Supraspinal fatigue after normoxic and hypoxic exercise in humans.
Supraspinal fatigue after normoxic and hypoxic exercise in humans.
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DOI：
10.1113/jphysiol.2012.228890
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发表时间：
2012-06-01
期刊：
影响因子：
--
通讯作者：
Romer LM
中科院分区：
文献类型：
--
作者：
Goodall S;González-Alonso J;Ali L;Ross EZ;Romer LM
脑氧供应不足已被认为是剧烈运动期间中枢疲劳发展的一个重要因素。在这里，我们测试的假设，脊髓上的疲劳过程将增加运动后，在急性缺氧相比，常氧，这种变化将与减少脑O2输送和组织氧合。9名经过耐力训练的自行车运动员以最大工作率的80%完成了三项恒定负荷自行车运动试验：（1）急性缺氧耐受极限;（2）相同时间但常氧（对照）;（3）常氧耐受极限。在每个试验中，前额叶皮质组织氧合和大脑中动脉血流速度（MCAV）分别使用近红外光谱和经颅多普勒超声进行评估。脑氧输送量计算为动脉氧含量和MCAV的乘积。在每次试验之前和之后立即获得对超大股神经刺激和经颅磁刺激的抽搐反应，以分别评估神经肌肉和皮质功能。与常氧相比，低氧运动时间减少了54%（3.6 ± 1.3 vs 8.1 ± 2.9 min; P < 0.001）。与对照组相比，缺氧组脑氧释放、脑氧合和最大摄氧量减少，而肌电活动增加（P < 0.05）。最大随意力和增强的股四头肌抽搐力在每个试验中运动后均低于基线;与对照组相比，缺氧组的下降幅度更大（P < 0.001），但在力竭试验中没有差异（P > 0.05）。在所有试验中，运动后皮层自主激活也降低，但低氧试验中的降低幅度（Δ18%）大于常氧试验中的降低幅度（Δ5-9%）（P < 0.05）。皮质自主激活的减少被大脑O2输送的减少所抵消。结果表明，在急性严重缺氧的运动性能的削减是由于，在一定程度上，从运动皮层的驱动失败，可能是由于大脑中的O2可用性减少。
Inadequate cerebral O2 availability has been proposed to be an important contributing factor to the development of central fatigue during strenuous exercise. Here we tested the hypothesis that supraspinal processes of fatigue would be increased after locomotor exercise in acute hypoxia compared to normoxia, and that such change would be related to reductions in cerebral O2 delivery and tissue oxygenation. Nine endurance-trained cyclists completed three constant-load cycling exercise trials at ∼80% of maximal work rate: (1) to the limit of tolerance in acute hypoxia; (2) for the same duration but in normoxia (control); and (3) to the limit of tolerance in normoxia. Throughout each trial, prefrontal cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assessed using near-infrared spectroscopy and transcranial Doppler sonography, respectively. Cerebral O2 delivery was calculated as the product of arterial O2 content and MCAV. Before and immediately after each trial, twitch responses to supramaximal femoral nerve stimulation and transcranial magnetic stimulation were obtained to assess neuromuscular and cortical function, respectively. Exercise time was reduced by 54% in hypoxia compared to normoxia (3.6 ± 1.3 vs. 8.1 ± 2.9 min; P < 0.001). Cerebral O2 delivery, cerebral oxygenation and maximum O2 uptake were reduced whereas muscle electromyographic activity was increased in hypoxia compared to control (P < 0.05). Maximum voluntary force and potentiated quadriceps twitch force were decreased below baseline after exercise in each trial; the decreases were greater in hypoxia compared to control (P < 0.001), but were not different in the exhaustive trials (P > 0.05). Cortical voluntary activation was also decreased after exercise in all trials, but the decline in hypoxia (Δ18%) was greater than in the normoxic trials (Δ5–9%) (P < 0.05). The reductions in cortical voluntary activation were paralleled by reductions in cerebral O2 delivery. The results suggest that curtailment of exercise performance in acute severe hypoxia is due, in part, to failure of drive from the motor cortex, possibly as a consequence of diminished O2 availability in the brain.
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影响因子：
3.3
作者：
Fowles, JR;Green, HJ;Roy, BD
通讯作者：
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3.3
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8.3
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