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OBJECTIVE--Whereas single assessments of cardiorespiratory fitness have been shown to predict lower incidence of type 2 diabetes, there are no data on long-term trends in fitness and risk. We investigated [...]

Nakagata, T, Yamada, Y, and Naito, H. Estimating energy cost of body weight resistance exercise using a multistage exercise test. J Strength Cond Res36(5): 1290–1296, 2022—The purpose of this study was to examine energy cost of body weight resistance exercises with slow movement in young men using a multistage exercise test. Fifteen men aged 21–29 years performed 3 exercises (heel-raise, squat, and push-up) at different frequencies (1, 2, 3, 4, 5, and 6 repetitions·min−1). Oxygen consumption was measured using indirect calorimetry; we then computed a simple linear regression between aerobic energy expenditure (EE) and repetition frequency. The slope coefficient in the regression represents the energy cost of those exercises; we compared the extrapolated EE for a frequency of 10 repetitions·min−1. Gross EE increased linearly with repetition frequency in all subjects (y= ax+ b). Energy cost was significantly greater in the case of the push-up than in the case of the squat {squat: 0.50 ± 0.14 (95% confidence interval [CI], 0.42–0.58); push-up: 0.77 ± 0.20 kcal (95% CI, 0.66–0.88); and the heel-raise elicited the lowest energy cost: 0.13 ± 0.04 kcal (95% CI, 0.11–0.15)}. Extrapolated EE at 10 repetitions·min−1was 2.7 ± 0.5 kcal (2.3 metabolic equivalents [METs]), 6.3 ± 1.4 kcal (5.4 METs), and 9.2 ± 2.1 kcal (7.8 METs), respectively, according to the regression based on aerobic EE. These results will be useful for health professionals in prescribing resistance exercise programs improving muscle fitness and considering for weight management.

This article examines the effects of endurance exercise training on concentrations of heat shock proteins in the striated muscle of aging rats. Findings indicate that endurance training results in similar increases in heat shock protein levels in young and old rats.

•Blood flow restriction at resting periods of high-intensity load exercise increases Pax7 expression.•miR-206 levels significantly decreased in the blood flow restriction leg compared to the control.•Blood flow restriction can cause DNA damage, judging from the increase in messenger RNA levels of Ku70.

Crystal structure design is important for the discovery of new highly functional materials because the crystal structure strongly influences material properties. Crystal structures are composed of space-filling polyhedra, which affect material properties such as ionic conductivity and the dielectric constant. However, most conventional methods of crystal structure prediction use random structure generation methods that do not take space-filling polyhedra into account, contributing to the inefficiency of materials development. In this work, we propose a crystal structure generation method based on discrete geometric analysis of polyhedra information. In our method, the shape and connectivity of a space-filling polyhedron are represented as a dual periodic graph, and the crystal structure is generated by the standard realization of this graph. We demonstrate that this method can correctly generate face-centered cubic, hexagonal close-packed, and body-centered cubic structures from dual periodic graphs. This work is a first step toward generating undiscovered crystal structures based on the target polyhedra, leading to major advances in materials design in areas such as electronics and energy storage.

Psoriasis is a chronic inflammatory skin disease characterized mainly by epidermal hyperplasia, scaling, and erythema; T helper 17 cells have a role in its pathogenesis. Although IL-26, known as a T helper 17 cytokine, is upregulated in psoriatic skin lesions, its precise role is unclear. We investigated the role of IL-26 in the imiquimod-induced psoriasis-like murine model using human IL-26transgenic mice. Erythema symptoms induced by daily applications of imiquimod increased dramatically in human IL-26transgenic mice compared with controls. Vascularization and immune cell infiltration were prominent in skin lesions of human IL-26transgenic mice. Levels of fibroblast growth factor (FGF) 1, FGF2, and FGF7 were significantly upregulated in the skin lesions of imiquimod-treated human IL-26transgenic mice and psoriasis patients. In vitro analysis demonstrated that FGF1, FGF2, and FGF7 levels were elevated in human keratinocytes and vascular endothelial cells following IL-26 stimulation. Furthermore, IL-26 acted directly on vascular endothelial cells, promoting proliferation and tube formation, possibly through protein kinase B, extracellular signal–regulated kinase, and NF-κB pathways. Moreover, similar effects of IL-26 were observed in the murine contact hypersensitivity model, indicating that these effects are not restricted to psoriasis. Altogether, our data indicate that IL-26 may be a promising therapeutic target in T cell–mediated skin inflammation, including psoriasis.

We tested the hypothesis that there are sex differences in hindlimb unloading-induced activation of the forkhead box subfamily O3a (FoxO3a) signaling pathway in rat soleus muscle. Age-matched male and female Wistar rats were subjected to hindlimb unloading, and the soleus muscle was removed before or 1 or 7 days after unloading. Female rats showed greater percent changes in relative soleus muscle weight than males. FoxO3a phosphorylation was lower in females than in males and was associated with higher levels of protein ubiquitination 7 days after unloading. Heat shock protein 72 (Hsp72) levels were lower in female rats and increased in males during unloading. Female rats showed slightly higher myostatin levels, which showed a non-significant decline in male rats following unloading. Thus, males and females show different responses to the FoxO3a/ubiquitin–proteasome pathway following hindlimb unloading in rat soleus muscle, which may be associated with differences in Hsp72 expression and myostatin signaling.

We examined the effect of a combination of astaxanthin (AX) supplementation, repeated heat stress, and intermittent reloading (IR) on satellite cells in unloaded rat soleus muscles. Forty-nine male Wistar rats (8-week-old) were divided into control, hind-limb unweighting (HU), IR during HU, IR with AX supplementation, IR with repeated heat stress (41.0–41.5 °C for 30 min), and IR with AX supplementation and repeated heat stress groups. After the experimental period, the antigravitational soleus muscle was analyzed using an immunohistochemical technique. Our results revealed that the combination of dietary AX supplementation and heat stress resulted in protection against disuse muscle atrophy in the soleus muscle. This protective effect may be partially due to a higher satellite cell number in the atrophied soleus muscle in the IR/AX/heat stress group compared with the numbers found in the other groups. We concluded that the combination treatment with dietary AX supplementation and repeated heat stress attenuates soleus muscle atrophy, in part by increasing the number of satellite cells.

Heat shock proteins (Hsps) have a critical role in maintaining cellular homeostasis and in protecting cells from a range of acute and chronic stressful conditions. Treadmill running exercise results in increased Hsp72 and Hsp25 levels in various tissues and heat production during exercise has been shown to be the main factor for the increased levels of Hsp72 in myocardium. Since the adrenal gland plays a vital role in general response to stress, regulation of Hsps in adrenal glands following stressful events seems to be critical for controlling the whole-body stress response appropriately. This study tested the hypothesis of whether elevation of temperature is solely responsible for exercise-induced adrenal Hsp72 and Hsp25 expression. Female Sprague–Dawley rats (3 months old) were randomly assigned to either a sedentary control group or one of two treadmill-running groups: a cold exercise group run in a cold room at 4 °C (CE), and a warm exercise group run at 25 °C temperature (WE). Animals were run 60 min a day at 30 m min−1speed for 4 consecutive days following adaptation to treadmill exercise. Exercise resulted in a significant elevation of body temperature only in the WE group (p< 0.05). Adrenal Hsp72 and Hsp25 levels were significantly higher in the WE group compare to the other groups (p< 0.05). These data demonstrated that exercise-related elevations of body temperature could be the only factor for the inductions of adrenal Hsp72 and Hsp25 expression.

Emphysema is defined pathologically as destruction of alveolar walls and permanent enlargement of the airspaces. Detection of localised emphysema is difficult using conventional methods because the parameters evaluate macroscopic lung function. In this study, the pulmonary kinematics of control and emphysema model mice were evaluated to investigate whether pulmonary kinematic analysis is useful for diagnosing localised emphysema. Emphysema model mice were induced by porcine pancreatic elastase treatment, and 3D micro-CT images were obtained during stepwise inflation and deflation. The pulmonary vessels and pleura were segmented at each pressure, and pulmonary deformation and volumetric strain between consecutive different pressures were calculated by non-rigid deformable registration. In particular, during low lung pressure, craniocaudal deformation and volumetric strain were higher in the regions where the alveolar enlargement was observed in emphysema model mice. Furthermore, volumetric strain of emphysema model mice was larger at alveolar enlargement. On the other hand, there were no significant differences between control and emphysema model mice in conventional macroscopic lung pressures and volume relationships. The present results indicate that pulmonary kinematic analysis, examining craniocaudal deformation, and volumetric strain may become useful for the clinical assessment of localised emphysema.

Intracellular signaling exhibits circadian variation in the suprachiasmatic nucleus and liver. However, it is unclear whether circadian regulation also extends to intracellular signaling pathways in the cardiac and skeletal muscles. Here, we examined circadian variation in the intracellular mammalian target of rapamycin (mTOR)/70 kDa ribosomal protein S6 kinase 1 (p70S6K) and extracellular signal-regulated kinase (ERK) pathways, which regulate protein synthesis in rat cardiac and skeletal muscles. Seven-week-old male Wistar rats were assigned to six groups: Zeitgeber time (ZT) 2, ZT6, ZT10, ZT14, ZT18, and ZT22 (ZT0, lights on; ZT12, lights off). The cardiac, plantaris, and soleus muscles were removed after a 12-h fasting period, and signal transducers involved in protein synthesis (mTOR, p70S6K, and ERK) were analyzed by western blotting. Circadian rhythms of signal transducers were observed in both cardiac (mTOR, p70S6K, and ERK) and plantaris (p70S6K and ERK) muscles (p<0.05), but not in the soleus muscle. In the cardiac muscle, the phosphorylation rate of mTOR was significantly higher at ZT6 (peak) than at ZT18 (bottom), and the phosphorylation rate of p70S6K was significantly higher at ZT2 (peak) than at ZT18 (bottom). In contrast, in the plantaris muscle, the phosphorylation rate of ERK was significantly lower at ZT2 (bottom) than at ZT18 (peak). Our data suggested that protein synthesis via mTOR/p70S6K and ERK signaling molecules exhibits circadian variation in rat cardiac and fast-type plantaris muscles.

Extended periods of skeletal muscle disuse results in muscle atrophy and weakness. Currently, no therapeutic treatment is available for the prevention of this problem. Nonetheless, growing evidence suggests that prevention of disuse-induced oxidative stress in inactive muscle fibers can delay inactivity-induced muscle wasting. Therefore, this study tested the hypothesis that dietary supplementation with the antioxidant astaxanthin would protect against disuse muscle atrophy, in part, by prevention of myonuclear apoptosis. Wistar rats (8 weeks old) were divided into control (CT, n= 9), hindlimb unloading (HU, n= 9), and hindlimb unloading with astaxanthin (HU + AX, n= 9) groups. Following 2 weeks of dietary supplementation, rats in the HU and HU + AX groups were exposed to unloading for 7 days. Seven-day unloading resulted in reduced soleus muscle weight and myofiber cross-sectional area (CSA) by ~30 and ~47 %, respectively. Nonetheless, relative muscle weights and CSA of the soleus muscle in the HU + AX group were significantly greater than those of the HU group. Moreover, astaxanthin prevented disuse-induced increase in the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei. We conclude that astaxanthin supplementation prior to and during hindlimb unloading attenuates soleus muscle atrophy, in part, by suppressing myonuclear apoptosis.

We investigated the protective effect of losartan, an angiotensin II type 1 receptor blocker, on soleus muscle atrophy. Age-matched male and female Wistar rats were subjected to hindlimb unloading, and the soleus muscle was removed on days 1 and 7 for analysis. Females showed greater reductions in relative weight and myofiber cross-sectional area of the soleus muscle than males on day 7 post-hindlimb unloading. Losartan partially protected females against muscle atrophy. Activation of the canonical TGF-β signaling pathway, assessed via Smad2/3 phosphorylation, was lower in females following losartan treatment and associated with lower levels of protein ubiquitination after 1 (myofibril) and 7 (cytosol) days of unloading. However, no effect was observed in non-canonical TGF-β signaling (p44/p42 and p38 MAPK phosphorylation) in males or females during unloading. Our results suggest that losartan provides partial protection against hindlimb unloading-induced soleus muscle atrophy in female rats, possibly associated with decreased canonical TGF-β signaling.

Chronic inflammation is considered as an etiology of obesity and type 2 diabetes. Brown adipose tissue (BAT) of obese animals shows increased inflammation. Regular exercise has anti-inflammatory effects; however, the effects of exercise training on BAT inflammation in obese animals remain unclear. Thus, this study aimed to investigate the effects of exercise training on inflammation-related signaling in the BAT of obese and diabetic rats. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an obese/diabetic rodent model, were randomly divided into either sedentary (n = 11) or exercise training (n = 8) groups. Long-Evans Tokushima Otsuka (LETO; n = 9) rats were used as the nondiabetic sedentary controls. Exercise training using a treadmill was conducted 4 days per week for 20 weeks, starting at 5 weeks old. As a result, exercise training attenuated the phosphorylation levels of p65 and mitogen-activated protein kinases in the BAT of OLETF rats, concurrently with the improvement of obesity and systemic glucose tolerance. Moreover, exercise training decreased oxidative stress and increased the antioxidant and anti-inflammatory protein levels in the BAT. Conversely, exercise training did not alter the expression levels of uncoupling protein-1 and oxidative phosphorylation-related proteins in the BAT, which were lower in the OLETF rats than the LETO rats. In conclusion, our data suggest that exercise training prevents the activation of inflammatory signaling in the BAT of obese/diabetic rats.

The effects of icing or heat stress on the regeneration of injured soleus muscle were investigated in male Wistar rats. Bupivacaine was injected into soleus muscles bilaterally to induce muscle injury. Icing (0 °C, 20 min) was carried out immediately after the injury. Heat stress (42 °C, 30 min) was applied every other day during 2–14 days after the bupivacaine injection. Injury-related increase in collagen deposition was promoted by icing. However, the level of collagen deposition in heat-stressed animals was maintained at control levels throughout the experimental period and was significantly lower than that in icing-treated animals at 15 and 28 days after bupivacaine injection. Furthermore, the recovery of muscle mass, protein content, and muscle fiber size of injured soleus toward control levels was partially facilitated by heat stress. These results suggest that, compared with icing, heat stress may be a beneficial treatment for successful muscle regeneration at least by reducing fibrosis.

The study described herein aimed to examine changes in HDAC4 and its downstream targets in immobilization-induced rat skeletal muscle atrophy. Eleven male Wistar rats were used, and one hindlimb was immobilized in the plantar flexion position using a plaster cast. The contralateral, non-immobilized leg served as an internal control. After 10 days, the gastrocnemius muscles were removed from both hindlimbs. Ten days of immobilization resulted in a significant reduction (−27.3 %) in gastrocnemius muscle weight. A significant decrease in AMPK phosphorylation was also observed in nuclear fractions from immobilized legs relative to the controls. HDAC4 expression was significantly increased in immobilized legs in both the cytoplasmic and nuclear fractions. Moreover, Myogenin and MyoD mRNA levels were upregulated in immobilized legs, resulting in increased Atrogin-1 mRNA expression. Our data suggest that nuclear HDAC4 accumulation is partly related to immobilization-induced muscle atrophy.

Aims/Introduction: Accumulation of intramyocellular lipid (IMCL) is associated with insulin resistance. However, the factors affecting the change in IMCL remain to be elucidated. The aim of the present study was to determine the factors that influence the change in IMCL level after high‐fat loading.

This study investigated the effect of heat stress (HS) on mammalian target of rapamycin (mTOR) signaling involved in translation initiation after resistance exercise in human skeletal muscle. Eight young male subjects performed four sets of six maximal repetitions of knee extension exercises, with or without HS, in a randomized crossover design. HS was applied to the belly of the vastus lateralis by using a microwave therapy unit prior to and during exercise. Muscle biopsies were taken from the vastus lateralis before, immediately after, and 1 h after exercise. HS significantly increased the phosphorylation of Akt/PKB, mTOR, and ribosomal protein S6 at 1 h after exercise (P< 0.05), and the 4E-BP1 phosphorylation level, which had initially decreased with exercise, had recovered by 1 h after exercise with HS. In addition, the phosphorylation of ribosomal S6 kinase 1 was significantly increased immediately after exercise with HS (P< 0.05). These results indicate that HS enhances mTOR signaling after resistance exercise in human skeletal muscle.

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control,2) 3 consecutive days of treadmill exercise [60 min/day at 60–70% maximal O2uptake (V˙o2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60–70%V˙o2 max), and 4) whole body heat stress (15 min at 42°C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P< 0.05) left ventricular developed pressure (LVDP), maximum rate of left venticular pressure development (+dP/dt), and maximum rate of left ventricular pressure decline (−dP/dt) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt, and −dP/dtat any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase (P< 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased (P< 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3–5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.

NAITO, H., S. K. POWERS, H. A. DEMIREL, and J. AOKI. Exercise training increases heat shock protein in skeletal muscles of old rats. Med. Sci. Sports Exerc., Vol. 33, No. 5, 2001, pp. 729–734. PurposeThe effects of chronic exercise training on the expression of heat shock protein (HSP) in skeletal muscle of senescent animals are unknown. Therefore, the purpose of this study was to investigate the effects of chronic exercise training on skeletal muscle HSP expression in both young and old rats.

This study tested the hypothesis that elevation of heat stress proteins by whole body hyperthermia is associated with a decrease in skeletal muscle atrophy induced by reduced contractile activity (i.e., hindlimb unweighting). Female adult rats (6 mo old) were assigned to one of four experimental groups (n= 10/group): 1) sedentary control (Con), 2) heat stress (Heat), 3) hindlimb unweighting (HLU), or 4) heat stress before hindlimb unweighting (Heat+HLU). Animals in the Heat and Heat+HLU groups were exposed to 60 min of hyperthermia (colonic temperature ∼41.6°C). Six hours after heat stress, both the HLU and Heat+HLU groups were subjected to hindlimb unweighting for 8 days. After hindlimb unweighting, the animals were anesthetized, and the soleus muscles were removed, weighed, and analyzed for protein content and the relative levels of heat shock protein 72 (HSP72). Compared with control and HLU animals, the relative content of HSP72 in the soleus muscle was significantly elevated (P< 0.05) in both the Heat and Heat+HLU animals. Although hindlimb unweighting resulted in muscle atrophy in both the HLU and Heat+HLU animals, the loss of muscle weight and protein content was significantly less (P< 0.05) in the Heat+HLU animals. These data demonstrate that heat stress before hindlimb unweighting can reduce the rate of disuse muscle atrophy. We postulate that HSP70 and/or other stress proteins play a role in the control of muscle atrophy induced by reduced contractile activity.

Endurance exercise training promotes a small but significant increase in antioxidant enzyme activity in the costal diaphragm (DIA) of rodents. It is unclear if these training-induced improvements in muscle antioxidant capacity are large enough to reduce oxidative stress during prolonged contractile activity. To test the hypothesis that training-related increases in DIA antioxidant capacity reduces contraction-induced lipid peroxidation, we exercise trained adult female Sprague-Dawley ( n?=?7) rats on a motor-driven treadmill for 12?weeks at ˜ 75% maximal O 2 consumption (90?min/day). Control animals ( n?=?8) remained sedentary during the same 12-week period. After training, DIA strips from animals in both experimental groups were excised and subjected to an in vitro fatigue contractile protocol in which the muscle was stimulated for 60?min at a frequency of 30?Hz, every 2?s, with a train duration of 330?m. Compared to the controls, endurance training resulted in an increase ( P?

This study investigated the effects of exercise training duration on the myosin heavy chain (MHC) isoform distribution in rat locomotor muscles. Female Sprague-Dawley rats (120 days old) were assigned to either a sedentary control group or to one of three endurance exercise training groups. Trained animals ran on a treadmill at ∼75% maximal O2uptake for 10 wk (4–5 days/wk) at one of three different exercise durations (30, 60, or 90 min/day). Training resulted in increases (P< 0.05) in citrate synthase activity in the soleus and extensor digitorum longus in both the 60 and 90 min/day duration groups and in the plantaris (Pla) in all three exercise groups. All durations of training resulted in a reduction (P< 0.05) in the percentage of MHCIIband an increase (P< 0.05) in the percentage of MHCIIain the Pla. The magnitude of change in the percentage of MHCIIbin the Pla increased as a function of the training duration. In the extensor digitorum longus, 90 min of daily exercise promoted a decrease (P< 0.05) in percentage of MHCIIband increases (P< 0.05) in the percentages of MHCI, MHCIIa, and MHCIId/x. Finally, training durations ≥60 min resulted in an increase (P< 0.05) in the percentage of MHCIand a concomitant decrease (P< 0.05) in the percentage of MHCIIain the soleus. These results demonstrate that increasing the training duration elevates the magnitude of the fast-to-slow shift in MHC phenotype in rat hindlimb muscles.

Exercise training reduces myocardial lipid peroxidation following short-term ischemia-reperfusion.Med. Sci. Sports Exerc.,Vol. 30, No. 8, pp. 1211-1216, 1998.

Aging is associated with a progressive loss of skeletal muscle mass and strength, resulting in frailty and lower quality of life in older individuals. At present, a standard of clinical or pharmacological care to prevent the adverse effects of aging does not exist. Determining the mechanism(s) responsible for muscular atrophy in disused aged muscle is a required key step for the development of effective countermeasures. Studies suggest an age-related differential response of genes and signalings to muscle disuse in both rodents and humans, implying the possibility that effective countermeasures to prevent disuse muscle atrophy may be age-specific. Notably, exercise preconditioning can attenuate disuse-induced muscular atrophy in rodent and human skeletal muscles; however, information on age-specific mechanisms of this exercise-induced protection remains limited. This mini-review aimed to summarize the protective effects of acute exercise preconditioning on muscular atrophy in aged muscle and provide potential mechanisms for its preventive effect on skeletal muscle wasting.

The relationship between long-term intensive training and brain plasticity in gymnasts has recently been reported. However, the relationship between abilities in different gymnastic events and brain structural changes has not been explored. This study aimed to evaluate the correlation between world-class gymnasts (WCGs)’ specific abilities in different gymnastics events and their gray matter (GM) volume. Ten right-handed Japanese male WCGs and 10 right-handed gender- and age-matched controls with no history of gymnastic training participated in this study. Whole brain three-dimensional T1-weighted images (magnetization-prepared rapid gradient-echo sequence) with 0.90 mm3voxels were obtained using a 3 T-MRI scanner from each subject. Volume-based morphometry (VolBM) was used to compare GM volume differences between WCGs and controls. We then explored the correlation between specific gymnastic abilities using different gymnastic apparatuses, and GM volume. Significantly higher GM volumes (false discovery rate-corrected p< 0.05) in the inferior parietal lobule, middle temporal gyrus, precentral gyrus, rostral middle frontal gyrus, and superior frontal gyrus were demonstrated in WCGs, compared with controls using VolBM. Moreover, significant positive correlations were observed between brain regions and the difficulty scores for each gymnastic event, for example, rings and inferior parietal lobule and parallel bars and rostral middle frontal gyrus. These results may reflect the neural basis of an outstanding gymnastic ability resulting from brain plasticity in areas associated with spatial perception, vision, working memory, and motor control.