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Maximum oxidative capacity of skeletal muscle measured by in vivo phosphorus magnetic resonance spectroscopy (³¹P-MRS) declines with age, and negatively affects whole-body aerobic capacity. However, it remains unclear whether the loss of oxidative capacity is caused by reduced volume and function of mitochondria or limited substrate availability secondary to impaired muscle perfusion. Therefore, we sought to elucidate the role of muscle perfusion on the age-related decline of muscle oxidative capacity and ultimately whole-body aerobic capacity. Muscle oxidative capacity was assessed by ³¹P-MRS post-exercise phosphocreatine recovery time (τ_PCr), with higher τ_PCr reflecting lower oxidative capacity, in 75 healthy participants (48 men, 22–89 years) of the Genetic and Epigenetic Signatures of Translational Aging Laboratory Testing study. Muscle perfusion was characterized as an index of blood volume at rest using a customized diffusion-weighted MRI technique and analysis method developed in our laboratory. Aerobic capacity (peak-VO₂) was also measured during a graded treadmill exercise test in the same visit. Muscle oxidative capacity, peak-VO₂, and resting muscle perfusion were significantly lower at older ages independent of sex, race, and body mass index (BMI). τ_PCr was significantly associated with resting muscle perfusion independent of age, sex, race, and BMI (p-value = 0.004, β = −0.34). τ_PCr was also a significant independent predictor of peak-VO₂ and, in a mediation analysis, significantly attenuated the association between muscle perfusion and peak-VO₂ (34% reduction for β in perfusion). These findings …