PDF(Pubmed)
Abstract：
Exercise elicits physiological adaptations, including hyperpnea. However, the mechanisms underlying exercise-induced hyperpnea remain unresolved. Skeletal muscle acts as a secretory organ, releasing irisin (IR) during exercise. Irisin can cross the blood-brain barrier, influencing muscle and tissue metabolism, as well as signaling in the central nervous system (CNS). We evaluated the effect of intracerebroventricular or intraperitoneal injection of IR in adult male rats on the cardiorespiratory and metabolic function during sleep-wake cycle under room air, hypercapnia and hypoxia. Central IR injection caused an inhibition on ventilation (VE) during wakefulness under normoxia, while peripheral IR reduced VE during sleep. Additionally, central IR exacerbates hypercapnic hyperventilation by increasing VE and reducing oxygen consumption. As to cardiovascular regulation, central IR caused an increase in heart rate (HR) across all conditions, while no change was observed following peripheral administration. Finally, central IR attenuated the hypoxia-induced regulated hypothermia and increase sleep episodes, while peripheral IR augmented CO2-induced hypothermia, during wakefulness. Overall, our results suggest that IR act mostly on CNS exerting an inhibitory effect on breathing under resting conditions, while stimulating the hypercapnic ventilatory response and increasing HR. Therefore, IR seems not to be responsible for the exercise-induced hyperpnea, but contributes to the increase in HR.
摘要：
运动引起生理适应，包括呼吸过度.然而,运动性呼吸过度的潜在机制仍未解决.骨骼肌作为分泌器官,在运动期间释放irisin（IR）。Irisin能穿过血脑屏障,影响肌肉和组织代谢，以及中枢神经系统（CNS）中的信号。我们评估了成年雄性大鼠在室内空气下的睡眠-觉醒周期中脑室内或腹膜内注射IR对心肺功能和代谢功能的影响，高碳酸血症和缺氧。中枢IR注射在常氧下清醒期间引起通气（VE）抑制，而睡眠期间外周IR降低VE。此外,中央IR通过增加VE和减少耗氧量来加剧高碳酸血症过度换气。至于心血管调节，在所有情况下，中央IR引起心率(HR)增加，而外周给药后没有观察到变化。最后,中枢IR减弱了缺氧诱导的调节低温，增加了睡眠发作，而外周IR增加CO2诱导的低体温，在清醒的时候。总的来说,我们的结果表明，IR主要作用于中枢神经系统，在静息条件下对呼吸产生抑制作用，同时刺激高碳酸血症的通气反应并增加HR。因此,IR似乎不是运动引起的呼吸过度的原因,但有助于增加人力资源。
