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

• Published in: Scandinavian Journal of Medicine & Science in Sports
• Main Authors: Boushel, R., Gnaiger, E., Larsen, F. J., Helge, J. W., González‐Alonso, J., Ara, I., Munch‐Andersen, T., van Hall, G., Søndergaard, H., Saltin, B., Calbet, J. A. L.
• Other Authors: Danmarks Grundforskningsfond
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2015
• Subjects: Arctic; Max Peak
• Online Access: http://dx.doi.org/10.1111/sms.12613; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fsms.12613; https://onlinelibrary.wiley.com/doi/pdf/10.1111/sms.12613

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.