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Athletes train to improve strength and endurance to demonstrate maximum performance during competitions. Training methods vary but most focus on strength, endurance, or both. Concurrent training is a combination of two different modes of training. In this study, we combined resistance exercise (RE) and high-intensity interval exercise (HIIE) to investigate the influence of the order of the concurrent training on signal molecules on hypertrophy and glycolysis in the skeletal muscle. The phosphorylation levels of mechanistic target of rapamycin (mTOR) signals, p70 S6 kinase (p70S6 K), ribosomal protein S6 (S6), and glycogen synthase kinase beta (GSK-3β) were significantly increased in the HIIE first group compared with the control group. The combined training course did not affect the glycogen content and expression levels of proteins concerning glycolytic and metabolic capacity, suggesting that a combination of HIIE and RE on the same day, with HIIE prior to RE, improves hypertrophy response and glycolysis enhancement., (© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

For many ball games, both resistance and endurance training are necessary to improve muscle strength and endurance capacity. Endurance training has been reported to inhibit muscle strength and hypertrophy, but some studies have reported that endurance exercise (EE) does not inhibit the effects of resistance exercise. Here, we examined the effect of short- or long-duration EE on mouse skeletal muscle hypertrophy induced by functional overload (OL) at the molecular level. Plantaris muscle hypertrophy was induced by OL with synergist ablation in mice. Body mass was reduced with endurance training, but EE duration (30 or 90 min) had no effect. The ratio of plantaris muscle weight to body weight was higher in the OL and EE for 30 min (OL+EE30) and OL and EE for 90 min (OL+EE90) groups compared with the OL group. Expression of mechanistic target of rapamycin signaling proteins, which is related to protein synthesis and hypertrophy, was increased in the OL+EE30 group. Expression of Forkhead box-containing protein O1, which is related to protein breakdown and atrophy, remained unchanged. However, microtubule-associated protein 1 light chain 3, a known marker of autophagy, and MAFbx, which is related to protein breakdown, were significantly increased in the OL+EE90 group. Furthermore, markers of oxidative stress, ubiquitin and 4-hydroxynonenal were also significantly increased in the OL+EE90 group compared with other groups. In conclusion, EE duration did not affect body mass and plantaris mass and did not interfere with mechanistic target of rapamycin signaling, but it did increase ubiquitinated proteins and oxidative stress. It is therefore necessary to consider training durations for EE when combining endurance and resistance training., (© 2020 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)

Concurrent training involves a combination of two different modes of training. In this study, we conducted an experiment by combining resistance and endurance training. The purpose of this study was to investigate the influence of the order of concurrent training on signal molecules in skeletal muscle. The phosphorylation levels of p70 S6 kinase, S6 ribosomal protein, and 4E-binding protein 1, which are related to hypertrophy signaling, increased significantly in the resistance-endurance order group as compared with in control group not the endurance-resistance order group. The gene expressions related to metabolism were not changed by the order of concurrent training. The mitochondrial respiratory chain complex was evaluated by western blot. Although both groups of concurrent training showed a significant increase in MTCO1, UQCRC2, and ATP5A protein levels, we could not detect a difference based on the order of concurrent training. In conclusion, a concurrent training approach involving resistance training before endurance training on the same day is an effective way to activate both mTOR signaling and mitochondria biogenesis., (© 2020 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

It is known that repeated bouts of high-intensity interval training (HIIT) lead to enhanced levels of glycolysis, glycogenesis, and lactate transport proteins in skeletal muscle; however, little is known about the molecular mechanisms underlying these adaptations. To decipher the mechanism leading to improvement of skeletal muscle glycolytic capacity associated with HIIT, we examined the role of hypoxia-inducible factor-1α (Hif-1α), the major transcription factor regulating the expression of genes related to anaerobic metabolism, in the adaptation to HIIT. First, we induced Hif-1α accumulation using ethyl 3,4-dihydroxybenzoate (EDHB) to assess the potential role of Hif-1α in skeletal muscle. Treatment with EDHB significantly increased the protein levels of Hif-1α in gastrocnemius muscles, accompanied by elevated expression of genes related to glycolysis, glycogenesis, and lactate transport. Daily administration of EDHB for 1 wk resulted in elevated glycolytic enzyme activity in gastrocnemius muscles. Second, we examined whether a single bout of HIIT could induce Hif-1α protein accumulation and subsequent increase in the expression of genes related to anaerobic metabolism in skeletal muscle. We observed that the protein levels of Hif-1α and expression of the target genes were elevated 3 h after an acute bout of HIIT in gastrocnemius muscles. Last, we examined the effects of long-term HIIT. We found that long-term HIIT increased the basal levels of Hif-1α as well as the glycolytic capacity in gastrocnemius muscles. Our results suggest that Hif-1α is a key regulator in the metabolic adaptation to high-intensity training., (Copyright © 2015 the American Physiological Society.)

Objective: To evaluate the effects of a single incremental exercise test (IET) on mRNA expression and protein content of monocarboxylate transporter (MCT) 1 and MCT4 in the gluteus medius muscle of Thoroughbreds., Animals: 12 Thoroughbreds (6 males and 6 females; age, 3 to 4 years)., Procedures: Horses underwent an IET before and after 18 weeks of high-intensity exercise training (HIT). Horses were exercised at 90% of maximal oxygen consumption for 3 minutes during the initial 10 weeks of HIT and 110% of maximal oxygen consumption for 3 minutes during the last 8 weeks of HIT. Gluteus medius muscle biopsy specimens were obtained from horses before (baseline), immediately after, and at 3, 6, and 24 hours after the IET., Results: Expression of MCT1 and MCT4 mRNA was upregulated at 3 and 6 hours after the IET in muscle specimens obtained from horses prior to HIT (untrained horses) and at 6 hours after the IET in muscle specimens obtained from horses after HIT (trained horses). For both untrained and trained horses, MCT1 and MCT4 protein contents were increased at 6 hours after the IET and did not differ at 24 hours after the IET, compared with those at baseline., Conclusions and Clinical Relevance: Results indicated that a single IET resulted in transient increases in MCT1 and MCT4 mRNA expression and protein content in untrained and trained horses. These results may be important for the elucidation of exercise-induced alterations in lactate metabolism.

Objective: To investigate the effects of high-intensity training (HIT) on carbohydrate and fat metabolism in Thoroughbreds., Animals: 12 Thoroughbreds (3 to 4 years old; 6 males and 6 females)., Procedures: Horses performed HIT for 18 weeks. They ran at 90% or 110% of maximal oxygen consumption ((V)O(2max)) for 3 minutes (5 d/wk) and were subjected to incremental exercise testing (IET) before and after training. Blood samples were collected during IET, and muscle samples were obtained from the gluteus medius muscle immediately after IET. Phosphofructokinase, citrate synthase, and β-3-hydroxyacyl CoA dehydrogenase (β-HAD) activities were measured to determine glycolytic and oxidative capacities. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and fatty acid translocase (FAT/CD36) protein contents were detected via western blotting. Metabolome analysis was performed via capillary electrophoresis-electrospray ionization mass spectrometry to measure substrate concentrations related to carbohydrate metabolism., Results: Peak speed during IET and (V)O(2max) increased after HIT. Activities of citrate synthase and β-HAD increased after HIT, whereas phosphofructokinase activity remained unchanged. The PGC-1α and FAT/CD36 protein contents increased after HIT, but plasma lactate concentration and the respiratory exchange ratio decreased after HIT. The plasma free fatty acid concentration increased after HIT, whereas the glucose concentration was not altered. Fructose 1,6-diphosphate, phosphoenolpyruvate, and pyruvate concentrations decreased after HIT., Conclusions and Clinical Relevance: HIT caused an increase in oxidative capacity in equine muscle, which suggested that there was a decreased reliance on carbohydrate utilization and a concomitant shift toward fatty acid utilization during intensive exercise.

The aim of this study was to investigate the effects of training and detraining on the monocarboxylate transporter (MCT) 1 and MCT4 levels in the gluteus medius muscle of Thoroughbred horses. Twelve Thoroughbred horses were used for the analysis. For 18 weeks, all the horses underwent high-intensity training (HIT), with running at 90-110% maximal oxygen consumption (VO2 max ) for 3 min, 5 days week(-1). Thereafter, the horses either underwent detraining for 6 weeks by either 3 min of moderate-intensity training (MIT) at 70% VO2 max, 5 days week(-1) (HIT-MIT group) or stall rest (HIT-SR group). The horses underwent an incremental exercise test, VO2 max was measured and resting muscle samples were obtained from the middle gluteus muscle at 0, 18 and 24 weeks. The content of MCT1 and MCT4 proteins increased after 18 weeks of HIT. At the end of this period, an increase was noted in the citrate synthase activity, while phosphofructokinase activity remained unchanged. After 6 weeks of detraining, all these indexes returned to the pretraining levels in the HIT-SR group. However, in the HIT-MIT group, the increase in the MCT1 protein content and citrate synthase activity was maintained after 6 weeks of MIT, while the MCT4 protein content decreased to the pretraining value. These results suggest that the content of MCT1 and MCT4 proteins increases after HIT in Thoroughbred horses. In addition, the increase in the MCT1 protein content and oxidative capacity induced by HIT can be maintained by MIT of 70% VO2 max, but the increase in the MCT4 protein content cannot be maintained by MIT.

During high-intensity exercise, the concentration of ammonia is augmented in skeletal muscle. Ammonia activates phosphofructokinase and prevents oxidation of pyruvate to acetyl CoA, thus leading to exhaustion. Citrulline is an amino acid component of the urea cycle in the liver, along with ornithine and arginine. The aim of this study was to examine the effect of citrulline supplementation on fatigue and performance during high-intensity exercise. We constructed a swimming exercise protocol, in which mice were subjected to exhaustive swimming with a load of 5% body weight, and measured the time until exhaustion, the blood levels of lactate and ammonia, and the glycogen content of the gastrocnemius and biceps femoris muscles. Citrulline supplementation significantly increased the swimming time until exhaustion. Exercise-induced blood ammonia elevation was repressed by citrulline supplementation, and exercise-induced blood lactate increment in the citrulline-supplemented group was significantly lower than that in the non-supplemented group. Citrulline supplementation may facilitate the detoxification of ammonia via the urea cycle and inhibit additional glycolysis. Our findings suggest that citrulline supplementation may be useful for improving the exercise performance of athletes.

The effects of 3-week exercise training on the functions of peritoneal macrophages from BALB/c mice were investigated. Lipopolysaccharide (LPS)-stimulated nitric oxide (NO) and proinflammatory cytokine production in macrophages from trained mice was markedly higher than those from control mice. Meanwhile, exercise training decreased the steady state level of beta(2)-adrenergic receptor (beta(2)AR) mRNA in macrophages. Overexpression of beta(2)AR in the macrophage cell line RAW264 by transfecting with beta(2)AR cDNA suppressed NO synthase (NOS) II expression but dose not influenced proinflammatory cytokine expression. When expression of transfected beta(2)AR in RAWar cells was downregulated by a tetracycline repressor-regulated mammalian expression system, NOS II mRNA expression was significantly increased; this suggested that the changes in the beta(2)AR expression level in macrophages associated with exercise training play a role in the regulation of NO production following LPS stimulation. These findings indicate that exercise training improves macrophage innate immune function in a beta(2)AR-dependent and -independent manner.

Peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) promotes the expression of oxidative enzymes in skeletal muscle. We hypothesized that activation of the p38 MAPK (mitogen-activated protein kinase) in response to exercise was associated with exercise-induced PGC-1alpha and respiratory enzymes expression and aimed to demonstrate this under the physiological level. We subjected mice to a single bout of treadmill running and found that the exercise induced a biphasic increase in the expression of respiratory enzymes mRNA. The second phase of the increase was accompanied by an increase in PGC-1alpha protein, but the other was not. Administration of SB203580 (SB), an inhibitor of p38 MAPK, suppressed the increase in PGC-1alpha expression and respiratory enzymes mRNA in both phases. These data suggest that p38 MAPK is associated with the exercise-induced expression of PGC-1alpha and biphasic increase in respiratory enzyme mRNAs in mouse skeletal muscle under physiological conditions.