Busch Stephen A, Bruce Christina D, Skow Rachel J, Pfoh Jaime R, Day Trevor A, Davenport Margie H, Steinback Craig D
Neurovascular Health Laboratory, Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Edmonton, Alberta, Canada.
Department of Biology, Faculty of Science and Technology, Mount Royal University, Calgary, Alberta, Canada.
Physiol Rep. 2019 Jan;7(2):e13991. doi: 10.14814/phy2.13991.
Volitional Apnea produces a robust peak sympathetic response through several interacting mechanisms. However, the specific contribution of each mechanism has not been elucidated. Muscle sympathetic activity was collected in participants (n = 10; 24 ± 3 years) that performed four maximal volitional apneas aimed at isolating lung-stretch (mechanical) and chemoreflex drive: (Ainslie and Duffin ) end-expiratory breath-hold, (Ainslie et al. ) end-inspiratory breath-hold, (Alpher et al. ) prehyperventilation breath-hold, and (Andersson and Schagatay ) prehyperoxia breath-hold. A final repeated rebreathe breath-hold protocol was performed to measure the peak sympathetic response during successive breath-holds at increasing chemoreflex stress. Finally, the influence of dynamic ventilation was assessed through asphyxic rebreathe. Muscle sympathetic activity was calculated as the change in burst frequency (burst/min), burst incidence (burst/100 heart-beats), and amplitude (au) between baseline and prevolitional breakpoint. Rebreathe was analyzed at similar chemoreflex stress as inspiratory breath-hold. All maneuvers increased muscle sympathetic activity compared to baseline (P < 0.01). However, prehyperoxia exhibited a smaller increase (+22.18 ± 9.13 burst/min; +25.52 ± 11.7 burst/100 heart-beats) compared to inspiratory, expiratory, and prehyperventilation breath-holds. At similar chemoreflex strain, rebreathe sympathetic activity was blunted compared to inspiratory breath-hold (P < 0.01). Finally, muscle sympathetic activity was not different between the repeated rebreathe trials, despite elevated chemoreflex stress and lower breath-hold duration with each subsequent breath-hold. We have demonstrated an obligatory role of the peripheral, but not central, chemoreflex (prehyperventilation vs. prehyperoxia) in producing peak sympathetic responses. At similar chemoreflex stresses the act of dynamic ventilation, but not static lung stretch per se, blunts muscle sympathetic activity. Finally, similar peak sympathetic responses during successive repeated breath-holds suggest a sympathetic ceiling may exist.
自主性呼吸暂停通过多种相互作用的机制产生强烈的交感神经反应峰值。然而，每种机制的具体作用尚未阐明。在10名参与者（年龄24±3岁）中收集肌肉交感神经活动，这些参与者进行了四次最大自主性呼吸暂停，旨在分离肺扩张（机械性）和化学反射驱动：（安斯利和达芬）呼气末屏气、（安斯利等人）吸气末屏气、（阿尔弗等人）过度通气前屏气以及（安德森和沙加泰）高氧前屏气。进行了最后一个重复再呼吸屏气方案，以测量在化学反射应激增加时连续屏气期间的交感神经反应峰值。最后，通过窒息性再呼吸评估动态通气的影响。肌肉交感神经活动以基线和自主性呼吸暂停前断点之间的爆发频率变化（爆发/分钟）、爆发发生率（爆发/100次心跳）和幅度（任意单位）来计算。在与吸气末屏气相似的化学反射应激下分析再呼吸情况。与基线相比，所有操作均增加了肌肉交感神经活动（P<0.01）。然而，与吸气、呼气和过度通气前屏气相比，高氧前屏气的增加幅度较小（+22.18±9.13爆发/分钟；+25.52±11.7爆发/100次心跳）。在相似的化学反射应变下，与吸气末屏气相比，再呼吸时的交感神经活动减弱（P<0.01）。最后，尽管随着每次后续屏气化学反射应激增加且屏气持续时间缩短，但在重复再呼吸试验中肌肉交感神经活动并无差异。我们已经证明外周而非中枢化学反射（过度通气前与高氧前相比）在产生交感神经反应峰值中起必要作用。在相似的化学反射应激下，动态通气的行为而非静态肺扩张本身会减弱肌肉交感神经活动。最后，连续重复屏气期间相似的交感神经反应峰值表明可能存在交感神经上限。
