Exercise Increases Adiponectin Levels and Insulin Sensitivity in Humans
Adiponectin is an abundant circulating adipocytokine with anti-inflammatory properties (1) linked to cardiovascular disease, type 2 diabetes, and obesity (2–5). Numerous reports (3–5), including the present one, confirm plasma adiponectin levels to be inversely related to insulin resistance. Longer term, a rise in adiponectin has been shown to occur in response to weight loss and glitazone therapy, but not after chronic exercise training. However, understanding of the shorter-term regulation of adiponectin in particular remains unclear. As an extension to a previously reported exercise intervention in sedentary males by our group (6), we have now examined the effects of this training intervention on adiponectin levels in overweight males. We demonstrate that the short-term exercise training increased circulating adiponectin levels with accompanied improved insulin sensitivity.
Twenty-six overweight males participated in an exercise program, as previously described (6). Full data were available on 19 subjects who completed the entire program. At baseline and postexercise intervention, all subjects were assessed for anthropometric measures (dual-energy X-ray absorptiometry, magnetic resonance imaging, and BMI), insulin sensitivity (insulin clamp), and indirect calorimetry (for fat oxidation rates), and overnight fasting plasma samples were collected for adiponectin levels. Briefly, exercise consisted of aerobic exercise (brisk walking mixed with light jogging) 4–5 days per week for 40 min per session (∼55–70% Vℴ2max) over 10 weeks (6). Plasma adiponectin was determined using a radioimmunoassay kit (Linco Research, St. Charles, MO). Two-tailed paired Student’s t tests were used for comparisons between time points before and after exercise, and associations between continuous variables were investigated using simple regression analyses. Analyses were performed using StatView software (version 4.5; Abacus Concepts, Berkeley, CA).
The subjects’ mean age was 37.1 ± 1.3 years, and before exercise mean BMI was 30.7 ± 0.7 kg/m2 and Vℴ2max was 48.4 ± 0.8 ml · kg fat-free mass (FFM)−1 · min−1. Correlations between glucose infusion rate (GIR), a measure of insulin sensitivity, and indexes of adiposity in the sedentary males were highly significant (allP < 0.0001). Fasting plasma adiponectin levels were strongly inversely related to insulin resistance in these subjects (r = −0.52, P = 0.0007) and to total fat (r = −0.39, P = 0.015), central subcutaneous fat (r = −0.37, P = 0.02), and visceral fat mass (r = −0.32, P = 0.05). Two to three bouts of moderately intense aerobic exercise performed within ∼1 week of baseline assessments resulted in a mean 23% increase in GIR (35.0 ± 2.7 vs. 43.0 ± 2.8 μmol · min−1 · kg FFM−1, P < 0.0001) and a mean 37% increase in basal fat oxidation rate (1.05 ± 0.14 vs. 1.44 ± 0.08 g · day−1 · kg FFM−1). These effects were maintained after 10 weeks of exercise training (42.4 ± 3.1 μmol · min−1 · kg FFM−1 and 1.35 ± 0.07 g · day−1 · kg FFM−1, respectively). Body weight was unchanged after two to three bouts of exercise (93.5 ± 1.9 vs. baseline 93.4 ± 1.8 kg) and was not significantly reduced at 10 weeks (92.6 ± 1.9 kg, P = 0.08) in this cohort.
Adiponectin levels rose by 260% after two to three bouts of exercise (∼1 week) (7.0 ± 0.7 vs. 18.2 ± 1.9 μg/ml, P < 0.0001) despite unchanged body weight and remained elevated (16.4 ± 1.9 μg/ml, P < 0.0001) after 10 weeks. However, individual changes in adiponectin levels after two to three bouts (∼1 week) and after 10 weeks of exercise were not correlated with the respective changes in insulin sensitivity or fat oxidation rate. Our results contrast with Hulver et al. (7) where adiponectin is unaltered with exercise training despite enhanced insulin action. However, we assessed the acute effect of exercise after two to three bouts of exercise (6), whereas they took their “basal” samples 6 weeks after a ramping exercise period before the 6-month endurance exercise training program (7). Our data indicate that elevated adiponectin levels are first apparent after 1 week (two to three bouts) of moderately intense exercise. We suggest that it is likely that this short-term moderate exercise training can modify regulation of adiponectin, and this could be postulated to provide another mechanism by which exercise reduces atherogenic risk, at least in overweight males.
We acknowledge the assistance of the nursing staff of the Clinical Research Facility, laboratory technicians of the Diabetes Research Group, Dr. Judith Freund and technicians of the Nuclear Medicine Department, St Vincent’s Hospital Sydney, and volunteers who participated in this study.
- DIABETES CARE