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全身低温对屈肘肌的表现有中枢和外周影响。

Whole-body hypothermia has central and peripheral influences on elbow flexor performance.

机构信息

Health Leisure and Human Performance Research Institute, Faculty of Kinesiology and Recreation Management, University of Manitoba, Winnipeg, Manitoba, Canada.

出版信息

Exp Physiol. 2011 May;96(5):528-38. doi: 10.1113/expphysiol.2010.054973. Epub 2011 Mar 4.

Abstract

The superimposed twitch technique was used to study the effect of whole-body hypothermia on maximal voluntary activation of elbow flexors. Seven subjects [26.4 ± 4 years old (mean ± SD)] were exposed to 60 min of either immersion in 8°C water (hypothermia) or sitting in 22°C air (control). Voluntary activation was assessed during brief (3 s) maximal voluntary contractions (MVCs) and then during a 2 min fatiguing sustained MVC. Hypothermia (core temperature 34.8 ± 0.9°C) decreased maximal voluntary torque from 98.2 ± 1.0 to 82.8 ± 5.8% MVC (P < 0.001) and increased central conduction time from 7.9 ± 0.4 to 9.1 ± 0.7 ms (P < 0.05). Hypothermia also decreased maximal resting twitch amplitude from 17.6 ± 4.0 to 10.0 ± 1.7% MVC (P < 0.005) and increased the time-to-peak twitch tension from 55.4 ± 4.0 to 79.0 ± 11.7 ms (P < 0.001). During the 2 min contraction, hypothermia decreased initial torque (P < 0.01) but attenuated the subsequent rate of torque decline (control from 95.5 ± 4 to 29.4 ± 8% MVC; and hypothermia from 85.3 ± 8 to 37.3 ± 5% MVC; P < 0.01). Cortical superimposed twitches increased as fatigue developed but were always lower in the hypothermic conditions. Cortical superimposed twitches increased from a value of 0.4 ± 0.3% MVC prefatigue to 3.9 ± 1.4% MVC postfatigue (P < 0.001) in the hypothermic conditions and from 1.7 ± 0.9 to 5.5 ± 2.3% MVC in control conditions. Our results suggest that hypothermia decreases MVCs primarily via peripheral mechanisms and attenuates the rate of fatigue development by reducing central fatigue.

摘要

叠加抽搐技术用于研究全身低温对肘屈肌最大自主激活的影响。7 名受试者[26.4±4 岁(均值±标准差)]分别暴露于 8°C 水中 60 分钟(低温组)或 22°C 空气中(对照组)。在短暂(3 秒)最大自主收缩(MVC)期间评估自主激活,然后在 2 分钟疲劳持续 MVC 期间评估自主激活。低温(核心温度 34.8±0.9°C)使最大自主扭矩从 98.2±1.0% MVC 降低至 82.8±5.8% MVC(P<0.001),并使中枢传导时间从 7.9±0.4 ms 增加至 9.1±0.7 ms(P<0.05)。低温还使最大静息抽搐幅度从 17.6±4.0% MVC 降低至 10.0±1.7% MVC(P<0.005),并使峰值抽搐张力的时间从 55.4±4.0 ms 增加至 79.0±11.7 ms(P<0.001)。在 2 分钟收缩过程中,低温降低了初始扭矩(P<0.01),但减轻了随后的扭矩下降速度(对照组从 95.5±4% MVC 降至 29.4±8% MVC;低温组从 85.3±8% MVC 降至 37.3±5% MVC;P<0.01)。皮质叠加抽搐随着疲劳的发展而增加,但在低温条件下总是较低。在低温条件下,皮质叠加抽搐从疲劳前的 0.4±0.3% MVC 增加到疲劳后的 3.9±1.4% MVC(P<0.001),而在对照组条件下从 1.7±0.9% MVC 增加到 5.5±2.3% MVC。我们的结果表明,低温主要通过外周机制降低 MVCs,并通过降低中枢疲劳来减轻疲劳发展的速度。

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