Abstract

The cellular mechanisms for the age‐related loss in muscle power output and increased fatigability during dynamic contractions remain unresolved. We recently observed that the depressive effects of fatiguing levels of acidosis (H+: pH 6.2) and inorganic phosphate (Pi: 30 mM) did not differ in muscle fibers from young compared with old men. However, the effects of these metabolites may have been saturated in the severe fatigue‐mimicking condition, potentially masking any age differences in the sensitivity of the cross‐bridge to these metabolites. Therefore, in this study we compared the contractile mechanics of myofibers (n = 327) from the vastus lateralis of 13 young (20‐32 years, 7 women) and 12 older adults (70‐90 years, 6 women) in conditions mimicking quiescent muscle and a range of fatiguing levels of acidosis (pH 6.8, 6.6, 6.2) and Pi(12, 20, 30 mM). The knee extensors of the older adults demonstrated hallmark signs of aging muscle including 19% lower thigh lean mass, 60% lower absolute power output, and ~1.8‐fold greater fatigability compared with young. Single fiber force, shortening velocity, and power decreased progressively with increasing concentrations of H+ and Pi; however, there were no age or sex differences in the depressive effects of these metabolites in any of the fatigue‐mimicking conditions. The cross‐sectional area of the fast fibers was 41% smaller in older compared with young adults, which corresponded with lower absolute fiber power. In contrast, there were no differences in fast fiber size‐specific power, indicating the age‐related decline in absolute fiber power was explained entirely by the differences in fiber size. Estimates of the amount of fast muscle in the thigh were associated with age‐related differences in whole‐muscle power output (r=0.78). These data suggest that the age‐related loss in whole‐muscle power output is primarily determined by the atrophy of fast fibers for both men and women, but that the age‐related increase in fatigability cannot be explained by an increased sensitivity of the cross‐bridge to H+ and Pi.

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