Adipokine responses to acute resistance exercise in trained and untrained men.

INTRODUCTION Adipose tissue-derived hormones act as key mediators that may link active lifestyles to improved cardiovascular function. This study tested the hypothesis that a single weight training session would beneficially modulate adipokine profile in a way that would exert protection against endothelial dysfunction, in trained but not sedentary subjects. METHODS Male subjects (n = 43) were categorized into four separate groups based on exercise history: 1) sedentary, 2) weight trainers, 3) runners, or 4) weight trainer + runners. All subjects underwent a single progressive leg press weight training session (low weight for two sets of 8-12 repetitions each and then near-maximal exertion for three sets of 8-12 repetitions each). RESULTS There were no differences between groups for age, body weight, BMI, waist circumference, or percent body fat. Adiponectin increased (P < 0.05) by 30% and 37%, whereas resistin decreased (P < 0.05) by 35% and 34% in the weight trainers and weight trainer + runners, respectively, after training. Flow-mediated dilation (FMD) was impaired (P < 0.05) in sedentary subjects (-1.1 +/- 0.3%) but not in the athletic groups (1.7 +/- 0.4%). Improvements in FMD were associated with increased adiponectin (r = 0.61, P = 0.01), and decreased resistin (r = -0.56, P = 0.01) in weight trainers only. Leptin was not altered by acute resistance training in any group. There were no differences after training for total, LDL, HDL cholesterol, triglycerides, C-reactive protein levels, and systolic or diastolic blood pressure. Increased adiponectin was related to higher levels of HDL cholesterol after intervention (r = 0.71, P = 0.001). CONCLUSIONS These findings suggest that habitual resistance training may modulate adipokine profiles in a way that is protective against endothelial dysfunction.

[1]  C. Lavie,et al.  Exercise training and cardiac rehabilitation in primary and secondary prevention of coronary heart disease. , 2009, Mayo Clinic proceedings.

[2]  J. Danesh,et al.  Clinical ResearchCoronary Artery DiseaseLeptin and Coronary Heart Disease: Prospective Study and Systematic Review , 2009 .

[3]  K. Chamari,et al.  Review on leptin and adiponectin responses and adaptations to acute and chronic exercise , 2008, British Journal of Sports Medicine.

[4]  Y. Jang,et al.  Association between serum resistin and carotid intima media thickness in hypertension patients. , 2008, International journal of cardiology.

[5]  G. Lembo,et al.  Resistin Impairs Insulin-Evoked Vasodilation , 2008, Diabetes.

[6]  William L Haskell,et al.  Resistance exercise in individuals with and without cardiovascular disease: 2007 update: a scientific statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism. , 2007, Circulation.

[7]  M. Quon,et al.  Adiponectin and cardiovascular disease: response to therapeutic interventions. , 2007, Journal of the American College of Cardiology.

[8]  J. Tune,et al.  Resistin impairs endothelium-dependent dilation to bradykinin, but not acetylcholine, in the coronary circulation. , 2006, American journal of physiology. Heart and circulatory physiology.

[9]  J. Bełtowski,et al.  Leptin and atherosclerosis. , 2006, Atherosclerosis.

[10]  D. Gutterman,et al.  The effect of exertional hypertension evoked by weight lifting on vascular endothelial function. , 2006, Journal of the American College of Cardiology.

[11]  A. Burska,et al.  Increased serum resistin in elite endurance athletes with high insulin sensitivity , 2006, Diabetologia.

[12]  A. Jamurtas,et al.  The effects of acute exercise on serum adiponectin and resistin levels and their relation to insulin sensitivity in overweight males , 2006, European Journal of Applied Physiology.

[13]  E. Picano,et al.  Peripheral vascular endothelial function testing for the diagnosis of coronary artery disease. , 2004, American heart journal.

[14]  S. Kihara,et al.  Selective Suppression of Endothelial Cell Apoptosis by the High Molecular Weight Form of Adiponectin , 2004, Circulation research.

[15]  Hui Chen,et al.  Adiponectin Stimulates Production of Nitric Oxide in Vascular Endothelial Cells* , 2003, Journal of Biological Chemistry.

[16]  Ary L Goldberger,et al.  Diurnal and ultradian dynamics of serum adiponectin in healthy men: comparison with leptin, circulating soluble leptin receptor, and cortisol patterns. , 2003, The Journal of clinical endocrinology and metabolism.

[17]  R. Kraemer,et al.  Leptin and Exercise , 2002, Experimental biology and medicine.

[18]  M. Watkins,et al.  Risk Stratification for Postoperative Cardiovascular Events via Noninvasive Assessment of Endothelial Function: A Prospective Study , 2002, Circulation.

[19]  G. Garcı́a-Cardeña,et al.  Biological action of leptin as an angiogenic factor. , 1998, Science.

[20]  Y. Ouchi,et al.  Modulation of endothelium-dependent flow-mediated dilatation of the brachial artery by sex and menstrual cycle. , 1995, Circulation.

[21]  D. Sale,et al.  Arterial blood pressure response to heavy resistance exercise. , 1985, Journal of applied physiology.

[22]  D. Costill,et al.  Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. , 1974, Journal of applied physiology.

[23]  A. Pfeiffer,et al.  Adiponectin oligomers in human serum during acute and chronic exercise: relation to lipid metabolism and insulin sensitivity. , 2007, International journal of sports medicine.

[24]  Response to Therapeutic Interventions , 2022 .