Resistance training enhances insulin-mediated glucose disposal with minimal effect on the tumor necrosis factor-alpha system in older hypertensives

Resistance training enhances insulin-mediated glucose disposal with minimal effect on the tumor... 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-α), soluble TNF-α 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-α, sTNF R1, and sTNF R2 were not significantly altered by RT (TNF-α: 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-α, sTNF R1, and sTNF R2 in older hypertensive subjects. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Metabolism Elsevier

Resistance training enhances insulin-mediated glucose disposal with minimal effect on the tumor necrosis factor-alpha system in older hypertensives

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Publisher
Elsevier
Copyright
Copyright © 2004 Elsevier Inc.
ISSN
0026-0495
D.O.I.
10.1016/j.metabol.2003.09.017
Publisher site
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Abstract

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-α), soluble TNF-α 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-α, sTNF R1, and sTNF R2 were not significantly altered by RT (TNF-α: 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-α, sTNF R1, and sTNF R2 in older hypertensive subjects.

Journal

MetabolismElsevier

Published: Mar 1, 2004

References

  • Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors
    Aderka, D.; Engelmann, H.; Maor, Y.
  • Exercise, glucose transport, and insulin sensitivity
    Goodyear, L.J.; Kahn, B.B.
  • The independent and combined effects of weight loss and aerobic exercise on blood pressure and oral glucose tolerance in older men
    Dengel, D.R.; Galecki, A.T.; Hagberg, J.M.
  • Strength training increases insulin action in healthy 50- to 65-yr old men
    Miller, J.P.; Pratley, R.E.; Goldberg, A.P.
  • Effects of resistance exercise on glucose tolerance in normal and glucose-intolerant subjects
    Fluckey, J.D.; Hickey, M.S.; Brambrink, J.K.
  • Aerobic exercise training improves insulin sensitivity independent of plasma tumor necrosis factor-alpha levels in older hypertensives
    Reynolds, T.H.; Brown, M.D.; Supiano, M.A.

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