Locher Chrystèle, Raux Mathieu, Fiamma Marie-Noelle, Morélot-Panzini Capucine, Zelter Marc, Derenne Jean-Philippe, Similowski Thomas, Straus Christian
Université Pierre et Marie Curie-Paris 6, UPRES EA 2397, Paris, France.
BMC Physiol. 2006 Jul 29;6:7. doi: 10.1186/1472-6793-6-7.
Breathing in humans is dually controlled for metabolic (brainstem commands) and behavioral purposes (suprapontine commands) with reciprocal modulation through spinal integration. Whereas the ventilatory response to chemical stimuli arises from the brainstem, the compensation of mechanical loads in awake humans is thought to involve suprapontine mechanisms. The aim of this study was to test this hypothesis by examining the effects of inspiratory resistive loading on the response of the diaphragm to transcranial magnetic stimulation.
Six healthy volunteers breathed room air without load (R0) and then against inspiratory resistances (5 and 20 cmH2O/L/s, R5 and R20). Ventilatory variables were recorded. Transcranial magnetic stimulation (TMS) was performed during early inspiration (I) or late expiration (E), giving rise to motor evoked potentials (MEPs) in the diaphragm (Di) and abductor pollicis brevis (APB). Breathing frequency significantly decreased during R20 without any other change. Resistive breathing had no effect on the amplitude of Di MEPs, but shortened their latency (R20: -0.903 ms, p = 0.03) when TMS was superimposed on inspiration. There was no change in APB MEPs.
Inspiratory resistive breathing facilitates the diaphragm response to TMS while it does not increase the automatic drive to breathe. We interpret these findings as a neurophysiological substratum of the suprapontine nature of inspiratory load compensation in awake humans.
人类的呼吸受代谢(脑干指令)和行为目的(脑桥以上指令)双重控制,并通过脊髓整合进行相互调节。虽然对化学刺激的通气反应起源于脑干,但清醒人类对机械负荷的补偿被认为涉及脑桥以上机制。本研究的目的是通过检查吸气阻力负荷对膈肌对经颅磁刺激反应的影响来验证这一假设。
六名健康志愿者在无负荷(R0)状态下呼吸室内空气,然后在有吸气阻力(5和20 cmH₂O/L/s,R5和R20)的情况下呼吸。记录通气变量。在吸气早期(I)或呼气晚期(E)进行经颅磁刺激(TMS),在膈肌(Di)和拇短展肌(APB)中产生运动诱发电位(MEP)。在R20期间呼吸频率显著降低,无其他变化。阻力呼吸对Di MEP的幅度没有影响,但当TMS叠加在吸气上时,缩短了其潜伏期(R20:-0.903 ms,p = 0.03)。APB MEP没有变化。
吸气阻力呼吸促进膈肌对TMS的反应,而不增加自主呼吸驱动力。我们将这些发现解释为清醒人类吸气负荷补偿的脑桥以上性质的神经生理基础。