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New Findings: What is the central question of this study?Is stretch–shortening contraction effective to attenuate skeletal muscle atrophy and hepatic dysfunction in a rat model of peptidoglycan–polysaccharide (PG‐PS)‐induced inflammation (PG‐PS rat)?What are the main findings and their importance?Stretch–shortening contraction attenuates skeletal muscle atrophy in the trained leg and increases circulating interleukin‐10 in PG‐PS rats. Stretch–shortening contraction also ameliorates liver dysfunction in PG‐PS rats, possibly via increased blood interleukin‐10. These findings are important because they suggest that stretch–shortening contraction is effective to maintain liver function in addition to exercised skeletal muscle mass. Stretch–shortening contraction (SSC) is an effective modality to improve skeletal muscle mass. However, the beneficial effects of SSC in the presence of chronic inflammation remain unclear. Here, we imposed five SSC sessions unilaterally on the triceps surae in young female Lewis rats. Rats were injected with vehicle or peptidoglycan–polysaccharide (PG‐PS) to induce long‐lasting inflammation. The PG‐PS reduced gastrocnemius muscle mass in both legs, but that of the SSC‐trained leg was significantly greater than that of the contralateral leg. Circulating pro‐inflammatory cytokines, such as IL‐1β, were significantly increased by PG‐PS injection, even if carrying out SSC. The circulating anti‐inflammatory cytokine IL‐10 increased with SSC in both healthy and inflammatory conditions. Stretch–shortening contraction also prevented increases in serum aspartate aminotransferase activity and plasma free phenylalanine concentration induced by PG‐PS, in comparison to the control resistance exercise consisting of isometric contractions. Moreover, aspartate aminotransferase and phenylalanine concentrations demonstrated a significant and negative correlation with IL‐10/IL‐1β values (r = −0.61, P = 0.017, and r = −0.66, P = 0.008, respectively). These results suggest that SSC training is effective to reduce both muscle atrophy and the hepatic dysfunction induced by PG‐PS, mediated, at least in part, through an increase in circulating IL‐10. [ABSTRACT FROM AUTHOR]

Cancer cachexia is the result of complex interorgan interactions initiated by cancer cells and changes in patient behavior such as decreased physical activity and energy intake. Therefore, it is crucial to distinguish between the direct and indirect effects of cancer cells on muscle mass regulation and bioenergetics to identify novel therapeutic targets. In this study, we investigated the direct effects of Colon-26 cancer cells on the molecular regulating machinery of muscle mass and its bioenergetics using a coculture system with C2C12 myotubes. Our results demonstrated that coculture with Colon-26 cells induced myotube atrophy and reduced skeletal muscle protein synthesis and its regulating mechanistic target of rapamycin complex 1 signal transduction. However, we did not observe any activating effects on protein degradation pathways including ubiquitin-proteasome and autophagy-lysosome systems. From a bioenergetic perspective, coculture with Colon-26 cells decreased the complex I-driven, but not complex II-driven, mitochondrial ATP production capacity, while increasing glycolytic enzyme activity and glycolytic metabolites, suggesting a shift in energy metabolism toward glycolysis dominance. Gene expression profiling by RNA sequencing showed that the increased activity of glycolytic enzymes was consistent with changes in gene expression. However, the decreased ATP production capacity of mitochondria was not in line with the gene expression. The potential direct interaction between cancer cells and skeletal muscle cells revealed in this study may contribute to a better fundamental understanding of the complex pathophysiology of cancer cachexia. NEW & NOTEWORTHY: We explored the potential direct interplay between colon cancer cells (Colon-26) and skeletal muscle cells (C2C12 myotubes) employing a noncontact coculture experimental model. Our findings reveal that coculturing with Colon-26 cells substantially impairs the protein synthesis rate, concurrently instigating a metabolic shift toward glycolytic dominance in C2C12 myotubes. This research unveils critical insights into the intricate cellular cross talk underpinning the complex pathophysiology of cancer cachexia. [ABSTRACT FROM AUTHOR]

High‐intensity exercise stimulates glycolysis, subsequently leading to elevated lactate production within skeletal muscle. While lactate produced within the muscle is predominantly released into the circulation via the monocarboxylate transporter 4 (MCT4), recent research underscores lactate's function as an intercellular and intertissue signalling molecule. However, its specific intracellular roles within muscle cells remains less defined. In this study, our objective was to elucidate the effects of increased intramuscular lactate accumulation on skeletal muscle adaptation to training. To achieve this, we developed MCT4 knockout mice and confirmed that a lack of MCT4 indeed results in pronounced lactate accumulation in skeletal muscle during high‐intensity exercise. A key finding was the significant enhancement in endurance exercise capacity at high intensities when MCT4 deficiency was paired with high‐intensity interval training (HIIT). Furthermore, metabolic adaptations supportive of this enhanced exercise capacity were evident with the combination of MCT4 deficiency and HIIT. Specifically, we observed a substantial uptick in the activity of glycolytic enzymes, notably hexokinase, glycogen phosphorylase and pyruvate kinase. The mitochondria also exhibited heightened pyruvate oxidation capabilities, as evidenced by an increase in oxygen consumption when pyruvate served as the substrate. This mitochondrial adaptation was further substantiated by elevated pyruvate dehydrogenase activity, increased activity of isocitrate dehydrogenase – the rate‐limiting enzyme in the TCA cycle – and enhanced function of cytochrome c oxidase, pivotal to the electron transport chain. Our findings provide new insights into the physiological consequences of lactate accumulation in skeletal muscle during high‐intensity exercises, deepening our grasp of the molecular intricacies underpinning exercise adaptation. Key points: We pioneered a unique line of monocarboxylate transporter 4 (MCT4) knockout mice specifically tailored to the ICR strain, an optimal background for high‐intensity exercise studies.A deficiency in MCT4 exacerbates the accumulation of lactate in skeletal muscle during high‐intensity exercise.Pairing MCT4 deficiency with high‐intensity interval training (HIIT) results in a synergistic boost in high‐intensity exercise capacity, observable both at the organismal level (via a treadmill running test) and at the muscle tissue level (through an ex vivo muscle contractile function test).Coordinating MCT4 deficiency with HIIT enhances both the glycolytic enzyme activities and mitochondrial capacity to oxidize pyruvate. [ABSTRACT FROM AUTHOR]

Belt electrode-skeletal muscle electrical stimulation (B-SES) involves the use of belt-shaped electrodes to contract multiple muscle groups simultaneously. Twitch contractions have been demonstrated to protect against denervation-induced muscle atrophy in rats, possibly through mitochondrial biosynthesis. This study examined whether inducing tetanus contractions with B-SES suppresses muscle atrophy and identified the underlying molecular mechanisms. We evaluated the effects of acute (60 Hz, 5 min) and chronic (60 Hz, 5 min, every alternate day for one week) B-SES on the tibialis anterior (TA) and gastrocnemius (GAS) muscles in Sprague–Dawley rats using belt electrodes attached to both ankle joints. After acute stimulation, a significant decrease in the glycogen content was observed in the left and right TA and GAS, suggesting that B-SES causes simultaneous contractions in multiple muscle groups. B-SES enhanced p70S6K phosphorylation, an indicator of the mechanistic target of rapamycin complex 1 activity. During chronic stimulations, rats were divided into control (CONT), denervation-induced atrophy (DEN), and DEN + electrically stimulated with B-SES (DEN + ES) groups. After seven days of treatment, the wet weight (n = 8–11 for each group) and muscle fiber cross-sectional area (CSA, n = 6 for each group) of the TA and GAS muscles were reduced in the DEN and DEN + ES groups compared with that in the CON group. The DEN + ES group showed significantly higher muscle weight and CSA than those in the DEN group. Although RNA-seq and pathway analysis suggested that mitochondrial biogenesis is a critical event in this phenomenon, mitochondrial content showed no difference. In contrast, ribosomal RNA 28S and 18S (n = 6) levels in the DEN + ES group were higher than those in the DEN group, even though RNA-seq showed that the ribosome biogenesis pathway was reduced by electrical stimulation. The mRNA levels of the muscle proteolytic molecules atrogin-1 and MuRF1 were significantly higher in DEN than those in CONT. However, they were more suppressed in DEN + ES than those in DEN. In conclusion, tetanic electrical stimulation of both ankles using belt electrodes effectively reduced denervation-induced atrophy in multiple muscle groups. Furthermore, ribosomal biosynthesis plays a vital role in this phenomenon. [ABSTRACT FROM AUTHOR]

Our previous studies demonstrated that an 8-week intake of 5% (w/w) apple polyphenol (APP) in the diet improves muscle endurance of young-adult rats. In order to identify a lower limit of the dietary contribution of APP to the effect, the experiments were designed for lower-dose supplementation (8-week feeding of 0.5% APP in AIN-93G diet) to 12-week-old male Sprague-Dawley rats. Results clearly showed that the 0.5% APP diet significantly up-regulates slower myosin-heavy-chain (MyHC) isoform ratios (IIx and IIa relative to total MyHC) and myoglobin expression in lower hind-limb muscles examined ( P < 0.05). There was a trend to increased fatigue resistance detected from measurements of relative isometric plantar-flexion force torque generated by a stimulus train delivered to the tibial nerve ( F(98, 1372) = 1.246, P = 0.0574). Importantly, there was no significant difference in the animal body-phenotypes or locomotor activity shown as total moving distance in light and dark periods. Therefore, the present study encourages the notion that even low APP-intake may increase the proportions of fatigue-resistant myofibers, and has promise as a strategy for modifying performance in human sports and improving function in age-related muscle atrophy. [ABSTRACT FROM AUTHOR]

Summary: We investigated the effects of volume‐matched resistance training (RT) with different training loads and rest intervals on acute responses and long‐term muscle and strength gains. Ten subjects trained with short rest (30 s) combined with low load (20 RM) (SL) and ten subjects performed the same protocol with long rest (3 min) and high load (8 RM) (LH). Cross‐sectional area (CSA) of the upper arm was measured by magnetic resonance imaging before and after 8 weeks of training. Acute stress markers such as growth hormone (GH) and muscle thickness (MT) changes have been assessed pre and post a single RT session. Only the SL group demonstrated significant increases in GH (7704·20 ± 11833·49%, P<0·05) and MT (35·2 ± 16·9%, P<0·05) immediately after training. After 8 weeks, the arm CSA s in both groups significantly increased [SL: 9·93 ± 4·86% (P<0·001), LH: 4·73 ± 3·01% (P<0·05)]. No significant correlation between acute GH elevations and CSA increases could be observed. We conclude that short rest combined with low‐load training might induce a high amount of metabolic stress ultimately leading to improved muscle hypertrophy while long rest with high‐load training might lead to superior strength increases. Acute GH increases seem not to be directly correlated with muscle hypertrophy. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated the beneficial effects of apple polyphenol (AP) intake on muscle endurance. Since mitochondria are critical for muscle endurance, we investigated mitochondrial enzyme activity, biogenesis, degradation and protein quality control. Twenty‐four Wistar rats were randomly fed a 5% AP diet (5% AP group, n = 8), a 0.5% AP diet (0.5% AP group, n = 8), or a control diet (control group, n = 8). After a 4‐week feeding period, the expression level of peroxisome proliferator‐activated receptor γ coactivator‐1α, a mitochondrial biosynthetic factor, did not increase, whereas that of transcription factor EB, another regulator of mitochondrial synthesis, significantly increased. Moreover, the mitochondrial count did not differ significantly between the groups. In contrast, mitophagy‐related protein levels were significantly increased. The enzymatic activities of mitochondrial respiratory chain complexes II, III and IV were significantly higher in the AP intake group than in the control group. We conclude that AP feeding increases the activity of respiratory chain complex enzymes in rat skeletal muscles. Moreover, mitochondrial biosynthesis and degradation may have increased in AP‐treated rats. New Findings: What is the central question of this study?Does the administration of apple polyphenols (AP) affect mitochondrial respiratory chain complex enzyme activity, biogenesis, degradation and protein quality control in rat skeletal muscles?What is the main finding and its importance?AP feeding increases respiratory chain complex enzyme activity in rat skeletal muscle. Moreover, AP administration increases transcription factor EB activation, and mitophagy may be enhanced to promote degradation of dysfunctional mitochondria, but mitochondrial protein quality control was not affected. [ABSTRACT FROM AUTHOR]

Background: Although muscle dysfunction caused by unfamiliar lengthening contraction is one of most important issues in sports medicine, there is little known about the molecular events on regeneration process. The purpose of this study was to investigate the temporal and spatial expression patterns of myogenin, myoD, pax7, and myostatin after acute lengthening contraction (LC)-induced injury in the rat hindlimb.Methods: We employed our originally developed device with LC in rat gastrocnemius muscle (n = 24). Male Wistar rats were anesthetized with isoflurane (aspiration rate, 450 ml/min, concentration, 2.0%). The triceps surae muscle of the right hindlimb was then electrically stimulated with forced isokinetic dorsi-flexion (180°/sec and from 0 to 45°). Tissue contents of myoD, myogenin, pax7, myostatin were measured by western blotting and localizations of myoD and pax7 was measured by immunohistochemistry. After measuring isometric tetanic torque, a single bout of LC was performed in vivo.Results: The torque was significantly decreased on days 2 and 5 as compared to the pre-treatment value, and recovered by day 7. The content of myoD and pax7 showed significant increases on day 2. Myogenin showed an increase from day 2 to 5. Myostatin on days 5 and 7 were significantly increased. Immunohistochemical analysis showed that myoD-positive/pax7-positive cells increased on day 2, suggesting that activated satellite cells play a role in the destruction and the early recovery phases.Conclusion: We, thus, conclude that myogenic events associate with torque recovery after LC-induced injury. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the effect of eicosapentaenoic and docosahexaenoic acids-rich fish oil (EPA + DHA) supplementation on eccentric contraction-induced muscle damage.Methods: Twenty-four healthy men were randomly assigned to consume the EPA + DHA supplement (EPA, n = 12) or placebo (PL, n = 12) by the double-blind method. Participants consumed EPA + DHA or placebo supplement for 8 weeks prior to exercise and continued it until 5 days after exercise. The EPA group consumed EPA + DHA-rich fish oil containing 600 mg EPA and 260 mg DHA per day. Subjects performed five sets of six maximal eccentric elbow flexion exercises. Changes in the maximal voluntary contraction (MVC) torque, range of motion (ROM), upper arm circumference, muscle soreness as well as serum creatine kinase, myoglobin, IL-6, and TNF-α levels in blood were assessed before, immediately after, and 1, 2, 3, and 5 days after exercise.Results: MVC was significantly higher in the EPA group than in the PL group at 2-5 days after exercise (p < 0.05). ROM was also significantly greater in the EPA group than in the PL group at 1-5 days after exercise (p < 0.05). At only 3 days after exercise, muscle soreness of the brachialis was significantly greater in the PL group than in the EPA group (p < 0.05), with a concomitant increase in serum IL-6 levels in the PL group.Conclusion: Eight-week EPA + DHA supplementation attenuates strength loss and limited ROM after exercise. The supplementation also attenuates muscle soreness and elevates cytokine level, but the effect is limited. [ABSTRACT FROM AUTHOR]

Belt electrode skeletal muscle electrical stimulation (B-SES) can simultaneously contract multiple muscle groups. Although the beneficial effects of B-SES in clinical situations have been elucidated, its molecular mechanism remains unknown. In this study, we developed a novel rodent B-SES ankle stimulation system to test whether low-frequency stimulation prevents denervation-induced muscle atrophy. Electrical stimulations (7‒8 Hz, 30 min) with ankle belt electrodes were applied to Sprague–Dawley rats daily for one week. All animals were assigned to the control (CONT), denervation-induced atrophy (DEN), and DEN + electrical stimulation (ES) groups. The tibialis anterior (TA) and gastrocnemius (GAS) muscles were used to examine the effect of ES treatment. After seven daily sessions of continuous stimulation, muscle wet weight (n = 8–11), and muscle fiber cross-sectional area (CSA, n = 4–6) of TA and GAS muscles were lower in DEN and DEN + ES than in CON. However, it was significantly higher in DEN than DEN + ES, showing that ES partially prevented muscle atrophy. PGC-1α, COX-IV, and citrate synthase activities (n = 6) were significantly higher in DEN + ES than in DEN. The mRNA levels of muscle proteolytic molecules, Atrogin-1 and Murf1, were significantly higher in DEN than in CONT, while B-SES significantly suppressed their expression (p < 0.05). In conclusion, low-frequency electrical stimulation of the bilateral ankles using belt electrodes (but not the pad electrodes) is effective in preventing denervation-induced atrophy in multiple muscles, which has not been observed with pad electrodes. Maintaining the mitochondrial quantity and enzyme activity by low-frequency electrical stimulation is key to suppressing muscle protein degradation. [ABSTRACT FROM AUTHOR]

Introduction: Sarcopenia is a complication of Chronic Obstructive Pulmonary Disease (COPD) that negatively affects physical activity and quality of life. However, the underlying mechanism by which COPD affects skeletal muscles remains to be elucidated. Therefore, we investigated the association between oxidative stress and structural alterations in muscles in elastase-induced emphysema mouse models. Materials and methods: Twelve-week-old male C57BL/6J mice were treated with either intratracheal porcine pancreatic elastase (PPE) dissolved in saline, or saline alone. The mice were euthanized 12 weeks after treatment, and the lungs and limb muscles were used for protein analysis of oxidative stress, p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and muscle atrophy signaling pathway related with oxidative stress. Furthermore, C57BL/6J mice treated with PPE or saline were analyzed for the effects of oral administration of astaxanthin or p38 inhibitor. Results: The weight of the soleus muscle, proportion of type I muscle fibers, and cross-sectional areas of muscle fibers in the PPE group were lower than those in the control group. Oxidative stress marker levels in the PPE group were elevated in skeletal muscles. The p38 MAPK signaling pathway was activated in the soleus muscles, leading to the activation of the ubiquitin–proteasome system and autophagy. Astaxanthin and p38 inhibitors attenuated alterations in muscle structure through the deactivation of the p38 MAPK signaling pathway. Conclusions: This study provides first evidence in COPD mouse model that oxidative stress trigger a series of muscle structural changes. Our findings suggest a novel target for sarcopenia in COPD. [ABSTRACT FROM AUTHOR]

The rs671 polymorphism is associated with the enzymatic activity of aldehyde dehydrogenase 2 (ALDH2), which is weakened by the A allele in East Asians. We recently reported the association of this polymorphism with the athletic status in athletic cohorts and the muscle strength of non-athletic cohorts. Therefore, we hypothesized the association of ALDH2 rs671 polymorphism with the performance in power/strength athletes. We aimed to clarify the relationship between the ALDH2 rs671 polymorphism and performance in power/strength athletes. Participants comprising 253 power/strength athletes (167 men and 86 women) and 721 healthy controls (303 men and 418 women) were investigated. The power/strength athletes were divided into classic powerlifting (n = 84) and weightlifting (n = 169). No differences in the genotypes and allele frequencies of the ALDH2 rs671 polymorphism and an association between performance and the ALDH2 rs671 genotype were observed in weightlifters. However, the relative values per body weight of the total record were lower in powerlifters with the GA + AA genotype than those with the GG genotype (7.1 ± 1.2 vs. 7.8 ± 1.0; p = 0.010, partial η2 = 0.08). Our results collectively indicate a role of the ALDH2 rs671 polymorphism in strength performance in powerlifters. [ABSTRACT FROM AUTHOR]

Aldehyde dehydrogenase (ALDH) is an enzyme that detoxifies aldehydes and is primarily involved in alcohol metabolism. Recently, we have shown that ALDH also plays an important role in skeletal muscle homeostasis. To better understand the role of ALDH in skeletal muscle, it is necessary to clarify the adaptability of ALDH. In this study, we examined the effects of endurance training, compensatory hypertrophy by synergist ablation (SA), and denervation-induced atrophy on gene expression and protein levels of selected ALDH isoforms in skeletal muscle. Ten-week-old C57BL/6J mice were subjected to each intervention, and the plantaris muscle was collected. Gene expression levels of Aldh1a1 were decreased by SA and denervation, but ALDH1A1 protein levels were not affected. Protein levels of ALDH1B1 increased after chronic endurance training, SA, and denervation interventions. However, the increase in Aldh1b1 gene expression was observed only after SA. The gene expression of Aldh2 was decreased after SA, but ALDH2 protein levels remained unchanged. Denervation increased both the Aldh2 gene and ALDH2 protein levels. Taken together, each isoform of ALDH undergoes unique quantitative adaptations in skeletal muscle under different conditions. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is Available in the Text. Terada, K, Kikuchi, N, Burt, D, Voisin, S, and Nakazato, K. Full title: Low-load resistance training to volitional failure induces muscle hypertrophy similar to volume-matched, velocity fatigue. J Strength Cond Res 36(6): 1576–1581, 2022—We investigated how resistance training (RT) to failure at low load affects acute responses and chronic muscle adaptations compared with low-load RT to velocity fatigue at equal work volume. Twenty-seven subjects performed 8 weeks of bench press twice weekly. Subjects were randomly assigned to one of 3 groups: low-load volitional failure (LVoF, n = 9), low-load velocity fatigue (LVeF, n = 8), and high-load (HL, n = 10). Resistance training comprised 3 sets to failure at 40% one repetition maximum (1RM) in the LVoF group, 3 sets to velocity fatigue (20% lifting velocity loss) at 40% 1RM in the LVeF group, and 3 sets of 8 repetitions at 80% 1RM in the HL group. We measured muscle strength, hypertrophy, endurance, and power at baseline and after the RT program. We also measured muscle swelling and blood lactate after each RT bout to investigate the acute response. There were no differences in total work volume between the LVoF and LVeF groups. Responses to RT were similar between LVoF and LVeF, whether looking at acute muscle swelling, increase in blood lactate, chronic hypertrophy, and strength gain. However, LVoF and LVeF RT triggered different responses to muscle function in comparison with HL training: LVoF and LVeF showed enhanced acute responses and greater chronic endurance gains, but lower chronic strength gains than HL. In conclusion, low-load RT to volitional failure induces muscle hypertrophy similar to volume-matched velocity fatigue. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine whether insulin-like growth factor (IGF-1) and Akt/mTOR/p70S6K pathway activity is altered by chronic eccentric exercise in rat medial gastrocnemius muscle. Male Wistar rats (n = 24) were randomly assigned to 1 of the 2 groups: eccentric exercise (ECC) group or shamoperated control (CON) group. Rats in the ECC group were trained every second day for 10 days (5 sessions in total) or 20 days (10 sessions in total). After either 5 or 10 exercise sessions, muscle specimens were dissected and weighed. The mRNA expression of IGF-1 and its variant, mechano growth factor (MGF), was evaluated using real time reverse transcriptasepolymerase chain reaction (RT-PCR). Tissue concentrations of Akt (P), mTOR (P), and p70S6K (P) were measured by using western blot analysis. The medial gastrocnemius muscle mass of the ECC group did not show any significant difference after 5 exercise sessions, whereas the muscle mass increased significantly after 10 exercise sessions with a concomitant increase in the cross-sectional area of muscle fibers (p < 0.05). The expression of IGF-1 mRNA and the tissue concentrations of Akt (P) and p70S6K (P) after 10 exercise sessions was significantly higher than those of the age-matched controls and the rats that received 5 exercise sessions. The expression of MGF mRNA in both ECC5S and ECC10S were significantly higher than that in each period-matched control (p < 0.01). The tissue concentration of mTOR (P) after 10 sessions showed a significant increase when compared with period-matched controls (p < 0.01). These results suggest that activation of the IGF-1/Akt/mTOR/p70S6K signaling pathway becomes dominant in the later phase of chronic exercise, when significant muscular hypertrophy is observed. [ABSTRACT FROM AUTHOR]

The article presents the study conducted regarding the sport-specific characteristics of trunk muscles and muscle strengths in the cross-sectional areas of the collegiate wrestlers and judokas. The study, administered to these players, will also examine the association of trunk muscles and strength to their athletic performance levels. The result shows that the players of both sports have different characteristics.

Online exercise is undoubtedly useful and important; however, chronic adaptations to online exercise, particularly strength gain, muscle hypertrophy, and cardiovascular parameters, remain unclear. We investigated the effect of online exercise training using Zoom on fitness parameters compared with the same exercises supervised directly. In the present study, 34 subjects (age: 42.9±14.4 years) were included. Twenty-three subjects performed 8 weeks of body mass-based exercise training online using Zoom, and eleven subjects performed the same exercise supervised directly as the control group. The subjects performed low-load resistance exercises twice a week for 8 weeks for a total of 16 sessions. The sessions included 9 exercises: leg raises, squats, rear raises, shoulder presses, rowing, dips, lunges, Romanian dead lifts, and push-ups. Chair-stand, push-up, and sit-and-reach tests were performed on all subjects. Overall, the home exercise program effectively increased strength and muscle mass and decreased blood pressure and arterial stiffness, but there were no differences between the groups. Changes in chair-stand and sit-and-reach test results were higher in the control group than in the online group. Our results show that there is a similar training response to body mass-based training in both groups, even with virtual experiences using Zoom. [ABSTRACT FROM AUTHOR]

BACKGROUND: Lumbar radiological abnormalities (LRA) and trunk muscle weakness are major causes of the low back pain (LBP). We reported that the prevalence of LRA was approximately 90% in middle- and heavyweight-judokas, independent to the occurrence of LBP. However, the trunk muscle weakness, especially the rotators, plays a key role in occurrence of LBP in heavyweight judokas. OBJECTIVE: To examine the trunk muscle strength (TMS) and LRA impact on LBP occurrence in lightweight judokas. METHOD: The strength of the trunk extensors, flexors, and rotators was measured in 32 lightweight male judokas. LBP and LRA were identified using a questionnaire, X-ray, and MRI. RESULTS: The occurrence rate of LBP and LRA were 40.6% and 62.5%, respectively, without any significant correlation. Among judokas without LRA, TMS of those with LBP were significantly lower than those without LBP (P < 0.05, the extensor; 60 ∘ /s: ES [d] = 1.38, 90 ∘ /s: ES [d] = 0.78, and 120 ∘ /s: ES [d] = 0.37, flexor; 60 ∘ /s: ES [d] = 1.48, dominant rotator; 60 ∘ /s: ES [d] = 1.66, and 90 ∘ /s: ES [d] = 1.87, non-dominant rotator; 90 ∘ /s: ES [d] = 0.17, and dominant/non-dominant rotator ratio; 90 ∘ /s: ES [d] = 1.55). Moreover, there were significant negative correlations between LBP severity and TMS (P < 0.05, the extensor; 90 ∘ /s: r = - 0.63, dominant rotator; 90 ∘ /s: r = - 0.648, and dominant/non-dominant rotator ratio; 90 ∘ /s: r = - 0.621) in judokas without LRA. RESULTS: The occurrence rate of LBP and LRA were 40.6% and 62.5%, respectively, without any significant correlation. Among judokas without LRA, the extensor (60, 90, and 120 ∘ /s), flexor (60 ∘ /s), dominant rotator (60 and 90 ∘ /s), non-dominant rotator (90 ∘ /s), and dominant/non-dominant rotator ratio (90 ∘ /s) of judokas with LBP were significantly lower than those of the judokas without LBP. Moreover, there were significant negative correlations (P < 0.05) between LBP severity and the extensor (90 ∘ /s; r = - 0.63) and dominant rotator (90 ∘ /s; r = - 0.648) strength, and dominant/non-dominant rotator ratio (90 ∘ /s; r = - 0.621) in judokas without LRA. CONCLUSION: Weak trunk musculature may be a co-factor in the occurrence of LBP in lightweight judokas without LRA. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare the frequency of COL1A1 rs1107946 polymorphism between sport climbers and controls from three ethnic groups (Japanese, Polish, and Russian) and investigate the effect of the COL1A1 rs1107946 polymorphism on the age-related decrease in flexibility in the general population. Study I consisted of 1929 healthy people (controls) and 218 climbers, including Japanese, Polish, and Russian participants. The results of the meta-analysis showed that the frequency of the AC genotype was higher in climbers than in the controls (p = 0.03). Study II involved 1093 healthy Japanese individuals (435 men and 658 women). Flexibility was assessed using a sit-and-reach test. There was a tendency towards association between sit-and-reach and the COL1A1 rs1107946 polymorphism (genotype: p = 0.034; dominant: p = 0.435; recessive: p = 0.035; over-dominant: p = 0.026). In addition, there was a higher negative correlation between sit-and-reach and age in the AA + CC genotype than in the AC genotype (AA + CC: r = −0.216, p < 0.001; AC: r = −0.089, p = 0.04; interaction p = 0.037). However, none of these results survived correction for multiple testing. Further studies are warranted to investigate the association between the COL1A1 gene variation and exercise-related phenotypes. [ABSTRACT FROM AUTHOR]

Purpose: This study was aimed at investigating the effect of eccentric contractions (ECCs) of flexor pollicis brevis muscles (FPBMs) on motor and sensory nerve functions as well as the ipsilateral repeated bout effect (IL-RBE) and contralateral (CL)-RBE of motor and sensory nerve conduction velocities following ECCs.Methods: Thirty-two young healthy men (age: 19.6 ± 0.2 years, height: 173.2 ± 1.2 cm, body mass: 69.7 ± 1.9 kg) performed two bouts of ECCs. During the first ECCs bout (ECCs-1), all participants performed 100 ECCs with 1 hand; for the second bout, 3 groups (2 weeks [W]: n = 11, 4W: n = 10, 8W: n = 11) performed ECCs with both hands 2, 4, or 8 weeks after ECCs-1. The maximal voluntary isometric contraction (MVC), range of motion (ROM), visual analog scale for pain (VAS), motor and sensory nerve conduction velocities were measured before, immediately after, and 1, 2, 3, and 5 days after ECCs.Results: ECCs-1 decreased the MVC, limited the ROM, developed VAS, and decreased the motor and sensory nerve conduction velocities compared to non-exercise hand (p < 0.05). The repeated bout effect was observed in the ROM for IL-RBE in 2W and 4W, VAS for IL-RBE in 2 W, and ROM and VAS for CL-RBE in 2W (p < 0.05). However, RBEs of MVC and motor and sensory nerve conduction velocities were not observed, and no differences were confirmed depending on the interval.Conclusion: In the present study, ECCs of the FPBM caused a sensory nerve dysfunction, while IL- or CL-RBE was not observed. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Is muscle protein synthesis (MPS) additionally activated following exercise when ribosomal capacity is increased after repeated bouts of resistance exercise (RE)?What is the main finding and its importance?Skeletal muscles with increased ribosome content through repeated RE bouts showed sufficient activation of MPS with lower mechanistic target of rapamycin complex 1 signalling. Thus, repeated bouts of RE possibly change the translational capacity and efficiency to optimize translation activation following RE. Resistance exercise (RE) activates ribosome biogenesis and increases ribosome content in skeletal muscles. However, it is unclear whether the increase in ribosome content subsequently causes an increase in RE‐induced activation of muscle protein synthesis (MPS). Thus, this study aimed to investigate the relationship between ribosome content and MPS after exercise using a rat RE model. Male Sprague–Dawley rats were categorized into three groups (n = 6 for each group): sedentary (SED) and RE trained with one bout (1B) or three bouts (3B). The RE stimulus was applied to the right gastrocnemius muscle by transcutaneous electrical stimulation under isoflurane anaesthesia. The 3B group underwent stimulation every other day. Our results revealed that 6 h after the last bout of RE, muscles in the 3B group showed an increase in total RNA and 18S+28S rRNA content per muscle weight compared with the SED and 1B groups. In both the 1B and 3B groups, MPS, estimated by puromycin incorporation in proteins, was higher than that in the SED group 6 h after exercise; however, no significant difference was observed between the 1B and 3B groups. In the 1B and 3B groups, phosphorylated p70S6K at Thr‐389 increased, indicating mechanistic target of rapamycin complex 1 (mTORC1) activity. p70S6K phosphorylation level was lower in the 3B group than in the 1B group. Finally, protein synthesis per ribosome (indicator of translation efficiency) was lower in the 3B group than in the 1B group. Thus, three bouts of RE changed the ribosome content and mTORC1 activation, but not the degree of RE‐induced global MPS activation. [ABSTRACT FROM AUTHOR]

The coronavirus disease 2019 (COVID‐19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), is threatening people's lives and impacting their health. It is still unclear whether people engaged in physical activity are at an increased risk of SARS‐CoV‐2 infection and severe forms of COVID‐19. In order to provide data to help answer this question, we, therefore, investigated the effects of endurance training on the levels of host proteins involved in SARS‐CoV‐2 infection in mice. Eight‐week‐old C57BL/6J mice were subjected to treadmill running (17–25 m/min, 60–90 min, 5 sessions/week, 8 weeks). After the intervention, the levels of angiotensin‐converting enzyme 2 (ACE2; host receptor for SARS‐CoV‐2), transmembrane protease serine 2 (TMPRSS2; host protease priming fusion of SARS‐CoV‐2 to host cell membranes), FURIN (host protease that promotes binding of SARS‐CoV‐2 to host receptors), and Neuropilin‐1 (host coreceptor for SARS‐CoV‐2) were measured in 10 organs that SARS‐CoV‐2 can infect (larynx, trachea, lung, heart, jejunum, ileum, colon, liver, kidney, and testis). Six organs (heart, lung, jejunum, liver, trachea, and ileum) showed changes in the levels of at least one of the proteins. Endurance training increased ACE2 levels in heart (+66.4%), lung (+37.1%), jejunum (+24.7%) and liver (+27.4%), and FURIN in liver (+17.9%) tissue. In contrast, endurance training decreased Neuropilin‐1 levels in liver (−39.7%), trachea (−41.2%), and ileum (−39.7%), and TMPRSS2 in lung (−11.3%). Taken together, endurance training altered the levels of host proteins involved in SARS‐CoV‐2 cell entry in an organ‐dependent manner. [ABSTRACT FROM AUTHOR]

Mechanistic target of rapamycin complex 1 (mTORC1) plays a central role in muscle protein synthesis and repeated bouts of resistance exercise (RE) blunt mTORC1 activation. However, the changes in the proteolytic signaling when recurrent RE bouts attenuate mTORC1 activation are unclear. Using a RE model of electrically stimulated rat skeletal muscle, this study aimed to clarify the effect of repeated RE bouts on acute proteolytic signaling, particularly the calpain, autophagy‐lysosome, and ubiquitin‐proteasome pathway. p70S6K and rpS6 phosphorylation, indicators of mTORC1 activity, were attenuated by repeated RE bouts. Calpain 3 protein was decreased at 6 h post‐RE in all exercised groups regardless of the bout number. Microtubule‐associated protein 1 light chain 3 beta‐II, an indicator of autophagosome formation, was increased at 3 h and repeated RE bouts increased at 6 h, post‐RE. Ubiquitinated proteins were increased following RE, but these increases were independent of the number of RE bouts. These results suggest that the magnitude of autophagosome formation was increased following RE when mTORC1 activity was attenuated with repeated bouts of RE. [ABSTRACT FROM AUTHOR]

Blackcurrant extract mainly contains anthocyanins. Several reports suggest that anthocyanins have beneficial effect for cardiovascular functions. The aim of this study was to examine the effect of 7-day intake of New Zealand blackcurrant (NZBC) extract on arterial functions, e.g. arterial stiffness, and serum lipids. A randomized, double-blind, placebo-controlled, crossover design study with a washout period of 28 days was conducted. Fourteen older adults participated in this study (age 73.3 ± 1.7 years). Participants took either a 7-day course of placebo or two capsules of NZBC extract (each 300 mg capsule contains 35% blackcurrant extract). Participants took one of the two trials first and then took the other after a washout period. Carotid-femoral pulse-wave velocity, an index of central arterial stiffness, and central blood pressure were measured at baseline and again at the end of the 7-day study period. Compared to baseline, carotid-femoral pulse-wave velocity (P =.03) and central blood pressure (P =.02) decreased significantly after the 7-day study period with NZBC intake. In addition, carotid-femoral pulse-wave velocity (P =.04) and central blood pressure (P =.001) in the NZBC intake trial decreased significantly more than in the placebo intake trial. No effects were observed on serum lipids. These results suggest that short-term NZBC intake reduces central arterial stiffness and central blood pressure in older adults. Therefore, anthocyanin-rich blackcurrants might be beneficial for maintaining or improving cardiovascular health as an alternative to pharmaceutical medications. Aix: augmentation index; BP: blood pressure; cfPWV: carotid–femoral pulse-wave velocity; CVD: cardiovascular diseases; DBP: diastolic blood pressure; faPWV: femoral-ankle pulse-wave velocity; FG: fasting glucose; HDL: high-density lipoprotein cholesterol; LDL: low-density lipoprotein cholesterol; MBP: mean blood pressure; NZBC: New Zealand blackcurrant; PP: pulse pressure; SBP: systolic blood pressure; TG: triglycerides. [ABSTRACT FROM AUTHOR]

Background: Eccentric contractions (ECCs) cause muscle damage. In addition, we showed that ECCs induce nerve dysfunction and damage with rats and human. Purpose: We aimed to evaluate motor nerve conduction velocity (MCV) for flexor pollicis brevis muscle (FPBM) after ECCs. Methods: Twelve men (years, 19.8 ± 1.7 years; height, 172.4 ± 7.0 cm; weight, 64.0 ± 8.6 kg) performed maximal 100 ECCs on their FPBM of non‐dominant hands with torque dynamometer. The dominant hands were control (CON). Maximal voluntary contraction (MVC), range of motion (ROM), DOMS, and MCV were assessed before, immediately post, and 1, 2, and 5 days after ECCs. MCV was calculated as the distance by stimulation divided by the latencies of the waveforms generated. Values were statistically analyzed by two‐way ANOVA, and the significance level was set at P <.05. Results: Decreases in MVC immediately (−32.9%) to 5 days after ECCs were significantly greater (P <.05) than for the CON group. ROM showed a significant decrease immediately (−21.6%) after ECCs compared with before ECCs and CON group (P <.05). DOMS after ECCs increased at 1 and 2 days (5.0 cm) after ECCs compared with before ECCs and CON (P <.05). Also, MCV after ECCs delayed significantly from immediately (−36.4%), 1, 2, and 5 days after ECCs compared with CON (P <.05), while no significant change in M‐wave amplitude was observed over time for both ECCs and CON. Conclusion: The present study showed that ECCs of the FPBM cause a significant delay in MCV of median nerve. [ABSTRACT FROM AUTHOR]

Abstract: Dietary apple polyphenols (AP) have been shown to exhibit beneficial effects on muscle endurance. Fast‐to‐slow change in the composition of myosin heavy chains was known as one of the molecular mechanisms. Here, we examined the effects of dietary AP on the capillaries and mitochondria in the rat skeletal muscle to elucidate the mechanisms underlying muscular endurance enhancement. Twenty‐four Wistar male rats were divided into three groups, namely, the control group, 0.5% AP group, and 5% AP group (n = 8 in each group). After a feeding period of 4 weeks, rats were dissected, gastrocnemius muscles were removed, and the density of capillaries and levels of mitochondrial proteins were analyzed. Capillary density of the gastrocnemius increased to 17.8% in rats fed with 5% AP as compared to the control rats. No significant change was observed in the mitochondrial content and dynamics (fusion/fission) of regulatory proteins. To investigate the mechanisms underlying the increase in the capillary density, positive (vascular endothelial cell growth factor, VEGF) and negative (thrombosponsin‐1, TSP‐1) factors of angiogenesis were analyzed. TSP‐1 expression significantly decreased in rats fed with 0.5% AP and 5% AP by approximately 25% and 40%, respectively, as compared with the control rats. There were no significant differences in VEGF expression. Thus, dietary AP may increase the muscle capillary density by decreasing TSP‐1 expression. We concluded that the increase in the capillary density and the fast‐to‐slow change in myosin heavy chains by AP feeding are the main causes for muscle endurance enhancement in Wistar rats. [ABSTRACT FROM AUTHOR]

High-intensity exercise has recently been shown to cause an increase in brain-derived neurotropic factor (BDNF) in the hippocampus. Some studies have suggested that myokines secreted from contracting skeletal muscle, such as irisin (one of the truncated form of fibronectin type III domain-containing protein 5 (FNDC5)), play important roles in this process. Thus, we hypothesized that locally evoked muscle contractions may cause an increase of BDNF in the hippocampus through some afferent mechanisms. Under anesthesia, Sprague-Dawley rats were fixed on a custom-made dynamometer and their triceps surae muscles were made to maximally contract via delivery of electric stimulations of the sciatic nerve (100 Hz with 1-ms pulse and 3-s duration). Following 50 repeated maximal isometric contractions, the protein expressions of BDNF and activation of its receptor in the hippocampus significantly increased compared with the sham-operated control rats. However, the expression of both BDNF and FNDC5 within stimulated muscles did not significantly increase, nor did their serum concentrations change. These results indicate that local muscular contractions under unconsciousness can induce BDNF expression in the hippocampus. This effect may be mediated by peripheral reception of muscle contraction, but not by systemic factors. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Purpose: Eccentric contractions (ECCs) induce muscle damage that is indicated by prolonged loss of muscle function and delayed onset muscle soreness. It is possible that ECCs affect motor nerves, and this may contribute to the prolonged decreases in force generating capability. The present study investigated the hypothesis that M-wave latency of biceps brachii would be increased after maximal elbow flexor ECCs resulting in prolonged loss of muscle strength.Methods: Fifteen women performed exercise consisting of 60 maximal ECCs of the elbow flexors using their non-dominant arm. M-wave latency was assessed by the time taken from electrical stimulation applied to the Erb's point to the onset of M-wave of the biceps brachii before, immediately after, and 1-4 days after exercise. Maximal voluntary isometric contraction (MVC) torque, range of motion (ROM) and muscle soreness using a numerical rating scale were also assessed before and after exercise.Results: Prolonged decreases in MVC torque (1-4 days post-exercise: -54 to -15 %) and ROM (1-2 days: -32 to -22 %), and increased muscle soreness (peak: 4.2 out of 10) were evident after exercise (p < 0.05). The M-wave latency increased (p < 0.01) from 5.8 ± 1.0 ms before exercise to 6.5 ± 1.7 ms at 1 day and 7.2 ± 1.5 ms at 2 days after exercise for the exercised arm only. No significant changes in M-wave amplitude were evident after exercise.Conclusion: The increased M-wave latency did not fully explain the prolonged decreases in MVC torque after eccentric exercise, but may indicate reversible motor nerve impairment. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? Does an acute bout of exercise alter vitamin D receptor expression in rat skeletal muscle?, What is the main finding and its importance? Resistance exercise but not endurance exercise increased intramuscular vitamin D receptor expression. Thus, resistance exercise may be an effective way to increase muscle vitamin D receptor expression., Vitamin D and vitamin D receptor (VDR) are involved in the maintenance of skeletal muscle mass and function. Although resistance exercise is well known to enhance muscle growth and improve muscle function, the effect of resistance exercise on VDR has been unclear. We investigated intramuscular VDR expression in response to an acute bout of resistance exercise or endurance exercise. Male adult Sprague-Dawley rats were subjected to either resistance exercise (isometrically exercised via percutaneous electrical stimulation for five sets of ten 3 s contractions, with a 7 s interval between contractions and 3 min rest intervals between sets) or endurance exercise (treadmill at 25 m min−1 for 60 min). Rats were killed immediately or 1, 3, 6 or 24 h after completion of the resistance or endurance exercise, and gastrocnemius muscles were removed. Non-exercised control animals were killed in a basal state (control group). Intramuscular VDR expression was significantly higher immediately after resistance exercise and elevated for 3 h after exercise compared with the control group ( P < 0.05), and the resistance exercise significantly increased phosphorylated ERK1/2 and Mnk1 expression ( P < 0.05), which may be associated with VDR expression, immediately after exercise. Additionally, intramuscular expression of cytochrome P450 27B1, an enzyme related to vitamin D metabolism, was significantly higher at 1 and 3 h after exercise ( P < 0.05) compared with the control group. In contrast, endurance exercise had no effect on any of the measured proteins. Our results indicate that resistance exercise may be an efficient way to increase intramuscular VDR and related enzyme expression. [ABSTRACT FROM AUTHOR]

We previously reported that low-intensity [50% of one repetition maximum (1RM)] resistance training with slow movement and tonic force generation (LST) causes muscle hypertrophy and strength gain in older participants. The aim of this study was to determine whether resistance training with slow movement and much more reduced intensity (30%1RM) increases muscle size and strength in older adults. Eighteen participants (60-77 years) were randomly assigned to two groups. One group performed very low-intensity (30% 1RM) knee extension exercise with continuous muscle contraction (LST: 3-s eccentric, 3-s concentric, and 1-s isometric actions with no rest between each repetition) twice a week for 12 weeks. The other group underwent intermitted muscle contraction (CON: 1-s concentric and 1-s eccentric actions with 1-s rest between each repetition) for the same time period. The 1RM, isometric and isokinetic strengths, and cross-sectional image of the mid-thigh obtained by magnetic resonance imaging were examined before and after the intervention. LST significantly increased the cross-sectional area of the quadriceps muscle (5·0%, P<0·001) and isometric and isokinetic knee extension strengths (P<0·05). CON failed to increase muscle size (1·1%, P = 0·12), but significantly improved its strength (P<0·05). These results indicate that even if the intensity is as low as 30% 1RM, LST can increase muscle size and strength in healthy older adults. The large total contraction time may be related to muscle hypertrophy and strength gain. LST would be useful for preventing sarcopenia in older individuals. [ABSTRACT FROM AUTHOR]

Introduction We examined the effects of gastrocnemius eccentric contractions (ECs) on the sciatic nerve in rats. Methods: Rats were divided randomly into the following 3 groups: control, 180EC (ECs with 180°/s angular velocity), and 30EC (ECs with 30°/s angular velocity). Twenty ECs were induced by electrical stimulation of the gastrocnemius. On days 3, 7, and 10 after the ECs, nerve conduction velocity (NCV) was measured, and sciatic nerve branches were harvested for analysis. Results: A significant decrease in NCV was observed between the control and day-7 180EC. Significant reduction in the levels of myelin sheath protein zero (p0) between day 7 and day 3 180EC and a significant increase of macrophage-related protein and tyrosine kinase receptor C were observed between day 7 180EC and day 7 30EC. Conclusions: ECs with fast angular velocities induce functional and structural damage in innervating nerve. Muscle Nerve 50: 87-94, 2014 [ABSTRACT FROM AUTHOR]

R40 --> 889.1 --> Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme of redox homeostasis and ethanol metabolism. Our recent work has indicated an important role for ALDH2 in regulating muscle homeostasis as well. However, the underlying mechanism and adaptability of ALDH2 in skeletal muscle remain highly elusive. We herein examined whether ALDH2 deficiency modifies mechanical overload‐induced muscle hypertrophy and related cellular process. Ten‐week‐old male ALDH2 knockout (background strain: C57BL/6J) and wild‐type littermates were involved in this work. Unilateral synergist ablation (SA; the surgical removal of gastrocnemius and soleus muscles) and sham surgery were performed as an experimental hypertrophy model. Seven days after surgery, plantaris muscles were collected. ALDH2 deficiency augmented SA‐induced activation of mTORC1 (a key regulator of muscle anabolism), based on the increase in phosphorylation of p70S6K at Thr389. Concomitantly, higher amounts of puromycin‐labeled peptides (a marker of protein synthesis rate) were observed in ALDH2 deficit muscle. These observations suggest that ALDH2 deficiency promotes SA‐induced muscle hypertrophy. Unexpectedly, there was no statistical difference in SA‐induced muscle hypertrophy between genotypes. To explore potential mechanisms underlying mismatch between protein synthesis signal and muscle size, we conducted RNA‐seq experiment. However, we couldn't detect any notable gene potentially affecting muscle mass between genotypes. In conclusion, ALDH2 deficiency enhances mechanical overload‐induced mTORC1 activity and protein synthesis but not muscle mass. Pathways other than protein synthesis and/or post‐transcriptional events may dominantly affect muscle mass in ALDH2 deficit mice. [ABSTRACT FROM AUTHOR]

R2683 --> 605.10 --> Neutral sphingomyelinase activation associated factor (Nsmaf) modulate ceramide production by activating neutral sphingomyelinase enzymes. Nsmaf also regulates tumor necrosis factor‐α (TNF‐α)‐induced signaling pathway. Since both ceramide metabolisms and TNF‐α signaling are key events during inflammation, Nsmaf might play a nodal role in inflammation‐induced events, such as muscle wasting. In the present study, we examined whether Nsmaf gene knock‐down effects on myogenesis in murine C2C12 myoblasts. C2C12 myoblasts were used in this study. In the growth phase, cells were maintained in DMEM and 10% FBS (growth medium: GM). For cell differentiation, the culture medium was switched to DMEM containing 1% HS (differentiation medium: DM). Small interfering RNA (siRNA) was used to induce Nsmaf gene Knock‐down (NsmafKD, n = 6). siRNA with a scrambled sequence was used as negative controls (Scr, n = 6). Gene knockdown was performed both in myoblasts and myotubes. After two‐day siRNA treatment, Western blotting was performed to examine protein expression levels. Laser scanning microscopy was used to investigate cell morphology. Even in the GM condition, differentiation markers, such as myogenin and myosin heavy chain (slow) were upregulated in the NsmafKD cells. In transfected myotubes, myotube diameter of the NsmafKD was about 50% smaller than that of the Scr. Both in myoblasts and myotubes, contents of a cell fusion mediator, myomixer, in the NsmafKD was significantly lower than that in the Scr. These data indicate that Nsmaf is a novel regulator of myogenesis. [ABSTRACT FROM AUTHOR]

The article highlights the study on whether muscle hypertrophy which promote effects are cross-transferred in resistance training with blood flow restriction which has been shown to evoke strong endocrine activation. According to the author, 15 untrained men are randomly assigned into the occlusive training group and the normal training group wherein they are to perform the same unilateral arm exercise at 50% of one-repetition maximum without occlusion. He emphasized that the result shows that when combined with resistance exercise with blood flow restriction for other muscle groups, the low-intensity resistance training increases muscular size and strength.

We and others have shown that apple polyphenols decrease adipose tissue mass. To better understand the underlying mechanisms and to expand clinical applicability, we herein examine whether apple polyphenols induce adipose thermogenic adaptations (browning) and prevent diet-induced obesity and related insulin resistance. In mice fed a standard diet, daily apple polyphenol consumption induced thermogenic adaptations in inguinal white adipose tissue (iWAT), based on increases in the expression of brown/beige adipocyte selective genes (Ucp1, Cidea, Tbx1, Cd137) and protein content of uncoupling protein 1 and mitochondrial oxidative phosphorylation enzymes. Among the upstream regulatory factors of browning, fibroblast growth factor 21 (FGF21) and peroxisome proliferator-activated receptor gamma coactivator 1 α (PGC-1α) levels were concomitantly up-regulated by apple polyphenols. In the primary cell culture experiment, the results did not support a direct action of apple polyphenols on beige adipogenesis. Instead, apple polyphenols increased tyrosine hydroxylase (a rate-limiting enzyme of catecholamine synthesis) in iWAT, which activates the adipocyte thermogenic program possibly via intratissue cellular communications. In high-fat fed mice, apple polyphenols induced beige adipocyte development in iWAT, reduced fat accumulation, and increased glucose disposal rates in the glucose and insulin tolerance tests. Taken together, dietary administration of apple polyphenols induced beige adipocyte development in iWAT possibly via activation/induction of the peripheral catecholamine synthesis-FGF21-PGC-1α cascade. Results from diet-induced obese mice indicate that apple polyphenols have therapeutic potential for obesity and related metabolic disorders. [ABSTRACT FROM AUTHOR]

The relationship between mechanistic target of rapamycin complex 1 (mTORC1) activation after resistance exercise and acetylcholine receptor (AChR) subunit gene expression remains largely unknown. Therefore, we aimed to investigate the effect of electrical stimulation-induced intense muscle contraction, which mimics acute resistance exercise, on the mRNA expression of AChR genes and the signalling pathways involved in neuromuscular junction (NMJ) maintenance, such as mTORC1 and muscle-specific kinase (MuSK). The gastrocnemius muscle of male adult Sprague-Dawley rats was isometrically exercised. Upon completion of muscle contraction, the rats were euthanized in the early (after 0, 1, 3, 6 or 24 h) and late (after 48 or 72 h) recovery phases and the gastrocnemius muscles were removed. Non-exercised control animals were euthanized in the basal state (control group). In the early recovery phase, Agrn gene expression increased whereas LRP4 decreased without any change in the protein and gene expression of AChR gene subunits. In the late recovery phase, Agrn, Musk, Chrnb1, Chrnd and Chrne gene expression were altered and agrin and MuSK protein expression increased. Moreover, mTORC1 and protein kinase B/Akt-histone deacetylase 4 (HDAC) were activated in the early phase but not in the late recovery phase. Furthermore, rapamycin, an inhibitor of mTORC1, did not disturb changes in AChR subunit gene expression after muscle contraction. However, rapamycin addition slightly increased AChR gene expression, while insulin did not impact it in rat L6 myotube. These results suggest that changes in the AChR subunits after muscle contraction are independent of the rapamycin-sensitive mTORC1 pathway., (© 2024 The Author(s). Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.)

Both ageing and exercise training affect the neuromuscular junction (NMJ) structure. Morphological alterations in the NMJ have been considered to influence neuromuscular transmission and myofibre properties, but the direct link between the morphology and function has yet to be established. We measured the neuromuscular transmission, myofibre composition and NMJ structure of 5-month-old (young) and 24-month-old untrained (aged control) and trained (aged trained) mice. Aged trained mice were subjected to 2 months of endurance training before the measurement. Neuromuscular transmission was evaluated in vivo as the ratio of ankle plantar flexion torque evoked by the sciatic nerve stimulation to that by direct muscle stimulation. The torque ratio was significantly lower in aged mice than in young and aged trained mice at high-frequency stimulations, showing a significant positive correlation with voluntary grip strength. The degree of pre- to post-synaptic overlap of the NMJ was also significantly lower in aged mice and positively correlated with the torque ratio. We also found that the proportion of fast-twitch fibres in the soleus muscle decreased with age, and that age-related denervation occurred preferentially in fast-twitch fibres. Age-related denervation and a shift in myofibre composition were partially prevented by endurance training. These results suggest that age-related deterioration of the NMJ structure impairs neuromuscular transmission and alters myofibre composition, but these alterations can be prevented by structural amelioration of NMJ with endurance training. Our findings highlight the importance of the NMJ as a major determinant of age-related deterioration of skeletal muscles and the clinical significance of endurance training as a countermeasure. KEY POINTS: The neuromuscular junction (NMJ) plays an essential role in neuromuscular transmission and the maintenance of myofibre properties. We show that neuromuscular transmission is impaired with ageing but recovered by endurance training, which contributes to alterations in voluntary strength. Neuromuscular transmission is associated with the degree of pre- to post-synaptic overlap of the NMJ. Age-related denervation of fast-twitch fibres and a shift in myofibre composition toward a slower phenotype are partially prevented by endurance training. Our study provides substantial evidence that age-related and exercise-induced alterations in neuromuscular transmission and myofibre properties are associated with morphological changes in the NMJ., (© 2024 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

Pulsed electromagnetic field (PEMF) therapy, a noninvasive treatment, has shown promise in mitigating nerve damage. However, unaccustomed exercises, such as eccentric contractions (ECCs), can damage both muscle and nerve tissue. This study investigated whether magnetic stimulation (MS) with PEMF could aid in nerve recovery after ECCs in the elbow flexors. Twenty participants were randomly assigned to either a control (CNT) or an MS group. Following ECCs, we measured the latency of the M-wave in the musculocutaneous nerve as an indicator of nerve function. Additionally, isometric torque, range of motion, and muscle pain were assessed for muscle function. Interestingly, only the CNT group exhibited a significant increase in latency on Day 2 (p < 0.05). The MS group, on the other hand, displayed an earlier recovery trend in isometric torque, range of motion, and muscle soreness. Notably, muscle soreness significantly decreased immediately after MS treatment compared to pretreatment levels. These findings suggest that MS treatment can effectively attenuate nerve damage induced by ECCs exercise., (© 2024 Bioelectromagnetics Society.)

Background/objectives: Monocarboxylate transporters (MCTs) comprise 14 known isoforms, with MCT1 being particularly important for lactate transport. Variations in lactate metabolism capacity and aerobic performance are associated with the T1470A polymorphism in MCT1 . We aimed to investigate the frequency of the T1470A polymorphism and compare relevant physiological parameters among long-distance runners, wherein these parameters are fundamental to athletic performance., Methods: We included 158 Japanese long-distance runners (LD) and 649 individuals from the general Japanese population (CON). The frequency of the T1470A polymorphism was compared between these groups and across athletic levels using the chi-square test. Additionally, physiological data were collected from 57 long-distance runners, and respiratory gas measurements were obtained using the mixing-chamber method during a graded incremental exercise test., Results: We observed a significant difference between the LD and CON groups in the dominant model and between the sub-28 min group and 28 min or above group in the recessive model. As the competitive level increased, the frequency of the AA genotype also increased. When comparing physiological parameters between the AA genotype and T allele, subjects with the AA genotype showed significantly higher values for oxygen uptake at lactate threshold ( p = 0.001), oxygen uptake at onset of blood lactate accumulation ( p = 0.01), maximal oxygen uptake ( p = 0.005), and maximal blood lactate concentration ( p = 0.038)., Conclusions: These results suggest that the AA genotype of the T1470A polymorphism of MCT1 is an effective genotype associated with athletic status and aerobic capacity in Japanese long-distance runners.

Ribosome biogenesis is an important regulator of skeletal muscle hypertrophy induced by repeated bouts of resistance exercise (RE). Hot-water immersion (HWI), a widely used post-exercise recovery strategy, activates the mechanistic target of rapamycin (mTOR) signaling, a key regulator of ribosome biogenesis in skeletal muscle. However, the effect of HWI on skeletal muscle ribosome biogenesis is not well understood. Here, we aimed to investigate the effects of HWI and post-exercise HWI on ribosome biogenesis using a rat RE model. Male Sprague-Dawley rats were randomly assigned to HWI and non-HWI groups. In both groups, the right leg was isometrically exercised using transcutaneous electrical stimulation, while the left leg was used as an internal non-RE control. Following RE, both limbs were immersed in hot water (41.2 ± 0.03°C) for 20 min under isoflurane anesthesia in the HWI group and the gastrocnemius muscles were sampled at 3- and 24-h post-exercise. HWI significantly increased mTOR signaling and c-Myc mRNA expression, whereas post-exercise HWI significantly increased transcription initiation factor-IA mRNA expression. However, neither HWI nor post-exercise HWI enhanced 45S pre-rRNA expression, ribosomal RNA, or ribosomal protein content. In addition, HWI tended to decrease 28S rRNA and 18S rRNA content, widely used markers of ribosome content. These results suggest that HWI as a post-exercise recovery is not effective in activating ribosome biogenesis. NEW & NOTEWORTHY Ribosome biogenesis is crucial in resistance exercise (RE)-induced skeletal muscle hypertrophy. This study examined the effects of hot-water immersion (HWI) on ribosome biogenesis after RE. HWI and post-exercise HWI increased c- Myc and transcription initiation factor-IA mRNA but did not alter ribosomal RNA transcription or ribosomal protein content. HWI tended to decrease 28S and 18S ribosomal RNA. These findings suggest that HWI, as a recovery strategy, does not effectively promote ribosome biogenesis or muscle protein synthesis.

Objective: This study explored the interaction among ACTN3 R577X polymorphism, muscle damage, and post-exercise inflammatory response by assessing changes over time in serum creatine kinase and interleukin-6 levels., Design: Ninety-five active Japanese participants (50 men and 45 women: 22.2 ± 2.3 years) who did not perform daily upper limb strength exercises were enrolled. Participants executed five sets of six maximal eccentric elbow flexion exercises. The exercise duration was 9 min, including rest between sets (90 s). Maximum voluntary isometric contraction, range of motion, muscle soreness, and serum creatine kinase and interleukin-6 levels were assessed pre and post and 1, 2, 3, and 5 d after exercise. Genotype groups were classified as RR + RX and XX based on the absence of ACTN3 expression., Results: A significant time and group interaction (p = 0.045) on creatine kinase levels was observed between the groups, indicating that the absence of ACTN3 significantly affects creatine kinase changes. Conversely, no significant interaction on change in interleukin-6, maximum voluntary isometric contraction, range of motion, and muscle soreness was observed between groups., Conclusion: The results highlight an interaction on creatine kinase activity post-exercise by ACTN3 R577X polymorphism, with elevated activity in the XX genotype., Competing Interests: The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Post-exercise muscle soreness and fatigue can negatively affect exercise performance. Thus, it is desirable to attenuate muscle soreness and fatigue and promote recovery even for daily exercise habits aimed at maintaining or improving health., Methods: This study investigated the effects of dietary collagen peptides (CPs) on post-exercise physical condition and fitness in healthy middle-aged adults unfamiliar with exercise. Middle-aged males ( n  = 20, 52.6 ± 5.8 years) received the active food (10 g of CPs per day) or the placebo food for 33 days in each period of the randomized crossover trial (registered at the University Hospital Medical Information Network Clinical Trials Registry with UMIN-CTR ID of UMIN000041441). On the 29th day, participants performed a maximum of five sets of 40 bodyweight squats. Muscle soreness as the primary outcome, fatigue, the maximum knee extension force during isometric muscle contraction of both legs, the range of motion (ROM), and the blood level of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were assessed before and after the exercise load., Results: The analysis set was the per-protocol set ( n  = 18, 52.6 ± 6.0 years) for efficacy and the full analysis set ( n  = 19, 52.8 ± 5.9 years) for safety. The visual analog scale (VAS) of muscle soreness immediately after the exercise load was significantly lower in the active group than in the placebo group (32.0 ± 25.0 mm versus 45.8 ± 27.6 mm, p  < 0.001). The VAS of fatigue immediately after the exercise load was also significantly lower in the active group than in the placebo group (47.3 ± 25.0 mm versus 59.0 ± 22.3 mm, p  < 0.001). Two days (48 hours) afterthe exercise load, muscle strength was significantly higher in the active group than in the placebo group (85.2 ± 27.8 kg versus 80.5 ± 25.3 kg, p  = 0.035). The level of CPK did not change over time. The level of LDH increased slightly but was not different between the groups. No safety-related issues were observed., Conclusions: These results showed that dietary CPs alleviated muscle soreness and fatigue and affected muscle strength after exercise load in healthy middle-aged males.