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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    ABSTRACT: Exercise-induced positive changes in skeletal muscle properties and metabolism decrease the risk for disability, cardiometabolic diseases and mortality. Here, we studied muscle properties and glucose homeostasis in a non-exercise stage in twin pairs with co-twins discordant for physical activity habits for at least 32 years of their adult lives. Isometric knee extension force, MR imaging of midthigh tissue composition and muscle volume, and fasting blood samples were acquired from 16 same-sex (seven monozygotic, nine dizygotic) middle-aged and older twin pairs. The consistently active twins had 20 % higher knee extension forces than their inactive co-twins (p = 0.006) although the active twins had only 4 % higher midthigh muscle cross-sectional areas (p = 0.072). These results were similar in intrapair analysis in which only the seven identical twin pairs were included. The ratio between the area of midthigh fat and muscle tissues was significantly lower among the active twins (0.65 vs. 0.48, p = 0.006). The active twins had also lower fasting plasma glucose levels (5.1 vs 5.6 mmol/l, p = 0.041). The area of midthigh intramuscular (extramyocellular) fat was associated with the markers of glucose homeostasis, especially with glycated hemoglobin, and these associations were emphasized by the diabetic and inactive twins. Regular exercise throughout the adult life retains muscle strength and quality but not necessarily mass. The regular use of muscles also prevents from the accumulation of intramuscular fat which might be related to maintained glucose metabolism and, thus, prevention of metabolic disorders.
    Age 11/2012; 35(5). DOI:10.1007/s11357-012-9486-7 · 3.45 Impact Factor
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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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    ABSTRACT: Type 2 diabetes mellitus (T2DM) is at virtually pandemic levels world-wide. Diabetes has been referred to as 'a geneticist's nightmare'. However, dramatic advances in our understanding of the genetics of T2DM have occurred in the past 5 years. While endurance exercise training and increased habitual physical activity levels have consistently been shown to improve or be associated with improved T2DM-related phenotypes, there is substantial interindividual variation in these responses. There is some evidence that T2DM-related phenotype responses to exercise training are heritable, indicating that they might have a genetic basis. Genome-wide linkage studies have not identified specific chromosomal loci that could account for these differences, and no genome-wide association studies have been performed relative to T2DM-related phenotype responses to exercise training. From candidate gene studies, there are relatively strong and replicated data supporting a role for the PPARγ Pro12Ala variant in the interindividual differences in T2DM-related phenotype responses to training. This is a potentially important candidate locus because it affects T2DM susceptibility, has high biological plausibility and is the target for the primary pharmaceutical method for treating T2DM. Is it time to conduct a hypothesis-driven large-scale exercise training intervention trial based on PPARγ Pro12Ala genotype with T2DM-related phenotypes as the primary outcome measures, while also assessing potential mechanistic changes in skeletal muscle and adipose tissue? Or would it be more appropriate to propose a smaller trial to address the specific skeletal muscle and adipose tissue mechanisms affected by the interaction between the PPARγ Pro12Ala genotype and exercise training?
    Acta Physiologica 06/2012; 205(4):456-71. DOI:10.1111/j.1748-1716.2012.02455.x · 4.25 Impact Factor
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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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    ABSTRACT: High-intensity interval training (HIT) has been proposed as a time-efficient alternative to traditional cardiorespiratory exercise training, but is very fatiguing. In this study, we investigated the effects of a reduced-exertion HIT (REHIT) exercise intervention on insulin sensitivity and aerobic capacity. Twenty-nine healthy but sedentary young men and women were randomly assigned to the REHIT intervention (men, n = 7; women, n = 8) or a control group (men, n = 6; women, n = 8). Subjects assigned to the control groups maintained their normal sedentary lifestyle, whilst subjects in the training groups completed three exercise sessions per week for 6 weeks. The 10-min exercise sessions consisted of low-intensity cycling (60 W) and one (first session) or two (all other sessions) brief 'all-out' sprints (10 s in week 1, 15 s in weeks 2-3 and 20 s in the final 3 weeks). Aerobic capacity ([Formula: see text]) and the glucose and insulin response to a 75-g glucose load (OGTT) were determined before and 3 days after the exercise program. Despite relatively low ratings of perceived exertion (RPE 13 ± 1), insulin sensitivity significantly increased by 28% in the male training group following the REHIT intervention (P < 0.05). [Formula: see text] increased in the male training (+15%) and female training (+12%) groups (P < 0.01). In conclusion we show that a novel, feasible exercise intervention can improve metabolic health and aerobic capacity. REHIT may offer a genuinely time-efficient alternative to HIT and conventional cardiorespiratory exercise training for improving risk factors of T2D.
    Arbeitsphysiologie 11/2011; 112(7):2767-75. DOI:10.1007/s00421-011-2254-z · 2.30 Impact Factor
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