Karolinska Institutet, Stockholm, Sweden.
Swedish Winter Sports Research Centre, Mid Sweden University, Östersund, Sweden.
J Physiol. 2017 Dec 15;595(24):7413-7426. doi: 10.1113/JP274870. Epub 2017 Oct 25.
We investigated whether intramuscular temperature affects the acute recovery of exercise performance following fatigue-induced by endurance exercise. Mean power output was better preserved during an all-out arm-cycling exercise following a 2 h recovery period in which the upper arms were warmed to an intramuscular temperature of ̴ 38°C than when they were cooled to as low as 15°C, which suggested that recovery of exercise performance in humans is dependent on muscle temperature. Mechanisms underlying the temperature-dependent effect on recovery were studied in intact single mouse muscle fibres where we found that recovery of submaximal force and restoration of fatigue resistance was worsened by cooling (16-26°C) and improved by heating (36°C). Isolated whole mouse muscle experiments confirmed that cooling impaired muscle glycogen resynthesis. We conclude that skeletal muscle recovery from fatigue-induced by endurance exercise is impaired by cooling and improved by heating, due to changes in glycogen resynthesis rate.
Manipulation of muscle temperature is believed to improve post-exercise recovery, with cooling being especially popular among athletes. However, it is unclear whether such temperature manipulations actually have positive effects. Accordingly, we studied the effect of muscle temperature on the acute recovery of force and fatigue resistance after endurance exercise. One hour of moderate-intensity arm cycling exercise in humans was followed by 2 h recovery in which the upper arms were either heated to 38°C, not treated (33°C), or cooled to ∼15°C. Fatigue resistance after the recovery period was assessed by performing 3 × 5 min sessions of all-out arm cycling at physiological temperature for all conditions (i.e. not heated or cooled). Power output during the all-out exercise was better maintained when muscles were heated during recovery, whereas cooling had the opposite effect. Mechanisms underlying the temperature-dependent effect on recovery were tested in mouse intact single muscle fibres, which were exposed to ∼12 min of glycogen-depleting fatiguing stimulation (350 ms tetani given at 10 s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2 h of recovery at 16-36°C. Recovery of submaximal force (30 Hz), the tetanic myoplasmic free [Ca ] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26°C) and improved by heating (36°C). In addition, glycogen resynthesis was faster at 36°C than 26°C in whole flexor digitorum brevis muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.
我们研究了在耐力运动引起疲劳后,肌内温度是否会影响运动表现的急性恢复。与冷却至低至 15°C 相比,在 2 小时恢复期内,将上臂加热至约 38°C 时,在全力手臂循环运动中,平均功率输出得到更好的保留,这表明人类运动表现的恢复取决于肌肉温度。在完整的单个鼠肌纤维中研究了温度依赖性恢复效果的机制,我们发现冷却(16-26°C)会恶化次最大力的恢复和疲劳抵抗力的恢复,而加热(36°C)会改善这种恢复。分离的整个鼠肌肉实验证实,冷却会损害肌肉糖原的合成。我们的结论是,由于糖原合成率的变化,耐力运动引起的疲劳后,骨骼肌的恢复会因冷却而受损,因加热而得到改善。
人们认为肌肉温度的调节可以改善运动后的恢复,冷却在运动员中尤为流行。然而,尚不清楚这种温度调节是否真的有积极作用。因此,我们研究了肌肉温度对耐力运动后力量和疲劳抵抗力的急性恢复的影响。在人类中进行 1 小时的中等强度手臂循环运动后,在 2 小时的恢复期内,上臂要么被加热到 38°C,要么不处理(33°C),要么冷却到约 15°C。在所有条件下(即不加热或冷却),通过在生理温度下进行 3 次×5 分钟的全力手臂循环运动来评估恢复期后的疲劳抵抗力。当肌肉在恢复期内加热时,在全力运动中输出的功率更好地维持,而冷却则产生相反的效果。在鼠完整的单个肌纤维中测试了温度依赖性恢复效果的机制,这些肌纤维经历了约 12 分钟的糖原消耗疲劳刺激(350ms 强直刺激,间隔 10s,直至力降至起始力的 30%)。在 16-36°C 的恢复期后 1-2 小时,纤维暴露于相同的疲劳刺激方案。在 30Hz 时,次最大力(30Hz)的恢复、肌浆内游离[Ca ](用荧光指示剂 indo-1 测量)和疲劳抵抗力均受到冷却(16-26°C)的损害,加热(36°C)则得到改善。此外,在整个屈趾短肌中,糖原的合成速度在 36°C 时比 26°C 时更快。我们的结论是,通过升高和降低肌肉温度可以加速从剧烈耐力运动后的恢复。