Article

Effects of exercise training on glucose homeostasis: the HERITAGE Family Study.

Laval University, Quebec City, Quebec, Canada
Diabetes Care (Impact Factor: 8.57). 02/2005; 28(1):108-14. DOI: 10.2337/diacare.28.1.108
Source: PubMed

ABSTRACT To determine the effect of a 20-week endurance training program in healthy, previously sedentary participants on measures derived from an intravenous glucose tolerance test (i.v.GTT).
An i.v.GTT was performed before and after a standardized training program in 316 women and 280 men (173 blacks and 423 whites). Participants exercised on cycle ergometers 3 days per week for 60 sessions. The exercise intensity was progressively increased from 55% VO2max for 30 min per session to 75% VO2max for 50 min per session.
Mean insulin sensitivity increased by 10% (P < 0.001) following the intervention, but the variability in the changes was high. Men had larger improvements than women (P = 0.02). Improvements in fasting insulin were transitory, disappearing 72 h after the last bout of exercise. There were also significant mean increases in the glucose disappearance index (3%, P = 0.02) and in glucose effectiveness (11%, P < 0.001), measures of glucose tolerance and of the capacity of glucose to mediate its own disposal, respectively. The acute insulin response to glucose, a measure of insulin secretion, increased by 7% in the quartile with the lowest baseline glucose tolerance and decreased by 14% in the quartile with the highest baseline glucose tolerance (P < 0.001). The glucose area below fasting levels during the i.v.GTT was reduced by 7% (P = 0.02).
Although the effects of structured regular exercise were highly variable, there were improvements in virtually all i.v.GTT-derived variables. In the absence of substantial weight loss, regular exercise is required for sustained improvements in glucose homeostasis.

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    • "However, although the number of mitochondria might be reduced in an insulin resistant skeletal muscle, the mitochondrial respiratory capacity can be maintained normal (Larsen et al. 2011). As such, the accumulation of ectopic " high-risk " fat and adipocyte function are important mechanisms in mediating the prolonged effects of life-long regular exercise on glucose metabolism (Goodpaster et al. 2000; Boule et al. 2005; Petersen and Shulman 2006; Dube et al. 2008; Leskinen et al. 2009b; Taube et al. 2009; Rector and Thyfault 2011). Notably, the cotwins did not differ significantly in either body weight or BMI (see Table 1), and there were no differences in their fat intakes (Rintala et al. 2011), yet the inactive co-twins had significantly more visceral, intramuscular , and liver fat, as we have reported earlier (Leskinen et al. 2009b). "
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    • "However, one often overlooked point is that there still is substantial interindividual variability in this response. For example, while HERITAGE found that exercise training significantly improved glucose and insulin metabolism in the overall group, 42% of their participants did not change or actually had worse insulin sensitivity after exercise training (Boule et al. 2005). In addition, for their other measures of glucose and insulin metabolism, again ~50% of individuals either did not change or had worse measures after training. "
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    • "Alternatively, it could be that our small sample included several non-responders. Previous studies have comprehensively demonstrated that following a period of exercise training part of the population will not adapt for specific parameters (non-responders), and for insulin sensitivity this has been shown to be the case for up to 40% of the population (Boule et al. 2005; Vollaard et al. 2009; Bouchard and Rankinen 2001). Therefore, further studies with larger sample sizes will be needed to confirm or refute our initial observations. "
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