Shibasaki Manabu, Nakata Hiroki, Ogoh Shigehiko
Department of Engineering, Nara Women's University, Nara, JAPAN.
Department of Biomedical Engineering, Toyo University, Saitama, JAPAN.
Med Sci Sports Exerc. 2025 Apr 23;57(9):2001-8. doi: 10.1249/MSS.0000000000003740.
Excessive increases in body temperature impair voluntary force production and neuromuscular function, but the underlying central mechanisms remain unclear.
We investigated the effect of hyperthermia on neural activity associated with motor preparation using electroencephalographic event-related potentials (EEG-ERPs).
Two stimulus presentation methods were used: movement-related cortical potentials (MRCP) induced by self-initiated movement, and contingent negative variation (CNV) induced by externally-cued movement. The exercise intensity that elicited MRCP and CNV was set at 20% maximum voluntary contraction. Healthy young volunteers performed trials before and during whole-body heat stress on separate days.
Heat stress increased esophageal temperature by 1.5 ± 0.1 °C during the MRCP trial and 1.5 ± 0.2 °C during the CNV trial. Consistent with previous studies, the results of the Go/No-go tasks showed that the hyperthermia-induced impairment of brain activity was associated with executive and inhibitory processing during heat stress in both trials. In the MRCP trial, the amplitude of Bereitschaftspotential and the negative slope remained unchanged across all electrodes. However, CNV amplitudes in the middle and late phases were significantly reduced at Cz and Pz (both phases, P < 0.005), and C4 (late phase, P < 0.05), while early phase amplitudes were unchanged.
These findings indicate that neural activity for self-initiated movements is preserved under heat stress, whereas neural activity for externally-cued movements may be inhibited due to hyperthermia-induced central fatigue, potentially involving brain regions such as the prefrontal cortex. This alteration in the central mechanisms may contribute to the attenuated exercise performance under heat stress.
体温过度升高会损害自主力量产生和神经肌肉功能，但其潜在的中枢机制仍不清楚。
我们使用脑电图事件相关电位（EEG-ERPs）研究了热应激对与运动准备相关的神经活动的影响。
采用两种刺激呈现方法：自我发起运动诱发的运动相关皮层电位（MRCP），以及外部提示运动诱发的关联性负变（CNV）。诱发MRCP和CNV的运动强度设定为最大自主收缩的20%。健康年轻志愿者在不同日期分别在全身热应激前和热应激期间进行试验。
在MRCP试验期间，热应激使食管温度升高1.5±0.1°C，在CNV试验期间升高1.5±0.2°C。与先前的研究一致，Go/No-go任务的结果表明，在两个试验中，热应激期间热疗引起的大脑活动损害与执行和抑制过程有关。在MRCP试验中，所有电极上的 Bereitschaftspotential 振幅和负斜率均保持不变。然而，在 Cz 和 Pz 电极处，CNV 中期和晚期的振幅显著降低（两个阶段，P < 0.005），在 C4 电极处晚期振幅降低（P < 0.05），而早期振幅不变。
这些发现表明，在热应激下，自我发起运动的神经活动得以保留，而外部提示运动的神经活动可能由于热疗引起的中枢疲劳而受到抑制，可能涉及前额叶皮层等脑区。这种中枢机制的改变可能导致热应激下运动表现的减弱。
