Peters Carli M, Welch Joseph F, Dominelli Paolo B, Molgat-Seon Yannick, Romer Lee M, McKenzie Donald C, Sheel A William
School of Kinesiology, University of British Columbia, Vancouver, BC, Canada.
Centre for Human Performance, Exercise and Rehabilitation, College of Health and Life Sciences, Brunel University London, Uxbridge, UK.
Exp Physiol. 2017 Sep 1;102(9):1221-1233. doi: 10.1113/EP086346. Epub 2017 Jul 22.
What is the central question of this study? This study is the first to measure objectively both inspiratory and expiratory muscle fatigue after inspiratory resistive loading to determine whether the expiratory muscles are activated to the point of fatigue when specifically loading the inspiratory muscles. What is the main finding and its importance? The absence of abdominal muscle fatigue suggests that future studies attempting to understand the neural and circulatory consequences of diaphragm fatigue can use inspiratory resistive loading without considering the confounding effects of abdominal muscle fatigue. Expiratory resistive loading elicits inspiratory as well as expiratory muscle fatigue, suggesting parallel coactivation of the inspiratory muscles during expiration. It is unknown whether the expiratory muscles are likewise coactivated to the point of fatigue during inspiratory resistive loading (IRL). The purpose of this study was to determine whether IRL elicits expiratory as well as inspiratory muscle fatigue. Healthy male subjects (n = 9) underwent isocapnic IRL (60% maximal inspiratory pressure, 15 breaths min , 0.7 inspiratory duty cycle) to task failure. Abdominal and diaphragm contractile function was assessed at baseline and at 3, 15 and 30 min post-IRL by measuring gastric twitch pressure (P ) and transdiaphragmatic twitch pressure (P ) in response to potentiated magnetic stimulation of the thoracic and phrenic nerves, respectively. Fatigue was defined as a significant reduction from baseline in P or P . Throughout IRL, there was a time-dependent increase in cardiac frequency and mean arterial blood pressure, suggesting activation of the respiratory muscle metaboreflex. The P was significantly lower than baseline (34.3 ± 9.6 cmH O) at 3 (23.2 ± 5.7 cmH O, P < 0.001), 15 (24.2 ± 5.1 cmH O, P < 0.001) and 30 min post-IRL (26.3 ± 6.0 cmH O, P < 0.001). The P was not significantly different from baseline (37.6 ± 17.1 cmH O) at 3 (36.5 ± 14.6 cmH O), 15 (33.7 ± 12.4 cmH O) and 30 min post-IRL (32.9 ± 11.3 cmH O). Inspiratory resistive loading elicits objective evidence of diaphragm, but not abdominal, muscle fatigue. Agonist-antagonist interactions for the respiratory muscles appear to be more important during expiratory versus inspiratory loading.
本研究的核心问题是什么?本研究首次客观测量了吸气阻力负荷后吸气肌和呼气肌的疲劳情况,以确定在专门负荷吸气肌时,呼气肌是否会被激活至疲劳程度。主要发现及其重要性是什么?腹肌未出现疲劳表明,未来试图了解膈肌疲劳的神经和循环后果的研究可以采用吸气阻力负荷,而无需考虑腹肌疲劳的混杂影响。呼气阻力负荷会引发吸气肌和呼气肌疲劳,这表明在呼气过程中吸气肌存在平行共激活。目前尚不清楚在吸气阻力负荷(IRL)期间,呼气肌是否同样会被共激活至疲劳程度。本研究的目的是确定IRL是否会引发呼气肌以及吸气肌疲劳。9名健康男性受试者接受了等碳酸血症性IRL(60%最大吸气压力,每分钟15次呼吸,吸气占空比0.7)直至任务失败。在基线以及IRL后3、15和30分钟,分别通过测量对胸神经和膈神经进行强化磁刺激时的胃抽搐压力(P )和跨膈抽搐压力(P )来评估腹肌和膈肌的收缩功能。疲劳定义为P 或P 相较于基线显著降低。在整个IRL过程中,心率和平均动脉血压随时间增加,提示呼吸肌代谢性反射被激活。IRL后3分钟(23.2±5.7cmH O,P<0.001)、15分钟(24.2±5.1cmH O,P<0.001)和30分钟(26.3±6.0cmH O,P<0.001)时,P 显著低于基线(34.3±9.6cmH O)。IRL后3分钟(36.5±14.6cmH O)、15分钟(33.7±12.4cmH O)和30分钟(32.9±11.3cmH O)时,P 与基线(37.6±17.1cmH O)相比无显著差异。吸气阻力负荷引发了膈肌而非腹肌疲劳的客观证据。呼吸肌的 agonist - antagonist 相互作用在呼气负荷与吸气负荷期间似乎更为重要。