Age-related reduction in bone mineral density (BMD) is generally accelerated in women after menopause, and could be even more pronounced in individuals with sarcopenia. Light-load power training with a low number of repetitions would increase BMD, significantly reducing bone loss in individuals at risk of osteoporosis. This study investigated the effects of low-repetition, light-load power training on BMD in Japanese postmenopausal women with sarcopenia. The training group (n = 7) followed a progressive power training protocol that increased the load with a weighted vest, for two sessions per week, over the course of 6 weeks. The training exercise comprised five kinds of exercises (squats, front lunges, side lunges, calf raises, and toe raises), and each exercise contained eight sets of three repetitions with a 15-s rest between each set. The control group (n = 8) did not undergo any training intervention. We measured BMD, muscle strength, and anthropometric data. Within-group changes in pelvis BMD and knee extensor strength were significantly greater in the training group than the control group (p = 0.029 and 0.030 for pelvis BMD and knee extensor strength, respectively). After low-repetition, light-load power training, we noted improvements in pelvis BMD (1.6%) and knee extensor strength (15.5%). No significant within- or between-group differences were observed for anthropometric data or forearm BMD. Six weeks of low-repetition, light-load power training improved pelvis BMD and knee extensor strength in postmenopausal women with sarcopenia. Since this training program does not require high-load exercise and is therefore easily implementable as daily exercise, it could be an effective form of exercise for sedentary adults at risk for osteoporosis who are fearful of heavy loads and/or training that could cause fatigue. This trial was registered with the University Hospital Medical Information Network on 31 October 2016 ( UMIN000024651 ).

The effects of chronic Dioscorea esculenta administration and exercise training on muscle sex steroid hormone levels and insulin resistance in type 2 diabetes rats was assessed. Twenty‐week‐old male Otsuka Long Evans Tokushima Fatty (OLETF) rats were assigned randomly to the control, D. esculenta treatment, D. esculenta with 5α‐reductase inhibitor treatment, or the exercise training groups (running at 25 m/min for 1 h, 5 d/wk; n = 10 each group). Eight weeks of D. esculenta treatment or exercise training significantly attenuated the increase in plasma insulin and fasting glucose levels. Plasma and muscle concentrations of dehydroepiandrosterone and 5adihydrotestosterone (DHT) and the expression of 5α‐reductase increased significantly in the D. esculenta ‐treated and exercise training groups, and both treatments led to the upregulation of glucose transporter‐4 translocation with concomitant increases in PKB and PKC‐ζ/λ phosphorylation. Furthermore, the glucose metabolic clearance rate, which represents insulin sensitivity, increased significantly in both the D. esculenta ‐treated and exercise training groups. These effects were suppressed by administration of the DHT synthetic inhibitor. Together, these findings suggest that the D. esculenta ‐induced increase in muscle sex steroid hormone levels helps decrease insulin resistance in type 2 diabetes.—Sato, K., Fujita, S., Iemitsu, M. Dioscorea esculenta ‐induced increase in muscle sex steroid hormones is associated with enhanced insulin sensitivity in a type 2 diabetes rat model. FASEB J. 31, 793–801 (2017). http://www.fasebj.org

Dietary protein intake is critical for the maintenance of skeletal muscle mass. Plasma amino acid concentrations increase with protein intake and increases in muscle protein synthesis are dependent on leucine concentrations. We aimed to investigate the effect of a mixed meal and free amino acids intake on plasma leucine concentrations. In this randomized crossover study, 10 healthy young men (age 25 ± 1 years, height 1.73 ± 0.02 m, weight 65.8 ± 1.5 kg) underwent tests under different conditions—intake of 2 g of leucine (LEU), intake of a mixed meal (protein 27.5 g, including 2.15 g of leucine, protein: fat: carbohydrate ratio—22:25:53) only (MEAL), intake of 2 g of leucine immediately after a mixed meal (MEAL-LEU) and intake of 2 g of leucine 180 min after a mixed meal (MEAL-LEU180). Blood samples were collected within 420 min (240 min for LEU only) after intake and changes in amino acid concentrations were evaluated. Although the maximum plasma leucine concentration increased to 442 ± 24 µM for LEU, it was lower at 347 ± 16 µM (p < 0.05 vs. LEU) for MEAL-LEU, 205 ± 8 µM (p < 0.05 vs. LEU) for MEAL. The maximum plasma leucine concentration for MEAL-LEU180 increased to 481 ± 27 µM and compared to LEU there was no significant difference (p > 0.1). The observation that rapid elevations in plasma leucine concentrations are suppressed when leucine is ingested at the same time as a meal suggests that the timing of its intake must be considered to maximize the anabolic response.

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants to prevent combustion in consumer products, such as electronics, construction materials, and textiles and, therefore, have become important commercial substances. PBDEs were also detected in maternal blood, breast milk, umbilical cord blood, and cord tissue, thereby indicating that fetuses were also exposed to PBDEs. The purpose of this study is to identify the effect of PBDEs on human umbilical vein endothelial cells (HUVECs). Cultured HUVECs were exposed to a commercial mixture of penta-BDE (DE71), octa-BDE (DE79), and deca-BDE (DE83). Each gene expression that was altered in DNA microarray was confirmed by real-time reverse transcription—polymerase chain reaction and Western blotting analysis. The results indicated that gene expressions concerning antioxidant system, i.e., thioredoxin family, 24-dehydrocholesterol reductase (DHCR24), and tumor suppressor protein p53, were altered by PBDEs exposure in HUVECs. Moreover, it was demonstrated that thioredoxin-interacting protein (TXNIP) was a target gene in exposure to DE71 and DE79 in HUVECs, by drastically decreasing time-dependent TXNIP expression in HUVECs.