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Exercise-induced changes in insulin action and glycogen metabolism in elderly adults
Coker RH, Hays NP, Williams RH, Brown AD, Freeling SA, Kortebein PM, Sullivan DH, Starling RD, Evans WJ
Medicine and Science in Sports and Exercise 2006 Mar;38(3):433-438
clinical trial
3/10 [Eligibility criteria: Yes; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: No; Adequate follow-up: No; Intention-to-treat analysis: No; Between-group comparisons: No; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

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 VO2max) exercise training (MI) versus high-intensity (75% of VO2max) exercise training (HI) on insulin-stimulated glucose disposal (ISGD) in elderly individuals. METHODS: Following medical examinations, 21 overweight (body mass index = 29 +/- 1 kg/m2) 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 1,000 kcal/wk. 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-H2 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/kg FFM/min). However, ISGD did not change (delta of -0.4 +/- 0.1 mg/kg FFM/min) with MI and was not different (delta of -0.2 +/- 0.1 mg/kg FFM/min) in the control group. Nonoxidative glucose disposal increased with HI (delta of 1.4 +/- 0.5 mg/kg FFM/min), 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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