Effects Of Aerobic Exercise Training And Exercise Intensity On Skeletal Muscle Metabolic Function In Premenopausal Women

Abstract

BACKGROUND: Aerobic training has been shown to improve mitochondrial bioenergetics and up-regulate proteins related to lipid metabolism. However, whether improvements in mitochondrial oxidation and translational proteins associated mitochondrial biogenesis and fatty acid transport (FA) occurs independent of negative energy balance (EB) is unclear. PURPOSE: To assess mitochondrial fatty acid (FA) and carbohydrate (CHO) oxidation in permeabilized muscle fibers, and proteins associated with mitochondrial biogenesis and FA transport under rigorously controlled EB conditions pre- and 12-weeks post aerobic exercise training (AET), and after an acute bout of moderate (MOD) or high (HI) intensity exercise in premenopausal women. METHODS: Participants were 7 women (age = 31±5; weight = 72 ± 11kg; BMI = 26 ± 4kg/m2). Testing was done prior to and after 12-weeks of aerobic exercise training (AET), and after an acute bout of moderate (MOD) or high (HI) intensity exercise in premenopausal women. Muscle biopsies were collected at baseline, 12-wks post, MOD, and HI. Mitochondrial FAO and CHO oxidation were quantified in permeabilized muscle fibers. Western blots were performed to determine PGC1α and carnitine palmitoyltransferase 1B (CPT1B) protein expression. Pre-test conditions were rigorously controlled for EB. RESULTS: Compared to baseline significant increases were observed following 12-wks post, MOD, and HI for State 3 (154%, 115%, and 163%), 4 (90%, 80%, and 128%), and maximum uncoupled respiration (137%, 97%, and 174%) rates when normalized to wet weight using malate and palmitoyl-carnitine as substrates (P 0.05). Importantly, there were no significant differences between 24-hr energy intake and EE across all time points, demonstrating tight control of EB over the 24hr period. CONCLUSION: These data demonstrate an enhanced mitochondrial fatty acid metabolism following 12-weeks of AET, and after a MOD or HI bout of acute exercise without any changes in EB. The increase in mitochondrial FA oxidation appears to be due to mitochondrial biogenesis after training and not intrinsic changes within existing mitochondria. These improvements occurred without any significant increases in PGC1α or CPT1B protein expression measured 24hrs following exercise, suggesting other potential mechanisms in which aerobic exercise may enhance mitochondrial FA oxidation.