NINDL, B. C., W. J. KRAEMER, P. J. ARCIERO, N. SAMATALLEE, C. LEONE, M. MAYO, and D. HAFEMAN. Leptin concentrations experience a delayed reduction after resistance exercise in men. Med. Sci. Sports Exerc., Vol. 34, No. 4, pp. 608–613, 2002.
Purpose: Leptin is an important metabolic hormone providing the brain with information concerning energy balance. Most studies have reported that circulating leptin concentrations are unaltered by acute, moderate exercise. We hypothesized that these studies have been limited by short sampling schemes (<4 h) postexercise and may have missed a time-delayed reduction in circulating leptin concentrations.
Methods: Ten men (age = 21 ± 1 yr, height = 177 ± 2 cm, body mass = 79 ± 3 kg, body fat = 11 ± 1%BF, V̇O2max = 51 ± 1 mL·kg−1·min−1) completed an acute heavy-resistance exercise protocol (AHREP) (50 total sets comprised of the squat, bench press, leg press, and lat pull-down) from 1500 to 1700 h. Blood was sampled hourly postexercise until 0600 h the next morning and also during a time-matched control period. Leptin concentrations were measured by an immunoradiometric assay. Resting energy expenditure (REE) was measured via indirect calorimetry using a ventilated hood beginning ∼0600 h after both overnight conditions.
Results: The estimated caloric expenditure from the AHREP was 856 ± 114 kcal. No significant differences (P > 0.05) between the control and exercise conditions were observed for serum leptin concentrations until 9 h postexercise. Significant interaction effects (P < 0.05) indicated lower serum leptin concentrations postexercise at hours 9 (2.9 vs 2.2 ng·mL−1), 10 (2.7 vs 2.0 ng·mL−1), 12 (2.5 vs 1.8 ng·mL−1), and 13 (2.6 vs 1.8 ng·mL−1). This delayed reduction was accompanied by a 12% elevation (P < 0.05) in morning-after REE (0.25 ± 0.02 vs 0.28 ± 0.02 L·min−1).
Conclusion: Leptin concentrations experience a delayed (∼ 9 h) reduction in the systemic circulation after acute resistance exercise. This decline is likely associated with the disruption in metabolic homeostasis created by the high-intensity, long-duration, energy expenditure and subsequent excess post oxygen consumption from the AHREP and is not due to losses in fat mass.
Intercollege Graduate Program in Physiology and General Clinical Research Center at Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, PA; Military Performance Division and Central Laboratory, Research Support Division, United States Army Research Institute of Environmental Medicine, Natick, MA; The Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT; and Department of Exercise Science, Skidmore College, Saratoga Springs, NY
Submitted for publication March 2001.
Accepted for publication August 2001.