Reduced muscle oxidative capacity is independent of O2 availability in elderly people
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Impaired O2 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) O2 availability or mitochondrial capacity limits the maximal rate of mitochondrial ATP synthesis in vivo in sedentary elderly individuals. We used 31P-magnetic resonance spectroscopy (31P-MRS) to examine the PCr recovery kinetics in six young (26ᱰ years) and six older (69᳠years) sedentary subjects following 4 min of dynamic plantar flexion exercise under different fractions of inspired O2 (FiO2, normoxia 0.2; hyperoxia 1.0). End-exercise pH was not significantly different between old (7.04ᰮ10) and young (7.05ፊ0.04) and was not affected by breathing hyperoxia (old 7.08ᰮ08, P>0.05 and young 7.05ᰮ03). Likewise, end-exercise PCr was not significantly different between old (19ᴠmM) and young (24ᵠmM) and was not changed in hyperoxia. The PCr recovery time constant was significantly longer in the old (36Ṡs) compared to the young in normoxia (23Ḡs, P<0.05) and was not significantly altered by breathing hyperoxia in both the old (35Ṡs) and young (29ᱰ s) groups. Therefore, this study reveals that the muscle oxidative capacity of both sedentary young and old individuals is independent of O2 availability and that the decline in oxidative capacity with age is most likely due to limited mitochondrial content and/or mitochondrial dysfunction and not O2 availability.
Medical Physiology not elsewhere classified