Regular exercise (3×45 min/wk) decreases plasma viscosity in sedentary obese, insulin resistant patients parallel to an improvement in fitness and a shift in substrate oxidation balance
Affiliations: Service Central de Physiologie Clinique, Centre d'Exploration et de Réadaptation des Anomalies du Métabolisme Musculaire (CERAMM), CHU Lapeyronie 34295 Montpellier‐cédex 5, France Tel.: +334 67 33 82 84; Fax: +334 67 33 89 86; Telex: CHR MONTP 480 766 F; E‐mail: drjfbrun.@aol.com
Note: [] Corresponding author: Dr J.F. Brun, MD, PhD, Service Central de Physiologie Clinique, Centre d'Exploration et de Réadaptation des Anomalies du Métabolisme Musculaire (CERAMM), CHU Lapeyrone 34295 Montpellier‐cédex 5, France. Tel.: +334 67 33 82 84; Fax: +334 67 33 89 86; Telex: CHR MONTP 480 766 F; E‐mail: drjfbrun.@aol.com.
Abstract: 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. Subjects: Thirty‐two obese insulin resistant subjects were tested before and after 2 months. Twenty‐one of them were trained (3×45 min/wk) at a level defined by exercise calorimetry and corresponding to the power at which lipid oxidation reaches a maximum (LIPOXmax ) 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 ηpl (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 (LIPOXmax ) before: 16.5±1.4 watts; after: 21.4±1.3 watts, p<0.001) and VO2max increased by 74% (p<0.01). Consistent with observations in athletes, the metabolic and ergometric improvements induced by training reduces ηpl 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 ηpl as simple and unexpensive marker of efficiency of training in insulin resistant patients should be further evaluated.
