Stellingwerff Trent, Leblanc Paul J, Hollidge Melanie G, Heigenhauser George J F, Spriet Lawrence L
Dept. of Human Health and Nutritional Sciences, Univ. of Guelph, Guelph, ON, N1G 2W1, Canada.
Am J Physiol Endocrinol Metab. 2006 Jun;290(6):E1180-90. doi: 10.1152/ajpendo.00499.2005. Epub 2006 Jan 10.
The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia (60% inspired O2) vs. room air is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate production and efflux. We measured pyruvate oxidation via PDH, muscle pyruvate and lactate accumulation, and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise. We hypothesized that 60% O2 would decrease muscle glycogenolysis, resulting in decreased pyruvate and lactate contents, leading to decreased muscle pyruvate and lactate release with no change in PDH activity. Seven active male subjects cycled for 40 min at 70% VO2 peak on two occasions when breathing 21 or 60% O2. Arterial and femoral venous blood samples and blood flow measurements were obtained throughout exercise, and muscle biopsies were taken at rest and after 10, 20, and 40 min of exercise. Hyperoxia had no effect on leg O2 delivery, O2 uptake, or RQ during exercise. Muscle glycogenolysis was reduced by 16% with hyperoxia (267 +/- 19 vs. 317 +/- 21 mmol/kg dry wt), translating into a significant, 15% reduction in total pyruvate production over the 40-min exercise period. Decreased pyruvate production during hyperoxia had no effect on PDH activity (pyruvate oxidation) but significantly decreased lactate accumulation (60%: 22.6 +/- 6.4 vs. 21%: 31.3 +/- 8.7 mmol/kg dry wt), lactate efflux, and total lactate production over 40 min of cycling. Decreased glycogenolysis in hyperoxia was related to an approximately 44% lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise. Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization. The tighter metabolic match between pyruvate production and oxidation resulted in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia.
本研究的目的是确定与呼吸室内空气相比，高氧（吸入60%氧气）运动期间肌肉和血乳酸水平降低是否是由于肌肉糖原分解减少，导致丙酮酸和乳酸生成及流出减少。我们通过丙酮酸脱氢酶（PDH）测量丙酮酸氧化、肌肉丙酮酸和乳酸积累以及乳酸和丙酮酸流出，以估计运动期间丙酮酸和乳酸的总生成量。我们假设60%氧气会减少肌肉糖原分解，导致丙酮酸和乳酸含量降低，从而使肌肉丙酮酸和乳酸释放减少，而PDH活性不变。七名活跃男性受试者在呼吸21%或60%氧气的两种情况下，以70%的最大摄氧量（VO2峰值）进行40分钟的骑行。在整个运动过程中采集动脉和股静脉血样并测量血流量，在静息状态以及运动10、20和40分钟后进行肌肉活检。高氧对运动期间腿部的氧气输送、氧气摄取或呼吸商（RQ）没有影响。高氧使肌肉糖原分解减少了16%（267±19 vs. 317±21 mmol/kg干重），在40分钟的运动期间，丙酮酸总生成量显著减少了15%。高氧期间丙酮酸生成减少对PDH活性（丙酮酸氧化）没有影响，但显著降低了乳酸积累（60%氧气组：22.6±6.4 vs. 21%氧气组：31.3±8.7 mmol/kg干重）、乳酸流出以及40分钟骑行期间的乳酸总生成量。高氧时糖原分解减少与肾上腺素浓度降低约44%以及运动期间强力磷酸化酶激活剂二磷酸腺苷（ADP）和一磷酸腺苷（AMP）的积累减弱有关。高氧期间更高的磷酸化电位与磷酸肌酸（PCr）利用率显著降低有关。丙酮酸生成与氧化之间更紧密的代谢匹配导致高氧期间40分钟运动中乳酸总生成量和流出量减少。
