Hunter Gary R, Moellering Douglas R, Carter Stephen J, Gower Barbara A, Bamman Marcas M, Hornbuckle Lyndsey M, Plaisance Eric P, Fisher Gordon
1Department of Human Studies, University of Alabama at Birmingham, Birmingham, AL; 2Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL; 3Diabetes Research Center Bioanalytical Redox Biology (BARB) Core, University of Alabama at Birmingham, Birmingham, AL; 4Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL; and 5Department of Kinesiology, Recreation, and Sport Studies, University of Tennessee, Knoxville, TN.
Med Sci Sports Exerc. 2017 Dec;49(12):2414-2421. doi: 10.1249/MSS.0000000000001386.
Resting energy expenditure (REE) increases after an intense exercise; however, little is known concerning mechanisms.
The purpose of this study was to determine effects of a single bout of moderate-intensity continuous (MIC) aerobic exercise, or high-intensity interval (HII) exercise on REE under energy balance conditions.
Thirty-three untrained premenopausal women were evaluated at baseline, after 8-16 wk of training, 22 h after either MIC (50% peak V˙O2) or HII (84% peak V˙O2). Participants were in a room calorimeter during and after the exercise challenge. Food intake was adjusted to obtain energy balance across 23 h. REE was measured after 22 h after all conditions. Twenty-three-hour urine norepinephrine concentration and serum creatine kinase activity (CrKact) were obtained. Muscle biopsies were obtained in a subset of 15 participants to examine muscle mitochondrial state 2, 3, and 4 fat oxidation.
REE was increased 22 h after MIC (64 ± 119 kcal) and HII (103 ± 137 kcal). Markers of muscle damage (CrKact) increased after HII (9.6 ± 25.5 U·L) and MIC (22.2 ± 22.8 U·L), whereas sympathetic tone (urine norepinephrine) increased after HII (1.1 ± 10.6 ng·mg). Uncoupled phosphorylation (states 2 and 4) fat oxidation were related to REE (r = 0.65 and r = 0.55, respectively); however, neither state 2 nor state 4 fat oxidation increased after MIC or HII. REE was not increased after 8 wk of aerobic training when exercise was restrained for 60 h.
Under energy balance conditions, REE increased 22 h after both moderate-intensity and high-intensity exercise. Exercise-induced muscle damage/repair and increased sympathetic tone may contribute to increased REE, whereas uncoupled phosphorylation does not. These results suggest that moderate- to high-intensity exercise may be valuable for increasing energy expenditure for at least 22 h after the exercise.
高强度运动后静息能量消耗（REE）会增加；然而，其机制尚不清楚。
本研究旨在确定在能量平衡条件下，单次中等强度持续（MIC）有氧运动或高强度间歇（HII）运动对REE的影响。
33名未受过训练的绝经前女性在基线时、训练8 - 16周后、进行MIC（峰值摄氧量的50%）或HII（峰值摄氧量的84%）运动22小时后进行评估。运动挑战期间及之后，参与者处于房间量热计中。调整食物摄入量以在23小时内实现能量平衡。在所有条件结束22小时后测量REE。获取23小时尿去甲肾上腺素浓度和血清肌酸激酶活性（CrKact）。对15名参与者进行肌肉活检，以检查肌肉线粒体状态2、3和4的脂肪氧化情况。
MIC运动（64±119千卡）和HII运动（103±137千卡）后22小时REE增加。HII运动（9.6±25.5 U·L）和MIC运动（22.2±22.8 U·L）后肌肉损伤标志物（CrKact）增加，而HII运动后交感神经张力（尿去甲肾上腺素）增加（1.1±10.6 ng·mg）。解偶联磷酸化（状态2和4）脂肪氧化与REE相关（分别为r = 0.65和r = 0.55）；然而，MIC或HII运动后状态2和状态4的脂肪氧化均未增加。当运动限制60小时后，进行8周有氧运动训练后REE未增加。
在能量平衡条件下，中等强度和高强度运动后22小时REE均增加。运动诱导的肌肉损伤/修复和交感神经张力增加可能导致REE增加，而解偶联磷酸化则不然。这些结果表明，中高强度运动对于运动后至少22小时增加能量消耗可能具有重要价值。
