Abstract and Introduction
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; 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.
Elevated plasma triglyceride (TG) concentrations are associated with increased risk of CHD, particularly in women. Therefore, interventions that decrease or prevent an increase in plasma TG concentrations, such as exercise and diet, may help reduce CHD risk. It has long been known that exercise reduces total plasma TG concentration, almost exclusively because of the reduced concentration of TG in VLDL. This effect is not the result of repeated exercise sessions (i.e., training) but instead is acute and short lived because plasma TG concentrations are decreased 12–18 h after a single bout of exercise and remain lower than preexercise values for 2–3 d (8,39). Exercise-induced hypotriglyceridemia manifests above a certain threshold of exercise energy expenditure, independent of duration and intensity and plateaus with progressively more exercise. In a series of studies in healthy nonobese men, we have shown that a single bout of aerobic exercise reduces fasting plasma TG concentrations the next day by increasing the clearance rate of VLDL-TG from the circulation, without affecting VLDL-TG secretion rate from the liver. The exercise-induced increase in VLDL-TG plasma clearance rate also requires a certain energy expenditure threshold and plateaus thereafter. However, the mechanism by which a single bout of exercise reduces fasting plasma TG concentrations in women remains elusive. Previous studies have revealed major sex differences in basal VLDL-TG kinetics. For example, women have a much greater basal VLDL-TG secretion rate than men. It is thus possible that exercise-induced hypotriglyceridemia in women manifests via a different mechanism (e.g., reduced hepatic VLDL-TG secretion) than that in men.
Recent data indicate that negative energy balance is a critical factor for exercise-induced TG lowering. Acutely increasing dietary energy intake to compensate for the energy expended during exercise abolishes the reduction in fasting total plasma TG concentration, whereas a single day of calorie restriction to induce a similar energy deficit as that caused by exercise decreases fasting plasma VLDL-TG concentration to the same extent. Still, although changes in energy balance seem to account for most of the exercise-induced TGlowering, there are data suggesting that exercise is somewhat superior to calorie restriction in inducing hypotriglyceridemia. These observations suggest that the hypotriglyceridemic effect of exercise may be mediated by a mechanism other than, or in addition to, the negative energy balance and that dietary energy deficit may have an independent effect on the mechanisms regulating VLDL-TG homeostasis. Chronic dietary energy restriction leading to weight loss is accompanied by a reduction in hepatic VLDL-TG secretion rate. However, the effects of acute dietary-induced negative energy balance on VLDL-TG kinetics are not known.
The overall aim of the present study was to assess the acute effects of exercise and calorie restriction, each tailored to induce the same negative energy balance, on VLDL-TG metabolism in women. The specific study purposes were 1) to assess the mechanisms leading to exercise-induced hypotriglyceridemia in women and 2) to assess the independent hypotriglyceridemic effect of negative energy balance.