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Heat stress (HS) induces Akt/mTOR phosphorylation and FoxO3a signaling; however, whether a prior increase in heat shock protein 72 (HSP72) expression affects intracellular signaling following eccentric exercise remains unclear. We analyzed the effects of HS pretreatment on intramuscular signaling in response to acute exercise in 10‐week‐old male Wistar rats (n = 24). One leg of each rat was exposed to HS and the other served as an internal control (CT). Post‐HS, rats were either rested or subjected to downhill treadmill running. Intramuscular signaling responses in the red and white regions of the gastrocnemius muscle were analyzed before, immediately after, or 1 h after exercise (n = 8/group). HS significantly increased HSP72 levels in both deep red and superficial white regions. Although HS did not affect exercise‐induced mTOR signaling (S6K1/ERK) responses in the red region, mTOR phosphorylation in the white region was significantly higher in CT legs than in HS legs after exercise. Thr308 phosphorylation of Akt showed region‐specific alteration with a decrease in the red region and an increase in the white region immediately after downhill running. Overall, a prior increase in HSP72 expression elicits fiber type‐specific changes in exercise‐induced Akt and mTOR phosphorylation in rat gastrocnemius muscle. [ABSTRACT FROM AUTHOR]

Objective: Evidence suggests that acquiring a high level of handgrip strength early in life and maintaining that strength throughout life may be important for health. In addition, it is thought that sports activities performed during the developmental period are effective in improving handgrip strength, but it is unknown what types of sports are more effective. As a first step, we conducted a cross‐sectional study to compare handgrip strength across different sports (upper‐body gripping sports vs. lower body) in early adulthood. Methods: We used the Juntendo Fitness Plus Study data from 1973 to 2018 and selected two types of sporting events with matching physiques (soccer, baseball, and kendo) but different degrees of gripping. Data on 7344 male first‐year sports university students included 1127 soccer, 297 Kendo, and 698 baseball players. Results: Those in the lower body‐only (soccer) sports had −3.78 (95% CI: −4.27, −3.29) kg lower handgrip strength than those in the lower + upper (kendo and baseball). Comparing each individual sport found that each sport was different from each other with Kendo > Baseball > Soccer (between each sport, p <.001). In addition, the difference between sports has become greater across time. Conclusions: In early adulthood, handgrip strength is greatest in those participating in sports with upper‐body movements compared to those participating in sports that mainly involved lower‐body movements. The three sports we selected are natural activities that do not directly train handgrip strength. Therefore, sport may be one potential method to improve low handgrip strength in children/adolescents during the developmental period. [ABSTRACT FROM AUTHOR]

This study investigated the impact of long‐term physical inactivity on hepatic cytoprotective‐ and inflammatory‐related protein expressions in young rats and the subsequent apoptotic response during microgravity stress simulated by tail suspension. Four‐week‐old male Wistar rats were randomly assigned to the control (CT) and physical inactivity (IN) groups. The floor space of the cages provided to the IN group was reduced to half of that provided to the CT group. After 8 weeks, rats in both groups (n = 6–7) underwent tail suspension. Their livers were harvested immediately before (0 day) or 1, 3, and 7 days after tail suspension. Levels of hepatic heat shock protein 72 (HSP72), an anti‐apoptotic protein, reduced over 7 days of tail suspension in the IN group than in the CT group (p < 0.01). Fragmented nucleosomes in the cytoplasmic fraction of the liver, an apoptotic index, were drastically increased by physical inactivity and tail suspension, and this change was significantly greater after 7 days of tail suspension in the IN group than in the CT group (p < 0.01). The apoptotic response was accompanied by the upregulation of pro‐apoptotic proteins (cleaved caspase‐3 and ‐7). Moreover, the levels of other pro‐apoptotic proteins (tumor necrosis factor‐1α and histone deacetylase 5) were also significantly higher in the IN than in the CT group (p < 0.05). Our results indicated that 8 weeks of physical inactivity decreased hepatic HSP72 levels and promoted hepatic apoptosis during the subsequent 7 days of tail suspension. [ABSTRACT FROM AUTHOR]

This study aimed to assess (1) blood pressure between young, current athletes, and non‐athletes early in life; (2) hypertension prevalence between former athletes and the general population later in life; and (3) understand the mechanisms between exercise training and hypertension risks in the form of DNA methylation. Study 1: A total of 354 young male participants, including current athletes, underwent blood pressure assessment. Study 2: The prevalence of hypertension in 1269 male former athletes was compared with that in the Japanese general population. Current and former athletes were divided into three groups: endurance‐, mixed‐, and sprint/power‐group. Study 3: We analyzed the effect of aerobic‐ or resistance‐training on DNA methylation patterns using publicly available datasets to explore the possible underlying mechanisms. In young, current athletes, the mixed‐ and sprint/power‐group exhibited higher systolic blood pressure, and all groups exhibited higher pulse pressure than non‐athletes. In contrast, the prevalence of hypertension in former athletes was significantly lower in all groups than in the general population. Compared to endurance‐group (reference), adjusted‐hazard ratios for the incidence of hypertension among mixed‐ and sprint/power‐group were 1.24 (0.87–1.84) and 1.50 (1.04–2.23), respectively. Moreover, aerobic‐ and resistance‐training commonly modified over 3000 DNA methylation sites in skeletal muscle, and these were suggested to be associated with cardiovascular function‐related pathways. These findings suggest that the high blood pressure induced by exercise training at a young age does not influence the development of future hypertension. Furthermore, previous exercise training experiences at a young age could decrease the risk of future hypertension. [ABSTRACT FROM AUTHOR]

Objective: The previous results from cross‐sectional studies indicate that there could be alterations across time in handgrip strength (HGS) asymmetry. One way to investigate this is to test the same children multiple times. Therefore, we aimed to evaluate the laterality of HGS in healthy young children at two different time points separated by a year. Methods: A total of 165 preschool children (79 males and 87 females) between the ages of 4.5 and 5.6 years participated and performed maximal voluntary HGS in both hands using a Smedley handgrip dynamometer. We ran a paired sample t‐test on the difference scores (right – left vs. right – left) to determine if HGS (right vs. left) differed across time. Results: The difference between hands (t = −4.804, p <.0001) did differ between time points. At the initial test, the mean value of the HGS in the right hand was approximately 15% higher than that of the left hand. This difference between hands was reduced following a year. The mean bias between tests (second test – initial test) and the 95% limits of agreement was −0.84 (−5.27, 3.58) kg. Conclusion: Contrary to our hypothesis, HGS asymmetry during the initial test (at age 5) was not observed in the second test completed a year later (at age 6). These results suggest that HGS asymmetry is uncertain in children between 5 and 6 years. In this short‐term study, it was impossible to ascertain when HGS asymmetry first appeared. Longer term studies are required to better determine when these changes occur. [ABSTRACT FROM AUTHOR]

Less is known about how compliance with 24‐hour movement guidelines for physical activity (PA), sedentary behavior, and sleep affects adiposity in young people. The purposes of this study were to compare compliance with 24‐hour movement guidelines in Asian adolescents and to examine the associations between compliance with 24‐hour movement guidelines and body fat percentage. A sample of 12 590 adolescents aged 13.63 (± 1.01) years from eight Asian metropolitan cities including Bangkok (Thailand), Hong Kong SAR, Kuala Lumpur (Malaysia), Seoul (South Korea), Shanghai (China), Singapore, Taipei (Taiwan), and Tokyo (Japan) completed interviewer‐administered questionnaires to assess moderate‐to‐vigorous PA, recreational screen time, sleep duration, and covariates. Body fat percentage was measured using bioelectrical impedance analysis. We found that compliance with 24‐hour movement guidelines differed in Asian adolescents across the eight cities. Adjusting for covariates, there was a negative association between number of the guidelines being met and body fat percentage in Asian adolescents. In addition, meeting only the sleep guideline and both the PA and sleep guidelines had negative associations with body fat percentage compared with no guidelines being met. Our findings improve the understanding about how compliance with 24‐hour movement guidelines benefit a healthy body weight in adolescents, as well as contribute to development of evidence‐based 24‐hour movement guidelines for Asian young people. Future research is needed to gain better insights into the directionality of the associations between compliance with 24‐hour movement guidelines and adiposity, as well as the mechanisms underlying the associations in Asian adolescents. [ABSTRACT FROM AUTHOR]

Key points Silent mating type information regulation 2 homologue 1 (SIRT1) activity and content increased significantly in overload-induced hypertrophy., SIRT1-mediated signalling through Akt, the endothelial nitric oxide synthase mediated pathway, regulates anabolic process in the hypertrophy of skeletal muscle., The regulation of catabolic signalling via forkhead box O 1 and protein ubiquitination is SIRT1 dependent., Overload-induced changes in microRNA levels regulate SIRT1 and insulin-like growth factor 1 signalling., Abstract Significant skeletal muscle mass guarantees functional wellbeing and is important for high level performance in many sports. Although the molecular mechanism for skeletal muscle hypertrophy has been well studied, it still is not completely understood. In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus and gastrocnemius muscles in rats. Two weeks of muscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant increase in silent mating type information regulation 2 homologue 1 (SIRT1) content and activity ( P < 0.001). SIRT1-regulated Akt, endothelial nitric oxide synthase and GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels. Alternatively, decreased forkhead box O 1 (FOXO1) and increased K48 polyubiquitination also suggest that SIRT1 could be involved in the catabolic process of hypertrophy. Furthermore, increased levels of K63 and muscle RING finger 2 (MuRF2) protein could also be important enhancers of muscle mass. We report here that the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, SIRT1 and Nampt levels. Our results reveal a strong correlation between SIRT1 levels and activity, SIRT1-regulated pathways and overload-induced hypertrophy. These findings, along with the well-known regulatory roles that SIRT1 plays in modulating both anabolic and catabolic pathways, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overload-induced hypertrophy of skeletal muscle. This hypothesis will now require rigorous direct and functional testing. [ABSTRACT FROM AUTHOR]

Aim Here, we aimed to compare the effect of a combination of body mass-based resistance exercise and moderate-intensity (55% peak oxygen uptake [ [ABSTRACT FROM AUTHOR]

Recent studies have shown that activation of Toll-like receptor (TLR)4 signaling may be an important factor in muscle atrophy and excessive inflammatory response associated with immobilization. To examine the role of TLR4 signaling on cast immobilization-induced skeletal muscle atrophy, we tested the hypothesis that muscle atrophy and inflammation after cast immobilization is reduced in TLR4-defective mice. TLR4-defective (C3H/HeJ) and wild type (C3H/HeN) mice were divided into control and cast-immobilization groups. Cast immobilization was imposed for 14 days. Cast immobilization increased TLR4 mRNA expression in the gastrocnemius and decreased muscle mass and cross-sectional area (CSA) of the gastrocnemius fibers. However, there was no difference in the gastrocnemius muscle mass and CSA between TLR4-defective and wild type mice. Cast immobilization-induced increase in ubiquitin E3 ligases (MAFbx/Atrogin-1 and MuRF1), inflammatory cytokines, and macrophage/monocyte marker mRNAs were unaffected by defective TLR4. Our findings in C3H/HeJ mice suggested that TLR4 signaling might not play an essential role in immobilization-induced muscle atrophy. [ABSTRACT FROM AUTHOR]

Aim: Recent meta-analyses of the literature confirmed the association between the RR+RX genotype of theACTN3R577X polymorphism and elite sprint/power athletic status in Europeans but not in Asians and Africans, while the association between the R577X genotype and elite endurance athlete status is less convincing. The aim of the present study was to investigate the association between theACTN3R577X genotype and elite athlete status in a large Asian (Japanese) cohort of track and field athletes. Methods: One-thousand fifty-seven Japanese track and field athletes (627 sprint/power athletes and 430 endurance athletes) and 810 Japanese controls were genotyped for theACTN3R577X polymorphism (rs1815739) by using the TaqMan® SNP Genotyping Assay. Results: Elite sprint/power athletes had a higher frequency of the RR+RX genotype than the controls (OR: 1.59, 95% CI: 1.16–2.18;P = .003). A significant linear correlation was found between the RR + RX genotype and athlete status (i.e. regional < national < international) in sprint/power athletes (regional: 71%, national: 81%, international: 84%;P = .001 for trend) and long-distance runners (regional: 65%, national: 72%, international: 82%;P = .030 for trend). Conclusions: The data obtained for this large Asian (Japanese) cohort of track and field athletes served to confirm the association between the RR + RX genotype of theACTN3R577X polymorphism and elite sprint/power athlete status and also the association between theACTN3RR + RX genotype and long-distance running athletic status. [ABSTRACT FROM PUBLISHER]

Astaxanthin is a carotenoid pigment and has been shown to be an effective inhibitor of oxidative damage. We tested the hypothesis that astaxanthin intake would attenuate immobilization-induced muscle atrophy in rats. Male Wistar rats (14-week old) were fed for 24 days with either astaxanthin or placebo diet. After 14 days of each experimental diet intake, the hindlimb muscles of one leg were immobilized in plantar flexion position using a plaster cast. Following 10 days of immobilization, both the atrophic and the contralateral plantaris muscles were removed and analyzed to determine the level of muscle atrophy along with measurement of the protein levels of CuZnsuperoxide dismutase (CuZn-SOD) and selected proteases. Compared with placebo diet animals, the degree of muscle atrophy in response to immobilization was significantly reduced in astaxanthin diet animals. Further, astaxanthin supplementation significantly prevented the immobilization-induced increase in the expression of CuZn-SOD, cathepsin L, calpain, and ubiquitin in the atrophied muscle. These results support the postulate that dietary astaxanthin intake attenuates the rate of disuse muscle atrophy by inhibiting oxidative stress and proteolysis via three major proteolytic pathways. [ABSTRACT FROM AUTHOR]

We examined the effect of repeated heat stress on muscle atrophy, and apoptotic and proteolytic regulation in unloaded rat slow- and fast-type skeletal muscles. Forty male Wistar rats (11 week-old) were divided into control ( CT), hindlimb unweighting ( HU), intermittent weight-bearing during HU ( HU + IWB), and intermittent weight-bearing with heat stress during HU (41-41.5°C for 30 min; HU + IWB + HS) groups. The HU + IWB + HS and HU + IWB groups were released from unloading for 1 h every second day, during which the HU + IWB + HS group underwent the heating. Our results revealed that repeated bouts of heat stress resulted in protection against disuse muscle atrophy in both soleus and plantaris muscles. This heat stress-induced protection against disuse-induced muscular atrophy may be partially due to reduced apoptotic activation in both muscles, and decreased ubiquitination in only the soleus muscle. We concluded that repeated heat stress attenuated skeletal muscle atrophy via suppressing apoptosis but the response to proteolytic systems depend on the muscle phenotype. [ABSTRACT FROM AUTHOR]

Abstract: Here we describe the interaction of phosphorylated ∼40kDa protein with phosphorylated Akt which is a serine/threonine kinase resulting from increased blood glucose in rat cardiac muscle. Mass spectrometry analysis revealed that this protein was glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Furthermore, increase in Akt and GAPDH phosporylation and induction of their association were both observed after insulin stimulation in the H9c2 cell line derived from embryonic rat ventricle. Moreover, the activation of GAPDH was upregulated when the GAPDH phosphorylation was increased. Our data suggest that GAPDH phosphorylation and association with Akt by insulin treatment have some bearing on the enhancement of GAPDH activity. Structured summary: MINT-7891324, MINT-7891304, MINT-7891314: GAPDH (uniprotkb:P04797) physically interacts (MI:0915) with Akt (uniprotkb:P47196) by anti bait coimmunoprecipitation (MI:0006) [Copyright &y& Elsevier]

A healthy diet and regular exercise are among the major factors that influence quality of life (QOL) in old age. Exercise is believed to be beneficial to improve QOL, retarding age-related decline of physiological functions and preventing age-related diseases. Regular physical exercise can possibly improve age-related functional decline and delay onset of age-related diseases by attenuating potentially harmful oxidative damage and suppressing inflammatory processes even in older age. [ABSTRACT FROM AUTHOR]

The duathlon is an endurance multisport event that consists of sequential running, cycling, and further running. Imbalance in the redox homeostasis is associated with fatigued status and underperformance in various sports; however, there are no corresponding reports regarding the duathlon. The purpose of this study was to examine the changes in the blood redox balance during a simulated duathlon race and to determine the relationship between performance and the redox balance. Eight male triathletes participated in a simulated race, consisting of a 5‐km run, 30 km cycling, and a further 5‐km run, with 5 min rest between two parts to collect the blood samples. The serum levels of reactive oxygen metabolites (d‐ROMs) and biological antioxidant potential (BAP) were measured and BAP/d‐ROMs ratio and oxidative stress index (OSI) were calculated. The d‐ROMs levels after the first Run were significantly increased compared with the levels observed before the race. Moreover, BAP levels increased significantly over the race. The BAP/d‐ROMs ratio also gradually increased through the race, while the OSI was gradually decreased. In addition, a significant relationship was observed only between d‐ROMs levels after the first Run and the first Run performance. These results suggest that the redox balance shifts toward reduction (antioxidation) during the duathlon race and increased oxidant potential levels are negatively correlated with performance in the early stages of the race. [ABSTRACT FROM AUTHOR]

Objective Methods Results Conclusion This study aimed to compare the current handgrip strength (HGS) of Kendo athletes with their HGS when they were in university (up to 50 years).Eighty male graduates who were Kendo club members during their university days performed anthropometric and HGS measurements, and these HGS were compared with those measured during their university days (mean age of 19.5 years old).There was no evidence of a statistical difference in HGS between the current measurement and the measurement taken during university [−0.64 (−1.9, 0.67) kg, p = .336]. There was, however, evidence that the difference in HGS depended upon the current age of the individual (t = −6.43, p < .001). When probing the interaction, there were statistical differences between the ages of 24.6 and 38.2 years and between the ages of 47.4 and 69.9 years. Strength increased across time in the younger participants and decreased for those who were older. Between the ages of 38.9 and 46.1 years, there was no evidence of a statistical difference indicating a maintenance of strength.The HGS of Kendo club graduates, which they acquired during their formative years, continued to increase even after they graduated from university and entered their 30s. However, their HGS decreased from age 50, even though they practiced Kendo. [ABSTRACT FROM AUTHOR]

Provides information on a study which tested the hypothesis that age-associated increases in reactive oxygen species production and nuclear factor-κB activation are attenuated by regular exercise even in old age. Examination of the nuclear protein levels of p50 and p65; Conclusions.