Resistance training enhances insulin-mediated glucose disposal with minimal effect on the tumor necrosis factor-alpha system in older hypertensives.
The purpose of the present study was to determine if the improvement in insulin sensitivity after resistance training (RT) is associated with a decline in plasma levels of tumor necrosis factor-alpha (TNF-alpha), soluble TNF-alpha receptor 1 (sTNF R1), and soluble TNF receptor 2 (sTNF R2). Eleven older hypertensives (5 men/6 women, 67 +/- 2 years) participated in a 4-month RT program. Following RT there was a significant increase in upper body (P =.029) and lower body strength (P =.001), assessed by the bench press 1-repetition maximum (1RM) and leg press 1RM, respectively. The RT program produced a significant increase in lean body mass (LBM) (P =.029), a trend for a decline in percent body fat (P =.083), and no change in total body mass (P =.958). Insulin-mediated glucose disposal, assessed by the hyperinsulinemic euglycemic clamp procedure, significantly increased following RT (P =.026). Despite the increase in insulin action, plasma levels of TNF-alpha, sTNF R1, and sTNF R2 were not significantly altered by RT (TNF-alpha: P =.118, sTNF R1: P =.184, sTNF R2: P =.168). In conclusion, a 4-month RT program significantly increased insulin-mediated glucose disposal and LBM without a significant reduction in plasma levels of TNF-alpha, sTNF R1, and sTNF R2 in older hypertensive subjects.
Reynolds
Thomas H
TH
Department of Internal Medicine, Division of Geriatric Medicine, University of Michigan, Ann Arbor, MI, USA.
Supiano
Mark A
MA
Dengel
Donald R
DR
D000368:Aged; D015308:Anaerobic Threshold / Q000502:physiology; D015703:Antigens, CD / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001823:Body Composition / Q000187:drug effects; D005260:Female; D005947:Glucose / Q000378:metabolism*; D015309:Glucose Clamp Technique; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D010809:Physical Fitness / Q000502:physiology*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014891:Weight Lifting / Q000502:physiology*
D015703:Antigens, CD; D007004:Hypoglycemic Agents; D007328:Insulin; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose