Purpose: The mechanisms by which exercise reduces fasting plasma triglyceride (TG) concentrations in women and the effect of negative energy balance independent of muscular contraction are not known.
The aim of this study was to evaluate the effects of equivalent energy deficits induced by exercise or calorie restriction on basal VLDL-TG metabolism in women.
Methods: Eleven healthy women (age = 23.5 ± 2.7 yr, body mass index = 21.6 ± 1.4 kg·m−2; mean ± SD) underwent a stable isotopically labeled tracer infusion study to determine basal VLDL-TG kinetics after performing, in random order, three experimental trials on the previous day: (i) a single exercise bout (brisk walking at 60% of peak oxygen consumption for 123 ± 18 min, with a net energy expenditure of 2.06 ± 0.39 MJ, ∼500 kcal), (ii) dietary energy restriction of 2.10 ± 0.41 MJ, and (iii) a control day of isocaloric feeding and rest (zero energy balance).
Results: Fasting plasma VLDL-TG concentration was approximately 30% lower after the exercise trial compared with the control trial (P < 0.001), whereas no significant change was detected after the calorie restriction trial (P = 0.297 vs control). Relative to the control condition, exercise increased the plasma clearance rate of VLDL-TG by 22% (P = 0.001) and reduced hepatic VLDL-TG secretion rate by approximately 17% (P = 0.042), whereas hypocaloric diet had no effect on VLDL-TG kinetics (P > 0.2).
Conclusion: (i) Exercise-induced hypotriglyceridemia in women manifests through a different mechanism (increased clearance and decreased secretion of VLDL-TG) than that previously described in men (increased clearance of VLDL-TG only), and (ii) exercise affects TG homeostasis by eliciting changes in VLDL-TG kinetics that cannot be reproduced by an equivalent diet-induced energy deficit, indicating that these changes are independent of the exercise-induced negative energy balance but instead are specific to muscular contraction.
1Laboratory of Nutrition and Clinical Dietetics, Department of Nutrition and Dietetics, Harokopio University, Athens, GREECE; 2Human Performance Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, Arkansas; 3Department of Internal Medicine, Center for Human Nutrition and Atkins Center of Excellence in Obesity Medicine, Washington University School of Medicine, St. Louis, MO; and 4Department of Internal Medicine, Sealy Center on Aging, Institute for Translational Sciences and Shriners Hospital for Children, University of Texas Medical Branch at Galveston, TX
Address for correspondence: Labros S. Sidossis, Ph.D., University of Texas Medical Branch at Galveston, 301 University Blvd, 6.128 Rebecca Sealy Hospital, Galveston, TX 77555-0177; E-mail: email@example.com.
Submitted for publication July 2012.
Accepted for publication October 2012.