Taurine supplementation enhances endurance capacity by delaying blood glucose decline during prolonged exercise in rats.

Taurine enhances physical performance; however, the underlying mechanism remains unclear. This study examined the effect of taurine on the overtime dynamics of blood glucose concentration (BGC) during endurance exercise in rats. Male F344 rats were subjected to transient treadmill exercise until exhaustion following 3 weeks of taurine supplementation or non-supplementation (TAU and CON groups). Every 10 min during exercise, BGC was measured in blood collected through cannulation of the jugular vein. Gluconeogenesis-, lipolysis-, and fatty acid oxidation-related factors in the plasma, liver, and skeletal muscles were also analyzed after 120-min run. Exercise time to exhaustion was significantly longer with taurine supplementation. BGC in the two groups significantly increased by 40 min and gradually and significantly decreased toward the respective exhaustion point. The decline in BGC from the peak at 40 min was significantly slower in the TAU group. The time when the once-increased BGC regressed to the 0-time level was significantly and positively correlated with exercise time until exhaustion. At the 120-min point, where the difference in BGC between the two groups was most significant, plasma free fatty acid concentration and acetyl-carnitine and N-acetyltaurine concentrations in skeletal muscle were significantly higher in the TAU group, whereas glycogen and glucogenic amino acid concentrations and G6Pase activity in the liver were not different between the two groups. Taurine supplementation enhances endurance capacity by delaying the decrease in BGC toward exhaustion through increases of lipolysis in adipose tissues and fatty acid oxidation in skeletal muscles during endurance exercise.

Relationship between early-onset muscle soreness and indirect muscle damage markers and their dynamics after a full marathon.

BACKGROUND/OBJECTIVE: Muscle soreness and damage occurs after completing a full marathon. Here we refer to muscle soreness induced by prolonged running as early-onset muscle soreness (EOMS) because muscle soreness and damage markers induced after prolonged running are different from delayed-onset muscle soreness (DOMS) and muscle damage markers induced after eccentric contraction, such as resistance exercise. The dynamics and relationship between muscle damage markers and EOMS are unclear; therefore, in this study, we aimed to elucidate the relationship between EOMS and indirect muscle damage markers, and their dynamics after a full marathon. METHODS: The following measurements were performed in 19 subjects who completed a full marathon: perceived muscle soreness (using a numeric rating scale), thigh circumference (CIR), hip joint range of motion (ROM), jump height (JH) and muscle damage marker activities in the blood (CK, AST, LDH, ALD) before (Pre), after (Post) and every day for 4 days after a full marathon (D1-4). RESULTS: EOMS was induced, as determined by the numeric rating scale score peaking immediately after a full marathon. ROM and JH significantly decreased and all muscle damage markers significantly increased after a full marathon. Serum CK and AST peaked at D1. Serum LDH and ALD peaked at Post and D3. Each marker showed different dynamics. CIR significantly decreased after a full marathon. CONCLUSION: Muscle soreness peaked and muscle damage markers in the blood showed different dynamics after a full marathon. In other words, this is different from DOMS.

The Production of a Rat Model That Inhibits Phosphoenolpyruvate Carboxykinase (PEPCK), a Rate-Limiting Enzyme of Hepatic Gluconeogenesis.

We previously showed that taurine administration contributed to the extension of time to exhaustion through exercise-induced hypoglycemia restraint, and we suggested that the activation of hepatic gluconeogenesis was initiated before the exercise with the taurine administration. We hypothesize that the extension effect of exercise duration with the taurine administration is restrained in the rats which inhibited hepatic gluconeogenesis. In this study, we aimed to produce a rat model that inhibited hepatic gluconeogenesis as a first step in testing our hypothesis.F344 male rats of 8 weeks after birth were purchased. The blood samples were collected via jugular vein catheter to perform the pyruvate tolerance test (PTT) with the intraperitoneal administration, and to determine the optimal time point of blood glucose measurement. 3-mercaptopicolinic acids (3MPA) was used as an inhibitor of PEPCK. The rats were divided into three groups, Non-dosage control (CON) group, 30 mg/kg・BW 3MPA (3MPA 30) group, and 300 mg/kg・BW 3MPA (3MPA 300) group.The blood glucose level showed a significant peak 15 min after pyruvate administration. The change of the blood glucose level after the PTT in 3MPA 300 group was significantly smaller than that of the CON group at this time point. These results show we could prepare the rat model that inhibited hepatic gluconeogenesis.

Effects of Taurine Supplementation on Vascular Endothelial Function at Rest and After Resistance Exercise.

High-intensity resistance exercise has been shown to increase arterial stiffness and reduce vascular endothelial function. Taurine supplementation has a favorable effect on maintaining vascular function. We had previously reported that taurine supplementation attenuated increases in resistance exercise-induced arterial stiffness. In the present study, we further investigate the effects of taurine supplementation on vascular endothelial function at rest and after resistance exercise.Twenty-nine healthy men were recruited and randomly assigned to either the placebo supplement group (n = 14) or the taurine supplement group (n = 15) in a double-blinded manner. Subjects were required to ingest 6 g of either a placebo or the taurine supplement for 2 weeks prior to and 3 days following the exercise. Two weeks after the commencement of supplementation, the subjects were asked to perform 2 sets of 20 repetitive unilateral maximal-effort resistance exercise of the elbow flexors on a Biodex isokinetic dynamometer, with each contraction lasting 3 s, with 1 repetition performed every 9 s and 4 min rest in between sets. We evaluated the changes in brachial artery flow-mediated dilation (FMD) in the non-exercised arm as an index of vascular endothelial function. Relative and absolute FMDs were measured prior to supplementation, before exercise, and 24, 48, and 96 h after exercise.Two weeks of taurine supplementation significantly increased both relative and absolute FMDs. Baseline diameter significantly increased at 96 h following the exercise in both groups. However, there was no change in the peak diameter. Consequently, both relative and absolute FMDs were significantly reduced at 96 h after the exercise in both groups. Taurine supplementation does not affect resistance exercise-induced reduction in FMD.Two weeks of taurine supplementation (6 g/day) significantly increased vascular endothelial function at rest; however, taurine supplementation did not improve resistance exercise-induced reduction in FMD.

Increased N-Acetyltaurine in the Skeletal Muscle After Endurance Exercise in Rat.

Taurine is metabolized to a novel metabolite, N-acetyltaurine (NAT), through N-acetylation with acetate. Furthermore, NAT production increases when the endogenous production of acetate is elevated in some situations, such as alcohol catabolism and endurance exercise. We have previously reported that both the serum concentration and urinary excretion of NAT from humans were increased after endurance exercise, and that NAT was secreted by cultured skeletal muscle cells exposed to both acetate and taurine. The present study evaluated the hypothesis that NAT is synthesized in the skeletal muscle after endurance exercise. Normal rats were loaded to a transient treadmill running until exhaustion. Serum, skeletal muscle, and liver were collected immediately after the exercise. The NAT concentration in the plasma and in the soleus muscle from the exercised rats was significantly increased compared to that in the samples from the sedentary control rats. There was a significant positive correlation in the NAT concentration between the plasma and soleus muscle. The NAT concentration in the liver was unchanged after the endurance exercise. These results confirm that the significantly increased NAT in both the serum and urine after endurance exercise is derived from NAT synthesis in the skeletal muscle.

Additional effects of taurine on the benefits of BCAA intake for the delayed-onset muscle soreness and muscle damage induced by high-intensity eccentric exercise.

Taurine (TAU) has a lot of the biological, physiological, and pharmocological functions including anti-inflammatory and anti-oxidative stress. Although previous studies have appreciated the effectiveness of branched-chain amino acids (BCAA) on the delayed-onset muscle soreness (DOMS), consistent finding has not still convinced. The aim of this study was to examine the additional effect of TAU with BCAA on the DOMS and muscle damages after eccentric exercise. Thirty-six untrained male volunteers were equally divided into four groups, and ingested a combination with 2.0 g TAU (or placebo) and 3.2 g BCAA (or placebo), thrice a day, 2 weeks prior to and 4 days after elbow flexion eccentric exercise. Following the period after eccentric exercise, the physiological and blood biochemical markers for DOMS and muscle damage showed improvement in the combination of TAU and BCAA supplementation rather than in the single or placebo supplementations. In conclusion, additional supplement of TAU with BCAA would be a useful way to attenuate DOMS and muscle damages induced by high-intensity exercise.

Design of Antioxidant Nanoparticle, which Selectively Locates and Scavenges Reactive Oxygen Species in the Gastrointestinal Tract, Increasing The Running Time of Mice.

Excess reactive oxygen species (ROS) produced during strong or unfamiliar exercise cause exercise-induced gastrointestinal syndrome (EIGS), leading to poor health and decreased exercise performance. The application of conventional antioxidants can neither ameliorate EIGS nor improve exercise performance because of their rapid elimination and severe side effects on the mitochondria. Hence, a self-assembling nanoparticle-type antioxidant (RNPO ) that is selectively located in the gastrointestinal (GI) tract for an extended time after oral administration is developed. Interestingly, orally administered RNPO significantly enhances the running time until exhaustion in mice with increasing dosage, whereas conventional antioxidants (TEMPOL) tends to reduce the running time with increasing dosage. The running (control) and TEMPOL groups show severe damage in the GI tract and increased plasma lipopolysaccharide (LPS) levels after 80 min of running, resulting in fewer red blood cells (RBCs) and severe damage to the skeletal muscles and liver. However, the RNPO group is protected against GI tract damage and elevation of plasma LPS levels, similar to the nonrunning (sedentary) group, which prevents damage to the whole body, unlike in the control and TEMPOL groups. Based on these results, it is concluded that continuous scavenging of excessive intestinal ROS protects against gut damage and further improves exercise performance.

Improvement of low-intensity long-time running performance in rats by intake of glucosyl hesperidin.

Recently, the use of ergogenic aids in sports by both athletes and fans has increased. Moreover, the overall demand for new ergogenic aids has increased. Hesperidin is a polyphenol that is useful for improving exercise performance by activating energy generation through ß-oxidation and oxidative phosphorylation in skeletal muscles. However, it is difficult to use this compound as an ergogenic aid because of its poor water solubility and low bioavailability. Glucosyl hesperidin is formed when one molecule of glucose is transferred to hesperidin via glycosyl-transferase. It is 10,000× more soluble and has 3.7× higher bioavailability than hesperidin. In this study, we assessed whether continuous (14 days) intake of glucosyl hesperidin improves the aerobic exercise capacity of rats during long-term acute exercise. Although glucosyl hesperidin intake did not improve the performance of high-intensity running (30 m/min), we did observe improvement in low-intensity running (15 m/min) (p < 0.05). We demonstrate that in sedentary rats, glucosyl hesperidin intake increased ß-oxidation and oxidative phosphorylation in the skeletal muscle (p < 0.05 and p < 0.01, respectively). Glucosyl hesperidin intake may have created a metabolic state useful for long-term exercise. In conclusion, the continuous intake of glucosyl hesperidin improved the aerobic exercise capacity of rats during long-term acute exercise.

Long-Term Habitual Exercise and Combination of ß-Hydroxy-ß-Methylbutyrate plus Black Ginger Alter the Autophagy and Mitochondria Related Genes in SAMP8 Mice.

Muscle mass and strength decrease with aging; however, habitual exercise can maintain muscle health. ß-Hydroxy-ß-methyl butyrate calcium (HMB) and black ginger (BG) improve muscle protein metabolism and energy production. Combining these two molecules, which have similar effects, may have a synergistic effect. Senescence-accelerated mouse-prone 8 (SAMP8) is a useful model of muscle aging. Therefore, we explored how the combination of habitual exercise, HMB, and BG affected muscle aging. We used 28-wk-old (28w) SAMP8 mice divided into six groups: 28 wk (28w), 44 wk (44w, Con), exercise (Ex), Ex+BG, Ex+HMB, and Ex+BG+HMB (Ex+Comb). Mice were required to run on a treadmill for 16 wk for 5 d per week. In 28w and 44w mice, grip strength tests and dissection were conducted. Muscle weight was measured, and qPCR and immunoblotting were conducted. Muscle mass and strength were declined in the 44w group. Exercise with HMB or BG alone had no effect, whereas muscle mass and strength were augmented in the Ex+Comb group. Similarly, levels of mitochondrial function- and biogenesis-related genes were increased. Autophagy-related protein (Atg3, 7, 16L1 and Beclin1) were altered in the Ex+Comb group. These results suggest that Ex+Comb affects autophagy. Overall, the combination of habitual exercise and HMB+BG may enhance muscle mass and strength by affecting the mitochondrial and autophagy systems in SAMP8.

Effect of taurine supplementation on the alterations in amino Acid content in skeletal muscle with exercise in rat.

Taurine included abundantly in skeletal muscle, particularly in the slow-twitch fibers, enhances exercise performance. However, the exact mechanisms for this effect have been unclear. The present study investigated the influence of taurine supplementation on amino acids profile in skeletal muscles as one of mechanisms in the enhancement of exercise performance induced by taurine. In the rats that received taurine solution, amino acids concentrations were comprehensively quantified in two portions with different fiber compositions in the fast-twitch fiber dominant (FFD) gastrocnemius muscle after 2 weeks, and in the gastrocnemius and additional other FFD muscles, liver, and plasma with exhausted exercise after 3 weeks. In the FFD muscles after 2 weeks, a common phenomenon that decreased concentrations of threonine (-16%), serine (-15~-16%), and glycine (-6~-16%) were observed, and they are categorized in the pyruvate precursors for hepatic gluconeogenesis rather than biosynthesis, polar, and side-chain structures. The decreases in the three amino acids were significantly emphasized after an additional week of taurine supplementation in the FFD muscles (p values in three amino acids in these tissues were less than 0.001-0.05), but not in the liver and plasma, accompanied with significantly increase of running time to exhaustion (p <0.05). In contrast, the three amino acids (threonine and serine; p < 0.05, glycine; p < 0.01) and alanine (p < 0.01) in the liver were significantly decreased and increased, respectively, following the exhaustive exercise. In conclusion, the taurine-induced reductions of these amino acids in skeletal muscle might be one of the mechanisms which underpin the enhancement of exercise performance by taurine. Key pointsTaurine ingestion significantly decreased certain amino acids in skeletal muscles accompanied with enhanced exercise performance.The decreased amino acids in common were threonine, serine, and glycine, but not alanine; pyruvate precursor for gluconeogenesis.The alteration of three amino acids in muscles was maintained after exhausted exercise.The muscular alterations of them might be one of taurine-induced roles on exercise performance.

An Antioxidant Nanoparticle Enhances Exercise Performance in Rat High-intensity Running Models.

Although the adverse effects of excessively generated reactive oxygen species (ROS) on the body during aerobic exercise have been debated, there are few reports on the remarkable effects of the application of conventional antioxidants on exercise performance. The conventional antioxidants could not enhance exercise performance due to their rapid excretion from the body and serious adverse effects on the cellular respiratory system. In this study, impact of the original antioxidant self-assembling nanoparticle, redox-active nanoparticle (RNP), is investigated on the exercise performance of rats during running experiments. With an increase in the dose of the administered RNP, the all-out time of the rat running extends in a dose-dependent manner. In contrast, with an increase in the dose of the low-molecular-weight (LMW) antioxidant, the all-out running time of the rats decreases. The control group and LMW antioxidant treated group decrease in the number of red blood cells (RBCs) and increase oxidative stress after running. However, the RNP group maintains a similar RBC level and oxidative stress as that of the sedentary group. The results suggest that RNP, which shows long-blood circulation without disturbance of mitohormesis, effectively removes ROS from the bloodstream to suppresses RBC oxidative stress and damage, thus improving exercise performance.

Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study.

OBJECTIVE: Excessive exercise increases the production of reactive oxygen species in skeletal muscles. Sulforaphane activates nuclear factor erythroid 2-related factor 2 (Nrf2) and induces a protective effect against oxidative stress. In a recent report, sulforaphane intake suppressed exercise-induced oxidative stress and muscle damage in mice. However, the effect of sulforaphane intake on delayed onset muscle soreness after eccentric exercise in humans is unknown. We evaluated the effect of sulforaphane supplement intake in humans regarding the delayed onset muscle soreness (DOMS) after eccentric exercise. RESEARCH METHODS & PROCEDURES: To determine the duration of sulforaphane supplementation, continuous blood sampling was performed and NQO1 mRNA expression levels were analyzed. Sixteen young men were randomly divided into sulforaphane and control groups. The sulforaphane group received sulforaphane supplements. Each group performed six set of five eccentric exercise with the nondominant arm in elbow flexion with 70% maximum voluntary contraction. We assessed muscle soreness in the biceps using the visual analog scale, range of motion (ROM), muscle damage markers, and oxidative stress marker (malondialdehyde; MDA). RESULTS: Sulforaphane supplement intake for 2 weeks increased NQO1 mRNA expression in peripheral blood mononuclear cells (PBMCs). Muscle soreness on palpation and ROM were significantly lower 2 days after exercise in the sulforaphane group compared with the control group. Serum MDA showed significantly lower levels 2 days after exercise in the sulforaphane group compared with the control group. CONCLUSION: Our findings suggest that sulforaphane intake from 2 weeks before to 4 days after the exercise increased NQO1, a target gene of Nrf2, and suppressed DOMS after 2 days of eccentric exercise.

N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises.

During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl moiety of mitochondrial acetyl-CoA derived from the short- and long-chain fatty acids of skeletal muscles during endurance exercises. In human subjects, the serum concentrations of acetylated forms of taurine (NAT) and carnitine (ACT), which are the metabolites of acetyl-CoA buffering, significantly increased after a full marathon. In the culture medium of primary human skeletal muscle cells, NAT and ACT concentrations significantly increased when they were cultured with taurine and acetate or with carnitine and palmitic acid, respectively. The increase in the mitochondrial acetyl-CoA/free CoA ratio induced by acetate and palmitic acid was suppressed by taurine and carnitine, respectively. Elevations of NAT and ACT in the blood of humans during endurance exercises might serve the buffering of the acetyl-moiety in mitochondria by taurine and carnitine, respectively. The results suggest that blood levels of NAT and ACT indicate energy production status from fatty acids in the skeletal muscles of humans undergoing endurance exercise.

Habitual Aerobic Exercise Diminishes the Effects of Sarcopenia in Senescence-Accelerated Mice Prone8 Model.

Loss of muscle mass and strength are progressing with aging. Exercise is a beneficial method to prevent physical dysfunction, and habitual exercise can improve the muscle quality. Therefore, we evaluated the effects of long-term habitual exercise's impact on sarcopenia utilizing the senescence-accelerated mice prone8 (SAMP8) model. Notably, 27 w SAMP8 were used in this study. Mice were classified into 28 (28 w) and 44 weeks old. The 44-week group was divided into the sedentary group (44 w) and a group exercising for 16 weeks (44 w + Ex). The 44 w + Ex performed habitual exercise from 28 to 44 weeks. Additionally, grip strength tests were performed with mice aged 28 and 44 weeks. Muscles were harvested and measured muscle weight at 44 w. Gastrocnemius decreased in 44 w, but was unchanged in 44 w + Ex. There was a trend for lower muscle grip strength in the 44 w group, but there was no change in 44 w + Ex. The phosphorylation levels of Akt and p70S6K as a protein synthesis marker were decreased in 44 w. Cytochrome c oxidase subunit IV (CoxIV) mRNA and protein levels decreased in 44 w. These results suggested that long-term habitual exercise attenuates muscle mass and strength decline, possibly through maintenance of muscle protein synthesis and mitochondrial maintenance.

LDH isoenzyme 5 is an index of early onset muscle soreness during prolonged running.

BACKGROUND: Muscle soreness is also induced during prolonged running such as a full marathon, and muscle soreness and increased damage markers are detected immediately after such a running. We named this muscle soreness, early onset muscle soreness (EOMS). Additionally, lactate dehydrogenase (LDH) level which has some isoenzyme is increased immediately after prolonged exercise. However, it is unclear that EOMS is related to muscle damage markers on prolonged running. This study aimed to determine at which point EOMS, and muscle damage markers are related to EOMS during prolonged running. METHODS: We studied 11 male subjects who habitually perform aerobic exercise. They ran 30 km at 90% of ventilatory threshold intensity. Every 10 km, we estimated perceived muscle soreness, and sampled blood to measure muscle and liver damage, inflammation, and oxidative stress (d-ROM and BAP) markers. RESULTS: Muscle soreness score lower limbs were significantly appeared at 20 km compared to that at 0 km. Serum lactate dehydrogenase (LDH) level increased at 30 km compared to that at 0 km. LDH isoenzymes 3, 4, and 5, and neutrophils significantly increased at 30 km compared to those at 0 km. Serum LDH isoenzyme 5 and change in aspartate aminotransferase significantly increased at 20 km. In addition, there was a significant correlation between the thigh NRS and amount of serum LDH isoenzyme 5 from 0 km to 20 km. d-ROM and BAP increased at 10 km compared to those at 0 km. CONCLUSIONS: EOMS started to occur at 20 km during a 30 km running task. Our data suggest that LDH isoenzyme 5 is a marker of occurrence in EOMS during prolonged running.

Effects of taurine administration on exercise.

Taurine concentration in rat skeletal muscles after endurance running, with and without taurine administration was studied. Taurine concentrations in skeletal muscles was significantly decreased in exercised groups without taurine administration. However, taurine administration reduced the decrease of taurine concentration in skeletal muscles in exercise. Oral administration of taurine has effect for maintaining taurine concentration in skeletal muscles in exercise. The duration of running time to exhaustion of rats, with and without taurine administration were studied. The duration of running time to exhaustion was significantly increased by taurine administration. Oral administration of taurine increases the ability of physical endurance. Rat urinary excretions of creatinine, creatine, 3-methylhistidine (3-MH) after treadmill running, with and without taurine administration were studied. Rat urinary excretions of creatinine, creatine, 3-MH after treadmill running was significantly decreased with taurine administration. Taurine administration was considered to reduce the exercise-induced muscle fatigue.

Effect of BCAA supplement timing on exercise-induced muscle soreness and damage: a pilot placebo-controlled double-blind study.

BACKGROUND: The aim of the present study was to compare the effects of branched-chain amino acid (BCAA) supplementation taken before or after exercise on delayed onset muscle soreness (DOMS) and exercise-induced muscle damage (EIMD). METHODS: Fifteen young men (aged 21.5±0.4 years) were given either BCAA (9.6 g·day-1) or placebo before and after exercise (and for 3 days prior to and following the exercise day) in three independent groups: the control group (placebo before and after exercise), the PRE group (BCAA before exercise and placebo after exercise), and the POST group (placebo before exercise and BCAA after exercise). Participants performed 30 repetitions of eccentric exercise with the non-dominant arm. DOMS, upper arm circumference (CIR), elbow range of motion (ROM), serum creatine kinase (CK), lactate dehydrogenase (LDH), and aldolase, BCAA, and ß-hydroxy-ß-methylbutyrate (3HMB) were measured immediately before and after the exercise and on the following 4 days. RESULTS: Serum BCAA and 3HMB concentrations increased significantly in the PRE group immediately after the exercise, recovering to baseline over the following days. In the days following the exercise day, DOMS, CIR, and ROM were significantly improved in the PRE group compared to the control group, with weaker effects in the POST group. Serum activities of CK, LDH, and aldolase in the days following the exercise day were significantly suppressed in the PRE group compared to control group. CONCLUSIONS: The present study confirmed that repeated BCAA supplementation before exercise had a more beneficial effect in attenuating DOMS and EIMD induced by eccentric exercise than repeated supplementation after exercise.

Influence of acute exercise on renalase and its regulatory mechanism.

AIMS: Renalase expression in the kidneys and liver is regulated by nuclear factor (NF)-κB, Sp1, and hypoxia-inducible factor (HIF)-1α. The dynamics of renalase expression in acute exercise, and its mechanism and physiological effects are unclear. We evaluated the effect of different exercise intensities on renalase expression and examined its mechanism and physiological effects. MAIN METHODS: 21 male Wistar rats ran for 30 min on a treadmill after resting for 15 min. The sedentary group rested on the treadmill while the exercise group ran for 30 min at 10 or 30 m/min. Skeletal muscles, the kidney, heart, liver, and blood samples were collected after exercise. The expression of renalase and phosphate IkB-α and Akt was measured by western blotting, while HIF-1α, Sp1, MuRF-1, and MAFbx were measured in the skeletal muscle by real-time RT-PCR. KEY FINDINGS: Renalase expression in skeletal muscles increased after acute exercise, while its expression in the kidneys, heart, and liver decreased. NF-κB regulated renalase expression in the plantaris muscle and that of HIF-1α in the soleus muscle. Phosphate Akt in the plantaris muscle significantly increased in the 30 m/min group compared with that in the sedentary group. MuRF-1 in the plantaris did not change between these groups. SIGNIFICANCE: Renalase expression in skeletal muscles increased after acute exercise but decreased in other tissues. This increase may be a response to exercise-induced oxidative stress. Furthermore, NF-κB in the plantaris muscle may mainly regulate renalase expression, and support a relationship with the cell protective effects of renalase.