Ramsook Andrew H, Molgat-Seon Yannick, Schaeffer Michele R, Wilkie Sabrina S, Camp Pat G, Reid W Darlene, Romer Lee M, Guenette Jordan A
Centre for Heart Lung Innovation, University of British Columbia and St. Paul's Hospital, Vancouver, British Columbia, Canada.
Department of Physical Therapy, University of British Columbia, Vancouver, British Columbia, Canada.
J Appl Physiol (1985). 2017 May 1;122(5):1267-1275. doi: 10.1152/japplphysiol.00046.2017. Epub 2017 Mar 2.
Inspiratory muscle training (IMT) has consistently been shown to reduce exertional dyspnea in health and disease; however, the physiological mechanisms remain poorly understood. A growing body of literature suggests that dyspnea intensity can be explained largely by an awareness of increased neural respiratory drive, as measured indirectly using diaphragmatic electromyography (EMGdi). Accordingly, we sought to determine whether improvements in dyspnea following IMT can be explained by decreases in inspiratory muscle electromyography (EMG) activity. Twenty-five young, healthy, recreationally active men completed a detailed familiarization visit followed by two maximal incremental cycle exercise tests separated by 5 wk of randomly assigned pressure threshold IMT or sham control (SC) training. The IMT group ( = 12) performed 30 inspiratory efforts twice daily against a 30-repetition maximum intensity. The SC group ( = 13) performed a daily bout of 60 inspiratory efforts against 10% maximal inspiratory pressure (MIP), with no weekly adjustments. Dyspnea intensity was measured throughout exercise using the modified 0-10 Borg scale. Sternocleidomastoid and scalene EMG was measured using surface electrodes, whereas EMGdi was measured using a multipair esophageal electrode catheter. IMT significantly improved MIP (pre: -138 ± 45 vs. post: -160 ± 43 cmHO, < 0.01), whereas the SC intervention did not. Dyspnea was significantly reduced at the highest equivalent work rate (pre: 7.6 ± 2.5 vs. post: 6.8 ± 2.9 Borg units, < 0.05), but not in the SC group, with no between-group interaction effects. There were no significant differences in respiratory muscle EMG during exercise in either group. Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by changes in the electrical activity of the inspiratory muscles. Exertional dyspnea intensity is thought to reflect an increased awareness of neural respiratory drive, which is measured indirectly using diaphragmatic electromyography (EMGdi). We examined the effects of inspiratory muscle training (IMT) on dyspnea, EMGdi, and EMG of accessory inspiratory muscles. IMT significantly reduced submaximal dyspnea intensity ratings but did not change EMG of any inspiratory muscles. Improvements in exertional dyspnea following IMT may be the result of nonphysiological factors or physiological adaptations unrelated to neural respiratory drive.
吸气肌训练（IMT）一直被证明能减轻健康人群和患病者的运动性呼吸困难；然而，其生理机制仍知之甚少。越来越多的文献表明，呼吸困难强度在很大程度上可以通过对神经呼吸驱动增加的感知来解释，这种感知通过膈肌肌电图（EMGdi）间接测量。因此，我们试图确定IMT后呼吸困难的改善是否可以通过吸气肌肌电图（EMG）活动的减少来解释。25名年轻、健康、有休闲运动习惯的男性完成了一次详细的熟悉流程，随后进行了两次最大递增式自行车运动测试，两次测试间隔5周，期间随机分配进行压力阈值IMT或假对照（SC）训练。IMT组（n = 12）每天进行两次30次最大重复强度的吸气努力。SC组（n = 13）每天进行一次60次吸气努力，对抗10%最大吸气压力（MIP），且每周不进行调整。在整个运动过程中，使用改良的0 - 10 Borg量表测量呼吸困难强度。使用表面电极测量胸锁乳突肌和斜角肌的EMG，而使用多对食管电极导管测量EMGdi。IMT显著改善了MIP（训练前：-138 ± 45 vs. 训练后：-160 ± 43 cmH₂O，P < 0.01），而SC干预则没有。在最高等效工作率时，呼吸困难显著减轻（训练前：7.6 ± 2.5 vs. 训练后：6.8 ± 2.9 Borg单位，P < 0.05），但SC组没有，且两组间没有交互作用。两组运动期间呼吸肌EMG均无显著差异。健康人IMT后呼吸困难强度评分的改善不能通过吸气肌电活动的变化来解释。运动性呼吸困难强度被认为反映了对神经呼吸驱动增加的感知增强，这种感知通过膈肌肌电图（EMGdi）间接测量。我们研究了吸气肌训练（IMT）对呼吸困难、EMGdi和辅助吸气肌EMG的影响。IMT显著降低了次最大呼吸困难强度评分，但没有改变任何吸气肌的EMG。IMT后运动性呼吸困难的改善可能是非生理因素或与神经呼吸驱动无关的生理适应的结果。
