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 (Boushel 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...

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Bibliographic Details
Published in:Scandinavian Journal of Medicine & Science in Sports
Main Authors: Boushel, Robert, Gnaiger, E., Larsen, F. J., Helge, J. W., González-Alonso, J., Ara, I., Munch-Andersen, T., van Hall, G., Søndergaard, Hans, Saltin, B., Calbet, J. A. L.
Format: Article in Journal/Newspaper
Language:English
Published: 2015
Subjects:
Arctic
Max Peak
Online Access:https://curis.ku.dk/portal/da/publications/maintained-peak-leg-and-pulmonary-vo2-despite-substantial-reduction-in-muscle-mitochondrial-capacity(d2a94ce4-adf1-4be7-966b-683964a7c4d0).html
https://doi.org/10.1111/sms.12613
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Summary:We recently reported the circulatory and muscle oxidative capacities of the arm after prolonged low-intensity skiing in the arctic (Boushel 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 O2 delivery (3.6 ± 0.2 L.min -1 pre vs 3.8 ± 0.4 post), O2 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.

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