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间歇引起的代谢紊乱决定了组织液向骨骼肌转移。

Interval-induced metabolic perturbation determines tissue fluid shifts into skeletal muscle.

机构信息

Department of Laboratory Medicine, Division of Clinical Physiology, Karolinska Institutet, and Unit of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.

AMRA Medical AB, Linköping, Sweden.

出版信息

Physiol Rep. 2021 Apr;9(7):e14841. doi: 10.14814/phy2.14841.

DOI:10.14814/phy2.14841
PMID:33904652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8077120/
Abstract

Intense interval exercise has proven to be as effective as traditional endurance exercise in improving maximal oxygen uptake. Shared by these two exercise regimes is an acute reduction in plasma volume, which is a suggested stimulus behind exercise-induced increases in blood volume and maximal oxygen uptake. This study aimed to link exercise-induced metabolic perturbation with volume shifts into skeletal muscle tissue. Ten healthy subjects (mean age 33 ± 8 years, 5 males and 5 females) performed three 30 s all-out sprints on a cycle ergometer. Upon cessation of exercise magnetic resonance imaging, Phosphorus magnetic resonance spectroscopy and blood samples were used to measure changes in muscle volume, intramuscular energy metabolites and plasma volume. Compared to pre-exercise, muscle volume increased from 1147.1 ± 35.6 ml to 1283.3 ± 11.0 ml 8 min post-exercise. At 30 min post-exercise, muscle volume was still higher than pre-exercise (1147.1 ± 35.6 vs. 1222.2 ± 6.8 ml). Plasma volume decreased by 16 ± 3% immediately post-exercise and recovered back to - 5 ± 6% after 30 min. Principal component analysis of exercise performance, muscle and plasma volume changes as well as changes in intramuscular energy metabolites showed generally strong correlations between metabolic and physiological variables. The strongest predictor for the volume shifts of muscle and plasma was the magnitude of glucose-6-phosphate accumulation post-exercise. Interval training leads to large metabolic and hemodynamic perturbations with accumulation of glucose-6-phosphate as a possible key event in the fluid flux between the vascular compartment and muscle tissue.

摘要

高强度间歇运动已被证明在提高最大摄氧量方面与传统耐力运动同样有效。这两种运动方式都有一个共同特点,即血浆容量急性减少,这被认为是运动引起的血容量和最大摄氧量增加的刺激因素。本研究旨在将运动引起的代谢紊乱与体积转移到骨骼肌组织联系起来。10 名健康受试者(平均年龄 33 ± 8 岁,5 名男性,5 名女性)在自行车测力计上进行了 3 次 30 秒的全力冲刺。运动停止后,使用磁共振成像、磷磁共振波谱和血液样本测量肌肉体积、肌肉内能量代谢物和血浆体积的变化。与运动前相比,运动后 8 分钟肌肉体积从 1147.1 ± 35.6ml 增加到 1283.3 ± 11.0ml。运动后 30 分钟,肌肉体积仍高于运动前(1147.1 ± 35.6 vs. 1222.2 ± 6.8ml)。运动后即刻血浆体积减少 16 ± 3%,30 分钟后恢复至-5 ± 6%。运动表现、肌肉和血浆体积变化以及肌肉内能量代谢物的主成分分析显示,代谢和生理变量之间通常具有很强的相关性。肌肉和血浆体积变化的最强预测因子是运动后 6-磷酸葡萄糖的积累量。间歇训练会导致代谢和血液动力学的剧烈变化,而 6-磷酸葡萄糖的积累可能是血管腔室和肌肉组织之间流体通量的关键事件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/5608c8021dcc/PHY2-9-e14841-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/a42be692da10/PHY2-9-e14841-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/26fb1b6e29dc/PHY2-9-e14841-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/8d9cedfeccfc/PHY2-9-e14841-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/0acbe9ff899a/PHY2-9-e14841-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/167af6d072b4/PHY2-9-e14841-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/e9e95499b063/PHY2-9-e14841-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/d5757e0adedb/PHY2-9-e14841-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/5608c8021dcc/PHY2-9-e14841-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/a42be692da10/PHY2-9-e14841-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/26fb1b6e29dc/PHY2-9-e14841-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/8d9cedfeccfc/PHY2-9-e14841-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/0acbe9ff899a/PHY2-9-e14841-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/167af6d072b4/PHY2-9-e14841-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/e9e95499b063/PHY2-9-e14841-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/d5757e0adedb/PHY2-9-e14841-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a39e/8077120/5608c8021dcc/PHY2-9-e14841-g002.jpg

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