Is practice rate rather than exercise intensity more important in health benefits of moderately obese postmenopausal women?

OBJECTIVE: The aim of this study was to evaluate the impact of brisk walking on physical fitness, body composition and fasting lipid-lipoprotein profile of women 50-65 years-old, once adherence or exercise intensity is considered. METHODS: A sample of 159 healthy, sedentary, obese postmenopausal women (body mass index [BMI]=29-35 kg/m2) was subjected to 3 sessions/week of 45 min-walking, at 60% of heart rate reserve (HRR), during 16 weeks. Body composition, physical fitness and fasting lipid-lipoprotein profile were assessed before and after the intervention. RESULTS: Among the three tertiles of adherence to exercise sessions (<71%, 71-87%,>87%) women displaying the greatest one were characterized by the highest reduction in body weight (-1.9±2.7 kg) (mean±SD), fat mass (-2.0±2.3 kg) and waist girth (-4.4±3.4 cm) and the best improvement in physical fitness (7.3±3.5 mL O2/kg/min), (P<0.0001). A comparable analysis based on tertiles of walking intensity (<56%, 56-63%,>63% HRR) did not show between-group differences in body composition or physical fitness. Also, the fasting lipid-lipoprotein profile was improved by a reduction of cholesterol, LDL cholesterol, and triglyceride levels and by an increase in HDL cholesterol, irrespective of the participants' adherence (0.05

Modification of mitochondrial metabolism in fibroblasts from mice with a skeletal muscle mutation (muscular dysgenesis). Evidence of embryonic communication between myoblasts and fibroblasts.

Muscle development during embryogenesis is a complex process involving many mechanisms. It requires a close communication among the different cellular types of the muscle, especially the fibroblasts and myoblasts. Indeed, any abnormality in one cell type might influence the differentiation of the other. Thus, any disturbance altering the metabolism of the myoblasts might lead to modifications in the fibroblasts. To study this phenomenon, we used the dysgenic mouse (mdg-"muscular dysgenesis") carrying a homozygous recessive lethal mutation expressed only in skeletal muscle cells. First, we found that fibroblasts isolated from such mutant muscle (and not from mutant skin tissue) and grown in culture exhibited an altered metabolism. Secondly, muscle fibroblasts showed a lower capacity for proliferation. We also observed that respiration and ATP synthesis of dysgenic muscle fibroblasts were deficient, while respiratory chain enzymatic activities were normal. Finally, intracellular [Ca2+] levels of dysgenic fibroblasts are 50% of those of normal fibroblasts. These results support the hypothesis that certain characteristics of fibroblasts are determined by the surrounding cellular environment during embryonic organogenesis, and that such modifications are stable when the fibroblasts are isolated in vitro. Since fibroblast differentiation was disrupted permanently, this suggests, in the case of myopathies, that the modified cells, surrounding the muscle tissue, could contribute to the muscle pathology. Synergistic activities of this type should be considered when studying the course of pathologies in different types of muscle diseases.

M-calpain levels increase during fusion of myoblasts in the mutant muscular dysgenesis (mdg) mouse.

Previous studies have led to the hypothesis of a possible role for the calcium-dependent neutral protease m-calpain in myoblast fusion in culture. To evaluate this hypothesis, we chose as our model, the "muscular dysgenesis" mouse (mdg), which presents in vivo and in vitro characteristics of an elevated process of fusion (Yao and Essien, 1975; Dussartre, 1993; Ashby et al., 1993, Joffroy et al., 1999). The aim of this study was to demonstrate using myoblast cell lines and muscle biopsies from this mdg mutant, that the amount of m-calpain increases significantly as multinucleated myotubes are formed. Using immunoblot analysis, it was shown that the m-calpain concentration in a dysgenic cell line (GLT) increased 3-fold compared to what it was upon the introduction of the differentiation medium. On the other hand, in a normal cell line (NLT), the concentration of m-calpain did not vary significantly. Thus, when the transition from myoblasts to myotubes was slow, and the absolute level of fusion was reduced, as in the NLT cell line, the level of m-calpain was stable. In contrast, when the process of fusion was precocious and fast, and the level of fusion was elevated, such as in the GLT cell line, the concentration of m-calpain increased during fusion. Moreover, when myoblast fusion was prevented by the addition of calpain inhibitor II, the process was reduced by approximately 93%. Taking into account these observations, it is clear from our data that the muscular dysgenesis mouse provides a relevant model to study myoblast fusion and that m-calpain is involved in this process.