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Sleeping/Resting Energy Expenditure Is Significantly Increased Following an Acute Bout of High Intensity Interval Exercise: 2388 Board #135 May 29, 930 AM - 1100 AM

Hunter, Gary R. FACSM; Fisher, Gordon; Carter, Stephen J.; Bamman, Marcas M. FACSM; Moellering, Doug R.; Gower, Barbara A.

Medicine & Science in Sports & Exercise: May 2015 - Volume 47 - Issue 5S - p 642
doi: 10.1249/01.mss.0000478467.29276.b8
E-32 Free Communication/Poster - Energy Expenditure Friday, May 29, 2015, 7:30 AM - 12:30 PM Room: Exhibit Hall F

University of Alabama at Birmingham, Birmingham, AL.


(No relationships reported)

During exercise and 22 hours following, a single bout of high intensity interval exercise can increase expenditure (EE) to a greater extent than work-matched moderate intensity continuous exercise.

PURPOSE: The purpose of this study was to determine whether increased mitochondrial leak and/or urinary norepinephrine might contribute to differences in post-exercise sleeping (SEE) and resting (REE) energy expenditure.

METHODS: Twenty-five premenopausal women served as participants. Energy expenditure was evaluated in a room calorimeter across four time-points: 1) baseline (BL); 2) following 8-16 weeks of aerobic exercise training (TR); 3) 22 hours during/following continuous cycle ergometry at 50% VO2max (CC); 4) 22 hours during/following high intensity interval cycle ergometry (IC). Post-exercise testing conditions were randomly ordered. Standardized food was provided to ensure energy balance the day prior to evaluation and during the period spent in the room calorimeter. Muscle biopsies taken from the vastus lateralis of 13 participants were used to evaluate mitochondrial leak. Urinary norepinephrine was measured 22 hours following exercise. A repeated measures ANOVA was used to identify differences across each time points while Pearson Product correlations were used to identify relationships between variables.

RESULTS: Energy balance differences between the 4 conditions was < 22 kcals. There was a significant time effect for both SEE and REE. However, post hoc evaluations indicated that IC significantly increased SEE (31±103 kcal/day above TR) and REE (91±103 kcal/day above TR) compared to all other conditions. Contrary to our hypothesis, uncoupled mitochondrial phosphorylation was negatively related to SEE (r = -0.66) and REE (r = -0.60). Norepinephrine was positively related to SEE (0.56) but not REE. In addition, changes in norepinephrine were positively related to changes in SEE (0.63) but not changes in REE.

CONCLUSIONS: Greater proton mitochondrial leak is associated with decreased SEE, suggesting it may play a counterintuitive role in whole body REE and SEE. However, urinary norepinephrine may be influencing sleeping but not resting energy expenditure.

Supported by NIH Grants R01AG027084-01, R01AG027084-S, P30DK56336, P60DK079626, UL1RR025777.

© 2015 American College of Sports Medicine