Expression and Mechanism of TRPV1 Channel in Prefrontal Cortex after Acute Hypoxic Exercise

Objective This study aims to explore TRPV1's function in acute hypoxic exercise and the CNS's impact on initial exercise decline in high-altitude-trained athletes. Methods After acute hypoxia intervention, RTqPCR was employed to detect the content of transient receptor potential vanilloid subtype 1 (TRPV1) and 5-hydroxytryptamine1A(5-HT1A) in the rat prefrontal cortex; ELISA was used to measure the content of 5-hydroxytryptamine (5-HT) in the rat prefrontal cortex. Results Hypoxic conditions can shorten the time rats can perform increased load exercise, leading to an early onset of fatigue and a significant decline in exercise capacity. Acute hypoxic exercise has been observed to increase the expression of TRPV1, 5-HT and 5-HT1A in the prefrontal cortex, which may contribute to the decline in exercise capacity. Blocking TRPV1 and 5-HT1A further extending the time for increased load exercise under hypoxic conditions and enhancing exercise capacity. Conclusion Rats' initial decline in exercise during acute hypoxia may result from TRPV1 upregulation, which activates the 5-HT/5-HT1A pathway; TRPV1 blockade can alleviate the stress caused by hypoxic conditions, thereby reducing prefrontal cortex cell damage and apoptosis, and ultimately extending exercise time.