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急性常压性缺氧增加健康男性运动后的脂质氧化

Acute Normobaric Hypoxia Increases Post-exercise Lipid Oxidation in Healthy Males.

作者信息

Kelly Liam P, Basset Fabien A

机构信息

Faculty of Medicine, Memorial University of NewfoundlandSt. John's, NL, Canada.

School of Human Kinetics and Recreation, Memorial University of NewfoundlandSt. John's, NL, Canada.

出版信息

Front Physiol. 2017 May 17;8:293. doi: 10.3389/fphys.2017.00293. eCollection 2017.

DOI:10.3389/fphys.2017.00293
PMID:28567018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5434119/
Abstract

The primary objective of the current study was to determine the effect of moderate normobaric hypoxia exposure during constant load cycling on post-exercise energy metabolism recorded in normoxia. Indirect calorimetry was used to examine whole body substrate oxidation before, during, 40-60 min post, and 22 h after performing 60 min of cycling exercise at two different fractions of inspired oxygen (FO): (i) FO = 0.2091 (normoxia) and (ii) FO = 0.15 (hypoxia). Seven active healthy male participants (26 ± 4 years of age) completed both experimental trials in randomized order with a 7-day washout period to avoid carryover effects between conditions. Resting energy expenditure was initially elevated following cycling exercise in normoxia and hypoxia (Δ 0.14 ± 0.05, kcal min, = 0.037; Δ 0.19 ± 0.03 kcal min, < 0.001, respectively), but returned to baseline levels the next morning in both conditions. Although, the same absolute workload was used in both environmental conditions (157 ± 10 W), a shift in resting substrate oxidation occurred after exercise performed in hypoxia while post-exercise measurements were similar to baseline after cycling exercise in normoxia. The additional metabolic stress of hypoxia exposure was sufficient to increase the rate of lipid oxidation (Δ 42 ± 11 mg min, = 0.019) and tended to suppress carbohydrate oxidation (Δ -55 ± 26 mg min, = 0.076) 40-60 min post-exercise. This shift in substrate oxidation persisted the next morning, where lipid oxidation remained elevated (Δ 9 ± 3 mg min, = 0.0357) and carbohydrate oxidation was suppressed (Δ -22 ± 6 mg min, = 0.019). In conclusion, prior exercise performed under moderate normobaric hypoxia alters post-exercise energy metabolism. This is an important consideration when evaluating the metabolic consequences of hypoxia exposure during prolonged exercise, and future studies should evaluate its role in the beneficial effects of intermittent hypoxia training observed in persons with obesity and insulin resistance.

摘要

本研究的主要目的是确定在恒负荷骑行过程中进行中度常压缺氧暴露对常氧条件下记录的运动后能量代谢的影响。采用间接测热法,在吸入两种不同氧分数(FO)的情况下进行60分钟的骑行运动之前、期间、运动后40 - 60分钟以及22小时后,检测全身底物氧化情况:(i)FO = 0.2091(常氧)和(ii)FO = 0.15(缺氧)。七名活跃健康的男性参与者(26 ± 4岁)以随机顺序完成了两项实验试验,并有7天的洗脱期以避免不同条件之间的残留效应。在常氧和缺氧环境下进行骑行运动后,静息能量消耗最初均有所升高(分别为Δ 0.14 ± 0.05千卡/分钟,P = 0.037;Δ 0.19 ± 0.03千卡/分钟,P < 0.001),但在两种情况下第二天早晨均恢复到基线水平。尽管在两种环境条件下使用了相同的绝对工作量(157 ± 10瓦),但在缺氧环境下运动后静息底物氧化发生了变化,而在常氧环境下骑行运动后运动后测量结果与基线相似。缺氧暴露带来的额外代谢应激足以增加运动后40 - 60分钟的脂质氧化速率(Δ 42 ± 11毫克/分钟,P = 0.019),并倾向于抑制碳水化合物氧化(Δ -55 ± 26毫克/分钟,P = 0.076)。这种底物氧化的变化在第二天早晨仍然存在,脂质氧化仍然升高(Δ 9 ± 3毫克/分钟,P = 0.0357),碳水化合物氧化受到抑制(Δ -22 ± 6毫克/分钟,P = 0.019)。总之,在中度常压缺氧条件下进行的先前运动改变了运动后的能量代谢。在评估长时间运动期间缺氧暴露的代谢后果时,这是一个重要的考虑因素,未来的研究应评估其在肥胖和胰岛素抵抗患者中观察到的间歇性缺氧训练有益效果中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1764/5434119/f666e44ec8aa/fphys-08-00293-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1764/5434119/2a78e286f0c1/fphys-08-00293-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1764/5434119/f666e44ec8aa/fphys-08-00293-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1764/5434119/2a78e286f0c1/fphys-08-00293-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1764/5434119/f666e44ec8aa/fphys-08-00293-g0002.jpg

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