Shanghai Research Institute of Sports Science

Shanghai, China

Shanghai Research Institute of Sports Science

Shanghai, China
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Zhang Q.,Shanghai Research Institute of Sports Science | Zheng J.,Shanghai Research Institute of Sports Science | Qiu J.,Shanghai Research Institute of Sports Science | Wu X.,Shanghai Research Institute of Sports Science | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2017

Background: Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. Methods: We created transgenic mice expressing ALDH2 in skeletal muscles. Male wild-type C57/BL6 (WT) and ALDH2 transgenic mice (ALDH2-Tg), 8-weeks old, were challenged with exhaustive exercise for 1 week to induce skeletal muscle injury. Animals were sacrificed 24 h post-exercise and muscle tissue was excised. Results: ALDH2-Tg mice displayed significantly increased treadmill exercise capacity compared to WT mice. Exhaustive exercise caused an increase in mRNA levels of the muscle atrophy markers, Atrogin-1 and MuRF1, and reduced mitochondrial biogenesis and fusion in WT skeletal muscles; these effects were attenuated in ALDH2-Tg mice. Exhaustive exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of Beclin1 and Bnip3; the effects of which were mitigated by ALDH2 overexpression. In addition, ALDH2-Tg reversed the increase of an oxidative stress biomarker (4-hydroxynonenal) and decreased levels of mitochondrial antioxidant proteins, including manganese superoxide dismutase and NAD(P)H:quinone oxidoreductase 1, in skeletal muscle induced by exhaustive exercise. Conclusion: ALDH2 may reverse skeletal muscle mitochondrial dysfunction due to exhaustive exercise by regulating mitochondria dynamic remodeling and enhancing the quality of mitochondria. © 2017 Elsevier Inc.


Sun M.,Shanghai Research Institute of Sports Science | Shen W.,Shanghai JiaoTong University | Zhong M.,Shanghai JiaoTong University | Wu P.,Shanghai JiaoTong University | And 2 more authors.
Cardiovascular Research | Year: 2013

Aims In this study, we investigated the interaction between exercise-induced mitochondrial adaptation of large vessels and the effects of chronic anabolic androgenic steroids (AASs). Methods and results Four groups of SpragueDawley rats were studied: (i) sedentary, (ii) sedentary + nandrolone-treated, (iii) aerobic exercise trained, and (iv) trained + nandrolone-treated. Aerobic training increased the levels of aortic endothelial nitric oxide synthase (eNOS) and heme oxygenase-1 (HO-1) in accordance with improved acetylcholine-induced vascular relaxation. These beneficial effects were associated with induction of mitochondrial complexes I and V, increased mitochondrial DNA copy number, and greater expression of transcription factors involved in mitochondrial biogenesis/fusion. We also observed enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of beclin1 and autophagy-related protein-7 (ATG7). The levels of thiobarbituric acid-reactive substances and protein carbonyls remained unchanged, whereas significant increases in catalase and mitochondrial manganese superoxide dismutase (MnSOD) levels were observed in the aortas of trained animals, when compared with sedentary controls. Nandrolone increased oxidative stress biomarkers and inhibited exercise-induced increases of eNOS, HO-1, catalase, and MnSOD expression. In addition, it also attenuated elevated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1a) and mitofusin- 2 expression, and further up-regulated LC3II conversion, beclin1, ATG7, and dynamin-related protein-1 expression. Conclusion These results demonstrate that nandrolone attenuates aortic adaptations to exercise by regulating mitochondrial dynamic remodelling, including down-regulation of mitochondrial biogenesis and intensive autophagy. © 2013 © The Author 2013. Published by Oxford University Press on behalf of the European Society of Cardiology.


Huang X.-X.,Shanghai JiaoTong University | Wang C.,Shanghai Research Institute of Sports Science | Zhang Y.-L.,Shanghai JiaoTong University | Qian F.-L.,Shanghai Research Institute of Sports Science | And 2 more authors.
Journal of Shanghai Jiaotong University (Medical Science) | Year: 2014

Objective: To detect serum levels of copper, zinc, calcium, and iron for Shanghai elite athletes and to provide evidences for establishing serum element reference values for athletes. Methods: A total of 45 athletes were selected. The nutrients were investigated by the dietary survey and the serum levels of copper, zinc, calcium, and iron were detected by the atomic absorption sepectrophotometry. Results: The difference of serum copper of male and female athletes was statistically significant. The differences of serum iron of athletes of different sports were statistically significant. The differences of zinc, calcium, iron, protein, vitamin C, carbohydrate, and dietary fiber intakes of athletes of different sports were statistically significant. The serum copper was positively correlated to energy, carbohydrate, and vitamin C. The serum iron was positively correlated to serum calcium, dietary calcium, and carbohydrate. Conclusion: The reference ranges of serum elements of Shanghai elite athletes and normal people are not exactly the same. In order to ensure the health of athletes, reference ranges of serum copper, zinc, calcium, and iron for athletes of different sports and from different areas should be established. ©, 2014, Editorial Department of Journal of Shanghai Second Medical University. All right reserved.


Sun M.,Shanghai Research Institute of Sports Science | Huang C.,Shanghai JiaoTong University | Wang C.,Shanghai Research Institute of Sports Science | Zheng J.,Shanghai Research Institute of Sports Science | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Emerging evidence indicates exercise training could mediate mitochondrial quality control through the improvement of mitochondrial dynamics. Ginsenoside Rg3 (Rg3), one of the active ingredients in Panax ginseng, is well known in herbal medicine as a tonic and restorative agent. However, the molecular mechanism underlying the beneficial effects of Rg3 has been elusive. In the present study, we compared the effects of Rg3 administration with aerobic exercise on mitochondrial adaptation in cardiac muscle tissue of Sprague-Dawley (SD) rats. Three groups of SD rats were studied: (1) sedentary control, (2) Rg3-treated and (3) aerobic exercise trained. Both aerobic exercise training and Rg3 supplementation enhanced peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1α) and nuclear factor-E2-related factor 2 (Nrf2) protein levels in cardiac muscle. The activation of PGC-1α led to increased mRNA levels of mitochondrial transcription factor A (Tfam) and nuclear related factor 1(Nrf1), these changes were accompanied by increases in mitochondrial DNA copy number and complex protein levels, while activation of Nrf2 increased levels of phase II detoxifying enzymes, including nicotinamide adenine dinucleotide phosphate:quinone oxidoreductase 1(NQO1), superoxide dismutase (MnSOD) and catalase. Aerobic exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of beclin1 and autophagy-related protein 7 (ATG7), these effects of aerobic exercise are comparable to that of Rg3. These results demonstrate that Rg3 mimics improved cardiac adaptations to exercise by regulating mitochondria dynamic remodeling and enhancing the quantity and quality of mitochondria. © 2013 Elsevier Inc. All rights reserved.


Sun M.,Shanghai Research Institute of Sports Science | Qian F.,Shanghai Research Institute of Sports Science | Shen W.,Shanghai JiaoTong University | Shen W.,CAS Shanghai Institutes for Biological Sciences | And 4 more authors.
Scandinavian Journal of Medicine and Science in Sports | Year: 2012

The aim of this study was to investigate the effects of a combination of nutrients on physical performance, oxidative stress and mitochondrial biogenesis in rats subjected to exhaustive exercise. Rats were divided into sedentary control (SC), exhaustive exercise (EC) and exhaustive exercise with nutrient supplementation (EN). The nutrients include (mg/kg/day): R-α-lipoic acid 50, acetyl-l-carnitine 100, biotin 0.1, nicotinamide 15, riboflavin 6, pyridoxine 6, creatine 50, CoQ10 5, resveratrol 5 and taurine 100. Examination of running distances over the 4-week period revealed that EN rats ran significantly longer throughout the entire duration of the exhaustive exercise period compared with the EC rats. Nutrient supplementation significantly inhibited the increase in activities of alanine transaminase, lactate dehydrogenase and creatine kinase, reversed increases in malondialdehyde, inhibited decreases in glutathione S-transferase and total antioxidant capacity in plasma, and suppressed the elevation of reactive oxygen species and apoptosis in splenic lymphocytes. Nutrient supplementation increased the protein expression of mitochondrial complexes I, II and III, mtDNA number and transcription factors involved in mitochondrial biogenesis and fusion in skeletal muscle. These findings suggest that mitochondrial nutrient supplementation can reduce exhaustive exercise-induced oxidative damage and mitochondrial dysfunction, thus leading to enhancement of physical performance and of fatigue recovery. © 2011 John Wiley & Sons A/S.


PubMed | Shanghai Research Institute of Sports Science and Shanghai JiaoTong University
Type: | Journal: Scientific reports | Year: 2016

NLRP3 is involved in obesity-induced cardiac remodeling and dysfunction. In this study, we evaluated whether the cardiac protective effects of nebivolol relied on attenuating NLRP3 activation in a juvenile-adolescent animal model of diet-induced obesity. Weaning male Sprague-Dawley rats were fed with either a standard chow diet (ND) or a high-fat diet (HFD) for 8 weeks. The obese rats were subsequently subdivided into three groups: 1) HFD control group; 2) HFD with low-dose nebivolol (5mg/kg/d); 3) HFD with high-dose nebivolol (10mg/kg/d). Treatment with nebivolol prevented HFD-induced obesity associated excess cardiac lipid accumulation as well as myocardial mitochondrial dysfunction. Nebivolol attenuated pro-inflammatory cytokines secretion and NLRP3 inflammasome activation in myocardium of obese rats. In parallel, nebivolol treatment of obese animals increased cardiac 3-AR expression, reversing the reduction of endothelial nitric oxide synthase (eNOS). In vitro, nebivolol treatment of palmitate-incubated H9C2 cells suppressed autophagy, restored mitochondrial biogenesis, leading to decreased mitochondrial reactive oxygen species (mtROS) generation, and suppressed NLRP3 inflammasome activation. Meanwhile the presence of shRNA against 3-AR or against eNOS deteriorated the protective effects of nebivolol. These data suggest the beneficial effect of nebivolol on myocardial lipotoxicity contributing to inhibiting NLRP3 inflammasome activation possibly via improved mitochondrial dysfunction.


Wang B.,University of Texas at Austin | Wang B.,Shanghai Research Institute of Sports Science | Ding Z.,University of Texas at Austin | Wang W.,University of Texas at Austin | And 3 more authors.
European Journal of Applied Physiology | Year: 2015

Purpose: We previously reported that an amino acid mixture (AA) was able to lower the glucose response to an oral glucose challenge in both rats and humans. Increased glucose uptake and glycogen storage in muscle might be associated with the faster blood glucose clearance. We therefore tested the effect of two different doses of AA provided with a carbohydrate supplement on blood glucose homeostasis and muscle glycogen replenishment in human subjects after strenuous aerobic exercise.Methods: Ten subjects received a carbohydrate (1.2 g/kg body weight, CHO), CHO/HAA (CHO + 13 g AA), or CHO/LAA (CHO + 6.5 g AA) supplement immediately and 2 h after an intense cycling bout. Muscle biopsies were performed immediately and 4 h after exercise.Results: The glucose responses for CHO/HAA and CHO/LAA during recovery were significantly lower than CHO, as was the glucose area under the curve (CHO/HAA 1259.9 ± 27.7, CHO/LAA 1251.5 ± 47.7, CHO 1376.8 ± 52.9 mmol/L 4 h, p < 0.05). Glycogen storage rate was significantly lower in CHO/HAA compared with CHO, while it did not differ significantly between CHO/LAA or CHO (CHO/HAA 15.4 ± 2.0, CHO/LAA 18.1 ± 2.0, CHO 21.5 ± 1.4 µmol/g wet muscle 4 h). CHO/HAA caused a significantly higher insulin response and a greater effect on mTOR and Akt/PKB phosphorylation compared with CHO. Phosphorylation of AS160 and glycogen synthase did not differ across treatments. Likewise, there were no differences in blood lactate across treatments.Conclusions: The AA lowered the glucose response to a carbohydrate supplement after strenuous exercise. However, it was not effective in facilitating subsequent muscle glycogen storage. © 2015, Springer-Verlag Berlin Heidelberg.


Liu X.,Shanghai Research Institute of Sports Science | Xu L.,Shanghai Research Institute of Sports Science
Chinese Journal of Rehabilitation Medicine | Year: 2014

Objective: To explore whether the swimming or running affect the bone mineral density (BMD) of girls in puberty. Method: A sample of 58 girls with bone age 10-12 years participated in the study: 14 runners (RG), 25 swimmers (SG) and 19 age-matched controls (CG). BMD was determined by Lunar Prodigy DXA; bone age was assessed by CHN-05. Result: (1) After body surface area (BSA) controlled, the BMD of SG (0.552 g/cm2)in arms was higher than that of CG(0.517 g/cm2, 6.8%) and RG (0.511 g/cm2, 8.6%) (P<0.05). The BMD of RG (0.798 g/cm2) in legs was higher than that of SG (0.746 g/cm2, 7.0%) and CG (0.754 g/cm2, 5.8%) (P<0.05), there was no significant differnce among groups in total BMD and total BMD excluded skull. (2) The lean mass (LM) of SG was higher than that of RG and CG in arms, the LM of RG was higher in legs, the LM of CG was lower than that of RG and SG. (3) the extracurricular exercise time of CG was 111.1 min per week, lower than that of RG (661.4 min) and SG (705.6 min), P<0.01. Conclusion: Regular swimming or running can locally affect BMD of female adolescents. The effects are associated with sports-specificity. It suggested that different sports can affect BMD in early stages of the youth. It is recommend that female adolescents should take swimming or running regularly to improve BMD of arms or legs.


PubMed | Shanghai Research Institute of Sports Science
Type: Journal Article | Journal: Die Pharmazie | Year: 2012

Natural pulmonary surfactant (PS) and its artificial substitute phospholipid hexadecanol tyloxapol (PHT) are effective absorption enhancers on promoting recombinant human insulin (Rh-ins) absorption in vivo, but the in vitro efficacy and underlying mechanism remains unclear. In the current study, the permeation promoting effects of PS and PHT of insulin through Calu-3 monolayers in Transwell were evaluated. The viability of Calu-3 cells on conducting the permeation study was confirmed by TER and Electron Microscopy. Both PS and PHT significantly enhanced the permeation of Rh-ins and FD4 through calu-3 cells, with PS having a greater absorption enhancing effect than that of PHT. PS and PHT may interact directly with the tight junctions between cells and then result in intercellular permeation of peptide drugs. LDH release assay showed no significant acute toxicity of PS and PHT. The results indicated that these absorption enhancing agents may be useful as an absorption enhancer for pulmonary delivery of peptide and protein drugs.


PubMed | Shanghai Research Institute of Sports Science
Type: Journal Article | Journal: Cardiovascular research | Year: 2013

In this study, we investigated the interaction between exercise-induced mitochondrial adaptation of large vessels and the effects of chronic anabolic androgenic steroids (AASs).Four groups of Sprague-Dawley rats were studied: (i) sedentary, (ii) sedentary + nandrolone-treated, (iii) aerobic exercise trained, and (iv) trained + nandrolone-treated. Aerobic training increased the levels of aortic endothelial nitric oxide synthase (eNOS) and heme oxygenase-1 (HO-1) in accordance with improved acetylcholine-induced vascular relaxation. These beneficial effects were associated with induction of mitochondrial complexes I and V, increased mitochondrial DNA copy number, and greater expression of transcription factors involved in mitochondrial biogenesis/fusion. We also observed enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of beclin1 and autophagy-related protein-7 (ATG7). The levels of thiobarbituric acid-reactive substances and protein carbonyls remained unchanged, whereas significant increases in catalase and mitochondrial manganese superoxide dismutase (MnSOD) levels were observed in the aortas of trained animals, when compared with sedentary controls. Nandrolone increased oxidative stress biomarkers and inhibited exercise-induced increases of eNOS, HO-1, catalase, and MnSOD expression. In addition, it also attenuated elevated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1) and mitofusin-2 expression, and further up-regulated LC3II conversion, beclin1, ATG7, and dynamin-related protein-1 expression.These results demonstrate that nandrolone attenuates aortic adaptations to exercise by regulating mitochondrial dynamic remodelling, including down-regulation of mitochondrial biogenesis and intensive autophagy.

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