Maintained peak leg and pulmonary VO 2 despite substantial reduction in muscle mitochondrial capacity

We recently reported the circulatory and muscle oxidative capacities of the arm after prolonged low‐intensity skiing in the arctic ( B oushel et al., 2014). In the present study, leg VO 2 was measured by the Fick method during leg cycling while muscle mitochondrial capacity was examined on a biopsy of the vastus lateralis in healthy volunteers (7 male, 2 female) before and after 42 days of skiing at 60% HR max. Peak pulmonary VO 2 (3.52 ± 0.18 L.min −1 pre vs 3.52 ± 0.19 post) and VO 2 across the leg (2.8 ± 0.4L.min −1 pre vs 3.0 ± 0.2 post) were unchanged after the ski journey. Peak leg O 2 delivery (3.6 ± 0.2 L.min −1 pre vs 3.8 ± 0.4 post), O 2 extraction (82 ± 1% pre vs 83 ± 1 post), and muscle capillaries per mm 2 (576 ± 17 pre vs 612 ± 28 post) were also unchanged; however, leg muscle mitochondrial OXPHOS capacity was reduced (90 ± 3 pmol.sec −1 .mg −1 pre vs 70 ± 2 post, P  < 0.05) as was citrate synthase activity (40 ± 3 μmol.min −1 .g −1 pre vs 34 ± 3 vs P  < 0.05). These findings indicate that peak muscle VO 2 can be sustained with a substantial reduction in mitochondrial OXPHOS capacity. This is achieved at a similar O 2 delivery and a higher relative ADP‐stimulated mitochondrial respiration at a higher mitochondrial p50. These findings support the concept that muscle mitochondrial respiration is submaximal at VO 2max , and that mitochondrial volume can be downregulated by chronic energy demand.