Maintained peak leg and pulmonary VO2 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 (Boushel etal., 2014). In the present study, leg VO2 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 42days of skiing at 60% HR max.Peak pulmonary VO2 (3.52 +/- 0.18L.min(-1) pre vs 3.52 +/- 0.19 post) and VO2 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 +/- 0.2L.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 musclemitochondrial OXPHOS capacity was reduced (90 +/- 3pmol.sec(-1).mg(-1) pre vs 70 +/- 2 post, P<0.05) as was citrate synthase activity (40 +/- 3mol.min(-1).g(-1) pre vs 34 +/- 3 vs P<0.05). These findings indicate that peak muscle VO2 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 VO2max, and that mitochondrial volume can be downregulated by chronic energy demand.