Kinetics of oxygen consumption during maximal exercise at different muscle temperatures
Kinetics of oxygen consumption during maximal exercise at different muscle temperatures
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DOI：
10.1016/0034-5687(95)00071-2
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发表时间：
1995-12-01
期刊：
影响因子：
--
通讯作者：
Cerretelli, P
中科院分区：
文献类型：
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作者：
Ferretti, G;Binzoni, T;Cerretelli, P
本研究的目的是测试在最大运动的假设的温度依赖性的动力学的O-2消耗（V-O2）），预测更大的O-2赤字肌肉温度降低。6名男性受试者在常温（A）和浸水冷却大腿肌肉后（C）以最小功率引起最大O-2消耗（V-O 2 max）进行3 min运动。测量逐呼吸VO 2以及肌肉血流量（Qm）、血乳酸蓄积（“早期乳酸”，eLa）、心率和肌肉温度（Tm）。通过标准程序计算O-2赤字。C组和A组的净V-O2 max分别为2.92 ± 0.85（SD）和3.19 ± 0.71 l.min（-1）（P < 0.05）。相应地，C中的最大功率比A中低20 W。在运动开始时，A和C中的Tm分别为35.0 +/- 1.2和27.5 +/- 1.8 ℃。A和C的O-2亏缺分别为2.25 ± 0.53和3.05 ± 1.12 l。A和C中相应的eLa分别为7.7 +/- 2.5和13.8 +/- 2.5 mM（P < 0.05），而Qm分别为376 +/- 92和290 +/- 50 ml.kg（-1）min（-1）（P < 0.05）。C的eLa增加与受损的肌肉血流量和减少的肌肉O-2卸载有关，并且不能完全解释C中更大的O-2赤字。后者的原因不明的分数可能是占一个更大的净无乳O-2赤字，在协议的氧化反应的速度常数的温度依赖性降低，所建议的测试假设。
The aim of this study was to test at maximal exercise the hypothesis of the temperature-dependence of the kinetics of O-2 consumption (V-O2)) which predicts a greater O-2 deficit as muscle temperature is decreased. Six male subjects underwent 3 min exercise bouts at the minimum power eliciting maximum O-2 consumption (V-O2max), at normal temperature (A) and after cooling the thigh muscles by water immersion (C). Breath-by-breath VO2 was measured together with muscle blood flow (Qm), blood lactate accumulation (''early lactate'', eLa), heart rate and muscle temperature (Tm). The O-2 deficit was calculated by standard procedure. Net V-O2max was 2.92 +/- 0.85 (SD) and 3.19 +/- 0.71 l.min(-1) in C and A respectively (P < 0.05). Correspondingly, maximum power was 20 W lower in C than in A. At exercise start, Tm was 35.0 +/- 1.2 and 27.5 +/- 1.8 degrees C in A and C respectively. O-2 deficit was 2.25 +/- 0.53 and 3.05 +/- 1.12 l in A and C respectively. The corresponding eLa was 7.7 +/- 2.5 and 13.8 +/- 2.5 mM, (P < 0.05) while Qm was 376 +/- 92 and 290 +/- 50 ml.kg(-1) min(-1) (P < 0.05) in A and C, respectively. The eLa increase in C is associated with an impaired muscle blood flow and decreased muscle O-2 unloading, and does not completely explain the greater O-2 deficit in C. The unexplained fraction of the latter is perhaps accounted for by a greater net alactic O-2 deficit, in agreement with a temperature-dependent decrease of the velocity constants of oxidative reactions, as suggested by the tested hypothesis.