not significantly altered by breathing hyperoxia in both the old (35 +/- 9 s) and young (29 +/- 10 s) groups. Therefore, this study reveals that the muscle oxidative capacity of both sedentary young and old individuals is independent of O-2 availability and that the decline in oxidative capacity with age is most likely due to limited mitochondrial content and/or mitochondrial dysfunction and not O-2 availability.