Passive exercise is an effective alternative to HRT for restoring OVX induced mitochondrial dysfunction in skeletal muscle.

Background: Postmenopausal women are more prone to develop muscle weakness, which is strongly associated with impairment of mitochondrial function in skeletal muscle. This study aimed to examine the impact of a passive exercise modality, whole-body vibration training (WBVT), on muscle mitochondrial function in ovariectomized (OVX) mice, in comparison with 17ß-estradiol (E2) replacement. Methods: Female C57BL/6J mice were assigned to four groups: sham operation control group (Sham), ovariectomized group (OVX), OVX with E2 supplement group (OVX+E), and OVX with WBVT group (OVX+W). The estrous cycle, body weight, body composition, and muscle strength of the mice were monitored after the operation. Serum E2 level was assessed by enzyme-linked immunosorbent assay (ELISA). The ATP levels were determined using a luciferase-catalyzed bioluminescence assay. The activity of mitochondrial respiration chain complexes was evaluated using high-resolution respirometry (O2K). Expression levels of oxidative phosphorylation (OXPHOS), peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and mitochondrial transcription factor A (TFAM) were detected using western blotting. Results: We observed decreased muscle strength and impaired mitochondrial function in the skeletal muscle of OVX mice. The vibration training alleviated these impairments as much as the E2 supplement. In addition, the vibration training was superior to the ovariectomy and the estradiol replacement regarding the protein expression of PGC-1α and TFAM. Conclusion: WBVT improves the OVX-induced decline in muscle strength and impairment of mitochondrial function in the skeletal muscle. This passive exercise strategy may be useful as an alternative to E2 replacement for preventing menopausal muscular weakness. Further studies are needed to understand the effects of WBVT on various physiological systems, and precautions should be taken when implementing it in patient treatment.

From mitochondria to sarcopenia: role of 17ß-estradiol and testosterone.

Sarcopenia, characterized by a loss of muscle mass and strength with aging, is prevalent in older adults. Although the exact mechanisms underlying sarcopenia are not fully understood, evidence suggests that the loss of mitochondrial integrity in skeletal myocytes has emerged as a pivotal contributor to the complex etiology of sarcopenia. Mitochondria are the primary source of ATP production and are also involved in generating reactive oxygen species (ROS), regulating ion signals, and initiating apoptosis signals in muscle cells. The accumulation of damaged mitochondria due to age-related impairments in any of the mitochondrial quality control (MQC) processes, such as proteostasis, biogenesis, dynamics, and mitophagy, can contribute to the decline in muscle mass and strength associated with aging. Interestingly, a decrease in sex hormones (e.g., 17ß-estradiol and testosterone), which occurs with aging, has also been linked to sarcopenia. Indeed, 17ß-estradiol and testosterone targeted mitochondria and exhibited activities in regulating mitochondrial functions. Here, we overview the current literature on the key mechanisms by which mitochondrial dysfunction contribute to the development and progression of sarcopenia and the potential modulatory effects of 17ß-estradiol and testosterone on mitochondrial function in this context. The advance in its understanding will facilitate the development of potential therapeutic agents to mitigate and manage sarcopenia.

The Current Status, Prospects, and Challenges of Shape Memory Polymers Application in Bone Tissue Engineering.

Bone defects can occur after severe trauma, infection, or bone tumor resection surgery, which requires grafting to repair the defect when it reaches a critical size, as the bone's self-healing ability is insufficient to complete the bone repair. Natural bone grafts or artificial bone grafts, such as bioceramics, are currently used in bone tissue engineering, but the low availability of bone and high cost limit these treatments. Therefore, shape memory polymers (SMPs), which combine biocompatibility, biodegradability, mechanical properties, shape tunability, ease of access, and minimally invasive implantation, have received attention in bone tissue engineering in recent years. Here, we reviewed the various excellent properties of SMPs and their contribution to bone formation in experiments at the cellular and animal levels, respectively, especially for the repair of defects in craniomaxillofacial (CMF) and limb bones, to provide new ideas for the application of these new SMPs in bone tissue engineering.

17beta-estradiol alleviates contusion-induced skeletal muscle injury by decreasing oxidative stress via SIRT1/PGC-1α/Nrf2 pathway.

PURPOSE: This study aimed to investigate the role of 17ß-estradiol (E2) in the repair of contusion-induced myoinjury in mice and to identify the underlying molecular mechanisms. METHODS: In vivo, contusion protocol was performed for preparing mice myoinjury model, and Injection (i.p.) of 17ß-estradiol (E2) or estrogen receptor antagonist ICI 182,780, or ovariectomy (OVX), was used to alter estrogen level of animal models. In vitro, C2C12 myoblasts were treated with H2O2 (oxidative stress inducer), SIRT1 inhibitor EX527, or aromatase inhibitor anastrozole. Serum E2 level was assessed by enzyme-linked immunosorbent assay (ELISA). Muscle damage repair was evaluated by H&E staining and the activities of serum creatine kinase (CK) and lactate dehydrogenase (LDH). The oxidative stress was estimated by the levels of catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Western blot was performed to measure the protein expressions of SIRT1, PGC-1α, Nrf2, and HO-1. RESULTS: We observed the elevated serum E2 levels and the upregulated oxidative stress in damaged muscle in female mice after contusion-induction. The E2 administration in vivo alleviated contusion-induced myoinjury in OVX mice by reducing CK and LDH activities, suppressing oxidative stress, and enhancing the expression levels of SIRT1, PGC-1α, Nrf2, and HO-1. These effects were inhibited by treatment with an ERα/ß antagonist. Moreover, EX527 or anastrozole treatment exacerbated H2O2-induced growth inhibition and oxidative stress, and expression downregulation of SIRT1, PGC-1α, Nrf2, and HO-1 in C2C12 cells in vitro. CONCLUSION: Our results suggest that E2 is a positive intervention factor for muscle repair followed contusion-induced myoinjury, through its effects on suppressing oxidative stress via activating the SIRT1/PGC-1α/Nrf2 pathway.

Effects of neural-derived estradiol on actin polymerization and synaptic plasticity-related proteins in prefrontal and hippocampal cells of mice.

Neural-derived 17ß-estradiol (E2) plays an important role in the synaptic plasticity of the hippocampus and prefrontal cortex, but the mechanism is not well defined. This study was designed to explore the effect and mechanism of neural-derived E2 on synaptic plasticity of the hippocampus and prefrontal cortex. Primary cultured hippocampal and prefrontal cells in mice were randomly divided into the DMSO (D), aromatase (Rate-limiting enzymes for E2 synthesizes) inhibitor letrozole (L), and ERs antagonist (MPG) treated groups. After intervention for 48 h, the cell was collected, and then, the expressions of AMPA-receptor subunit GluR1 (GluR1), synaptophysin (SYN), p-21-Activated kinase (PAK) phosphorylation, Rho kinase (ROCK), p-Cofilin, F-actin, and G-actin proteins were detected. Letrozole or ER antagonists inhibited the expression of GluR1, F-actin/G-actin, p-PAK and p-Cofilin proteins in prefrontal cells significantly. And the expressions of GluR1 and F-actin/G-actin proteins were declined in hippocampal cells markedly after adding letrozole or ERs antagonists. In conclusion, neural-derived E2 and ERs regulated the synaptic plasticity, possibly due to promoting actin polymerization in prefrontal and hippocampal cells. The regional specificity in the effect of neural-derived E2 and ERs on the actin polymerization-related pathway may provide a theoretical basis for the functional differences between the hippocampus and prefrontal cortex.

Correction to: Runners' metabolomic changes following marathon.

[This corrects the article DOI: 10.1186/s12986-020-00436-0.].

Determination of testosterone/epitestosterone concentration ratio in human urine by capillary electrophoresis.

A novel method for determining the testosterone/epitestosterone concentration ratio in human urine was established by capillary electrophoresis with diode-array detector. The urine samples were firstly purified by the solid extraction. The optimal experimental conditions were: running buffer pH = 4.74, 15.0 mmol L-1 HAc-NaAc, separation voltage 25 kV, temperature 25 °C, sample injection pressure 3.43 × 103 Pa, and duration 10 s. The testosterone and epitestosterone linear range were determined as 8.0-960.0 ng mL-1, respectively. The testosterone and epitestosterone detection limits were determined as 4.6 and 4.5 ng mL-1, respectively. The relative standard deviation was less than 0.36%.

Runners' metabolomic changes following marathon.

INTRODUCTION: Marathon, as a long-distance aerobic exercise, has become a fashionable or popular sport. However, little is known about the holistic metabolic changes occurring within the serum metabolome of athletes after the completion of a marathon. OBJECTIVES: The goal of current study was to have an in-depth understanding of the impact of marathon on human metabolomics as well as the relationships among a variety of metabolites. METHODS: The 20 studied subjects were all adult males who participated in a marathon. The serum samples of these participants were collected before and after the marathon and the biochemical metabolites in the serum were identified by an untargeted two-dimensional gas chromatography time-of-flight mass spectrometry. RESULTS: All participants completed the marathon within 3 h. Compared to those before exercise, serum urea and creatine kinase, as well as cortisol, elevated significantly (p < 0.05), whereas testosterone decreased significantly (p < 0.01). Metabolomic analysis showed that, compared to those before the competition, metabolites pyruvic acid, glyceric acid, malic acid, cis-aconitic acid, galacturonic acid, methyl fumaric acid, maltotriose, and others increased significantly after the competition (p < 0.05), but glucosamine and O-succinyl-L-homoserine decreased significantly (p < 0.05). Amino acid indexes, such as alanine, L-tyrosine and phenylalanine, increased significantly after exercise compared with those before exercise (p < 0.05), whereas serine, valine and asparagine decreased significantly (p < 0.05). Lipid metabolism indexes, glycerol, glyceric acid, octanoic acid, and quinic acid increased significantly (p < 0.05). Theophylline, xanthine and other indicators of caffeine metabolism increased significantly (p < 0.05). Furthermore, marathon performance, fat percentage, VO2max, and hemoglobin were correlated with the serum metabonomic indicators, so were serum testosterone and cortisol. CONCLUSION: These results illustrate that the metabolism of glucose and lipid of the athletes was enhanced following the marathon match. In addition, the metabolism of glucosamine was decreased and the metabolism of caffeine was increased. Our data provide new insights for marathon performance and nutritional status.

Mechanical stretch activates glycometabolism-related enzymes via estrogen in C2 C12 myoblasts.

Moderate exercise improves glycometabolic disorder and type 2 diabetes mellitus in menopausal females. So far, the effect of exercise-induced estrogen on muscular glycometabolism is not well defined. The current study was designed to explore the effect of mechanical stretch-induced estrogen on glycometabolism in mouse C2 C12 myoblasts. The mouse C2 C12 myoblasts in vitro were assigned randomly to the control (C), stretch (S), and stretch plus aromatase inhibitor anastrozole (SA) groups. Cells in the S group were stretched by the Flexcell FX-5000™ system (15% magnitude, 1 Hz frequency, and 6-hr duration) whereas those in the SA group were treated with 400 µg/ml anastrozole before the same stretching. Glucose uptake, estradiol levels, PFK-1 levels, and oxygen consumption rate were determined, and the expression of HK, PI3K, p-AKT, AKT, and GLUT4 proteins were semiquantified with western blot analysis. Compared to the control, the estradiol level, oxygen consumption rate, expression of HK, PI3K, and PFK-1 proteins, the ratio of p-AKT to AKT, and the ratio of GLUT4 in the cell membrane to that in the whole cell were higher in the S group. On the other hand, the estradiol level, glucose uptake, expression of PFK-1 and GLUT4 proteins, oxygen consumption rate, expression of HK protein, and the ratio of p-AKT/AKT were lower in the myoblasts in the SA group than those in the S group. The level of estradiol was positively correlated with glucose uptake (p < .01, r = .818). Therefore, mechanical stretch-induced estrogen increased the expression of glycometabolism-related enzymes and proteins in the mouse C2 C12 myoblasts.

Mechanical stretch enhances sex steroidogenesis in C2C12 skeletal muscle cells.

Skeletal muscle contains estrogens and estrogen synthesis-related enzymes. However, it has not been reported whether myoblasts cultured in vitro also express these enzymes. The purpose of the current study was to address these issues and to explore the effects of mechanical stretch on the enzyme system. The in vitro cultured C2C12 mouse myoblasts were divided into the control, stretch, testosterone and stretch plus testosterone groups. Cells in the stretch and stretch plus testosterone groups were mechanically stretched with the Flexercell cell stress loading device at an amplitude of 10% and in a frequency of 0.5 Hz for 8 h. Cells in the testosterone and stretch plus testosterone groups were incubated with 100 nM testosterone for 24 h before distraction. Following the treatments, cell proliferation and estradiol levels, as well as the expressions of 17ß-hydroxysteroid (17ß-HSD), 3ß-hydroxysteroid (3ß-HSD) and aromatase were analyzed. Compared to the control, the cell proliferation in all experimental groups increased significantly, the estradiol levels in the mechanically stretched groups were significantly higher, and, moreover, the estradiol levels were positively correlated with the cell proliferation (r = 0.615, p < 0.01). Additionally, analyses of aromatase protein and mRNA showed that, compared to the control, their levels were significantly increased upon stretching and testosterone exposure. Similarly, the protein and mRNA levels of both 3ß-HSD and 17ß-HSD in the stretched cells differed significantly from the control. In the presence of aromatase and 5α-reductase inhibitors, the protein and mRNA levels of these enzymes altered significantly compared to the control. Conclusions: Steroid synthases were detected in the C2C12 myoblasts cultured in vitro, the synthesized estrogen was closely related to the cell proliferation, and mechanical stretch was the external factor that affected the expression of the estrogen synthesis-related enzymes.

Expression of aromatase and synthesis of sex steroid hormones in skeletal muscle following exercise training in ovariectomized rats.

Age-related muscle wasting (sarcopenia) is accompanied by a decrease in estrogen levels which can compromise the health of aging women. Recent studies have shown that the key enzyme of estrogen synthesis (aromatase) is detected in the skeletal muscle. The purpose of this study was to investigate the effects of exercise on the expression of aromatase and the synthesis of sex steroid hormones in skeletal muscle following exercise training. Ovariectomized rats were divided into two groups, treadmill running group (25 m/min, 60 min/day, 6 days/week) and sedentary group. We found that in ovariectomized rats, exercise training significantly increased the soleus and plantar muscles mass. The level of aromatase expression and 17-ß-estradiol (E2) were increased significantly in skeletal muscle following exercise training. In addition, activation of the down-stream Akt-FoxO1-MyoD signaling pathway was significantly increased in both soleus and plantaris muscles following exercise. These results demonstrate that exercise training increased the expression of aromatase and local estrogen production in skeletal muscle, which potentially influences skeletal muscle in ovariectomized rats through activation of the Akt-FoxO1-MyoD signaling pathway.

α-Klotho Expression in Mouse Tissues Following Acute Exhaustive Exercise.

α-Klotho, a multifunctional protein, has been demonstrated to protect tissues from injury via anti-oxidation and anti-inflammatory effects. The expression of α-klotho is regulated by several physiological and pathological factors, including acute inflammatory stress, oxidative stress, hypertension, and chronic renal failure. Exhaustive exercise has been reported to result in tissue damage, which is induced by inflammation, oxidative stress, and energy metabolism disturbance. However, little is known about the effects of exhaustive exercise on the expression of α-klotho in various tissues. To determine the effects, the treadmill exhaustion test in mice was performed and the mice were sacrificed at different time points following exhaustive exercise. Our results confirmed that the full-length (130 kDa) and shorter-form (65 kDa) α-klotho were primarily expressed in the kidneys. Moreover, we found that, except for the kidneys and brain, other tissues primarily expressed the shorter-form α-klotho, including liver, which was in contrast to previous reports. Furthermore, the shorter-form α-klotho was decreased immediately following the acute exhaustive exercise and was then restored to the pre-exercise level or even higher levels in the next few days. Our results indicate that α-klotho may play a key role in the body exhaustion and recovery following exhaustive exercise.

Exercise induced Right Ventricular Fibrosis is Associated with Myocardial Damage and Inflammation.

BACKGROUND AND OBJECTIVES: Intense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF. METHODS: Sprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin (IL)-1ß and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles. RESULTS: After IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of pro-inflammation factors including IL-1ß and MCP-1 in the RV. CONCLUSIONS: Right ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.

Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts.

Mechanical stretch may cause myoblasts to either proliferate or undergo apoptosis. Identifying the molecular events that switch the fate of a stretched cell from proliferation to apoptosis is practically important in the field of regenerative medicine. A recent study on vascular smooth muscle cells illustrated that identification of these events may be achieved by addressing the stretch-induced opposite cellular outcomes simultaneously within a single investigation. To define conditions or a model in which both proliferation and apoptosis can be studied at the same time, we exposed in vitro cultured C2C12 myoblasts to a cyclic mechanical stretch regimen of 15% elongation at a stretching frequency of 1 Hz for 0, 2, 4, 6, or 8 h every day, consecutively, for 3 days. Both proliferation and apoptosis were observed. Moreover, as the duration of the stretch was prolonged, cell proliferation increased until it peaked at the optimal stretching duration. Afterwards, apoptosis gradually prevailed. Therefore, we established a model in which stretch-induced cell proliferation and apoptosis can be studied simultaneously.

[Effects of laser stimulation with different power on oxygen consumption rate of C2C12 myoblasts in mice].

OBJECTIVE: To investigate the effects of 650 nm laser irradiation on cell oxygen consumption rate in C2C12 myoblasts following different doses. METHODS: C2C12 cells were irradiated with 650 nm laser(λ=650 nm, p=5 mW) with energy densities of 0, 0.4, and 0.8 J/cm2. Cell oxidative function was measured by oxygen consumption rate kit. Protein expression of myogenic determination factor (MyoD), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), mammalian target of rapamycin (mTOR) and its phosphorylation were detected by Western blot. RESULTS: Compared to the control group, the expression levels of MyoD, PGC-1α protein were increased and cell oxygen consumption rate was promoted in the low dose group(P<0.05). MyoD and PGC-1α protein expressions were also increased(P<0.05), the ratio of mTOR and its phosphorylationwere decreased significantly in the high dose group(P<0.05). CONCLUSIONS: 650 nm laser irradiation that dose is 0.4 J/cm2 enhances cell oxidative function, it related to that proper dose laser irradiation promoted the expression of PGC-1a protein.

The regulation of SKF38393 on the signaling pathway of dopamine D1 receptor in hippocampus during chronic sleep deprivation.

BACKGROUND: Hippocampal functions are sensitive to sleep deficiency. Dopamine D1 receptor (D1R) in hippocampus can regulate the expression of cAMP response element binding protein (CREB) through PKA, MAPK and phosphoinositide pathway, but which pathway plays the major role in hippocampus during Chronic sleep deprivation (CSD) is unclear. METHODS: The CSD model was created, SKF rats were administered the D1R agonist (SKF38363), and hippocampus from each animal was dissected for following molecular detection. The gene and protein levels of CREB and key molecules in D1R pathways were measured by real-time PCR and western blotting, respectively. RESULTS: Both the gene and protein expression of CREB in hippocampus decreased by CSD and improved significantly by SKF38393 (p<0.05). Both the gene and protein expression of PKA in hippocampus decreased by CSD and improved significantly by SKF38393 (p<0.05). SKF38393 just significantly improved the gene level of CaMK IV and the protein level of p-CaMK IV (p<0.05) in CSD rats, but it cannot improve the protein expression of ERK1/2 and p-ERK1/2. DISCUSSION: CSD significantly decreased the expression of CREB in hippocampus. As the key molecules, PKA and CaMK IV play an important role during the improvement of hippocampus by the activation of D1R, and this process might be improved during CSD through the PKA and phosphoinositide pathway.

[Effects of dietary corn peptide and exercise on hepatic ATGL and TNF-α in obese rats].

OBJECTIVE: To determine whether dietary corn peptides supplementation with or without exercise on body composition and fac-tors related to hepatic lipid metabolism in obese rats induced by a high fat diet. METHODS: Male SD rats were fed a high-fat diet (40% calorie as fat) for 8 weeks as a dietary induced obesity model (DIO, n=32). They were then randomly divided into four groups, control, corn pip-tide(CP) group, exercise group and CP + exercise group (n=8). Supplement (CP:200 g/kg) and exercise(tread mill Ex was performed 15 m/min for 60 min/d, 5 days a week) protocol for 4 weeks. Body weight and dietary levels of rats were monitored during the experimental peri-od. At the end of the 4th weeks, rats of all groups were sacrificed. Perirenal fat and liver were harvested, and hepatic adipose triglyceride li-pase(ATGL) and TNF-α were analyzed via Western blot. RESULTS: After 4 weeks, compared with DIO control group, body weight and perire-nal fat mass index in CP + exercise group were significantly decreased (P < 0.05). Hepatic ATGL was significantly higher in corn peptides supplementation, especially in combination with exercise (P < 0.05). At the same time, the values of TNF-α expression were decreased signif-icantly in exercise groups compared with DIO group (P < 0.05). CONCLUSIONS: Corn peptides combined with aerobic exercise has a weight re-duction by lowering adipose tissue in experimental animals, it may be related to the expression of ATGL and TNF-α in the liver, and promote lipid metabolism.

Lose dose genistein inhibits glucocorticoid receptor and ischemic brain injury in female rats.

Although acute bolus of genistein treatment has been shown to protect against neuronal damage in experimental brain injury animal models, chronic continuous low dose treatment of genistein on ischemic brain injury has not been well elucidated. In the present study, female rats were received either pure genistein (0.1mg/kg/day via osmotic minipumps) or placebo at the time of ovariectomy, and transient forebrain ischemia was induced 7days later. Results demonstrated that genistein treatment for 14days significantly improved ischemic neuronal survival in hippocampal CA1 region of ovariectomized rats. Glucocorticoid receptor (GR) is a member of the adrenal steroid hormone receptor, which is highly expressed in the rat hippocampus. Activation of the GR plays a critical role in the neuronal stress responses, including ischemic brain damage. This study therefore examined the potential mechanisms by which genistein regulates GR signaling, including the protein distribution and receptor activation in hippocampus following ischemic reperfusion (I/R). Results showed that GR expression in the ovariectomized rats was excessively increased both in neurons (I/R 6h) and activated microglial cells (I/R 7d) in hippocampal CA1 region. Genistein treatment significantly attenuated GR induction and the enhanced GR nuclear translocation and DNA-binding capacity. The effects of genistein on the GR levels was accompanied with decreased blood plasma levels of corticosterone (primary glucocorticoid in rodents) and coupled to an E3 ubiquitin ligase Mdm2 targeted proteasomal degradation of GR, because genistein treatment could enhance the GR-Mdm2 interaction and the ubiquitination level of GR protein. In addition, our results indicated that genistein markedly prevented the excessive activation of microglia in CA1 sector. These results demonstrate the neuroprotective action of chronic low dose genistein replacement against ischemic brain damage, and a potential mechanism associated with the inhibition of both neuronal and microglial GR signaling following ischemic stress.

[Swimming training enhances muscle growth and potentiates p70s6k, rpS6 protein expression in rat skeletal muscle].

OBJECTIVE: To illustrate the molecular mechanism of skeletal muscle growth by examining the effect of swimming training on skeletal muscle growth and p70s6k, rpS6 protein expression. METHODS: Twenty four male SD rats were used to establish swimming training models with a 15% body mass load. The training protocol adopted interval swimming training (every other day with 8 weeks). The gastrocnemius and soleus muscle were collected and weighed after training, and the protein expression of p70s6k, rpS6 and their phosphorylated forms were examined. RESULTS: After 8 weeks treatment, no significant change was observed in skeletal muscle mass between training group (T) and control group (C) (P > 0.05), but muscle mass in training rapamycin (TR) group has a significantly decrease compared with that in T and C groups (P < 0.05). Soleus and gastrocnemius muscle mass index in T group increased significantly compared with C group (P < 0.05). Compared with the C group, the ratio of P-p70s6k/p70s6k in T group increased with significant difference (P < 0.05), but the ratio in TR group was significantly reduced (P < 0.05). The ratio of P-rpS6/rpS6 had a significant difference between TR and T group (P < 0.05). CONCLUSION: These results suggest that the interval training protocol is helpful to increase the relative muscle hypertrophy, and has a role in promoting the expression of p70s6k and rpS6.