Boushel 2015 Scand J Med Sci Sports: Difference between revisions
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|journal=Scand J Med Sci Sports | |journal=Scand J Med Sci Sports | ||
|abstract=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 ''V''<sub>O2</sub> 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 ''V''<sub>O2</sub> (3.52 Β± 0.18 L.min<sup>-1</sup> pre vs 3.52 Β± 0.19 post) and ''V''<sub>O2</sub> across the leg (2.8 Β± 0.4 L.min<sup>-1</sup> pre vs 3.0 Β± 0.2 post) were unchanged after the ski journey. Peak leg O<sub>2</sub> delivery (3.6 Β± 0.2 L.min<sup>-1</sup> pre vs 3.8 Β± 0.4 post), O<sub>2</sub> extraction (82 Β± 1% pre vs 83 Β± 1 post), and muscle capillaries per mm<sup>2</sup> (576 Β± 17 pre vs 612 Β± 28 post) were also unchanged; however, leg muscle mitochondrial OXPHOS capacity was reduced (90 Β± 3 pmol.s<sup>-1</sup>.mg<sup>-1</sup> pre vs 70 Β± 2 post, ''P'' < 0.05) as was citrate synthase activity (40 Β± 3 Β΅mol.min<sup>-1</sup>.g<sup>-1</sup> pre vs 34 Β± 3; ''P'' < 0.05). These findings indicate that peak muscle ''V''<sub>O2</sub> can be sustained with a substantial reduction in mitochondrial OXPHOS capacity. This is achieved at a similar O<sub>2</sub> delivery and a higher relative ADP-stimulated mitochondrial respiration at a higher mitochondrial ''p''<sub>50</sub>. These findings support the concept that muscle mitochondrial respiration is submaximal at ''V''<sub>O2max</sub>, and that mitochondrial volume can be downregulated by chronic energy demand. | |abstract=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 ''V''<sub>O2</sub> 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 ''V''<sub>O2</sub> (3.52 Β± 0.18 L.min<sup>-1</sup> pre vs 3.52 Β± 0.19 post) and ''V''<sub>O2</sub> across the leg (2.8 Β± 0.4 L.min<sup>-1</sup> pre vs 3.0 Β± 0.2 post) were unchanged after the ski journey. Peak leg O<sub>2</sub> delivery (3.6 Β± 0.2 L.min<sup>-1</sup> pre vs 3.8 Β± 0.4 post), O<sub>2</sub> extraction (82 Β± 1% pre vs 83 Β± 1 post), and muscle capillaries per mm<sup>2</sup> (576 Β± 17 pre vs 612 Β± 28 post) were also unchanged; however, leg muscle mitochondrial OXPHOS capacity was reduced (90 Β± 3 pmol.s<sup>-1</sup>.mg<sup>-1</sup> pre vs 70 Β± 2 post, ''P'' < 0.05) as was citrate synthase activity (40 Β± 3 Β΅mol.min<sup>-1</sup>.g<sup>-1</sup> pre vs 34 Β± 3; ''P'' < 0.05). These findings indicate that peak muscle ''V''<sub>O2</sub> can be sustained with a substantial reduction in mitochondrial OXPHOS capacity. This is achieved at a similar O<sub>2</sub> delivery and a higher relative ADP-stimulated mitochondrial respiration at a higher mitochondrial ''p''<sub>50</sub>. These findings support the concept that muscle mitochondrial respiration is submaximal at ''V''<sub>O2max</sub>, and that mitochondrial volume can be downregulated by chronic energy demand. | ||
|editor=[[Gnaiger E]] | |||
|mipnetlab=CA Vancouver Boushel RC, AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS, ES CN Las Palmas Calbet JA | |mipnetlab=CA Vancouver Boushel RC, AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS, ES CN Las Palmas Calbet JA | ||
}} | }} | ||
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|topics=Oxygen kinetics | |topics=Oxygen kinetics | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
| | |pathways=F, N, S, NS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=MitoFitPublication, BMI, VO2max | |additional=MitoFitPublication, BMI, VO2max |
Revision as of 14:36, 7 November 2016
Boushel R, Gnaiger E, Larsen FJ, Helge JW, Gonzalez-Alonso J, Ara I, Munch-Andersen T, van Hall G, SΓΈndergaard H, Saltin B, Calbet JAL (2015) Maintained peak leg and pulmonary VO2 despite substantial reduction in muscle mitochondrial capacity. Scand J Med Sci Sports 25 (Suppl 4):135β43. |
Boushel R, Gnaiger E, Larsen FJ, Helge JW, Gonzalez-Alonso J, Ara I, Munch-Andersen T, van Hall G, Soendergaard H, Saltin B, Calbet JA (2015) Scand J Med Sci Sports
Abstract: 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 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 42 days of skiing at 60% HR max. Peak pulmonary VO2 (3.52 Β± 0.18 L.min-1 pre vs 3.52 Β± 0.19 post) and VO2 across the leg (2.8 Β± 0.4 L.min-1 pre vs 3.0 Β± 0.2 post) were unchanged after the ski journey. Peak leg O2 delivery (3.6 Β± 0.2 L.min-1 pre vs 3.8 Β± 0.4 post), O2 extraction (82 Β± 1% pre vs 83 Β± 1 post), and muscle capillaries per mm2 (576 Β± 17 pre vs 612 Β± 28 post) were also unchanged; however, leg muscle mitochondrial OXPHOS capacity was reduced (90 Β± 3 pmol.s-1.mg-1 pre vs 70 Β± 2 post, P < 0.05) as was citrate synthase activity (40 Β± 3 Β΅mol.min-1.g-1 pre vs 34 Β± 3; 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 O2 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.
β’ Bioblast editor: Gnaiger E β’ O2k-Network Lab: CA Vancouver Boushel RC, AT Innsbruck Gnaiger E, AT Innsbruck OROBOROS, ES CN Las Palmas Calbet JA
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Intact organ, Permeabilized tissue
Regulation: Oxygen kinetics Coupling state: OXPHOS Pathway: F, N, S, NS HRR: Oxygraph-2k
MitoFitPublication, BMI, VO2max