Potential Causes of Elevated REE following High-Intensity Exercise

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Resting energy expenditure (REE) increases following intense exercise; however, little is known concerning mechanisms.


Determine effects of a single bout of moderate-intensity continuous aerobic exercise (MIC), or high intensity interval exercise (HII) on REE under energy balance conditions.


Thirty-three untrained premenopausal women were evaluated at baseline, after 8-16 weeks of training, 22 hours following either MIC (50% peak VO2) or HII (84% peak VO2). Participants were in a room calorimeter during and following the exercise challenge. Food intake was adjusted to obtain energy balance across 23 hours. REE was measured after 22 hours following 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 hours following MIC (64±119 kcal) and HII (103±137 kcal). Markers of muscle damage (CrKact) increased following HII (9.6±25.5 units/liter) and MIC (22.2±22.8 units/liter) while sympathetic tone (urine norepinephrine) increased following HII (1.1±10.6 ng/mg). Uncoupled phosphorylation (states 2 and 4) fat oxidation were related to REE (respectively r=0.65 and r=0.55); however, neither state 2 or 4 fat oxidation increased following MIC or HII. REE was not increased following 8 weeks of aerobic training when exercise was restrained for 60 hours.


Under energy balance conditions REE increased 22 hours following 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 hours following the exercise.

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