Kounalakis Stylianos N, Keramidas Michail E, Eiken Ola, Mekjavic Igor B
Department of Physical & Cultural Education, Evelpidon Hellenic Army Academy, Vari, Greece.
Division of Environmental Physiology, KTH Royal Institute of Technology, Swedish Aerospace Physiology Center, Stockholm, Sweden.
Exp Physiol. 2021 Jul;106(7):1498-1507. doi: 10.1113/EP089539. Epub 2021 Jun 2.
What is the central question of this study? Does a 35-day horizontal bedrest impair thermoeffector responses during whole-body submaximal exercise performed in temperate conditions? What is the main finding and its importance? Cardiovascular and muscular deconditioning ensuing from prolonged recumbency seems to augment, at least to a degree, exercise-induced increase in body core temperature, most likely due to an impairment in non-evaporative heat loss. The response is a function of the absolute exercise intensity imposed.
We examined the effects of a 35-day horizontal bedrest on thermoregulation during whole-body exercise. Fifteen healthy men were randomly assigned to either a bedrest (BR; n = 10) or a control (CON; n = 5) group. Prior to bedrest, both groups performed 40-min constant-load upright cycling at 30% of their peak workload (W ; PRE). One and 2 days after bedrest, the BR group performed, in a randomised counterbalanced order, two 40-min trials at 30% of (i) the pre-bedrest W (i.e., at a fixed absolute intensity; POST-A) and (ii) the post-bedrest W (i.e., at a fixed relative intensity; POST-R). The CON group conducted only the POST-A trial, at the same time intervals. During the trials, rectal (T ) and skin ( ) temperatures, and the forehead sweating rate (SwR) were monitored. In the CON group, no differences were observed between the trials. Bedrest potentiated moderately the T elevation during the latter part of POST-A (∼0.10°C; P ≤ 0.05), but not of POST-R (∼0.04°C; P = 0.11). In both post-bedrest trials, was attenuated by ∼1.5-2.0°C throughout (P < 0.01), whereas the forehead SwR was not modulated. T and were similar in POST-A and POST-R, yet the forehead SwR was more dependent on the relative workload imposed (P = 0.04). The present findings therefore suggest that the cardiovascular and muscular deconditioning ensuing from a 35-day bedrest may aggravate the exercise-induced increase in body core temperature when working at a given absolute intensity, most likely due to an impairment in non-evaporative heat loss.
本研究的核心问题是什么？在温带条件下进行全身次最大强度运动期间，35天的水平卧床休息是否会损害体温调节效应反应？主要发现及其重要性是什么？长时间卧床导致的心血管和肌肉失健状况似乎至少在一定程度上加剧了运动引起的体核温度升高，这很可能是由于非蒸发散热受损所致。这种反应是所施加的绝对运动强度的函数。
我们研究了35天水平卧床休息对全身运动期间体温调节的影响。15名健康男性被随机分为卧床休息组（BR；n = 10）或对照组（CON；n = 5）。在卧床休息前，两组均以其峰值工作量的30%进行40分钟的恒定负荷直立骑行（W；PRE）。卧床休息1天和2天后，BR组以随机平衡顺序进行了两项40分钟的试验，分别为（i）卧床休息前的W的30%（即固定绝对强度；POST - A）和（ii）卧床休息后的W的30%（即固定相对强度；POST - R）。CON组仅在相同时间间隔进行POST - A试验。在试验期间，监测直肠温度（T）、皮肤温度（ ）和额头出汗率（SwR）。在CON组中，各试验之间未观察到差异。卧床休息适度增强了POST - A后期的T升高（约0.10°C；P≤0.05），但未增强POST - R的T升高（约0.04°C；P = 0.11）。在两项卧床休息后的试验中，整个过程中 均降低了约1.5 - 2.0°C（P < 0.01），而额头SwR未受调节。POST - A和POST - R中的T和 相似，但额头SwR更依赖于所施加的相对工作量（P = 0 .04）。因此，目前的研究结果表明，35天卧床休息导致的心血管和肌肉失健状况可能会在以给定绝对强度工作时加剧运动引起的体核温度升高，这很可能是由于非蒸发散热受损所致。
