Jonathan L Warren1, Gary R Hunter1, Barbara A Gower1, Marcas M Bamman2, Samuel T Windham3, Douglas R Moellering1, Gordon Fisher4. 1. Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL. 2. Department of Cell Development and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL. 3. Department of Surgery, University of Alabama at Birmingham, Birmingham, AL. 4. Department of Human Studies, University of Alabama at Birmingham, Birmingham, AL.
Abstract
INTRODUCTION/ PURPOSE: Aerobic exercise training (AET) has been shown to improve mitochondrial bioenergetics and upregulate proteins related to lipid metabolism. However, it remains to be determined if these alterations associated with AET persist when measured in energy balance (EB) in the days after the last bout of training. The purpose of the study was to test the hypothesis that improvements in skeletal muscle mitochondrial function induced by AET observed in previous literature would persist when measured after restoring EB conditions 72 h removed from the last exercise bout. METHODS: Participants were 14 premenopausal women (age = 31.2 ± 6.7 yr, BMI = 26.6 ± 5.1 kg·m). The AET program required three monitored training sessions per week for 8-16 wk. Skeletal muscle biopsies were obtained at baseline and after 8-16 wk of AET (≥72 h after the last exercise bout). All food was provided for 72 h before biopsies, and EB was managed 24 h before testing within ±100 kcal of measured energy requirements using a whole-room calorimeter. Mitochondrial oxidative capacity was quantified in permeabilized muscle fibers from the vastus lateralis. RESULTS: We found that AET increased coupled respiration (154%) and uncoupled respiration (90%) rates using a fatty acid substrate (palmitoyl carnitine) (P < 0.05). However, when rates were normalized to complex IV activity (a marker of mitochondrial content), no significant differences were observed. In addition, there were no changes in proteins known to mediate mitochondrial biogenesis or lipid transport and metabolism after AET. CONCLUSION: Eight to 16 wk of AET improved mitochondrial capacity under fatty acid substrate when assessed in EB, which appears to be due to mitochondrial biogenesis.
INTRODUCTION/ PURPOSE: Aerobic exercise training (AET) has been shown to improve mitochondrial bioenergetics and upregulate proteins related to lipid metabolism. However, it remains to be determined if these alterations associated with AET persist when measured in energy balance (EB) in the days after the last bout of training. The purpose of the study was to test the hypothesis that improvements in skeletal muscle mitochondrial function induced by AET observed in previous literature would persist when measured after restoring EB conditions 72 h removed from the last exercise bout. METHODS: Participants were 14 premenopausal women (age = 31.2 ± 6.7 yr, BMI = 26.6 ± 5.1 kg·m). The AET program required three monitored training sessions per week for 8-16 wk. Skeletal muscle biopsies were obtained at baseline and after 8-16 wk of AET (≥72 h after the last exercise bout). All food was provided for 72 h before biopsies, and EB was managed 24 h before testing within ±100 kcal of measured energy requirements using a whole-room calorimeter. Mitochondrial oxidative capacity was quantified in permeabilized muscle fibers from the vastus lateralis. RESULTS: We found that AET increased coupled respiration (154%) and uncoupled respiration (90%) rates using a fatty acid substrate (palmitoyl carnitine) (P < 0.05). However, when rates were normalized to complex IV activity (a marker of mitochondrial content), no significant differences were observed. In addition, there were no changes in proteins known to mediate mitochondrial biogenesis or lipid transport and metabolism after AET. CONCLUSION: Eight to 16 wk of AET improved mitochondrial capacity under fatty acid substrate when assessed in EB, which appears to be due to mitochondrial biogenesis.
Authors: Gary R Hunter; C Scott Bickel; Pedro Del Corral; Nuala M Byrne; Andrew P Hills; D Enette Larson-Meyer; Marcas M Bamman; Bradley R Newcomer Journal: Eur J Appl Physiol Date: 2010-10-23 Impact factor: 3.078
Authors: Nicholas P Greene; James D Fluckey; Brad S Lambert; Elizabeth S Greene; Steven E Riechman; Stephen F Crouse Journal: Am J Physiol Endocrinol Metab Date: 2012-09-18 Impact factor: 4.310
Authors: Danny K Asami; Roger B McDonald; Kevork Hagopian; Barbara A Horwitz; David Warman; Aileen Hsiao; Craig Warden; Jon J Ramsey Journal: Exp Gerontol Date: 2008-09-30 Impact factor: 4.032
Authors: Stephen J Carter; TaShauna U Goldsby; Gordon Fisher; Eric P Plaisance; Barbara A Gower; Stephen P Glasser; Gary R Hunter Journal: Appl Physiol Nutr Metab Date: 2016-01-07 Impact factor: 2.665
Authors: R Sreekumar; J Unnikrishnan; A Fu; J Nygren; K R Short; J Schimke; R Barazzoni; K Sreekumaran Nair Journal: Am J Physiol Endocrinol Metab Date: 2002-07 Impact factor: 4.310