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−1) and MIC (22.2 ± 22.8 U·L−1), whereas sympathetic tone (urine norepinephrine) increased after HII (1.1 ± 10.6 ng·mg−1). 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.
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
Address for correspondence: Gary R. Hunter, Ph.D., Department of Human Studies, University of Alabama at Birmingham, Birmingham, AL 35294; E-mail: email@example.com.
Submitted for publication January 2017.
Accepted for publication July 2017.