John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, Wisconsin, USA.
J Appl Physiol (1985). 2010 Oct;109(4):966-76. doi: 10.1152/japplphysiol.00462.2010. Epub 2010 Jul 15.
We investigated the role of somatosensory feedback on cardioventilatory responses to rhythmic exercise in five men. In a double-blind, placebo-controlled design, subjects performed the same leg cycling exercise (50/100/150/325 ± 19 W, 3 min each) under placebo conditions (interspinous saline, L(3)-L(4)) and with lumbar intrathecal fentanyl impairing central projection of spinal opioid receptor-sensitive muscle afferents. Quadriceps strength was similar before and after fentanyl administration. To evaluate whether a cephalad migration of fentanyl affected cardioventilatory control centers in the brain stem, we compared resting ventilatory responses to hypercapnia (HCVR) and cardioventilatory responses to arm vs. leg cycling exercise after each injection. Similar HCVR and minor effects of fentanyl on cardioventilatory responses to arm exercise excluded direct medullary effects of fentanyl. Central command during leg exercise was estimated via quadriceps electromyogram. No differences between conditions were found in resting heart rate (HR), ventilation [minute ventilation (VE)], or mean arterial pressure (MAP). Quadriceps electromyogram, O(2) consumption (VO(2)), and plasma lactate were similar in both conditions at the four steady-state workloads. Compared with placebo, a substantial hypoventilation during fentanyl exercise was indicated by the 8-17% reduction in VE/CO(2) production (VCO(2)) secondary to a reduced breathing frequency, leading to average increases of 4-7 Torr in end-tidal PCO(2) (P < 0.001) and a reduced hemoglobin saturation (-3 ± 1%; P < 0.05) at the heaviest workload (∼90% maximal VO(2)) with fentanyl. HR was reduced 2-8%, MAP 8-13%, and ratings of perceived exertion by 13% during fentanyl vs. placebo exercise (P < 0.05). These findings demonstrate the essential contribution of muscle afferent feedback to the ventilatory, cardiovascular, and perceptual responses to rhythmic exercise in humans, even in the presence of unaltered contributions from other major inputs to cardioventilatory control.
我们研究了体感反馈对 5 名男性进行节奏性运动时的心呼吸反应的作用。在一项双盲、安慰剂对照设计中，受试者在安慰剂条件（棘突间盐水，L3-L4）和腰椎鞘内芬太尼下进行相同的腿部踏车运动（50/100/150/325±19 W，3 分钟/次），以干扰脊髓阿片受体敏感肌肉传入纤维的中枢投射。芬太尼给药前后股四头肌力量相似。为了评估芬太尼的向头侧迁移是否影响脑干的心血管控制中心，我们比较了每次注射后静息呼吸对高碳酸血症（HCVR）的反应和手臂与腿部踏车运动对心血管的反应。相似的 HCVR 和芬太尼对手臂运动心血管反应的轻微影响排除了芬太尼对延髓的直接作用。通过股四头肌肌电图评估腿部运动时的中枢命令。在静息心率（HR）、通气[分钟通气量（VE）]或平均动脉压（MAP）方面，两种条件之间没有差异。在两种条件下，股四头肌肌电图、耗氧量（VO2）和血浆乳酸在四个稳定工作负荷下均相似。与安慰剂相比，芬太尼运动时 VE/CO2 产生（VCO2）减少 8-17%，提示通气明显减少，导致呼吸频率降低，终末 PCO2 平均增加 4-7 Torr（P<0.001），血红蛋白饱和度降低（-3±1%；P<0.05），在最繁重的工作负荷（~90%最大 VO2）时芬太尼。与安慰剂相比，HR 降低 2-8%，MAP 降低 8-13%，运动时的感知用力降低 13%（P<0.05）。这些发现表明，即使在其他主要心血管控制输入的作用不变的情况下，肌肉传入反馈对人类节奏性运动的通气、心血管和感知反应也具有重要贡献。
