title: Leptin concentrations experience a delayed reduction after resistance exercise in men.
abstract: OBJECTIVE
  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, .VO(2max) = 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 approximately 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).
  
  
  CONCLUSIONS
  Leptin concentrations experience a delayed ( approximately 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.
authors.affiliation: Intercollege Graduate Program in Physiology, Department of Kinesiology, The Pennsylvania State University, University Park, PA, USA. Bradley.Nindl@NA.AMEDD.Army.Mil
authors.forename: Bradley C
authors.initials: BC
authors.lastname: Nindl
authors.forename: William J
authors.initials: WJ
authors.lastname: Kraemer
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Arciero
authors.forename: Naeem
authors.initials: N
authors.lastname: Samatallee
authors.forename: Cara D
authors.initials: CD
authors.lastname: Leone
authors.forename: Michele F
authors.initials: MF
authors.lastname: Mayo
authors.forename: Doreen L
authors.initials: DL
authors.lastname: Hafeman
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D004734:Energy Metabolism; D015444:Exercise / Q000502:physiology*; D006801:Humans; D020738:Leptin / Q000097:blood* / Q000502:physiology; D008297:Male; D010101:Oxygen Consumption; D011930:Reaction Time; D013997:Time Factors; D014891:Weight Lifting
chemical_list: D020738:Leptin