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The present study was performed to investigate the involvement of SNARK in physical activity levels in mice. To examine the acute effect of SNARK deficiency on voluntary running, Snark-deficient mice ([Snark.sup.+/-] : n = 16) and their wild-type counterparts ([Snark.sup.+/+] : n = 16) were assigned to sedentary or exercise (1 wk voluntary wheel running) groups. In addition, to clarify the differences in voluntary running activity and its effect between genotypes, mice ([Snark.sup.+/+] : n = 16; [Snark.sup.+/-] : n = 16) were also kept in individual cages with/without a running wheel for 5 mo. Unexpectedly, in both voluntary running experiments, running distances were increased in [Snark.sup.+/-] mice compared with [Snark.sup.+/+] mice. Under sedentary conditions, body and white adipose tissue weights were increased significantly in [Snark.sup.+/-] mice. However, no significant differences were observed between the two genotypes under exercise conditions, and the values were significantly less than those under sedentary conditions in the long-term experiment. In the short-term experiment, serum interleukin-6 level in exercised [Snark.sup.+/+] mice was the same as that in sedentary [Snark.sup.+/+] mice, whereas that in sedentary [Snark.sup.+/-] mice was significantly lower than in the other groups. In contrast, serum leptin level was reduced significantly in exercised [Snark.sup.+/-] mice compared with sedentary [Snark.sup.+/-] mice. The results of this study demonstrated that exposure to an environment that allows voluntary exercise promotes increased running activity and prevents obesity in Snark-deficient mice. SNARK; adenosine 5'-monophosphate-activated protein kinase; voluntary running activity; adipose tissue; adipokine

This study examined whether the exercise-increased extracellular heat shock protein 72 (eHsp72) levels in rats was associated with body temperature elevation during exercise. In all, 26 female Sprague-Dawley rats (3 mo old) were assigned randomly to control (CON; n = 8), exercise under warm temperature (WEx; n = 9), or exercise under cold temperature (CEx; n = 9). The WEx and CEx were trained at 25[degrees]C or 4[degrees]C, respectively, for nine days using a treadmill. Before and immediately after the final exercise bout, the colonic temperatures were measured as an index of body temperature. The animals were subsequently anesthetized, and blood samples were collected and centrifuged. Plasma samples were obtained to assess their eHsp72 levels. Only the colonic temperature in WEx was increased significantly (P < 0.05) by exercise. The eHsp72 level in WEx was significantly higher (P < 0.05) than that of either the CON or CEx. However, no significant difference was found between CON and CEx. Regression analyses revealed that the eHsp72 level increased as a function of the body temperature. In another experiment, the eHsp72 level of animals with body temperature that was passively elevated through similar kinetics to those of the exercise was studied. Results of this experiment showed that mere body temperature elevation was insufficient to induce eHsp72 responses. Collectively, our results suggest that body temperature elevation during exercise is important for induction of exercise-increased eHsp72. In addition, the possible role of body temperature elevation is displayed when the exercise stressor is combined with it. running exercise; warm; cold; ELISA; stress proteins

Obesity and aging reduce skeletal muscle contractile function. However, it remains unclear whether obesity additively promotes muscle contractile dysfunction in the setting of aging. In this study, we investigated skeletal muscle contractile function ex vivo and intracellular Ca 2+ release in male C57BL/6J mice fed a low-fat diet (LFD) or a high-fat diet (HFD) for 4 or 20 mo. Tetanic force production in the extensor digitorum longus muscle was decreased by aging or HFD feeding, and the further reduction was observed in aged HFD mice. The 20-mo HFD-fed mice, not the 20-mo LFD-fed mice or 4-mo HFD-fed mice, showed reduced intracellular Ca 2+ peak levels by high concentration of caffeine (25 mM) compared with 4-mo LFD mice. Aging and HFD feeding additively increased intramyocellular lipid (IMCL) levels and were associated with the degree of impaired muscle contractile force and peak Ca 2+ level. These data suggest that impairment in the contractile force in aged muscle is aggravated by HFD, which may be due, at least in part, to dysfunction in intracellular Ca 2+ release. The IMCL level may be a marker for impaired muscle contractile force caused by aging and HFD. NEW & NOTEWORTHY The aim of this study was to examine the effect of high-fat diet (HFD)-induced obesity on contractile function and Ca 2+ release capacity in aged skeletal muscle. Not only were the force production and peak Ca 2+ levels decreased by aging and HFD feeding, respectively, but also, these interventions had an additive effect in aged HFD-fed mice. These data suggest that the impairment in the contractile force in aged muscle is aggravated by a HFD, which may be due to synergistic dysfunction in intracellular Ca 2+ release.

Type 2 diabetes is characterized by reduced contractile force production and increased fatigability of skeletal muscle. While the maintenance of Ca 2+ homeostasis during muscle contraction is a requisite for optimal contractile function, the mechanisms underlying muscle contractile dysfunction in type 2 diabetes are unclear. Here, we investigated skeletal muscle contractile force and Ca 2+ flux during contraction and pharmacological stimulation in type 2 diabetic model mice ( db/db mice). Furthermore, we investigated the effect of treadmill exercise training on muscle contractile function. In male db/db mice, muscle contractile force and peak Ca 2+ levels were both lower during tetanic stimulation of the fast-twitch muscles, while Ca 2+ accumulation was higher after stimulation compared with control mice. While 6 wk of exercise training did not improve glucose tolerance, exercise did improve muscle contractile dysfunction, peak Ca 2+ levels, and Ca 2+ accumulation following stimulation in male db/db mice. These data suggest that dysfunctional Ca 2+ flux may contribute to skeletal muscle contractile dysfunction in type 2 diabetes and that exercise training may be a promising therapeutic approach for dysfunctional skeletal muscle contraction. NEW & NOTEWORTHY The purpose of this study was to examine muscle contractile function and Ca 2+ regulation as well as the effect of exercise training in skeletal muscle in obese diabetic mice ( db/db). We observed impairment of muscle contractile force and Ca 2+ regulation in a male type 2 diabetic animal model. These dysfunctions in muscle were improved by 6 wk of exercise training.