Background: Low muscle strength has been focused on as an essential characteristic of sarcopenia, and the 30-s chair stand test (CS-30) could be a particularly useful test for assessing muscle strength. While it is speculated to be a beneficial tool for the assessment of sarcopenia, this remains to be verified. In this study, we examined the reliability and optimal diagnostic score of the CS-30 for assessing sarcopenia in elderly Japanese participants. Methods: This cross-sectional study included 678 participants (443 females and 235 males) who underwent the test for sarcopenia as per the Asian Working Group for Sarcopenia (AWGS) 2019, the CS-30 test, and the isometric knee-extension muscle strength test. ROC analysis was used to estimate the optimal CS-30 scores at which sarcopenia was detected. Results: CS-30 scores were positively associated with sarcopenia (OR: 0.88; 95% CI:0.82–0.93). The AUC of the CS-30 for sarcopenia definition were 0.84 (p < 0.001) for females and 0.80 (p < 0.001) for males. The optimal number of stands in the CS-30 that predicted sarcopenia was 15 for females (sensitivity, 76.4%; specificity, 76.8%) and 17 for males (sensitivity, 75.0%; specificity, 71.7%). Conclusions: The CS-30 was found to be a reliable test for sarcopenia screening in the elderly Japanese population.

Insulin resistance of peripheral muscle is implicated in the etiology of metabolic syndrome in obesity. Although accumulation of glycerolipids, such as triacylglycerol and diacylglycerol (DAG), in muscle contributes to insulin resistance in obese individuals, endurance-trained athletes also have higher glycerolipid levels but normal insulin sensitivity. We hypothesized that the difference in insulin sensitivity of skeletal muscle between athletes and obese individuals stems from changes in fatty acid composition of accumulated lipids. Here, we evaluated the effects of intense endurance exercise and high-fat diet (HFD) on the accumulation and composition of lipid molecular species in rat skeletal muscle using a lipidomic approach. Sprague-Dawley female rats were randomly assigned to three groups and received either normal diet (ND) in sedentary conditions, ND plus endurance exercise training, or HFD in sedentary conditions. Rats were fed ND or HFD between 4 and 12 wk of age. Rats in the exercise group ran on a treadmill for 120 min/day, 5 days/wk, for 8 wk. Soleus muscle lipidomic profiles were obtained using liquid chromatography/tandem mass spectrometry. Total DAG levels, particularly those of palmitoleate-containing species, were increased in muscle by exercise training. However, whereas the total DAG level in the muscle was also increased by HFD, the levels of DAG molecular species containing palmitoleate were decreased by HFD. The concentration of phosphatidylethanolamine molecular species containing palmitoleate was increased by exercise but decreased by HFD. Our results indicate that although DAG accumulation was similar levels in trained and sedentary obese rats, specific changes in molecular species containing palmitoleate were opposite.

Background: Skeletal muscle inflammation and oxidative stress are associated with aging‐related loss of muscle mass and may be attributable to alterations in the number and types of leukocytes in skeletal muscle. Here, we tested the hypothesis that aging changes the number and composition of leukocyte subsets in skeletal muscle tissue.Methods: Skeletal muscle was sampled from 4‐mo‐old (young) and 27‐mo‐old (old) C57BL/6J mice. Mononuclear cells of the gastrocnemius muscle were isolated, and flow cytometry was used to characterize the number and types of immune cells.Results: The number of neutrophils and Ly‐6C+ inflammatory macrophages in the skeletal muscle was significantly higher in old mice than in young mice. Inflammation and oxidative stress (measured using the markers phosphorylated JNK and nitrotyrosine) were also higher in the skeletal muscle of old mice than in that of young mice.Conclusions: Increasing age promotes skeletal muscle inflammation and oxidative stress, as well as infiltration of inflammatory macrophages and neutrophils.

Muscle satellite cells are committed myogenic progenitors capable of contributing to myogenesis to maintain adult muscle mass and function. Several experiments have demonstrated that muscle satellite cells can differentiate into adipocytes in vitro, supporting the mesenchymal differentiation potential of these cells. Moreover, muscle satellite cells may be a source of ectopic muscle adipocytes, explaining the lipid accumulation often observed in aged skeletal muscle (sarcopenia) and in muscles of patients` with diabetes. Quercetin, a polyphenol, is one of the most abundant flavonoids distributed in edible plants, such as onions and apples, and possesses antioxidant, anticancer, and anti-inflammatory properties. In this study, we examined whether quercetin inhibited the adipogenesis of muscle satellite cells in vitro with primary cells from rat limbs by culture in the presence of quercetin under adipogenic conditions. Morphological observations, Oil Red-O staining results, triglyceride content analysis, and quantitative reverse transcription polymerase chain reaction revealed that quercetin was capable of inhibiting the adipogenic induction of muscle satellite cells into adipocytes in a dose-dependent manner by suppressing the transcript levels of adipogenic markers, such as peroxisome proliferator-activated receptor-γ and fatty acid binding protein 4. Our results suggested that quercetin inhibited the adipogenesis of muscle satellite cells in vitro by suppressing the transcription of adipogenic markers.

Background: Oestrogen deficiency reduces skeletal muscle mass and force generation in postmenopausal women. Muscle mass is maintained by satellite cells, which are regulated by oestrogen. Although oestrogen therapy enhances muscle hypertrophy induced by resistance training in postmenopausal women, the molecular mechanism is unclear.Methods: Adult female rats (10 weeks old) were divided into six groups: sham sedentary (Sham‐Sed), sham climbing training (Sham‐CT), ovariectomy sedentary (OVX‐Sed), ovariectomy climbing training (OVX‐CT), ovariectomy plus oestrogen treatment sedentary (OVX+E‐Sed), and ovariectomy plus oestrogen treatment climbing training (OVX+E‐CT). At 8 weeks after ovariectomy, rats in the training group were trained (one session every 3 days for 8 weeks) to climb a ladder while bearing a load. Oestrogen treatment involved subcutaneous insertion of a 17β‐oestradiol pellet. After 8 weeks, the flexor hallucis longus muscle was collected and analysed.Results: Following climbing training, the flexor hallucis longus muscle mass and muscle‐to‐body weight ratios were dramatically increased by training (main effect of training, P < 0.01); the OVX+E‐CT group showed the highest values (main effect of group, P < 0.01). The cross‐sectional area of all muscle fibre types was increased by training (main effect of training, P < 0.01). Particularly, the cross‐sectional area of MHC IIa in the OVX+E‐CT group was significantly larger than that in the Sham‐CT and OVX‐CT groups. Satellite cell numbers were increased in all training groups (main effect of training, P < 0.05), and the myonuclear number was increased by training (main effect of training, P < 0.01), but there was no main group effect. The myonuclear domain size of all muscle fibre types and MHC IIa was increased in all training groups (main effect of training, P < 0.01) and showed a main group effect (P < 0.01). The myonuclear domain sizes of all muscle fibre types and MHC IIa in the OVX+E‐CT group were significantly larger than those in the Sham‐CT and OVX‐CT groups. The total RNA contents revealed main effects of training and the group (P < 0.01); the OVX+E‐CT group showed the highest contents (main effect of group, P < 0.01). The mRNA and protein levels of rpS6 were increased in the OVX+E‐Sed and CT groups (main effects of group, P < 0.05). Particularly, the 28S ribosomal RNA content in OVX+E‐Sed group was significantly higher than that in the OVX‐Sed group.Conclusions: Oestrogen enhanced the resistance training‐induced increase in myonuclear domain size but did not affect satellite cells and ribosome biogenesis.