Effect of acute exercise and dietary manipulation on hepatic triglycerides

Introduction: Exercise fat oxidation is increased with exercise duration and when exercise is preceded by short-term low-carbohydrate high-fat diet. However, the relative contribution of tissue lipids to fat oxidation remains unclear and cannot be accounted for by the oxidation of adipose-derived free fatty acids (FFAs). This has implicated a role for other fat sources such as muscle and/or hepatic triglycerides in exercise metabolism. No study has measured hepatic triglyceride concentration (HTGC) before and after exercise in humans. In rodents, acute exercise has been shown significantly reduce HTGC during the hours following exercise cessation. Demonstration of a reduction in HTGC during and/or after exercise in humans may have important implications for non-alcoholic fatty liver disease (NAFLD). Methods: Five endurance-trained men (VO2max 63.3 ± 6.0 ml kg−1 min−1; body mass 75.5 ± 4.3 kg; age 30.4 ± 3.8 years) undertook two bouts of prolonged cycling exercise (65% of VO2max) after 67 h of a: (1) mixed diet (50% carbohydrate; 35% fat; 15% protein) (Mixed) and (2) low-carbohydrate high-fat diet (2% carbohydrate; 83% fat; 15% protein) (LCHO), via a double-blinded cross-over design. HTGC was measured before and after exercise by localised magnetic resonance spectroscopy. All participants were informed of the study protocol and risks before providing their written consent. The study was approved by the Human Research Ethics Committee of The University of Sydney. Results: Fat oxidation was significantly higher during exercise in LCHO versus Mixed (p < 0.01). The rise in FFAs was greater in LCHO versus Mixed (p < 0.05). There was no effect of diet on HTGC before or after exercise (p > 0.05) yet HTGC increased during exercise in both conditions and was significantly higher than pre-exercise 4.5 hrs after exercise cessation (p < 0.05). Conclusion: Hepatic triglyceride concentration is not altered by short-term dietary manipulation but is increased during and following prolonged aerobic exercise in endurance-trained humans. This increase may reflect the fact that exercise increases adipose-derived plasma FFAs, whose uptake into the liver may exceed hepatic triglyceride removal via oxidation and/or triglyceride export. These data suggest that the benefit of regular exercise in NAFLD is not due to acute benefits.

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