Severity of arterial hypoxaemia affects the relative contributions of peripheral muscle fatigue to exercise performance in healthy humans
Severity of arterial hypoxaemia affects the relative contributions of peripheral muscle fatigue to exercise performance in healthy humans
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DOI：
10.1113/jphysiol.2007.129700
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发表时间：
2007-05-15
影响因子：
5.5
通讯作者：
Dempsey, Jerome A.
中科院分区：
文献类型：
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作者：
Amann, Markus;Romer, Lee M.;Dempsey, Jerome A.
我们研究了缺氧严重程度对运动表现的外周和中枢决定因素的影响。8名骑自行车的人在不同分数的吸入O-2分数（F-IO2 0.21/0.15/0.10）下进行持续负荷运动至疲惫。在任务失败（踏板频率< 70%目标）时，通过急性O-2补充（F-IO2 = 0.30）可以暗中逆转动脉低氧血症，并鼓励受试者继续锻炼。外周疲劳是通过增强股四头肌抽搐力（δ Q(tw,pot)）的变化来评估的，该变化是在运动前和运动后对股上端神经刺激的反应。在正常缺氧（血红蛋白饱和度（s - po2）接近94%，656 +/- 82秒）和中度缺氧（s - po2接近82%，278 +/- 16秒）的任务失败情况下，高氧对延长耐力时间没有显著影响。然而，在严重缺氧（s - po2，类似67%；125 +/- 6 s）的任务失败后，高氧引起了到衰竭时间的显著延长（176.1 %）。三个试验中，衰竭时的aq （tw,pot）的大小没有差异（-35%至-36%，P = 0.8）。此外，在运动过程中，股四头肌综合肌电图、血乳酸、心率和努力感都显著上升，在所有水平的动脉氧合高氧后的疲劳状态下也有相似的程度。由于高氧作用仅在严重缺氧时延长运动时间，我们重复了该试验，并在高氧作用前评估了任务失败后的周围疲劳（125 +/- 6秒）。虽然Q（tw,pot）较运动前基线降低（-23%;P < 0.01），但与正常缺氧和中度缺氧任务失败相比，外周疲劳明显减少（P < 0.01）。我们得出结论，在正常缺氧到严重缺氧的范围内，中枢运动输出和运动表现的主要决定因素从主要的外周疲劳来源转变为缺氧敏感的疲劳中心成分，可能涉及大脑缺氧对努力感知的影响。
We examined the effects of hypoxia severity on peripheral versus central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various fractions of inspired O-2 fraction (F-IO2 0.21/0.15/0.10). At task failure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O-2 supplementation (F-IO2 = 0.30) and subjects were encouraged to continue exercising. Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (Delta Q(tw,pot)) as measured pre- versus post-exercise in response to supramaximal femoralnerve stimulation. At task failure in normoxia (haemoglobin saturation (S-pO2) similar to 94%, 656 +/- 82 s) and moderate hypoxia (S-pO2 similar to 82%, 278 +/- 16 s), hyperoxygenation had no significant effect on prolonging endurance time. However, following task failure in severe hypoxia (S-pO2, similar to 67%; 125 +/- 6 s), hyperoxygenation elicited a significant prolongation of time to exhaustion (171 6 1 %). The magnitude of A Q(tw,pot) at exhaustion was not different among the three trials (-35% to -36%, P = 0.8). Furthermore, quadriceps integrated EMG, blood lactate, heart rate, and effort perceptions all rose significantly throughout exercise, and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe hypoxia, we repeated this trial and assessed peripheral fatigue following task failure prior to hyperoxygenation (125 +/- 6 s). Although Q(tw,pot) was reduced from pre-exercise baseline (-23%; P < 0.01), peripheral fatigue was substantially less (P < 0.01) than that observed at task failure in normoxia and moderate hypoxia. We conclude that across the range of normoxia to severe hypoxia, the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxia-sensitive central component of fatigue, probably involving brain hypoxic effects on effort perception.