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Regular exercise (3x45 min/wk) decreases plasma viscosity in sedentary obese, insulin resistant patients parallel to an improvement in fitness and a shift in substrate oxidation balance.

内科学 内分泌学 红细胞压积 脂质氧化 胰岛素 化学 胰岛素抵抗 有氧运动 血液粘度 体质指数 交叉研究 红细胞 医学 动物科学 抗氧化剂 生物化学 生物 替代医学 病理 安慰剂
作者
M Dumortier,A. Pérez‐Martin,E. Pierrisnard,Jacques Mercier,J.‐F. Brun
出处
期刊:PubMed 卷期号:26 (4): 219-29 被引量:14
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Exercise training decreases blood viscosity in athletes parallel with metabolic improvements mostly characterized by an increase in insulin sensitivity. Patients with low insulin sensitivity exhibit a host of metabolic disorders that may also benefit from regular training. However, the hemorheologic aspects of training in such subjects are not known and we aimed at characterizing them.Thirty-two obese insulin resistant subjects were tested before and after 2 months. Twenty-one of them were trained (3x45 min/wk) at a level defined by exercise calorimetry and corresponding to the power at which lipid oxidation reaches a maximum (LIPOX(max )) and eleven served as controls. The two groups were matched for age and body mass index. There was no weight change in controls while the 2 months training period decreased weight by 2.5 kg (p<0.02). This change was totally explained by a loss in fat mass (-2.7 kg, p<0.02) while fat free mass remained unchanged. Blood rheology was unchanged in the control group while training improved plasma viscosity eta(pl) (before: 1.43+/-0.03 mPa.s; after: 1.35+/-0.03 mPa.s, p<0.02). There was no change in either hematocrit, red cell rigidity or red cell aggregation. The balance of substrates oxidation shifted towards a higher use of lipids (point of crossover where subjects oxidize 70% carbohydrates 30% lipids: before 39.3+/-6.9 watts; after 70.8+/-6 watts, p<0.001; point where lipid oxidation is maximal (LIPOX(max )) before: 16.5+/-1.4 watts; after: 21.4+/-1.3 watts, p<0.001) and V(O(2max )) increased by 74% (p<0.01). Consistent with observations in athletes, the metabolic and ergometric improvements induced by training reduces eta(pl) in sedentary, insulin resistant patients, but at those low levels training does not appear to induce "autohemodilution" (as reflected by hematocrit) neither it improves red cell deformability or aggregation. The reliability of eta(pl) as simple and unexpensive marker of efficiency of training in insulin resistant patients should be further evaluated.

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