持续间歇运动中工作和恢复时间对骨骼肌氧合和燃料使用的影响。

M A Christmass, B Dawson, P G Arthur
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引用次数: 84

摘要

本研究的目的是比较两种间歇运动方案中底物的氧化率,在相同的跑步机速度和总工作时间下,减少因素差异的影响,如肌纤维类型激活、激素反应、肌肉葡萄糖摄取和非酯化脂肪酸(NEFA)可用性对底物利用比较的影响。受试者(n = 7)在不同的天完成40分钟的间歇性高强度跑步,要求工作:恢复比为6秒:9秒(短间隔运动,SE)或24秒:36秒(长间隔运动,LE)。另一项实验使用近红外光谱(RunMan, NIM)比较了东南(10分钟)和东南(10分钟)运动时股外侧肌的O(2)可用性。费城,美国)。整体(即工作和恢复)O(2)消耗(VO(2))和能量消耗较低(P < 0.01, P < 0.05)。总体运动强度,以峰值有氧能力(VO2(峰值))的比例表示,[mean (SEM)]为64.9 (2.7)% VO2(峰值)(LE)和71.4 (2.4)% VO2(峰值)(SE)。脂肪氧化降低3倍(P < 0.01),碳水化合物氧化升高1.3倍(P < 0)。01),尽管整体运动强度较低。血浆乳酸保持不变,在整个运动过程中升高[平均(SEM) 5.33 (0.53) mM, LE;3.28 (0.31) mM, SE;P < 0.001)。血浆丙酮酸较高,甘油较低[215 (17)μ m, 151 (13) μ m, P < 0.05,丙酮酸;197(19)微米,246(19)微米,P < 0.05,甘油]。血浆NEFA浓度(n = 4)或血浆去甲肾上腺素和肾上腺素无差异。两种方案的肌肉氧合均下降(P < 0.001),但LE时的最低点较低[52.04(0.05)]。60)%]与SE相比[61.85 (0.51)%;P < 0.001]。工作时肌肉氧合下降与平均乳酸浓度相关(r = 0.68;P < 0.05;N = 12)。脂肪氧化水平降低的同时,碳水化合物代谢加速,乳酸和丙酮酸增加,肌肉O(2)利用率降低。尽管跑步机速度和总工作时间相同,但这些变化与工作时间和恢复时间成比例地延长有关。在这些条件下,肌纤维内的代谢调节因子延缓脂肪氧化的建议得到了当前研究结果的支持。
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Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise.

The purpose of this study was to compare rates of substrate oxidation in two protocols of intermittent exercise, with identical treadmill speed and total work duration, to reduce the effect of differences in factors such as muscle fibre type activation, hormonal responses, muscle glucose uptake and non-esterified fatty acid (NEFA) availability on the comparison of substrate utilisation. Subjects (n = 7) completed 40 min of intermittent intense running requiring a work:recovery ratio of either 6 s:9 s (short-interval exercise, SE) or 24 s:36 s (long-interval exercise, LE), on separate days. Another experiment compared O(2) availability in the vastus lateralis muscle across SE (10 min) and LE (10 min) exercise using near-infrared spectroscopy (RunMan, NIM. Philadelphia, USA). Overall (i.e. work and recovery) O(2) consumption (VO(2)) and energy expenditure were lower during LE (P < 0.01, P < 0.05, respectively). Overall exercise intensity, represented as a proportion of peak aerobic power (VO2(peak)), was [mean (SEM)] 64.9 (2.7)% VO2(peak) (LE) and 71.4 (2.4)% VO2(peak) (SE). Fat oxidation was three times lower (P < 0.01) and carbohydrate oxidation 1.3 times higher (P < 0. 01) during LE, despite the lower overall exercise intensity. Plasma lactate was constant and was higher throughout exercise in LE [mean (SEM) 5.33 (0.53) mM, LE; 3.28 (0.31) mM, SE; P < 0.001)]. Plasma pyruvate was higher and glycerol was lower in LE [215 (17) microM, 151 (13) microM, P < 0.05, pyruvate; 197 (19) microM, 246 (19) microM, P < 0.05, glycerol]. There was no difference between protocols for plasma NEFA concentration (n = 4) or plasma noradrenaline and adrenaline. Muscle oxygenation declined in both protocols (P < 0.001), but the nadir during LE was lower [52.04 (0. 60)%] compared to SE [61.85 (0.51)%; P < 0.001]. The decline in muscle oxygenation during work was correlated with mean lactate concentration (r = 0.68; P < 0.05; n = 12). Lower levels of fat oxidation occurred concurrent with accelerated carbohydrate metabolism, increases in lactate and pyruvate and reduced muscle O(2) availability. These changes were associated with proportionately longer work and recovery periods, despite identical treadmill speed and total work duration. The proposal that a metabolic regulatory factor within the muscle fibre retards fat oxidation under these conditions is supported by the current findings.

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