Exercise & Insulin Sensitivity I ~ IR in older populations

Just wanted to share two studies I came across relating exercise and cardiac fitness to insulin sensitivity.  I'm sure to add more to this series as I come across them.

I only have access to the abstracts for these studies.  If any of you have access to the full text, please consider sharing it with me via my email address in my profile.  Thanks!

Study 1:

Association of cardiorespiratory fitness with insulin sensitivity in overweight and obese postmenopausal women: a Montreal Ottawa New Emerging Team study

The purpose of this study was to examine the relation between insulin sensitivity and cardiorespiratory fitness in overweight and obese postmenopausal women. The study population consisted of 127 overweight and obese postmenopausal women (age, 57.7 ± 4.8 years; body mass index, 32.7 ± 4.7 kg/m2).

Subjects were classified by dividing the entire cohort into tertiles (T) based on insulin sensitivity expressed per kilograms of lean body mass (LBM) (T1, <10.9; T2, 10.9-12.9, T3, >12.9 mg/min per kilogram of LBM, respectively). Outcome measures were body composition (dual-energy x-ray absorptiometry), visceral adipose tissue (computed tomography), insulin sensitivity (hyperinsulinemic-euglycemic clamp), cardiorespiratory fitness (indirect calorimetry), lower-body muscle strength (1 maximal repetition), physical activity energy expenditure (doubly labeled water), fasting lipids, and inflammatory profile.

We found a significant positive relationship between insulin sensitivity and cardiorespiratory fitness (r = 0.25, P = .005). Moreover, cardiorespiratory fitness was higher in the T3 group compared to the T1 group (36.2 ± 6.1 vs 33.1 ± 5.0 mL/kg LBM per minute, respectively; P = .028). However, the difference was no longer significant after controlling for visceral adipose tissue or muscle strength.

Finally, cardiorespiratory fitness was an independent predictor of insulin sensitivity. High levels of cardiorespiratory fitness are associated with higher levels of insulin sensitivity in overweight and obese postmenopausal women. Moreover, visceral adipose tissue accumulation or muscle strength may be potential mediators of this relationship.

I'm presuming the more cardiorespiratory fit women got that way through some form of exercise, likely "cardio".  

Study 2:  Exercise-Induced Changes in Insulin Action and Glycogen Metabolism in Elderly Adults

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 V̇O_2max) exercise training (MI) versus high-intensity (75% of V̇O_2max) exercise training (HI) on insulin-stimulated glucose disposal (ISGD) in elderly individuals.

Methods: Following medical examinations, 21 overweight (body mass index = 29 ± 1 kg·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·wk^-1. ISGD was assessed using a hyperinsulinemic, euglycemic clamp pre- and postintervention. ISGD was corrected for hepatic glucose production (glucose R_a) using a constant rate infusion of [6,6-²H₂]glucose and determined during the last 30 min of the clamp by subtracting glucose R_a 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 (Δ of 1.4 ± 0.5 mg·kg^-1FFM·min^-1). However, ISGD did not change (Δ of -0.4 ± 0.1 mg·kg^-1 FFM·min^-1) with MI and was not different (Δ of -0.2 ± 0.1 mg·kg^-1 FFM·min^-1) in the control group. Nonoxidative glucose disposal increased with HI (Δ of 1.4 ± 0.5 mg·kg^-1 FFM·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.

This study looked at the influence of exercise on insulin resistance in weight-stable subjects - e.g. changes in IR cannot be attributed to weight loss.  It was the high intensity exercise that improved insulin sensitivity by increasing insulin stimulated glucose disposal, while medium intensity did not.  This is interesting because the activities were "standardized" to equivalent caloric expenditure of 1000 cal/week.  Since they were weight stable over 12 weeks, it is not mentioned in the abstract, but presumably intake was adjusted to compensate. Unfortunately, the abstract contains no details on the duration of exercise, although there's no mention that the HI was also interval training (HIIT).

Insulin resistance is associated with aging and menopause.  These two studies indicate exercise as a good strategy to maintain insulin sensitivity.