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Exercise-Induced Changes in Insulin Action and Glycogen Metabolism in Elderly Adults

  • Autores: Robert H. Coker, Nicholas P. Hays, Rick H. Williams
  • Localización: Medicine & Science in Sports & exercise: Official Journal of the American College of Sports Medicine, ISSN 0195-9131, Vol. 38, Nº. 3, 2006, págs. 433-438
  • Idioma: inglés
  • Texto completo no disponible (Saber más ...)
  • Resumen
    • Purpose: Although data suggest that physical activity is associated with decreased insulin resistance, recommendations for exercise training are not specific for age or level of obesity. Therefore, we examined the influence of moderate-intensity (50% of [latin capital V with dot above]O2max) exercise training (MI) versus high-intensity (75% of [latin capital V with dot above]O2max) exercise training (HI) on insulin-stimulated glucose disposal (ISGD) in elderly individuals.

      Methods: Following medical examinations, 21 overweight (body mass index = 29 +/- 1 kg[middle dot]m-2) elderly (74 +/- 1 yr) subjects were randomized to 1) HI, 2) MI, or a 3) nonexercising control group. Subjects enrolled in HI or MI completed a 12-wk exercise training regimen designed to expend 1000 kcal[middle dot]wk-1. ISGD was assessed using a hyperinsulinemic, euglycemic clamp pre- and postintervention. ISGD was corrected for hepatic glucose production (glucose Ra) using a constant rate infusion of [6,6-2H2]glucose and determined during the last 30 min of the clamp by subtracting glucose Ra from the exogenous glucose infusion rate. Nonoxidative glucose disposal was calculated using indirect calorimetry. Body composition testing was completed using dual energy x-ray absorptiometry.

      Results: ISGD increased by approximately 20% with HI ([DELTA] of 1.4 +/- 0.5 mg[middle dot]kg-1 FFM[middle dot]min-1). However, ISGD did not change ([DELTA] of -0.4 +/- 0.1 mg[middle dot]kg-1 FFM[middle dot]min-1) with MI and was not different ([DELTA] of -0.2 +/- 0.1 mg[middle dot]kg-1 FFM[middle dot]min-1) in the control group. Nonoxidative glucose disposal increased with HI ([DELTA] of 1.4 +/- 0.5 mg[middle dot]kg-1 FFM[middle dot]min-1), but there was no change in nonoxidative glucose disposal with MI or in the control group. No change in body weight or percentage of body fat was observed in any group.

      Conclusion: In weight-stable subjects, MI resulted in no change in ISGD, and the improvement in ISGD with HI was completely reliant on improvements in nonoxidative glucose disposal


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