Post-exercise recovery of contractile function and endurance in humans and mice is accelerated by heating and slowed by cooling skeletal muscle

被引:59
作者
Cheng, Arthur J. [1 ]
Willis, Sarah J. [2 ]
Zinner, Christoph [2 ]
Chaillou, Thomas [1 ,3 ]
Ivarsson, Niklas [1 ]
Ortenblad, Niels [4 ]
Lanner, Johanna T. [1 ]
Holmberg, Hans-Christer [1 ,2 ]
Westerblad, Hakan [1 ]
机构
[1] Karolinska Inst, Stockholm, Sweden
[2] Mid Sweden Univ, Swedish Winter Sports Res Ctr, Ostersund, Sweden
[3] Orebro Univ, Orebro, Sweden
[4] Univ Southern Denmark, Odense, Denmark
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2017年 / 595卷 / 24期
基金
瑞典研究理事会;
关键词
cold-water immersion; fatigue; glycogen; recovery; skeletal muscle; temperature; COLD-WATER IMMERSION; FREQUENCY FORCE DEPRESSION; FAST-TWITCH MUSCLE; GLYCOGEN-CONTENT; CA2+ RELEASE; PHYSIOLOGICAL-MECHANISMS; FATIGUING STIMULATION; GLUCOSE-UPTAKE; EXERCISE; FIBERS;
D O I
10.1113/JP274870
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 2h recovery in which the upper arms were either heated to 38 degrees C, not treated (33 degrees C), or cooled to approximate to 15 degrees C. Fatigue resistance after the recovery period was assessed by performing 3x5min 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 approximate to 12min of glycogen-depleting fatiguing stimulation (350ms tetani given at 10s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2h of recovery at 16-36 degrees C. Recovery of submaximal force (30Hz), the tetanic myoplasmic free [Ca2+] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26 degrees C) and improved by heating (36 degrees C). In addition, glycogen resynthesis was faster at 36 degrees C than 26 degrees 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. 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 2h recovery period in which the upper arms were warmed to an intramuscular temperature of ? 38 degrees C than when they were cooled to as low as 15 degrees 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 degrees C) and improved by heating (36 degrees 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.
引用
收藏
页码:7413 / 7426
页数:14
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