首页> 外文期刊>The Journal of Physiology >Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists.
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Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists.

机译:在训练有素的自行车手中,呼吸肌血流对运动诱发的fatigue肌疲劳的贡献。

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We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.
机译:我们调查了先前在训练有素的运动员缺氧(与正常氧相比)中更大程度的运动诱发的diaphragm肌疲劳是否可能是由于呼吸肌血流受限所致。七名训练有素的自行车手完成了三个恒定负荷5分钟的运动测试,并以平衡的顺序分别获得了O3(2)分数(FIO2)0.13、0.21和1.00。选择工作率以在每个FIO2处产生相同的潮气量,呼吸频率和呼吸肌负荷(分别为常氧最大工作率的63 +/- 1、78 +/- 1和87 +/- 1%)。使用吲哚花青绿染料分别在左第7肋间隙和左外侧阔肌上通过近红外光谱法测量肋间和股四头肌的血流量(分别为IMBF和QMBF)。在这三个运动测试中,隔膜的平均压力时间乘积与呼吸功没有差异。低氧运动后,trans横dia肌压力降低了33.3 +/- 4.8%,比常氧运动(降低25.6 +/- 3.5%)和高氧运动(降低26.6 +/- 3.3%)明显降低(P <0.05),这证实了缺氧时疲劳加剧。尽管在缺氧状态下小腿功率输出较低,但心输出量和QMBF均未显着(分别为27.6 +/- 1.2 l min(-1)和100.4 +/- 8.7 ml(100 ml)(-1)min(-1))与高氧(分别为28.4 +/- 1.9 l min(-1)和94.4 +/- 5.2 ml(100 ml)(-1)min(-1)和高氧(27.8 +/- 1.6 l min( -1)和95.1 +/- 7.8 ml(100 ml)(-1)min(-1))。 IMBF在缺氧,常氧和高氧状态下均无差异(分别为53.6 +/- 8.5、49.9 +/- 5.9和52.9 +/- 5.9 ml(100 ml)(-1)min(-1))。我们得出的结论是,当常氧和低氧之间的呼吸肌能量需求没有差异时,低氧时diaphragm肌疲劳会更大,因为肋间肌血流量没有增加(与正常氧相比)以补偿PaO2的减少,从而进一步损害了O(2)供给呼吸肌肉。

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