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Oxidative capacity interacts with oxygen delivery to determine maximal O2 uptake in rat skeletal muscles in situ

By Russell T Hepple, Jason L Hagen and Dan J Krause


Based on proportional changes in V̇O2,max with alterations in O2 delivery, it is widely held that O2 availability limits V̇O2,max. In contrast, reductions in V̇O2,max are also seen when mitochondrial oxidative capacity is reduced. Taken collectively, these prior results are consistent with the notion that there is not a single-step limitation to V̇O2,max. We used a pump-perfused rat hindlimb model to test the hypothesis that combining moderate reductions in O2 delivery and mitochondrial oxidative capacity would yield a greater reduction in V̇O2,max than seen when performing each intervention independently, demonstrating an interaction between O2 supply and mitochondrial oxidative capacity in determining V̇O2,max. Four groups of animals were studied: two in high O2 delivery conditions (hindlimb O2 delivery: 88 ± 1 μmol O2 min−1; mean ± s.e.m.) and two in moderately reduced O2 delivery conditions (66 ± 2 μmol O2 min−1). One group at each level of O2 delivery was treated with 0.1 μM myxothiazol to reduce mitochondrial oxidative capacity via competitive inhibition of NADH cytochrome c reductase. V̇O2,max in control animals (no myxothiazol) was 29 % lower in the moderately reduced O2 delivery group (592 ± 24 mmol O2 min−1 (100 g)−1); P < 0.05) than in the high O2 delivery group (833 ± 63 μmol O2 min−1 (100 g)−1). Similarly, V̇O2,max was reduced by 29 % (594 ± 22 μmol O2 min−1 (100 g)−1); P < 0.05) in myxothiazol-treated animals in high O2 delivery conditions compared to control animals in high O2 delivery conditions. When myxothiazol treatment was combined with moderately reduced O2 delivery, V̇O2,max was reduced by an additional 18 % (484 ± 21 μmol O2 min−1 (100 g)−1); P < 0.05) compared to either intervention performed independently. These results show that O2 supply and mitochondrial oxidative capacity interact to determine V̇O2,max

Topics: Original Articles
Publisher: Blackwell Science Inc
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Provided by: PubMed Central
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