期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 109, 期 1, 页码 101-111出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00782.2009
关键词
deconditioning; microgravity; near-infrared spectroscopy; gas exchange kinetics; skeletal muscle bioenergetics
资金
- Agenzia Spaziale Italiana (ASI) [I/007/06/0-Workpackage 1B-32-1]
Porcelli S, Marzorati M, Lanfranconi F, Vago P, Pisot R, Grassi B. Role of skeletal muscles impairment and brain oxygenation in limiting oxidative metabolism during exercise after bed rest. J Appl Physiol 109: 101-111, 2010. First published April 15, 2010; doi:10.1152/japplphysiol.00782.2009.-Central and peripheral limitations to oxidative metabolism during exercise were evaluated in 10 young males following a 35-day horizontal bed rest (BR). Incremental exercise (IE) and moderate-and heavy-intensity constant-load exercises (CLE) were carried out on a cycloergometer before and 1-2 days after BR. Pulmonary gas exchange, cardiac output (Q.; by impedance cardiography), skeletal muscle (vastus lateralis), and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined. After BR, peak (values at exhaustion during IE) workload, peak O-2 uptake ((V) over dotO(2peak)), peak stroke volume, (Q) over dot(peak), and peak skeletal muscle O-2 extraction were decreased (-18, -18, -22, -19, and -33%, respectively). The gas exchange threshold was similar to 60% of (V) over dotO(2peak) both before and after BR. At the highest workloads, brain oxygenation data suggest an increased O-2 extraction, which was unaffected by BR. (V) over dotO(2) kinetics during CLE (same percentage of peak workload before and after BR) were slower (time constant of the fundamental component: 31.1 +/- 2.0 s before vs. 40.0 +/- 2.2 s after BR); the amplitude of the slow component was unaffected by BR, thus it would be greater, after BR, at the same absolute workload. A more pronounced overshoot of skeletal muscle O-2 extraction during CLE was observed after BR, suggesting an impaired adjustment of skeletal muscle O-2 delivery. The role of skeletal muscles in the impairment of oxidative metabolism during submaximal and maximal exercise after BR was identified. The reduced capacity of peak cardiovascular O-2 delivery did not determine a competition for the available O-2 between skeletal muscles and brain.
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