Morrison Shawnda A, Sleivert Gordon G, Neary J Patrick, Cheung Stephen S
Human Performance Laboratory, Faculty of Kinesiology, University of New Brunswick, P.O. Box 4400, Fredericton, NBE3B5A3, Canada.
Appl Physiol Nutr Metab. 2009 Feb;34(1):66-74. doi: 10.1139/H08-139.
We investigated the role of passive hyperthermia upon motor unit activation and prefrontal cortex oxygenation. Six healthy males were passively heated, using a liquid conditioning garment in a hot environment (35 degrees C, 50% relative humidity). Maximal force output and voluntary activation were examined during a 10 s maximal isometric knee extension. Of the initial 6 subjects, 1 experienced syncope at a rectal temperature (Tre) of 38.0 degrees C and was removed from the study. The remaining 5 subjects completed heating and testing to a Tre of 38.5 degrees C (n = 1), 39.0 degrees C (n = 3), or 39.5 degrees C (n = 1), and then were cooled back to baseline. Force production decreased from 553 +/- 133 to 430 +/- 176 N (p < 0.01) with passive heating, as did voluntary activation (from 90 +/- 5% to 84 +/- 7%). Percent heart rate reserve increased from 8 +/- 5% to 59 +/- 3% before returning to 4 +/- 8% (p < 0.001). Although mean arterial pressure remained unchanged, there were significant decreases in diastolic blood pressure with heating (80 +/- 3 to 63 +/- 8 mm Hg). Passive heating did not alter prefrontal cortex oxygenation, but cooling back to baseline core temperature attenuated cerebral oxygenated and total hemoglobin levels (p < 0.05). Passive heating to the point of voluntary exhaustion elevated cardiovascular and thermal strain and subjective perceptions of thermal discomfort. However, while this resulted in a marked decrement in maximal isometric force production and central voluntary activation, no concomitant changes in cerebral oxygenation were observed, suggesting that overall cerebrovascular regulation was maintained.
我们研究了被动热疗对运动单位激活和前额叶皮层氧合作用的影响。六名健康男性在炎热环境（35摄氏度，相对湿度50%）中使用液体调节服装进行被动加热。在10秒的最大等长膝关节伸展过程中检测最大力量输出和自主激活情况。最初的6名受试者中，有1名在直肠温度（Tre）为38.0摄氏度时发生晕厥，被排除在研究之外。其余5名受试者完成加热并测试至Tre为38.5摄氏度（n = 1）、39.0摄氏度（n = 3）或39.5摄氏度（n = 1），然后冷却至基线水平。被动加热时，力量产生从553±133牛顿降至430±176牛顿（p < 0.01），自主激活情况也如此（从90±5%降至84±7%）。心率储备百分比在恢复到4±8%之前从8±5%增加到59±3%（p < 0.001）。尽管平均动脉压保持不变，但加热时舒张压显著下降（从80±3毫米汞柱降至63±8毫米汞柱）。被动加热未改变前额叶皮层氧合情况，但冷却至基线核心温度会减弱脑氧合血红蛋白和总血红蛋白水平（p < 0.05）。被动加热至自主疲劳会增加心血管和热应激以及热不适的主观感受。然而，虽然这导致最大等长力量产生和中枢自主激活显著下降，但未观察到脑氧合的相应变化，表明整体脑血管调节得以维持。
