Guy's, King's & St Thomas' School of Medical Education, Faculty of Life Sciences & Medicine, King's College London, London, UK.
Centre for Human & Applied Physiological Sciences, School of Basic & Medical Biosciences, Faculty of Life Sciences & Medicine, King's College London, London, UK.
Exp Physiol. 2020 May;105(5):842-851. doi: 10.1113/EP088180. Epub 2020 Apr 1.
What is the central question of this study? What are the mechanisms underlying impaired muscular endurance and accelerated fatigue during acute hypoxia? What is the main finding and its importance? Hypoxia had no effect on the electrochemical latency associated with muscle contraction elicited by supramaximal electrical motor nerve stimulation in vivo. This provides greater insight into the effects of hypoxia and fatigue on the mechanisms of muscle contraction in vivo.
Acute hypoxia impairs muscle endurance and accelerates fatigue, but the underlying mechanisms, including any effects on muscle electrical activation, are incompletely understood. Electromyographic, mechanomyographic and force signals, elicited by common fibular nerve stimulation, were used to determine electromechanical delay (EMD ) of the tibialis anterior muscle in normoxia and hypoxia ( 0.125) at rest and following fatiguing ankle dorsiflexor exercise (60% maximum voluntary contraction, 5 s on, 3 s off) in 12 healthy participants (mean (SD) age 27.4 (9.0) years). EMD was determined from electromyographic to force signal onset, electrical activation latency from electromyographic to mechanomyographic (EMD ) and mechanical latency from mechanomyographic to force (EMD ). Twitch force fell significantly following fatiguing exercise in normoxia (46.8 (14.7) vs. 20.6 (14.3) N, P = 0.0002) and hypoxia (52.9 (15.4) vs. 28.8 (15.2) N, P = 0.0006). No effect of hypoxia on twitch force at rest was observed. Fatiguing exercise resulted in significant increases in mean (SD) EMD in normoxia (Δ 4.7 (4.57) ms P = 0.0152) and hypoxia (Δ 3.7 (4.06) ms P = 0.0384) resulting from increased mean (SD) EMD only (normoxia Δ 4.1 (4.1) ms P = 0.0391, hypoxia Δ 3.4 (3.6) ms P = 0.0303). Mean (SD) EMD remained unchanged during normoxic (Δ 0.6 (1.08) ms) and hypoxic (Δ 0.25 (0.75) ms) fatiguing exercise. No differences in percentage change from baseline for twitch force, EMD , EMD and EMD between normoxic and hypoxic fatigue conditions were observed. Hypoxia in isolation or in combination with fatigue had no effect on the electrochemical latency associated with electrically evoked muscle contraction.
本研究的核心问题是什么？急性低氧时肌肉耐力下降和疲劳加速的潜在机制是什么？主要发现及其重要性是什么？低氧对体内最大电刺激诱发的肌肉收缩的电化学潜伏期没有影响。这为深入了解低氧和疲劳对体内肌肉收缩机制的影响提供了更多的见解。
急性低氧会降低肌肉耐力并加速疲劳，但潜在机制，包括对肌肉电激活的任何影响，尚不完全清楚。使用腓肠神经刺激引起的肌电图、肌动图和力信号，在 12 名健康参与者（平均（SD）年龄 27.4（9.0）岁）中，在常氧和低氧（ 0.125）下休息时和疲劳性踝背屈运动后（60%最大自主收缩，5 s 开，3 s 关）测定胫骨前肌的机电延迟（EMD）。EMD 是从肌电图到力信号起始确定的，电激活潜伏期是从肌电图到肌动图（EMD）确定的，机械潜伏期是从肌动图到力（EMD）确定的。在常氧和低氧下，疲劳运动后，抽搐力明显下降（分别为 46.8（14.7）和 20.6（14.3）N，P=0.0002 和 52.9（15.4）和 28.8（15.2）N，P=0.0006）。在休息时，低氧对抽搐力没有影响。疲劳运动导致常氧（Δ 4.7（4.57）ms，P=0.0152）和低氧（Δ 3.7（4.06）ms，P=0.0384）的平均（SD）EMD 显著增加，这是由于平均（SD）EMD 仅增加（常氧Δ 4.1（4.1）ms，P=0.0391，低氧Δ 3.4（3.6）ms，P=0.0303）。常氧（Δ 0.6（1.08）ms）和低氧（Δ 0.25（0.75）ms）疲劳运动期间，平均（SD）EMD 保持不变。在常氧和低氧疲劳条件下，从基线的抽搐力、EMD、EMD 和 EMD 的百分比变化没有差异。低氧单独或与疲劳结合对电诱发肌肉收缩的电化学潜伏期没有影响。
