Rupp Thomas, Mallouf Thibault Le Roux, Perrey Stéphane, Wuyam Bernard, Millet Guillaume Y, Verges Samuel
1HP2 Laboratory, Université Grenoble Alpes, Grenoble, FRANCE; 2U1042, INSERM, Grenoble, FRANCE; 3Laboratoire de Physiologie de l'Exercice, Université Savoie Mont Blanc, Chambéry, FRANCE; 4Movement To Health, Montpellier-I University, Euromov, Montpellier, FRANCE; 5Université de Lyon, Saint-Etienne, FRANCE; and 6Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, AB, CANADA.
Med Sci Sports Exerc. 2015 Dec;47(12):2513-24. doi: 10.1249/MSS.0000000000000724.
The central nervous system can play a critical role in limiting exercise performance during hypoxic conditions. Hypocapnia, which is associated with hypoxia-induced hyperventilation, may affect cerebral perfusion. We hypothesized that CO2 clamping during hypoxic isometric knee extensions would improve cerebral oxygenation and reduce central fatigue.
Fifteen healthy men (mean ± SD: age, 25 ± 8 yr; body mass, 72 ± 11 kg; height, 179 ± 7 cm) performed intermittent isometric knee extensions at ∼50% of maximal voluntary contraction to task failure in normoxia, hypoxia with CO2 clamping (arterial O2 saturation, 80% ± 2%; end-tidal CO2 partial pressure, 40 ± 2 mm Hg), and hypoxia without CO2 clamping (arterial O2 saturation, 80% ± 3%). Transcranial magnetic stimulation and femoral nerve electrical stimulation were used to assess central and peripheral determinants of fatigue. Prefrontal cortex and quadriceps femoris oxygenation were monitored by multichannel near-infrared spectroscopy.
Exercise duration was reduced to a similar extent in hypoxia with CO2 clamping (997 ± 460 s) or hypoxia without CO2 clamping (929 ± 412 s) compared to normoxia (1473 ± 876 s; P < 0.001). Prefrontal cortex and quadriceps oxygenation were increased (+5.3 ± 8.6 and +2.6 ± 3.0 μmol·cm at task failure, respectively; P < 0.01) during hypoxia with CO2 clamping compared to hypoxia without CO2 clamping. Transcranial magnetic stimulation maximal voluntary activation decreased to a greater extent at task failure in hypoxia without CO2 clamping (-18% ± 8%) compared to hypoxia with CO2 clamping (-9% ± 9%; P < 0.01) and normoxia (-10% ± 7%; P < 0.05). Conversely, exercise-induced peripheral fatigue was larger in hypoxia with CO2 clamping than in hypoxia without CO2 clamping (e.g., Db10-to-Db100 ratio of 0.54 ± 0.12 and 0.63 ± 0.11 at task failure, respectively; P < 0.05).
The results demonstrate that CO2 clamping can alter central and peripheral mechanisms that contribute to neuromuscular fatigue during hypoxic isometric knee extensions in men. Hypocapnia impairs cerebral oxygenation and central drive but exerts a protective effect against fatigability in muscles.
中枢神经系统在低氧条件下限制运动表现方面可能发挥关键作用。低碳酸血症与低氧诱导的过度通气相关,可能影响脑灌注。我们假设在低氧等长伸膝过程中进行二氧化碳钳制可改善脑氧合并减轻中枢疲劳。
15名健康男性(平均±标准差:年龄,25±8岁;体重,72±11千克;身高,179±7厘米)在常氧、有二氧化碳钳制的低氧(动脉血氧饱和度,80%±2%;呼气末二氧化碳分压,40±2毫米汞柱)和无二氧化碳钳制的低氧(动脉血氧饱和度,80%±3%)条件下,以约最大自主收缩的50%进行间歇性等长伸膝,直至任务失败。采用经颅磁刺激和股神经电刺激评估疲劳的中枢和外周决定因素。通过多通道近红外光谱监测前额叶皮质和股四头肌的氧合情况。
与常氧(1473±876秒;P<0.001)相比,有二氧化碳钳制的低氧(997±460秒)或无二氧化碳钳制的低氧(929±412秒)条件下运动持续时间缩短程度相似。与无二氧化碳钳制的低氧相比,有二氧化碳钳制的低氧在任务失败时前额叶皮质和股四头肌的氧合增加(分别为+5.3±8.6和+2.6±3.0微摩尔·厘米;P<0.01)。与有二氧化碳钳制的低氧(-9%±9%;P<0.01)和常氧(-10%±7%;P<0.05)相比,无二氧化碳钳制的低氧在任务失败时经颅磁刺激最大自主激活下降幅度更大(-18%±8%)。相反,有二氧化碳钳制的低氧条件下运动诱导的外周疲劳比无二氧化碳钳制的低氧更大(例如,任务失败时Db10至Db100比率分别为0.54±0.12和0.63±0.11;P<0.05)。
结果表明,在男性低氧等长伸膝过程中,二氧化碳钳制可改变导致神经肌肉疲劳的中枢和外周机制。低碳酸血症损害脑氧合和中枢驱动,但对肌肉疲劳性具有保护作用。