Abstract

It is unclear whether the full oxygen (O2) consuming capacity of skeletal muscle mitochondria (mitoVO2max) is utilized during whole-body, maximal aerobic exercise. PURPOSE: We sought to determine if muscle O2 delivery limitations during cycling exercise prevent mitochondria from reaching mitoVO2max and if augmenting mass-specific O2 delivery, by reducing the amount of exercising muscle with single leg knee extension (KE), would allow muscle VO2max to reach mitoVO2max. METHODS: mitoVO2max (i.e convergent State 3 respiration) was assessed in permeabilized fibers biopsied from the vastus lateralis of 11 young males of varying aerobic fitness (pulmonary VO2max: 32-64 ml/kg/min). Muscle VO2max and O2 delivery during cycling and KE were determined with blood drawn from catheters placed in the femoral artery and vein and blood flow was simultaneously measured by Doppler ultrasound. Leg muscle mass was measured anthropometrically. RESULTS: During cycling exercise muscle O2 delivery (157± 17 ml/kg/min) failed to reach rates similar to mitoVO2max (551 ± 56 ml/kg/min; P<0.05) which yielded a muscle VO2max of 144 ± 7 ml/kg/min that was only to 29 ± 3% of mitoVO2max. During KE muscle O2 delivery was significantly elevated compared to cycling (512 ± 31 ml/kg/min; P<0.05) which resulted in a much greater muscle VO2max (385± 28 ml/kg/min; P<0.05). However, despite the augmented O2 delivery during KE muscle VO2max was still significantly less than mitoVO2max (73±7% of mitoVO2max, P<0.05). Interestingly, the greater a subject’s aerobic fitness, the less they utilized their full mitochondrial capacity (r=-0.60, P<0.05). CONCLUSIONS: Increasing mass-specific O2 delivery by switching from large to small muscle mass exercise within the same limb allowed muscle VO2max to approach mitoVO2max, suggesting that limited O2 delivery prevents mitochondria from maximally respiring during whole-body maximal aerobic exercise. Surprisingly, even during maximal KE, a modality reported to elicit the highest mass-specific rates of O2 consumption, much of the mitochondria’s potential to consume oxygen, especially among endurance-trained subjects, was left unrealized. The function of this untapped mitochondrial respiratory capacity is unclear, but may be related to substrate utilization and endurance performance.

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