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

Abstract

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 31 P-magnetic resonance spectroscopy ( 31 P-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.

Assessment of in vivo skeletal muscle mitochondrial respiratory capacity in humans by near‐infrared spectroscopy: a comparison with in situ measurements

“…; Layec et al . ), while others suggest declines in respiratory capacity with age may be more closely associated with reduced physical activity levels (Larsen et al . , b ).…”

The role and regulation of erythropoietin (EPO) and its receptor in skeletal muscle: how much do we really know?

“…However, these mice displayed a 100-fold higher serum EPO concentration when compared to WT; therefore, the physiological relevance of such results is questionable. On the other hand, it has previously been shown that hyperoxia could augment muscle oxidative capacity (Ploutz-Snyder et al, 1996), although other studies have failed to reproduce similar results (Perry et al, 2007; Layec et al, 2012). It can therefore be hypothesized that an EPO-induced increase in oxygen supply could mediate a shift towards a more oxidative muscle, especially at supraphysiological EPO concentrations.…”

In vivoevidence of an age-related increase in ATP cost of contraction in the plantar flexor muscles

“…Using a hyperoxic mixture, our group recently reported that muscle oxidative capacity in the calf muscle of older individuals was independent of O 2 availability [70], implying further that peripheral O 2 supply to the lower leg is well preserved with age. Somewhat in contrast with this work and the present study, Wray et al [11], also from our group, reported decreased post-exercise tissue perfusion measured by ASL (arterial spin labelling) imaging in the calf muscle of elderly subjects.…”