The glucose metabolism improved both in the IGT(slow) and IGT(fast) group during the 2-year exercise and dietary intervention. The change was more prominent in the IGT(fast) group than in the IGT(slow) group, associated with the decrease of the GSK-alphabeta protein expression in skeletal muscle. The exercise training improved both glycolytic and oxidative capacity in the vastus lateralis muscle. The glycolytic capacity improved in the IGT(slow) group and the oxidative capacity in both groups.

BackgroundInsulin resistance and diabetes are associated with increased oxidative stress and impairment of cellular defence systems. Our purpose was to investigate the interaction between glucose metabolism, antioxidative capacity and heat shock protein (HSP) defence in different skeletal muscle phenotypes among middle-aged obese subjects during a long-term exercise and dietary intervention. As a sub-study of the Finnish Diabetes Prevention Study (DPS), 22 persons with impaired glucose tolerance (IGT) taking part in the intervention volunteered to give samples from the vastus lateralis muscle. Subjects were divided into two sub-groups (IGTslow and IGTfast) on the basis of their baseline myosin heavy chain profile. Glucose metabolism, oxidative stress and HSP expressions were measured before and after the 2-year intervention.ResultsExercise training, combined with dietary counselling, increased the expression of mitochondrial chaperones HSP60 and glucose-regulated protein 75 (GRP75) in the vastus lateralis muscle in the IGTslow group and that of HSP60 in the IGTfast group. In cytoplasmic chaperones HSP72 or HSP90 no changes took place. In the IGTslow group, a significant positive correlation between the increased muscle content of HSP60 and the oxygen radical absorbing capacity values and, in the IGTfast group, between the improved VO2max value and the increased protein expression of GRP75 were found. Serum uric acid concentrations decreased in both sub-groups and serum protein carbonyl concentrations decreased in the IGTfast group.ConclusionThe 2-year intervention up-regulated mitochondrial HSP expressions in middle-aged subjects with impaired glucose tolerance. These improvements, however, were not correlated directly with enhanced glucose tolerance.

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The cellular energy metabolism in human musculus gluteus medius (MGM) under normal conditions and hip osteoarthritis (OA) was explored. The functions of oxidative phosphorylation and energy transport systems were analyzed in permeabilized (skinned) muscle fibers by oxygraphy, in relation to myosin heavy chain (MHC) isoform distribution profile analyzed by SDS-PAGE, and to creatine kinase (CK) and adenylate kinase (AK) activities measured spectrophotometrically in the intact muscle. The results revealed high apparent Km for ADP in regulation of respiration that decreased after addition of creatine in MGM of traumatic patients (controls). OA was associated with increased sensitivity of mitochondrial respiration to ADP, decreased total activities of AK and CK with major reduction in mi-CK fraction, and attenuated effect of creatine on apparent Km for ADP compared with control group. It also included a complete loss of type II fibers in a subgroup of patients with the severest disease grade. It is concluded that energy metabolism in MGM cells is organized into functional complexes of mitochondria and ATPases. It is suggested that because of degenerative remodeling occurring during development of OA, these complexes become structurally and functionally impaired, which results in increased access of exogenous ADP to mitochondria and dysfunction of CK-phosphotransfer system.

Viscoelastic properties of skeletal muscle are associated with a complex network of cytoskeletal proteins where titin and nebulin play a substantial role. The need for evaluation of muscle viscoelastic properties is widely accepted in clinical use to evaluate the effect of treatment or progression of muscle pathology (atrophy). We tested the hypothesis that the viscoelastic properties (elasticity, tone and stiffness) change in atrophied muscles with concomitant changes in cytoskeletal proteins (titin, nebulin) and contractile protein (myosin heavy chain) proportion. Sixteen 24-week-old male rats of the Wistar strain were randomly allocated to two groups: dexamethasone group treated each day for 10 consecutive days with dexamethasone in order to induce atrophy and control group. Skeletal muscle viscoelastic properties (elasticity, tone and stiffness) were determined using a myotonometer. Titin, nebulin and myosin heavy chain content were quantified using SDS-PAGE electrophoresis. We found that glucocorticoid-induced muscle atrophy is accompanied by reduced elasticity and increased tone and stiffness, with concomitant changes in titin, nebulin and myosin heavy chain content. The elasticity decreased by 10.9% (P < 0.05), tone increased from 26.69 Hz to 37.73 Hz (P < 0.05), and stiffness was significantly lower in dexamethasone group (627.3 N/m vs 758.6 N/m); (P < 0.05). Compared with the control group, the content of titin, nebulin and myosin heavy chain in atrophied muscle was 76.4%, 70.6% and 82.3%, respectively. Our results may lead to a better understanding of the mechanism of muscle atrophy and provide better guidance for rehabilitation practices and help to find rational therapeutic intervention in the future.