Goulding Richie P, Roche Denise M, Marwood Simon
School of Health Sciences, Liverpool Hope University, Liverpool, UK.
Exp Physiol. 2019 Jul;104(7):1061-1073. doi: 10.1113/EP087599. Epub 2019 May 27.
What is the central question of this study? Critical power is a fundamental parameter defining high-intensity exercise tolerance and is related to the phase II time constant of pulmonary oxygen uptake kinetics ( ). To test whether this relationship is causal, we assessed the impact of hyperoxia on and critical power during supine cycle exercise. What is the main finding and its importance? The results demonstrate that hyperoxia increased muscle oxygenation, reduced (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that is a determinant of the upper limit for steady-state exercise, i.e. critical power.
The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics ( ) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, and absolute concentrations of oxyhaemoglobin ([HbO ]; via near-infrared spectroscopy) were determined via four constant-power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O = 0.5). A 6 min bout of moderate-intensity exercise (70% of gas exchange threshold) was also undertaken before each severe-intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, [HbO ] was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 μm versus normoxia, 63 ± 11 μm; P = 0.020). The was significantly related to CP in hyperoxia (R = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, reduced and CP increased in hyperoxia compared with normoxia, suggesting that is an independent determinant of CP. The finding that was related to CP in hyperoxia but not normoxia also supports this notion.
本研究的核心问题是什么?临界功率是定义高强度运动耐力的一个基本参数,并且与肺氧摄取动力学的II期时间常数( )相关。为了检验这种关系是否具有因果性,我们评估了高氧对仰卧位蹬车运动期间的 和临界功率的影响。主要发现及其重要性是什么?结果表明,与常氧相比,高氧增加了肌肉氧合,降低了 (即加快了氧摄取动力学),随后增加了临界功率。因此,这些结果表明 是稳态运动上限即临界功率的一个决定因素。
本研究确定了高氧对仰卧位蹬车运动期间肺氧摄取动力学的II期时间常数( )和临界功率(CP)的影响。八名健康男性完成了递增测试以确定最大摄氧量和气体交换阈值。随后进行了八次单独的访视试验,通过四次恒定功率测试直至力竭来确定CP、 和氧合血红蛋白的绝对浓度([HbO ];通过近红外光谱法),每种条件下均重复测试一次常氧和一次高氧(吸入氧分数 = 0.5)。在两种条件下,每次高强度运动前还进行了6分钟的中等强度运动(气体交换阈值的70%)。与常氧相比,高氧条件下剧烈运动时临界功率更高(高氧,148±29W;常氧,134±27W;P = 0.006), 降低(高氧,33±12秒;常氧,52±22秒,P = 0.007)。此外,与常氧相比,高氧条件下[HbO ]升高(高氧,67±10μm;常氧,63±11μm;P = 0.020)。在高氧条件下, 与CP显著相关(R = 0.89,P < 0.001),但在常氧条件下未观察到相关性(r = 0.07,P = 0.68)。与常氧相比,高氧条件下肌肉氧合增加, 降低,CP增加,表明 是CP的一个独立决定因素。 在高氧条件下与CP相关而在常氧条件下不相关这一发现也支持了这一观点。