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Effects Of Aerobic Exercise Training And Exercise Intensity On Mitochondrial Function And Insulin Sensitivity In Premenopausal Women: 1987 Board #273 May 29, 330 PM - 500 PM

Fisher, Gordon; Gower, Barbara A.; Moellering, Douglas R.; Ovalle, Fernando; Windham, Samuel T.; Hunter, Gary R. FACSM

Medicine & Science in Sports & Exercise: May 2014 - Volume 46 - Issue 5S - p 545
doi: 10.1249/01.mss.0000495099.93574.4a
D-39 Free Communication/Poster - Exercise, Diabetes, and Glucose Thursday, May 29, 2014, 1:00 PM - 6:00 PM Room: WB1

University of Alabama at Birmingham, Birmingham, AL.

(No relationships reported)

BACKGROUND: It is well known that aerobic exercise can improve skeletal muscle insulin sensitivity (SI). Similarly, aerobic training has been reported to improve mitochondrial bioenergetics. However, whether these improvements occur independent of negative energy balance (EB) is not clear

PURPOSE: To assess SI and mitochondrial fatty acid (FA) and carbohydrate (CHO) oxidation in permeabilized muscle fibers 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 18 women (age = 31±5; weight = 72 ± 11kg; BMI = 26 ± 4kg/m2). SI was assessed using euglycemic clamp. Mitochondrial FAO and CHO oxidation were quantified in permeabilized muscle fibers. Pre-test conditions were rigorously controlled for EB. 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

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). However, when normalized to mitochondrial content, no significant differences were observed. No significant changes in respiration were observed for either carbohydrate driven protocols. A significant improvement in SI occurred following 12-wks post, MOD, and HI (baseline SI clamp = 8.5 ± 4.3; 12wks-post = 10.7 ± 4.6; MOD = 12.3 ± 6.5, and HI = 11.8 ± 5.1; P < 0.05). No significant differences in SI were observed between the three post-time points. Importantly, there were no significant differences between 24-hr energy intake and EE across all time points.

CONCLUSION: These data demonstrate an enhanced mitochondrial fatty acid metabolism and increase in SI 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.

© 2014 American College of Sports Medicine