The influence of icing on muscle regeneration after crush injury was examined in the rat extensor digitorum longus. After the injury, animals were randomly divided into nonicing and icing groups. In the latter, ice packs were applied for 20 min. Due to the icing, degeneration of the necrotic muscle fibers and differentiation of satellite cells at early stages of regeneration were retarded by ∼1 day. In the icing group, the ratio of regenerating fibers showing central nucleus at 14 days after the injury was higher, and cross-sectional area of the muscle fibers at 28 days was evidently smaller than in the nonicing group. Besides, the ratio of collagen fibers area at 14 and 28 days after the injury in the icing group was higher than in the nonicing group. These findings suggest that icing applied soon after the injury not only considerably retarded muscle regeneration but also induced impairment of muscle regeneration along with excessive collagen deposition. Macrophages were immunohistochemically demonstrated at the injury site during degeneration and early stages of regeneration. Due to icing, chronological changes in the number of macrophages and immunohistochemical expression of transforming growth factor (TGF)-β1 and IGF-I were also retarded by 1 to 2 days. Since it has been said that macrophages play important roles not only for degeneration, but also for muscle regeneration, the influence of icing on macrophage activities might be closely related to a delay in muscle regeneration, impairment of muscle regeneration, and redundant collagen synthesis.

A novel method is used to develop a functional 3D integumentary organ system, including appendage organs from iPS cells.

This study investigated the injured region-specific alterations of factors related to the "repeated bout effect" (RBE), i.e., when the first bout of eccentric exercise generates resistance to injuries from the second bout of the same exercise. Wistar rats were divided into single injury (SI) and repeated injury (RI) groups. The right gastrocnemius muscle was subjected to a bout of eccentric contractions (ECs) at the age of 14 weeks in the SI group and 10 and 14 weeks in the RI group. The number of injured fibers after the last bout of ECs was lower in RI than in SI. In the SI group, injured fibers after ECs were mainly located in the superficial region of muscle and expressed myosin heavy chain (MHC) IIx and IIb. Prior to the second bout of ECs, the fiber-type composition in the RI group showed decreased MHC IIx and IIb fibers and increased MHC IIa fibers compared with those in the SI group. However, most regenerating fibers showed either MHC IIx or IIb expression. Heat shock protein 72 and total collagen contents in whole muscle were higher in the RI group than in the SI group; however, only the collagen expression in the RI group was more intense than that in the SI group in the superficial region of muscle. These findings suggest that increased collagen may play a more important role in the injured region of muscle than the other factors in RBE.

Resistance exercise training induces muscle hypertrophy, and recovery between sessions is one of the major determinants of this effect. However, the effect of the recovery period between sessions on muscle hypertrophy following resistance exercise training remains unclear. To elucidate the effect of recovery period on hypertrophy, in the present study, we investigated changes in protein degradation systems and hypertrophic responses in rat skeletal muscle to resistance training with variable recovery periods. In the conventional recovery group (exercised every 72 h) and a shorter recovery group (exercised every 24 h), 18 bouts of resistance exercise consisting of 50 repetitions of a 3‐sec maximal isometric contraction caused muscle hypertrophy and slight activation of muscle protein degradation systems. By contrast, in an excessively shorter recovery group (exercised every 8 h), 18 bouts of resistance exercise did not cause hypertrophy and markedly activated protein degradation systems, accompanied by inflammatory responses. These observations indicate that excessive shortening of recovery between sessions does not cause skeletal muscle hypertrophy, likely due to the activation of proteolysis induced by inflammatory responses to resistance exercise training.

Glucocorticoid action in target organs is regulated by relative activities of 11b-HSD type 1 (HSD11B1) that mainly converts cortisone to active cortisol and type 2 (HSD11B2) that inactivates cortisol to cortisone. HSD11Bs have been shown to be expressed in the ovary of various species. However, little is known about the expression and activity of HSD11Bs in the bovine cumulus-oocyte complex (COC). In the present study, we investigated the expression and activities of HSD11Bs in in vitro-matured (IVM) bovine COCs. Bovine COCs were matured in M199 supplemented with or without FSH and FCS. The expression of HSD11B1 and HSD11B2 was measured by using quantitative RT-PCR in denuded oocytes (DO) and cumulus cells (CC). Reductive and oxidative activities of HSD11Bs were determined by radiometric conversion assay using labeled cortisol, cortisone or dexamethasone in intact COCs, DO or CC in the presence or absence of 11-keto-progesterone (11kP), a selective inhibitor of HSD11B2. The presence of HSD11Bs in the oocyte was examined by immunofluorescence microscopy. Oocytes exclusively expressed HSD11B2 and its expression and activity were largely unchanged during IVM. CC, on the other hand, exclusively expressed HSD11B1 and its expression and activity were upregulated as IVM progressed. As a result, the net glucocorticoid metabolism shifted from inactivation to activation towards the end of IVM. These results indicate that the bovine COC is capable of modulating local glucocorticoid concentration and, by doing so, may create an environment that is favorable to ovulating oocyte for maturation, fertilization and subsequent development.

The recovery period between bouts of exercise is one of the major factors influencing the effects of resistance exercise, in addition to exercise intensity and volume. However, the effects of shortening the recovery time between bouts of resistance exercise on subsequent protein synthesis remain unclear. In this study, we investigated the consequences of shortening the recovery time between bouts of resistance exercise on protein synthesis and related processes in mouse skeletal muscles. Eighteen male C57BL/6J mice were randomly subjected to three bouts of resistance exercise with 72 (72H), 24 (24H), or 8 h (8H) of recovery periods between bouts. Resistance exercise, consisting of five sets of 3 s × 10 isometric contractions with 3 min rest between sets, was elicited on the right tibialis anterior muscle via percutaneous electrical stimulation on the deep peroneal nerve under isoflurane anesthesia. The left muscle served as an internal control. Six hours after the third bout of exercise, protein synthesis was found to be activated in the 72H and 24H groups, but not in the 8H group. Phosphorylation of p70S6K at Thr 389, a marker of mammalian target of rapamycin (mTOR) signaling, was increased in all groups, with the 8H group showing the highest magnitude. In contrast, protein carbonylation was observed only in mice in the 8H group. These results suggest that repeated bouts of resistance exercise with 8 h of recovery periods do not effectively increase the levels of muscle protein synthesis despite activation of the mTOR signaling pathway, which likely involves oxidative stress.

Ribosome biogenesis has been implicated in resistance exercise training (RET)-induced skeletal muscle hypertrophy. However, it is unclear how increasing bouts of RET affects ribosome content and biogenesis. This was investigated in the present study using simulated RET where rat skeletal muscle is subjected to increasing bouts of electrical stimulation. Sprague-Dawley rats were randomly assigned to the following seven groups: sedentary for 5 days (SED) or 6 wk (SED_6w), resistance-exercise trained with 1 bout (1B), 2 bouts (2B), 3 bouts (3B), 6 bouts (6B), and 18 bouts (18B). RET was simulated on the right gastrocnemius muscle by transcutaneous electric stimulation under isoflurane anesthesia, and a RET bout was given 3 times a week. Rats in 1B, 2B, and 3B groups showed increased 45S precursor (pre-) rRNA and 18S+28S rRNA content per muscle weight and elevated mRNA levels of c- myc and upstream binding factor (UBF). Increases in phosphorylated UBF and total cyclin D1 protein level were observed 48 h after RET; the former increased as a function of RET duration. In 3B, 6B, and 18B groups, the 18S+28S rRNA content per muscle weight was kept unchanged, and 45S pre-rRNA, cyclin D1, and phosphorylated UBF levels in 18B were lower than those in 3B. These results suggest that RET activates ribosome biogenesis and increases ribosome content through modulation of UBF and cyclin D1 activity at its early phase. Additional bouts of RET may not lead to a further increase in ribosome content per muscle weight through possibly the attenuation of transcription process. NEW & NOTEWORTHY Ribosome biogenesis has been implicated in resistance exercise training-induced skeletal muscle hypertrophy. However, it remains unclear how this is influenced by the volume of repeated bouts of resistance exercise training. Using resistance exercise training model with rat skeletal muscle, we provide evidence that ribosome biogenesis is stimulated by the initial few bouts of resistance exercise training with no additional effect of further increase in the exercise bout.

No abstract