Aspetar, Research and Education Centre, Qatar Orthopaedic and Sports Medicine Hospital, Doha, Qatar.
Med Sci Sports Exerc. 2011 Sep;43(9):1657-65. doi: 10.1249/MSS.0b013e3182148a9a.
Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined.
On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC.
Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05).
The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.
在长时间运动（ExH）和被动加热（PaH）期间诱导体温过高，以在热应激下分离运动对股四头肌最大自主等长收缩（MVC）期间神经肌肉功能的影响。还检查了心血管应变在限制热应激下耐力表现方面的影响。
在不同的日子里，8 名男性以 60%最大摄氧量的速度骑自行车直至力竭，或浸入水浴（约 41°C），直到直肠温度（Tre）升高至 39.5°C。ExH 和 PaH 干预在环境温度为 38°C和 60%相对湿度的条件下进行，Tre 在运动过程中升高至 39.8°C。在每个干预之前（对照）和之后，通过在 45 秒 MVC 期间叠加电刺激的强直收缩来评估自愿激活和力产生能力。
与对照相比，PaH 和 ExH 后力的产生立即下降，ExH 后下降幅度更大（P < 0.01）。两种干预后平均自愿激活也明显降低（P < 0.01 与对照）。然而，在 PaH 和 ExH MVC 期间，自愿激活的下降程度维持在约 90%。这种下降占力产生下降的 41.5%（PaH）和 33.1%（ExH）。此外，疲劳与 HR 显著增加（最大的约 96%）、心输出量减少（25%）和平均动脉压下降（10%）（P < 0.05）同时发生。
在体温过高期间，力产生能力的丧失源于中枢和外周疲劳因素，热应激和先前的收缩活动的结合加剧了下降的速度。因此，在 ExH 和 PaH 中观察到的热应激显著增加，损害了神经肌肉功能，并与心血管应变限制的运动表现增加有关。
