@article{MTMT:34658720, title = {Simultaneous effects of nanocurcumin supplementation and resistance training on TERF2 gene expression and p21-p53 axis in muscle tissue of male rats}, url = {https://m2.mtmt.hu/api/publication/34658720}, author = {Pourjafarian, J. and Kazemzadeh, Y. and Arshadi, S. and Banaefar, A. and Yahya, Mohammadnajad Panahkandi}, doi = {10.48307/FMSJ.2023.27.6.590}, journal-iso = {FEYZ MEDICAL SCIENCES JOURNAL}, journal = {FEYZ: JOURNAL OF KASHAN UNIVERSITY OF MEDICAL SCIENCES}, volume = {27}, unique-id = {34658720}, issn = {1029-7855}, abstract = {Background and Aim: Apoptosis is regulated by a complex interplay of gene products that either activate or inhibit this process. This study aimed at assessing the combined impact of nanocurcumin supplementation and resistance training on TERF2 (Telomeric Repeat Binding Factor 2) gene expression and the p21-p53 axis in the muscle tissue of male rats. Methods: In this experimental study, 24 male Wistar rats were randomly allocated into four groups: a healthy control group, a resistance training group, a nanocurcumin group, and a resistance training + nanocurcumin group. Resistance training was conducted over a 4-week period following a specific protocol. Concurrently, rats in the nanocurcumin groups received 80 mg of the supplement per kilogram of body weight. The expression levels of TERF2, p53, and p21 genes were assessed using the Real-Time PCR method. Results: The results showed significant differences in the expression levels of TERF2, p53, and p21 genes among the four groups (P<0.05). In the resistance training + nanocurcumin group, the expression of TERF2, p53, and p21 genes was significantly higher compared to the control group (P<0.05). Additionally, p53 gene expression in the resistance training group was significantly higher than in the nanocurcumin supplement group (P<0.05). The combined resistance training and nanocurcumin supplementation did not significantly affect the expression of the TERF2 gene in the muscle tissue of male rats compared to either training or supplementation alone (P<0.05). Furthermore, the synergistic effect of resistance training and supplementation significantly increased the expression of p21 and p53 genes (P<0.05). Conclusion: Resistance training and nanocurcumin supplementation enhance TERF2 gene expression, potentially reducing telomere shortening and aging. Moreover, the upregulation of p53 and p21 gene expression during resistance training and nanocurcumin supplementation may induce cell cycle arrest and apoptosis.}, year = {2024}, eissn = {2008-9821}, pages = {590-598} } @article{MTMT:34775622, title = {Resistance exercise exacerbates muscle atrophy of skeletal muscle-specific Beclin1 conditioned knockout (cKO) mice}, url = {https://m2.mtmt.hu/api/publication/34775622}, author = {Zeng, Zhengzhong and Zhang, Hu and Liang, Jiling and Lv, Jun and Wu, Liangwen and Chen, Ning}, doi = {10.1016/j.aehs.2024.03.001}, journal-iso = {ADVANCED EXERCISE AND HEALTH SCIENCE}, journal = {ADVANCED EXERCISE AND HEALTH SCIENCE}, unique-id = {34775622}, issn = {2950-273X}, year = {2024} } @article{MTMT:32975919, title = {The Role of Sirtuins in Sarcopenia and Frailty}, url = {https://m2.mtmt.hu/api/publication/32975919}, author = {Anwar, Masroor and Pradhan, Rashmita and Dey, Sharmistha and Kumar, Rahul}, doi = {10.14336/AD.2022.0622}, journal-iso = {AGING DIS}, journal = {AGING AND DISEASE}, volume = {14}, unique-id = {32975919}, issn = {2152-5250}, abstract = {The population of older individuals is increasing rapidly, but only a small fraction among them is able to experiences a healthy life. Due to lack of physical exercise and oxidative stress, aging leads to sarcopenia and finally end up with frailty. Sarcopenia is a component of the frailty and described as age related degenerative changes in the skeletal muscle mass, strength and quality. Though the loss of muscle strength and mass gradually seem inevitable during aging, it can be partially prevented or overcome by a deeper insight into the pathogenesis. Sirtuin protein leads to longevity across different organisms ranging from worms to mammals. Expression of sirtuin protein increases during physical exercise and thus strengthens muscle mass. Satellite cells leads to muscle repair in a SIRT1 dependent manner. In addition, SIRT1 improves insulin sensitivity and induces autophagy in the aged mice. The current review discussed the putative role of sirtuins in sarcopenia and frailty. Moreover, it highlighted the pathways by which sirtuins can inhibit ROS production, inflammation and mitochondrial dysfunctions and therefore confers a protective role against frailty and sarcopenia. The critical role of sirtuins in the sarcopenia and frailty pathogenesis can eventually fuel the development of novel interventions by targeting sirtuins.}, keywords = {Aging; SIRTUINS; Sarcopenia; Frailty; Oxidative stress}, year = {2023}, eissn = {2152-5250}, pages = {25-32} } @article{MTMT:34287694, title = {Oral administration of a locally isolated Lactobacillus rhamnosus (NR_113332.1) improves regeneration of extensor digitorum longus muscle in mice}, url = {https://m2.mtmt.hu/api/publication/34287694}, author = {Jabeen, Shamsa and Qazi, Javed Iqbal}, doi = {10.1016/j.nut.2023.112110}, journal-iso = {NUTRITION}, journal = {NUTRITION}, volume = {114}, unique-id = {34287694}, issn = {0899-9007}, abstract = {Objective: The aim of this study was to examine the effects of probiotic supplementation on extensor digitorum longus (EDL) regeneration after grafting in mice.Methods: EDL muscles were ortho-transplanted in mice. The experimental group was given 1 pound 108 colonyforming units/g body weight of Lactobacillus rhamnosus daily after EDL muscle transplantation surgeries. EDL muscle transplants were recovered after 3, 5, 7, and 14 d post-transplantation from the control as well as the experimental animals and processed for histologic analysis. Results: At day 3 post-transplantation, the inflammatory cells had infiltrated into the grafted EDL muscles and the central section of the grafted tissue contained necrotic fibers. At day 5 post-transplantation, the concentration of inflammatory cells increased further and degenerative muscle fibers were being replaced with centrally nucleated muscle cells. The average cross-sectional area non-grafted EDL and grafted muscle in the probiotic supplemented mice at day 7 increased to 48% and 23% (P = 0.002), respectively, compared with the respective values in the control animals. Whereas in non-grafted and grafted EDL muscle it could approach 8% and 36% (P = 0.008), respectively at 14 d compared with the corresponding values of the control EDL muscle transplants. The number of muscle fibers in the non-grafted and grafted probiotic-supplemented groups increased to12% and 20% (P = 0.045) at day 7 compared with the control EDL muscle. In non-grafted and grafted EDL muscle, the number of regenerated muscle fibers increased to 73% and 64% (P = 0.110) at day 14 compared with control EDL grafted muscle. Conclusion: Results of the present study regarding better regeneration of skeletal muscle fibers in the probiotic-supplemented mice than the control grafts warrant further molecular-level investigation to understand the underlying mechanism mediating the process of skeletal muscle fiber regeneration. Probiotics possibly modulate the process of muscle fiber regeneration by adjusting the composition of gut microbiota.(c) 2023 Published by Elsevier Inc.}, keywords = {regeneration; skeletal muscle; Probiotics; extensor digitorum longus; Muscle grafting}, year = {2023}, eissn = {1873-1244} } @article{MTMT:34263803, title = {Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction}, url = {https://m2.mtmt.hu/api/publication/34263803}, author = {Zhu, Yang and Zhou, Xuchang and Zhu, Aiyuan and Xiong, Shijing and Xie, Jun and Bai, Zhenmin}, doi = {10.3389/fphys.2023.1196426}, journal-iso = {FRONT PHYSIOL}, journal = {FRONTIERS IN PHYSIOLOGY}, volume = {14}, unique-id = {34263803}, abstract = {Sarcopenia is a chronic degenerative disease affecting primarily older adults. A growing aging population is gradually increasing the number of patients suffering from sarcopenia, placing increasing financial pressure on patients' families and society in general. There is a strong link between mitochondrial dysfunction and sarcopenia pathogenesis. As a result, treating sarcopenia by improving mitochondrial dysfunction is an effective strategy. Numerous studies have demonstrated that exercise has a positive effect on mitochondrial dysfunction when treating sarcopenia. Exercise promotes mitochondrial biogenesis and mitochondrial fusion/division to add new mitochondria or improve dysfunctional mitochondria while maintaining mitochondrial calcium homeostasis, mitochondrial antioxidant defense system, and mitochondrial autophagy to promote normal mitochondrial function. Furthermore, exercise can reduce mitochondrial damage caused by aging by inhibiting mitochondrial oxidative stress, mitochondrial DNA damage, and mitochondrial apoptosis. Exercise effectiveness depends on several factors, including exercise duration, exercise intensity, and exercise form. Therefore, Moderate-intensity exercise over 4 weeks potentially mitigates sarcopenia in older adults by ameliorating mitochondrial dysfunction. HIIT has demonstrated potential as a viable approach to addressing sarcopenia in aged rats. However, further investigation is required to validate its efficacy in treating sarcopenia in older adults.}, keywords = {Exercise; mitochondrial dysfunction; MITOCHONDRIAL BIOGENESIS; Sarcopenia; mitochondrial apoptosis}, year = {2023}, eissn = {1664-042X} } @article{MTMT:33035308, title = {Plant-derived compounds, vitagens, vitagenes and mitochondrial function}, url = {https://m2.mtmt.hu/api/publication/33035308}, author = {Franco, R. and Navarro, G. and Martínez-Pinilla, E.}, doi = {10.1016/j.phanu.2021.100287}, journal-iso = {PHARMANUTRITION}, journal = {PHARMANUTRITION}, volume = {19}, unique-id = {33035308}, issn = {2213-4344}, year = {2022} } @article{MTMT:33172187, title = {Ubiquitin Ligases in Longevity and Aging Skeletal Muscle}, url = {https://m2.mtmt.hu/api/publication/33172187}, author = {Hughes, David C. and Baehr, Leslie M. and Waddell, David S. and Sharples, Adam P. and Bodine, Sue C.}, doi = {10.3390/ijms23147602}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {23}, unique-id = {33172187}, issn = {1661-6596}, abstract = {The development and prevalence of diseases associated with aging presents a global health burden on society. One hallmark of aging is the loss of proteostasis which is caused in part by alterations to the ubiquitin-proteasome system (UPS) and lysosome-autophagy system leading to impaired function and maintenance of mass in tissues such as skeletal muscle. In the instance of skeletal muscle, the impairment of function occurs early in the aging process and is dependent on proteostatic mechanisms. The UPS plays a pivotal role in degradation of misfolded and aggregated proteins. For the purpose of this review, we will discuss the role of the UPS system in the context of age-related loss of muscle mass and function. We highlight the significant role that E3 ubiquitin ligases play in the turnover of key components (e.g., mitochondria and neuromuscular junction) essential to skeletal muscle function and the influence of aging. In addition, we will briefly discuss the contribution of the UPS system to lifespan. By understanding the UPS system as part of the proteostasis network in age-related diseases and disorders such as sarcopenia, new discoveries can be made and new interventions can be developed which will preserve muscle function and maintain quality of life with advancing age.}, keywords = {Healthspan; protein degradation; Sarcopenia; Proteostasis; E3 ubiquitin ligase}, year = {2022}, eissn = {1422-0067} } @article{MTMT:33015571, title = {Effect of 32-Weeks High-Intensity Interval Training and Resistance Training on Delaying Sarcopenia: Focus on Endogenous Apoptosis}, url = {https://m2.mtmt.hu/api/publication/33015571}, author = {Su, Hao and Wen, Tianhao and Liu, Dongsen and Shao, Jia and Zhao, Lei and Gao, Qi}, doi = {10.3389/fphys.2022.811369}, journal-iso = {FRONT PHYSIOL}, journal = {FRONTIERS IN PHYSIOLOGY}, volume = {13}, unique-id = {33015571}, abstract = {Sarcopenia caused by aging is an important factor leading to a decline in the quality of life of older people. Apoptosis in muscle atrophy accelerates the process of muscle loss in older populations. The present study aimed to investigate the effects of 32 weeks of high-intensity interval training (HIIT) and resistance training (RT) on the skeletal muscle-related indices and provide a theoretical basis for regulating the mitochondrial-mediated pathway to delay sarcopenia. We randomly selected 10 from eight-month-old male SD rats (N = 130) as the baseline group; after 1 week of adaptive feeding, the rats were sacrificed. The remaining rats were randomly assigned to one of three groups: control group (C, N = 40, natural aging for 32 weeks), HIIT group (H, N = 40, performed six loops of 3 min at 90% and 3 min at 50% VO2 max speed treadmill running, with 5 min at 70% VO2 max speed at the beginning and the end of the training, 3 times a week for 32 weeks), and resistance group (R, n = 40, 46 min per day, 3 days per week, with a 30% maximum load on a treadmill with a slope of 35 degrees, 15 m/min). The soleus muscles were collected for analysis at baseline and every 8 weeks. Aging resulted in decreased soleus muscle mass and Bcl-2 levels in the mitochondria, while the levels of reactive oxygen species (ROS) and Bax did not change. HIIT reversed the age-associated activation of pro-apoptotic processes, but RT did not. In addition, when rats were aged from 8 to 16 months, the level of Cyt-C did not change, the Caspase-9 levels and Caspase-3 levels decreased gradually in the soleus muscles, the rats of both the HIIT and RT groups had these indices decreased at 32 weeks. The results suggest that the age-associated loss of muscle mass was reversed by training, and the effect of RT was better than that of HIIT. Both the HIIT and RT rats showed a decrease in the apoptosis of skeletal muscle cells after 32 weeks of intervention. HIIT performed better for long-term intervention regarding the pro-apoptotic factors. This study warranted further research to delineate the underlying mechanism of effects of different exercise methods on the changes of aging skeletal muscle at in vivo level.}, keywords = {Aging; Sarcopenia; resistance exercise; HIIT; endogenous apoptosis}, year = {2022}, eissn = {1664-042X} } @article{MTMT:33216593, title = {A Preclinical Systematic Review of the Effects of Chronic Exercise on Autophagy-Related Proteins in Aging Skeletal Muscle}, url = {https://m2.mtmt.hu/api/publication/33216593}, author = {Wang, Cenyi and Liang, Jiling and Ren, Yuanyuan and Huang, Jielun and Jin, Baoming and Wang, Guodong and Chen, Ning}, doi = {10.3389/fphys.2022.930185}, journal-iso = {FRONT PHYSIOL}, journal = {FRONTIERS IN PHYSIOLOGY}, volume = {13}, unique-id = {33216593}, abstract = {Background: Exercise is one of the most effective interventions for preventing and treating skeletal muscle aging. Exercise-induced autophagy is widely acknowledged to regulate skeletal muscle mass and delay skeletal muscle aging. However, the mechanisms underlying of the effect of different exercises on autophagy in aging skeletal muscle remain unclear.}, year = {2022}, eissn = {1664-042X} } @article{MTMT:33010207, title = {The effect of resistance and endurance training with ursolic acid on atrophy-related biomarkers in muscle tissue of diabetic male rats induced by streptozotocin and a high-fat diet}, url = {https://m2.mtmt.hu/api/publication/33010207}, author = {Zolfaghari, Maryam and Faramarzi, Mohammad and Hedayati, Mehdi and Ghaffari, Mehdi}, doi = {10.1111/jfbc.14202}, journal-iso = {J FOOD BIOCHEM}, journal = {JOURNAL OF FOOD BIOCHEMISTRY}, volume = {46}, unique-id = {33010207}, issn = {0145-8884}, abstract = {In this study, the effect of resistance and endurance training with/without ursolic acid supplementation was evaluated to identify atrophy-related biomarkers in elderly rats induced by diabetes and a high-fat diet (HFD) based on in silico analysis algorithms and pharmaceutical methods. The visualizer software found differential gene expression levels in skeletal muscle atrophy via computed hub gene network parameters. Also, the impact of ursolic acid, as a potent inducer of the Trp53 protein in ameliorating decreased muscle mass, was analyzed in diabetic rats. Fifty-six-old male Wistar rats were randomly assigned into seven groups, including healthy control (Control), diabetic control (DM), Ursolic acid supplementation (UA), resistance training (RT), endurance training (ET), resistance training+ Ursolic acid supplementation (RT + U), and endurance training in combination with Ursolic acid supplementation (ET + U). Exercise intervention included 8 weeks of resistance or endurance training programs. Biomedical informatic outputs determined the P53 signaling pathway as a remarkable causative factor in the pathomechanism of atrophy. In addition, the results demonstrated that exercise and supplementation of UA impeded the interactions among p53/ATF4/p21. Moreover, ET and ursolic acid had a synergetic effect on the signaling pathway of p53/ATF4/p21 and probably could inhibit the aging process and modulate the p53/ATF4/p21 molecular pathway. The interaction between UA and endurance exercise significantly modified the activity of the p53/ATF4/p21 signaling pathway. Based on in silico studies, the p53/ATF4/p21 pathway plays an essential role in aging, and the inhibition of this pathway would be beneficial in decelerating the aging process. Practical applications Ursolic acid (UA) is a natural pentacyclic triterpenoid carboxylic acid found in apples (a major compound of apple wax) and other fruits; it is known to improve skeletal muscle function and reduce the muscular atrophy pathways. We indicated that p53/ATF4/p21 signaling is an essential factor in aging, and the suppression of this pathway could be beneficial in the deceleration of the aging process. Therefore, this work would shed light on understanding the effect of exercise and nutrition interventions on preventing atrophy markers of skeletal muscle in diabetic rats. Further studies are needed to seek the precise mechanism of the synergism between UA and exercise in ameliorating atrophy markers.}, keywords = {p53; ursolic acid; p21; endurance training; resistance training; ATF4}, year = {2022}, eissn = {1745-4514}, orcid-numbers = {Hedayati, Mehdi/0000-0001-5816-775X} } @article{MTMT:32331093, title = {Acute Low-Intensity Treadmill Running Upregulates the Expression of Intestinal Glucose Transporters via GLP-2 in Mice}, url = {https://m2.mtmt.hu/api/publication/32331093}, author = {Aoki, Kai and Suzuki, Takuji and Hui, Fang and Nakano, Takuro and Yanazawa, Koki and Yonamine, Masato and Fujita, Shinichiro and Sugasawa, Takehito and Yoshida, Yasuko and Omi, Naomi and Kawakami, Yasushi and Takekoshi, Kazuhiro}, doi = {10.3390/nu13051735}, journal-iso = {NUTRIENTS}, journal = {NUTRIENTS}, volume = {13}, unique-id = {32331093}, abstract = {The effects of exercise on nutrient digestion and absorption in the intestinal tract are not well understood. A few studies have reported that exercise training increases the expression of molecules involved in carbohydrate digestion and absorption. Exercise was also shown to increase the blood concentration of glucagon-like peptide-2 (GLP-2), which regulates carbohydrate digestion and absorption in the small intestine. Therefore, we investigated the effects of exercise on the expression of molecules involved in intestinal digestion and absorption, including GLP-2. Six-week-old male mice were divided into a sedentary (SED) and low-intensity exercise (LEx) group. LEx mice were required to run on a treadmill (12.5 m/min, 1 h), whereas SED mice rested. All mice were euthanized 1 h after exercise or rest, and plasma, jejunum, ileum, and colon samples were collected, followed by analysis via IHC, EIA, and immunoblotting. The levels of plasma GLP-2 and the jejunum expression of the GLP-2 receptor, sucrase-isomaltase (SI), and glucose transporter 2 (GLUT2) were higher in LEx mice. Thus, we showed that acute low-intensity exercise affects the expression of molecules involved in intestinal carbohydrate digestion and absorption via GLP-2. Our results suggest that exercise might be beneficial for small intestine function in individuals with intestinal frailty.}, keywords = {INTESTINE; glucose transporter 2; Glucagon-Like Peptide 2; Low-intensity exercise; Sodium-dependent glucose transporter}, year = {2021}, eissn = {2072-6643}, orcid-numbers = {Aoki, Kai/0000-0003-1872-099X; Suzuki, Takuji/0000-0002-7257-6792} } @article{MTMT:32331094, title = {Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1 alpha Signaling Pathway}, url = {https://m2.mtmt.hu/api/publication/32331094}, author = {Liang, Jiling and Zhang, Hu and Zeng, Zhengzhong and Wu, Liangwen and Zhang, Ying and Guo, Yanju and Lv, Jun and Wang, Cenyi and Fan, Jingjing and Chen, Ning}, doi = {10.3390/metabo11050323}, journal-iso = {METABOLITES}, journal = {METABOLITES}, volume = {11}, unique-id = {32331094}, issn = {2218-1989}, abstract = {Sarcopenia is an aging-induced syndrome characterized by a progressive reduction of skeletal muscle mass and strength. Increasing evidence has attested that appropriate and scientific exercise could induce autophagy or optimize the functional status of autophagy, which plays a critical role in senescent muscular dystrophy. As a publicly recognized strategy for extending lifespan and improving the health of the elderly, the underlying mechanisms of lifelong regular aerobic exercise for the prevention of sarcopenia have not been fully elucidated. To explore the role of lifelong aerobic exercise in the beneficial regulation of autophagic signaling pathways in senescent skeletal muscle, the natural aging mice were used as the sarcopenia model and subjected to lifelong treadmill running to evaluate corresponding parameters related to skeletal muscle atrophy and autophagic signaling pathways. Compared with the young control mice, the aged mice showed a significant reduction in skeletal muscle mass, gastrocnemius muscle weight/body weight (GMW/BW) ratio, and cross-sectional areas (CSA) of skeletal muscle fibers (p < 0.01). In contrast, lifelong aerobic exercise effectively rescued these reduced biomarkers associated with muscle atrophy. Moreover, as shown in the activated AMPK/PGC-1 alpha signaling pathway, lifelong aerobic exercise successfully prevented the aging-induced impairment of the ubiquitin-proteasome system (UPS), excessive apoptosis, defective autophagy, and mitochondrial dysfunction. The exercise-induced autophagy suppressed the key regulatory components of the UPS, inhibited excessive apoptosis, and optimized mitochondrial quality control, thereby preventing and delaying aging-induced skeletal muscle atrophy.}, keywords = {APOPTOSIS; UBIQUITIN-PROTEASOME SYSTEM; Autophagy; Sarcopenia; mitochondrial quality control; lifelong aerobic exercise}, year = {2021}, eissn = {2218-1989}, orcid-numbers = {Fan, Jingjing/0000-0002-1110-5735; Chen, Ning/0000-0002-8191-6744} } @article{MTMT:32331095, title = {Exercise-induced muscle damage: multi-parametric MRI quantitative assessment}, url = {https://m2.mtmt.hu/api/publication/32331095}, author = {Lyu, Xiaohong and Gao, Yue and Liu, Qiang and Zhao, Heng and Zhou, Huadong and Pan, Shinong}, doi = {10.1186/s12891-021-04085-z}, journal-iso = {BMC MUSCULOSKEL DIS}, journal = {BMC MUSCULOSKELETAL DISORDERS}, volume = {22}, unique-id = {32331095}, issn = {1471-2474}, abstract = {Background To explore the value of magnetic resonance quantitative analysis using diffusion tensor imaging, T2 mapping, and intravoxel incoherent motion in the evaluation of eccentric exercise-induced muscle damage and to compare the effects of various eccentric exercise modes at different time points in rats. Methods A total of 174 Sprague-Dawley male rats were randomly divided into five groups: control, once-only exercise, continuous exercise, intermittent exercise, and once-fatigue exercise groups. Each experimental group was divided into seven time-subgroups: 0.5 h, 24 h, 48 h, 72 h, 96 h, 120 h and 168 h after exercise. The quadriceps femoris muscles were then scanned using magnetic resonance imaging. The apparent diffusion coefficient and fractional anisotropy values of diffusion tensor imaging, T2 values of T2 mapping, D and D* values of intravoxel incoherent motion and optical density values of desmin were measured. Associations among different eccentric exercise programmes, magnetic resonance imaging findings, and histopathological results were evaluated. Dunnett's test, two-way repeated measures analysis of variance, and Pearson correlation analysis were used for statistical analysis. Results Diffusion tensor imaging showed that the number of muscle fibre bundles decreased to varying degrees with different time points and eccentric exercises. Apparent diffusion coefficient values of the exercise groups showed a trend that first increased and then decreased, the opposite of fractional anisotropy. The specimens in all eccentric exercise programmes showed high signal T2 values after exercise, the highest among which was in the once-fatigue exercise group. D and D* in the experimental groups were significantly higher than those in the control group at 0.5-48 h after exercise. The apparent diffusion coefficient, fractional anisotropy, T2, D and D* values correlated with the optical density values of desmin. Conclusions Diffusion tensor imaging, T2 mapping, and intravoxel incoherent motion technology accurately reflect the degree of skeletal muscle damage and recovery associated with eccentric exercise. The degree of muscle damage was the lowest in the continuous exercise group and the highest in the once-fatigue exercise group, which may provide more information and guidance for the formulation of physical and athletic training programmes.}, keywords = {RATS; ECCENTRIC EXERCISE; T2 mapping; DTI; IVIM; Skeletal muscle damage}, year = {2021}, eissn = {1471-2474} } @article{MTMT:31708129, title = {Habitual Aerobic Exercise Diminishes the Effects of Sarcopenia in Senescence-Accelerated Mice Prone8 Model}, url = {https://m2.mtmt.hu/api/publication/31708129}, author = {Aoki, Kai and Konno, Masaki and Honda, Katsunari and Abe, Takuya and Nagata, Takeshi and Takehara, Masaaki and Sugasawa, Takehito and Takekoshi, Kazuhiro and Ohmori, Hajime}, doi = {10.3390/geriatrics5030048}, journal-iso = {GERIATRICS-BASEL}, journal = {GERIATRICS}, volume = {5}, unique-id = {31708129}, abstract = {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.}, keywords = {Aging; Sarcopenia; SAMP8; Habitual exercise}, year = {2020}, eissn = {2308-3417}, orcid-numbers = {Aoki, Kai/0000-0003-1872-099X} } @article{MTMT:31694998, title = {Cashew (Anacardium occidentaleL.) Nuts Counteract Oxidative Stress and Inflammation in an Acute Experimental Model of Carrageenan-Induced Paw Edema}, url = {https://m2.mtmt.hu/api/publication/31694998}, author = {Cordaro, Marika and Siracusa, Rosalba and Fusco, Roberta and D'Amico, Ramona and Peritore, Alessio Filippo and Gugliandolo, Enrico and Genovese, Tiziana and Scuto, Maria and Crupi, Rosalia and Mandalari, Giuseppina and Cuzzocrea, Salvatore and Di Paola, Rosanna and Impellizzeri, Daniela}, doi = {10.3390/antiox9080660}, journal-iso = {ANTIOXIDANTS-BASEL}, journal = {ANTIOXIDANTS}, volume = {9}, unique-id = {31694998}, abstract = {Background:Anacardium occidentaleL. is a medicinal plant with powerful anti-oxidative and anti-inflammatory properties. Acute inflammatory events cause tissue alterations, decrease of anti-oxidative endogenous enzymes such as superoxide dismutase, catalase and glutathione, neutrophils infiltration, increase in the activities of myeloperoxidase, malondialdehyde, and pro-inflammatory release. Methods: Paw edema was induced by subplantar injection of carrageenan into the right hind paw in rats, but 30 min before a group of animals were orally treated with 100 mg/kg of cashew nuts to evaluate the anti-inflammatory and anti-oxidative response. Results: In the present work, we found that (1) cashew nuts reduced the development of carrageenan-induced paw edema limiting the formation of edema and pain; (2) cashew nuts ameliorated the diminutions of the anti-oxidative enzymes caused by carrageenan injection; (3) cashew nuts decreased myeloperoxidase malondialdehyde activity induced by carrageenan; and (4) cashew nuts acted by blocking pro-inflammatory cytokines response and nitrate/nitrite formation stimulated by carrageenan injection. Conclusions: The mechanisms of anti-inflammatory and analgesic effects exerted by cashew nuts were relevant to oxygen free radical scavenging, anti-lipid peroxidation, and inhibition of the formation of inflammatory cytokines.}, keywords = {Inflammation; ANTIOXIDANT; polyphenols; paw edema; analgesic; cashew nuts}, year = {2020}, eissn = {2076-3921}, orcid-numbers = {Cordaro, Marika/0000-0002-3980-0043; D'Amico, Ramona/0000-0003-0389-3871; Gugliandolo, Enrico/0000-0001-6840-3154; Scuto, Maria/0000-0003-1019-5158} } @article{MTMT:31236292, title = {The systemic role of SIRT1 in exercise mediated adaptation}, url = {https://m2.mtmt.hu/api/publication/31236292}, author = {Radák, Zsolt and Suzuki, Katsuhiko and Pósa, Anikó and Petrovszki, Zita and Koltai, Erika and Boldogh, Istvan}, doi = {10.1016/j.redox.2020.101467}, journal-iso = {REDOX BIOL}, journal = {REDOX BIOLOGY}, volume = {35}, unique-id = {31236292}, issn = {2213-2317}, year = {2020}, eissn = {2213-2317}, orcid-numbers = {Radák, Zsolt/0000-0003-1297-6804; Pósa, Anikó/0000-0003-2167-2888; Koltai, Erika/0000-0002-1370-2955} } @article{MTMT:31572357, title = {Sarcopenia: Tilting the Balance of Protein Homeostasis}, url = {https://m2.mtmt.hu/api/publication/31572357}, author = {Tan, Kuan Ting and Ang, Seok-Ting Jamie and Tsai, Shih-Yin}, doi = {10.1002/pmic.201800411}, journal-iso = {PROTEOMICS}, journal = {PROTEOMICS}, volume = {20}, unique-id = {31572357}, issn = {1615-9853}, abstract = {Sarcopenia, defined as age-associated decline of muscle mass and function, is a risk factor for mortality and disability, and comorbid with several chronic diseases such as type II diabetes and cardiovascular diseases. Clinical trials showed that nutritional supplements had positive effects on muscle mass, but not on muscle function and strength, demonstrating our limited understanding of the molecular events involved in the ageing muscle. Protein homeostasis, the equilibrium between protein synthesis and degradation, is proposed as the major mechanism underlying the development of sarcopenia. As the key central regulator of protein homeostasis, the mammalian target of rapamycin (mTOR) is proposed to be essential for muscle hypertrophy. Paradoxically, sustained activation of mTOR complex 1 (mTORC1) is associated with a loss of sensitivity to extracellular signaling in the elderly. It is not understood why sustained mTORC1 activity, which should induce muscle hypertrophy, instead results in muscle atrophy. Here, recent findings on the implications of disrupting protein homeostasis on muscle physiology and sarcopenia development in the context of mTOR/protein kinase B (AKT) signaling are reviewed. Understanding the role of these molecular mechanisms during the ageing process will contribute towards the development of targeted therapies that will improve protein metabolism and reduce sarcopenia.}, keywords = {AKT; Ageing; mTor; muscle atrophy; protein homeostasis}, year = {2020}, eissn = {1615-9861} } @article{MTMT:31702454, title = {Exercise-Induced Autophagy Suppresses Sarcopenia Through Akt/mTOR and Akt/FoxO3a Signal Pathways and AMPK-Mediated Mitochondrial Quality Control}, url = {https://m2.mtmt.hu/api/publication/31702454}, author = {Zeng, Zhengzhong and Liang, Jiling and Wu, Liangwen and Zhang, Hu and Lv, Jun and Chen, Ning}, doi = {10.3389/fphys.2020.583478}, journal-iso = {FRONT PHYSIOL}, journal = {FRONTIERS IN PHYSIOLOGY}, volume = {11}, unique-id = {31702454}, abstract = {Exercise training is one of the most effective interventional strategies for sarcopenia in aged people. Nevertheless, the underlying mechanisms are not well recognized. Increasing studies have reported abnormal regulation of autophagy in aged skeletal muscle. Our current study aims to explore the efficiency of exercise interventions, including treadmill exercise, resistance exercise, alternating exercise with treadmill running and resistance exercise, and voluntary wheel running, on 21-month-old rats with sarcopenia and to detect the underlying mechanisms. Results showed the declined mass of gastrocnemius muscle with deficient autophagy and excessive apoptosis as a result of up-regulated Atrogin-1 and MuRF1, declined Beclin1 level and LC3-II/LC3-I ratio, accumulated p62, increased Bax, and reduced Bcl-2 levels, and also exhibited a defective mitochondrial quality control due to declined PGC-1 alpha, Mfn2, Drp1, and PINK1 levels. However, 12-week exercise interventions suppressed the decline in mass loss of skeletal muscle, accompanied by down-regulated Atrogin-1 and MuRF1, increased Beclin1 level, improved LC3-II/LC3-I ratio, declined p62 level, and reduced Bax and increased Bcl-2 level, as well as enhanced mitochondrial function due to the increased PGC-1 alpha, Mfn2, Drp1, and PINK1 levels. Moreover, exercise interventions also down-regulated the phosphorylation of Akt, mTOR, and FoxO3a, and up-regulated phosphorylated AMPK to regulate the functional status of autophagy and mitochondrial quality control. Therefore, exercise-induced autophagy is beneficial for remedying sarcopenia by modulating Akt/mTOR and Akt/FoxO3a signal pathways and AMPK-mediated mitochondrial quality control, and resistance exercise exhibits the best interventional efficiency.}, keywords = {Autophagy; Sarcopenia; mitochondrial quality control; Exercise intervention; Akt/mTOR signal pathway; Akt/FoxO3a signal pathway}, year = {2020}, eissn = {1664-042X} } @article{MTMT:31460474, title = {Aging Induced p53/p21 in Genioglossus Muscle Stem Cells and Enhanced Upper Airway Injury}, url = {https://m2.mtmt.hu/api/publication/31460474}, author = {Zhu, Lu-Ying and Yu, Li-Ming and Zhang, Wei-Hua and Deng, Jia-Jia and Liu, Shang-Feng and Huang, Wei and Zhang, Meng-Han and Lu, Yan-Qin and Han, Xin-Xin and Liu, Yue-Hua}, doi = {10.1155/2020/8412598}, journal-iso = {STEM CELLS INT}, journal = {STEM CELLS INTERNATIONAL}, volume = {2020}, unique-id = {31460474}, issn = {1687-966X}, abstract = {Aging of population brings related social problems, such as muscle attenuation and regeneration barriers with increased aging. Muscle repair and regeneration depend on muscle stem cells (MuSCs). Obstructive sleep apnea (OSA) rises in the aging population. OSA leads to hypoxia and upper airway muscle injury. However, little is known about the effect of increasing age and hypoxia to the upper airway muscle. The genioglossus (GG) is the major dilator muscle to keep the upper airway open. Here, we reported that muscle fiber and MuSC function declined with aging in GG. Increasing age also decreased the migration and proliferation of GG MuSCs. p53 and p21 were high expressions both in muscle tissue and in GG MuSCs. We further found that hypoxia inhibited GG MuSC proliferation and decreased myogenic differentiation. Then, hypoxia enhanced the inhibition effect of aging to proliferation and differentiation. Finally, we investigated that hypoxia and aging interact to form a vicious circle with upregulation of p53 and p21. This vicious hypoxia plus aging damage accelerated upper airway muscle injury. Aging and hypoxia are the major damage elements in OSA patients, and we propose that the damage mechanism of hypoxia and aging in GG MuSCs will help to improve upper airway muscle regeneration.}, year = {2020}, eissn = {1687-9678} } @article{MTMT:30953227, title = {High-intensity interval training changes the expression of muscle RING-finger protein-1 and muscle atrophy F-box proteins and proteins involved in the mechanistic target of rapamycin pathway and autophagy in rat skeletal muscle}, url = {https://m2.mtmt.hu/api/publication/30953227}, author = {Cui, Xinwen and Zhang, Yimin and Wang, Zan and Yu, Jingjing and Kong, Zhenxing and Ruzic, Lana}, doi = {10.1113/EP087601}, journal-iso = {EXP PHYSIOL}, journal = {EXPERIMENTAL PHYSIOLOGY}, volume = {104}, unique-id = {30953227}, issn = {0958-0670}, abstract = {New FindingsWhat is the central question of this study?What are the adaptations of protein synthesis and degradation that occur in skeletal muscle in response to high-intensity interval training (HIIT), and what are the magnitudes of the changes in response to HIIT, compared to moderate-intensity continuous training (MICT), and the mechanisms underlying these changes? What is the main finding and its importance?HIIT is more effective than MICT in altering the expression of muscle RING-finger protein-1 and muscle atrophy F-box, and enhancing the autophagic flux in rat soleus muscle. In addition, HIIT could activate the mechanistic target of rapamycin pathway. These findings suggest that HIIT might be an effective exercise strategy for health promotion in skeletal muscle. This study aimed to investigate the impact of high-intensity interval training (HIIT) on the proteins involved in protein synthesis, the ubiquitin-proteasome system (UPS) and autophagy in skeletal muscle of middle-aged rats. Nine-month-old male Wistar rats (n = 56) were randomly divided into three groups: a control (C) group, a moderate-intensity continuous training (MICT) group and a HIIT group. Rats in the training groups ran on treadmills 5 days per week for 8 weeks. The MICT group ran for 50 min at 60% V?O2 max , while the HIIT group ran for 3 min at 80% of V?O2 max six times separated by 3-min periods at 40% V?O2 max . Aerobic endurance, number of autophagosomes and expression of proteins involved in protein synthesis and degradation in the soleus muscle were measured at three time points: before training, after 4 weeks and after 8 weeks of training. Compared to the C group, HIIT and MICT increased the expression of phosphorylated mechanistic target of rapamycin (mTOR) after 8 weeks (P P < 0.01, respectively). HIIT increased the expression of muscle RING-finger protein-1 (MuRF-1) after 4 weeks (P < 0.01), and decreased its expression after 8 weeks (P < 0.01). Both HIIT and MICT decreased the expression of muscle atrophy F-box (MAFbx) after 4 weeks (P < 0.05). HIIT improved the expression of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II (P < 0.05), and decreased the P62 content (P < 0.01) after 4 weeks. The LC3II/LC3I ratio was increased after 8 weeks (P < 0.01). This study demonstrated that HIIT could activate the mTOR pathway, alter the expression of MuRF-1 and MAFbx proteins, and enhance autophagic flux in soleus muscle of middle-aged rats.}, keywords = {UBIQUITIN-PROTEASOME SYSTEM; Autophagy; MTOR PATHWAY; High-intensity interval training}, year = {2019}, eissn = {1469-445X}, pages = {1505-1517} } @article{MTMT:30953226, title = {Effects of treadmill with different intensities on bone quality and muscle properties in adult rats}, url = {https://m2.mtmt.hu/api/publication/30953226}, author = {Liu, Zhehao and Gao, Jiazi and Gong, He}, doi = {10.1186/s12938-019-0728-0}, journal-iso = {BIOMED ENG ONLINE}, journal = {BIOMEDICAL ENGINEERING ONLINE}, volume = {18}, unique-id = {30953226}, issn = {1475-925X}, abstract = {BackgroundBone is a dynamically hierarchical material that can be divided into length scales of several orders of magnitude. Exercise can cause bone deformation, which in turn affects bone mass and structure. This study aimed to study the effects of treadmill running with different intensities on the long bone integrity and muscle biomechanical properties of adult male rats.MethodsForty-eight 5-month-old male SD rats were randomly divided into 4 groups: i.e., sedentary group (SED), exercise with speed of 12 m/min group (EX12), 16 m/min group (EX16), and 20 m/min group (EX20). The exercise was carried out for 30 min every day, 5 days a week for 4 weeks. The femurs were examined using three-point bending test, microcomputer tomography scanning and nanoindentation test; the soleus muscle was dissected for tensile test; ALP and TRACP concentrations were measured by serum analysis.ResultsThe failure load was significantly increased by the EX12 group, whereas the elastic modulus was not significantly changed. The microstructure and mineral densities of the trabecular and cortical bone were significantly improved by the EX12 group. The mechanical properties of the soleus muscle were significantly increased by treadmill exercise. Bone formation showed significant increase by the EX12 group. Statistically higher nanomechanical properties of cortical bone were detected in the EX12 group.ConclusionThe speed of 12 m/min resulted in significant changes in the microstructure and biomechanical properties of bone; besides, it significantly increased the ultimate load of the soleus muscle. The different intensities of treadmill running in this study provide an experimental basis for the selection of exercise intensity for adult male rats.}, keywords = {treadmill exercise; exercise intensity; Femurs; Multiscale analysis; Biomechanical properties}, year = {2019}, eissn = {1475-925X} } @article{MTMT:30542642, title = {Sarcopenia, frailty and their prevention by exercise}, url = {https://m2.mtmt.hu/api/publication/30542642}, author = {Nascimento, C. M. and Ingles, M. and Salvador-Pascual, A. and Cominetti, M. R. and Gomez-Cabrera, M. C. and Vina, J.}, doi = {10.1016/j.freeradbiomed.2018.08.035}, journal-iso = {FREE RADICAL BIO MED}, journal = {FREE RADICAL BIOLOGY AND MEDICINE}, volume = {132}, unique-id = {30542642}, issn = {0891-5849}, abstract = {Sarcopenia is a major component of the frailty syndrome, both being considered as strong predictors of morbidity, disability, and death in older people.}, keywords = {PROTEINS; ATROPHY; protein synthesis; malnutrition; Oxidative stress}, year = {2019}, eissn = {1873-4596}, pages = {42-49} } @article{MTMT:30953229, title = {Electromyostimulation with blood flow restriction enhances activation of mTOR and MAPK signaling pathways in rat gastrocnemius muscles}, url = {https://m2.mtmt.hu/api/publication/30953229}, author = {Natsume, Toshiharu and Yoshihara, Toshinori and Naito, Hisashi}, doi = {10.1139/apnm-2018-0384}, journal-iso = {APPL PHYSIOL NUTR ME}, journal = {APPLIED PHYSIOLOGY NUTRITION AND METABOLISM-PHYSIOLOGIE APPLIQUEE NUTRITION}, volume = {44}, unique-id = {30953229}, issn = {1715-5312}, abstract = {Neuromuscular electrical stimulation (NMES) combined with blood flow restriction (BFR) induces muscle hypertrophy. However, cellular mechanisms underlying the muscle hypertrophy induced by NMES combined with BFR remain unclear. We tested the hypothesis that NMES combined with BFR would enhance the mechanistic target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) signaling pathways. Age-matched male Wistar rats (6 months old, n = 7 per group) were assigned randomly to control, BFR alone (BFR), NMES alone (NMES), and NMES combined with BFR (NMES/BFR) groups. NMES induced 25 isometric contractions lasting 8 s with 4-s resting periods between contractions in the gastrocnemius muscle. Four sets in total were performed, with 1-min intervals between sets. A latex cuff was placed on the proximal portion of the hind limb and BFR at 200 mm Hg was conducted in 4 sets (each set 5 min) with 1-min rest intervals between sets. Venous blood was collected from the lateral tail vein to determine pH, H+ concentration, and lactate concentration before and immediately after the treatments. Expression levels of proteins related to muscle hypertrophy were determined by Western blot analysis. The application of NMES/BFR promoted muscle fatigue more than NMES alone. NMES/BFR induced greater changes in accumulation of metabolites and increase in gastrocnemius muscle weight. The phosphorylation of mTOR and MAPK signaling-related proteins was also enhanced following NMESIBFR, compared with other conditions. Thus, NMES enhanced the activation of mTOR and MAPK signaling pathways when combined with BFR.}, keywords = {PH; MYOSTATIN; LACTATE; muscle hypertrophy; KAATSU; hydrogen ion}, year = {2019}, eissn = {1715-5320}, pages = {637-644} } @article{MTMT:30319457, title = {Exercise effects on physiological function during aging}, url = {https://m2.mtmt.hu/api/publication/30319457}, author = {Radák, Zsolt and Torma, Ferenc Gergely and Berkes, István and Goto, Sataro and Mimura, Tatsuya and Pósa, Anikó and Balogh, László and Boldogh, Istvan and Suzuki, Katsuhiko and Higuchi, Mitsuru and Koltai, Erika}, doi = {10.1016/j.freeradbiomed.2018.10.444}, journal-iso = {FREE RADICAL BIO MED}, journal = {FREE RADICAL BIOLOGY AND MEDICINE}, volume = {132}, unique-id = {30319457}, issn = {0891-5849}, year = {2019}, eissn = {1873-4596}, pages = {33-41}, orcid-numbers = {Radák, Zsolt/0000-0003-1297-6804; Pósa, Anikó/0000-0003-2167-2888; Koltai, Erika/0000-0002-1370-2955} } @article{MTMT:30953228, title = {Antioxidant and Adaptative Response Mediated by Nrf2 during Physical Exercise}, url = {https://m2.mtmt.hu/api/publication/30953228}, author = {Vargas-Mendoza, Nancy and Morales-Gonzalez, Angel and Osiris Madrigal-Santillan, Eduardo and Madrigal-Bujaidar, Eduardo and Alvarez-Gonzalez, Isela and Fernando Garcia-Melo, Luis and Anguiano-Robledo, Liliana and Fregoso-Aguilar, Tomas and Morales-Gonzalez, Jose A.}, doi = {10.3390/antiox8060196}, journal-iso = {ANTIOXIDANTS-BASEL}, journal = {ANTIOXIDANTS}, volume = {8}, unique-id = {30953228}, abstract = {Nuclear factor erythroid 2-related factor 2 (Nrf2) is a powerful nuclear transcription factor that coordinates an antioxidant cytoprotector system complex stimulated by the increase in inoxidative stress (OS). In the present manuscript, we conduct a review on the evidence that shows the effect different modalities of physical exercise exert on the antioxidant metabolic response directed by Nrf2. During physical exercise, the reactive oxygen species (ROS) are increased; therefore, if the endogenous and exogenous antioxidant defenses are unable to control the elevation of ROS, the resulting OS triggers the activation of the transcriptional factor Nrf2 to induce the antioxidant response. On a molecular basis related to physical exercise, hormesis maintenance (exercise preconditioning) and adaptative changes in training are supported by a growing body of evidence, which is important for detailing the health benefits that involve greater resistance to environmental aggressions, better tolerance to constant changes, and increasing the regenerative capacity of the cells in such a way that it may be used as a tool to support the prevention or treatment of diseases. This may have clinical implications for future investigations regarding physical exercise in terms of understanding adaptations in high-performance athletes but also as a therapeutic model in several diseases.}, keywords = {antioxidants; Nrf2; Exercise training; adaptative response; Oxidative stress}, year = {2019}, eissn = {2076-3921} } @article{MTMT:27688528, title = {Autophagy and mitophagy flux in young and aged skeletal muscle following chronic contractile activity}, url = {https://m2.mtmt.hu/api/publication/27688528}, author = {Carter, Heather N and Kim, Yuho and Erlich, Avigail T and Zarrin-khat, Dorrin and Hood, David A}, doi = {10.1113/JP275998}, journal-iso = {J PHYSIOL-LONDON}, journal = {JOURNAL OF PHYSIOLOGY-LONDON}, volume = {596}, unique-id = {27688528}, issn = {0022-3751}, year = {2018}, eissn = {1469-7793}, pages = {3567-3584} } @article{MTMT:27477270, title = {Regulation of apoptosis and autophagy in mouse and human skeletal muscle with aging and lifelong exercise training}, url = {https://m2.mtmt.hu/api/publication/27477270}, author = {Dethlefsen, MM and Halling, JF and Møller, HD and Plomgaard, P and Regenberg, B and Ringholm, S and Pilegaard, H}, doi = {10.1016/j.exger.2018.07.011}, journal-iso = {EXP GERONTOL}, journal = {EXPERIMENTAL GERONTOLOGY}, volume = {111}, unique-id = {27477270}, issn = {0531-5565}, year = {2018}, eissn = {1873-6815}, pages = {141-153} } @article{MTMT:27595402, title = {Identification of pathways and genes associated with synovitis in osteoarthritis using bioinformatics analyses}, url = {https://m2.mtmt.hu/api/publication/27595402}, author = {Huang, Hui and Zheng, Jiaxuan and Shen, Ningjiang and Wang, Guangji and Zhou, Gang and Fang, Yehan and Lin, Jianping and Zhao, Jianning}, doi = {10.1038/s41598-018-28280-6}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {8}, unique-id = {27595402}, issn = {2045-2322}, year = {2018}, eissn = {2045-2322} } @article{MTMT:3396116, title = {Reactive Oxygen and Nitrogen Species Regulate Key Metabolic, Anabolic, and Catabolic Pathways in Skeletal Muscle}, url = {https://m2.mtmt.hu/api/publication/3396116}, author = {Nemes, R and Koltai, Erika and Taylor, AW and Suzuki, K and Győri, Ferenc József and Radák, Zsolt}, doi = {10.3390/antiox7070085}, journal-iso = {ANTIOXIDANTS-BASEL}, journal = {ANTIOXIDANTS}, volume = {7}, unique-id = {3396116}, abstract = {Reactive oxygen and nitrogen species (RONS) are important cellular regulators of key physiological processes in skeletal muscle. In this review, we explain how RONS regulate muscle contraction and signaling, and why they are important for membrane remodeling, protein turnover, gene expression, and epigenetic adaptation. We discuss how RONS regulate carbohydrate uptake and metabolism of skeletal muscle, and how they indirectly regulate fat metabolism through silent mating type information regulation 2 homolog 3 (SIRT3). RONS are causative/associative signaling molecules, which cause sarcopenia or muscle hypertrophy. Regular exercise influences redox biology, metabolism, and anabolic/catabolic pathways in skeletal muscle in an intensity dependent manner.}, year = {2018}, eissn = {2076-3921}, orcid-numbers = {Koltai, Erika/0000-0002-1370-2955; Győri, Ferenc József/0000-0002-9989-0028; Radák, Zsolt/0000-0003-1297-6804} } @article{MTMT:27601301, title = {Exercise training causes a partial improvement through increasing testosterone and eNOS for erectile function in middle-aged rats}, url = {https://m2.mtmt.hu/api/publication/27601301}, author = {Seo, Dae Yun and Lee, Sung Ryul and Kwak, Hyo Bum and Park, Hyuntea and Seo, Kyo Won and Noh, Yeon Hee and Song, Kang-Moon and Ryu, Ji-Kan and Ko, Kyung Soo and Rhee, Byoung Doo and Han, Jin}, doi = {10.1016/j.exger.2018.04.003}, journal-iso = {EXP GERONTOL}, journal = {EXPERIMENTAL GERONTOLOGY}, volume = {108}, unique-id = {27601301}, issn = {0531-5565}, year = {2018}, eissn = {1873-6815}, pages = {131-138} } @article{MTMT:27595404, title = {Effects of aerobic training, resistance training, or both on circulating irisin and myostatin in untrained women}, url = {https://m2.mtmt.hu/api/publication/27595404}, author = {Shabani, Ramin and Izaddoust, Fatemeh}, doi = {10.5507/ag.2018.007}, journal-iso = {ACTA GYMNICA}, journal = {ACTA GYMNICA}, volume = {48}, unique-id = {27595404}, issn = {2336-4912}, year = {2018}, eissn = {2336-4920}, pages = {47-55} } @article{MTMT:30531905, title = {Role of exercise in age-related sarcopenia}, url = {https://m2.mtmt.hu/api/publication/30531905}, author = {Yoo, Su-Zi and No, Mi-Hyun and Heo, Jun-Won and Park, Dong-Ho and Kang, Ju-Hee and Kim, So Hun and Kwak, Hyo-Bum}, doi = {10.12965/jer.1836268.134}, journal-iso = {J EXERC REHABIL}, journal = {JOURNAL OF EXERCISE REHABILITATION}, volume = {14}, unique-id = {30531905}, issn = {2288-176X}, abstract = {Sarcopenia is an age-associated decline of skeletal muscle mass and function and is known to lead to frailty, cachexia, osteoporosis, metabolic syndromes, and death. Notwithstanding the increasing incidence of sarcopenia, the molecular and cellular mechanisms driving age-related sarcopenia are not completely understood. This article reviews current definitions of sarcopenia, its potential mechanisms, and effects of exercise on sarcopenia. The pathogenesis of age-related sarcopenia is multifactorial and includes myostatin, inflammatory cytokines, and mitochondria-derived problems. Especially, age-induced mitochondrial dysfunction triggers the production of reactive oxygen species (ROS) by mitochondria, impedes mitochondrial dynamics, interrupts mitophagy, and leads to mitochondria-mediated apoptosis. Aerobic exercise provides at least a partial solution to sarcopenia as it ameliorates mitochondria-derived problems, and resistance exercise strengthens muscle mass and function. Furthermore, combinations of these exercise types provide the benefits of both. Collectively, this review summarizes potential mechanisms of age-related sarcopenia and emphasizes the use of exercise as a therapeutic strategy, suggesting that combined exercise provides the most beneficial means of combating age-related sarcopenia.}, keywords = {Mitochondria; skeletal muscle; Aging; Exercise; Sarcopenia}, year = {2018}, eissn = {2288-1778}, pages = {551-558} } @article{MTMT:27101630, title = {The emerging role of follistatin under stresses and its implications in diseases}, url = {https://m2.mtmt.hu/api/publication/27101630}, author = {Zhang, Lingda and Liu, Kangli and Han, Bing and Xu, Zhengping and Gao, Xiangwei}, doi = {10.1016/j.gene.2017.10.017}, journal-iso = {GENE}, journal = {GENE}, volume = {639}, unique-id = {27101630}, issn = {0378-1119}, year = {2018}, eissn = {1879-0038}, pages = {111-116} } @article{MTMT:26805122, title = {The effect of endurance training with and without vitamin E on expression of p53 and PTEN tumor suppressing genes in prostate glands of male rats}, url = {https://m2.mtmt.hu/api/publication/26805122}, author = {Dashtiyan, AA and Sepehrimanesh, M and Tanideh, N and Afzalpour, ME}, doi = {10.1016/j.biopen.2017.03.005}, journal-iso = {Biochimie Open}, journal = {Biochimie Open}, volume = {4}, unique-id = {26805122}, issn = {2214-0085}, year = {2017}, pages = {112-118} } @article{MTMT:26517299, title = {Spermidine coupled with exercise rescues skeletal muscle atrophy from D-gal-induced aging rats through enhanced autophagy and reduced apoptosis via AMPK-FOXO3a signal}, url = {https://m2.mtmt.hu/api/publication/26517299}, author = {Fan, Jingjing and Yang, Xiaoqi and Li, Jie and Shu, Ziyang and Dai, Jun and Liu, Xingran and Li, Biao and Jia, Shaohui and Kou, Xianjuan and Yang, Yi and Chen, Ning}, doi = {10.18632/oncotarget.15420}, journal-iso = {ONCOTARGET}, journal = {ONCOTARGET}, volume = {8}, unique-id = {26517299}, year = {2017}, eissn = {1949-2553}, pages = {17475-17490}, orcid-numbers = {Fan, Jingjing/0000-0002-1110-5735} } @article{MTMT:26769427, title = {Exercise restores muscle stem cell mobilization, regenerative capacity and muscle metabolic alterations via adiponectin/AdipoR1 activation in SAMP10 mice}, url = {https://m2.mtmt.hu/api/publication/26769427}, author = {Inoue, Aiko and Cheng, Xian Wu and Huang, Zhe and Hu, Lina and Kikuchi, Ryosuke and Jiang, Haiying and Piao, Limei and Sasaki, Takeshi and Itakura, Kohji and Wu, Hongxian and Zhao, Guangxian and Lei, Yanna and Yang, Guang and Zhu, Enbo and Li, Xiang and Sato, Kohji and Koike, Teruhiko and Kuzuya, Masafumi}, doi = {10.1002/jcsm.12166}, journal-iso = {J CACHEXIA SARCOPENIA MUSCLE}, journal = {JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE}, volume = {8}, unique-id = {26769427}, issn = {2190-5991}, year = {2017}, eissn = {2190-6009}, pages = {370-385} } @article{MTMT:26769430, title = {Sarcopenic obesity or obese sarcopenia: A cross talk between age-associated adipose tissue and skeletal muscle inflammation as a main mechanism of the pathogenesis}, url = {https://m2.mtmt.hu/api/publication/26769430}, author = {Kalinkovich, Alexander and Livshits, Gregory}, doi = {10.1016/j.arr.2016.09.008}, journal-iso = {AGEING RES REV}, journal = {AGEING RESEARCH REVIEWS}, volume = {35}, unique-id = {26769430}, issn = {1568-1637}, year = {2017}, eissn = {1872-9649}, pages = {200-221} } @article{MTMT:26769431, title = {Impact of Aging and Exercise on Mitochondrial Quality Control in Skeletal Muscle}, url = {https://m2.mtmt.hu/api/publication/26769431}, author = {Kim, Yuho and Triolo, Matthew and Hood, David A}, doi = {10.1155/2017/3165396}, journal-iso = {OXID MED CELL LONGEV}, journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY}, unique-id = {26769431}, issn = {1942-0900}, year = {2017}, eissn = {1942-0994} } @article{MTMT:3202563, title = {SIRT1 may play a crucial role in overload-induced hypertrophy of skeletal muscle}, url = {https://m2.mtmt.hu/api/publication/3202563}, author = {Koltai, Erika and Bori, Zoltán and Chabert, C and Dubouchaud, H and Naito, H and Machida, S and Davies, KJ and Murlasits, Zsolt and Fry, AC and Boldogh, I and Radák, Zsolt}, doi = {10.1113/JP273774}, journal-iso = {J PHYSIOL-LONDON}, journal = {JOURNAL OF PHYSIOLOGY-LONDON}, volume = {595}, unique-id = {3202563}, issn = {0022-3751}, abstract = {Significant skeletal muscle mass guarantees functional wellbeing and is important for high level performance in many sports. Although the molecular mechanism for skeletal muscle hypertrophy has been well-studied, it still is not completely understood. In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus, and gastrocnemius muscles in rats. Two weeks of muscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant increase in SIRT1 content and activity (P < 0.001). SIRT1-regulated Akt, eNOS, GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels. Alternatively, decreased FOXO1 and increased K48 polyubiquitination also suggest that SIRT1 could also be involved in the catabolic process of hypertrophy. Furthermore, increased levels of K63 and muscle RING finger 2 (MuRF2) protein could also be important enhancers of muscle mass. We report here that the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, SIRT1, and Nampt levels. Our results reveal a strong agreement between SIRT1 levels and activity, SIRT1 regulated pathways, and overload-induced hypertrophy. These findings, along with the well-known regulatory roles that SIRT1 plays in modulating both anabolic and catabolic pathways, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overload induced hypertrophy of skeletal muscle. This hypothesis will now require rigorous direct and functional testing. This article is protected by copyright. All rights reserved.}, year = {2017}, eissn = {1469-7793}, pages = {3361-3376}, orcid-numbers = {Koltai, Erika/0000-0002-1370-2955; Bori, Zoltán/0000-0003-1253-060X; Murlasits, Zsolt/0000-0003-4101-3417; Radák, Zsolt/0000-0003-1297-6804} } @article{MTMT:26912934, title = {Influence of anaerobic and aerobic exercise on age-related pathways in skeletal muscle}, url = {https://m2.mtmt.hu/api/publication/26912934}, author = {Navas-Enamorado, Ignacio and Bernier, Michel and Brea-Calvo, Gloria and de Cabo, Rafael}, doi = {10.1016/j.arr.2017.04.005}, journal-iso = {AGEING RES REV}, journal = {AGEING RESEARCH REVIEWS}, volume = {37}, unique-id = {26912934}, issn = {1568-1637}, year = {2017}, eissn = {1872-9649}, pages = {39-52} } @article{MTMT:27101631, title = {The role of declining adaptive homeostasis in ageing}, url = {https://m2.mtmt.hu/api/publication/27101631}, author = {Pomatto, Laura C D and Davies, Kelvin J A}, doi = {10.1113/JP275072}, journal-iso = {J PHYSIOL-LONDON}, journal = {JOURNAL OF PHYSIOLOGY-LONDON}, volume = {595}, unique-id = {27101631}, issn = {0022-3751}, year = {2017}, eissn = {1469-7793}, pages = {7275-7309} } @article{MTMT:26804424, title = {Resistance training regulates gene expression of molecules associated with intramyocellular lipids, glucose signaling and fiber size in old rats}, url = {https://m2.mtmt.hu/api/publication/26804424}, author = {Ribeiro, MBT and Guzzoni, V and Hord, JM and Lopes, GN and Marqueti, RDC and de Andrade, RV and Selistre-de-Araujo, HS and Durigan, JLQ}, doi = {10.1038/s41598-017-09343-6}, journal-iso = {SCI REP}, journal = {SCIENTIFIC REPORTS}, volume = {7}, unique-id = {26804424}, issn = {2045-2322}, year = {2017}, eissn = {2045-2322} } @article{MTMT:26769429, title = {Epigallocatechin-3-gallate increases autophagy signaling in resting and unloaded plantaris muscles but selectively suppresses autophagy protein abundance in reloaded muscles of aged rats}, url = {https://m2.mtmt.hu/api/publication/26769429}, author = {Takahashi, Hideyuki and Suzuki, Yutaka and Mohamed, Junaith S and Gotoh, Takafumi and Pereira, Suzette L and Alway, Stephen E}, doi = {10.1016/j.exger.2017.02.075}, journal-iso = {EXP GERONTOL}, journal = {EXPERIMENTAL GERONTOLOGY}, volume = {92}, unique-id = {26769429}, issn = {0531-5565}, year = {2017}, eissn = {1873-6815}, pages = {56-66} } @article{MTMT:26573021, title = {Mitochondrial Adaptations in Aged Skeletal Muscle: Effect of Exercise Training}, url = {https://m2.mtmt.hu/api/publication/26573021}, author = {Ziaaldini, M M and Hosseini, S R A and Fathi, M}, doi = {10.33549/physiolres.933329}, journal-iso = {PHYSIOL RES}, journal = {PHYSIOLOGICAL RESEARCH}, volume = {66}, unique-id = {26573021}, issn = {0862-8408}, year = {2017}, eissn = {1802-9973}, pages = {1-14} } @article{MTMT:26936283, title = {Biochemical Pathways of Sarcopenia and Their Modulation by Physical exercise: A Narrative Review}, url = {https://m2.mtmt.hu/api/publication/26936283}, author = {Ziaaldini, Mohammad Mosaferi and Marzetti, Emanuele and Picca, Anna and Murlasits, Zsolt}, doi = {10.3389/fmed.2017.00167}, journal-iso = {FRONT MED}, journal = {FRONTIERS IN MEDICINE}, volume = {4}, unique-id = {26936283}, year = {2017}, eissn = {2296-858X}, orcid-numbers = {Murlasits, Zsolt/0000-0003-4101-3417} } @article{MTMT:26517300, title = {The effect of intense intermittent training with and without taking vitamin E on mRNA expression of p53/PTEN tumor suppressing genes in prostate glands of male rats}, url = {https://m2.mtmt.hu/api/publication/26517300}, author = {Afzalpour, Mohammad Esmaeil and Tanideh, Nader and Sepehrimanesh, Masood and Dashtiyan, Amin Allah}, journal-iso = {INT J MED RES HEALTH SCI}, journal = {INTERNATIONAL JOURNAL OF MEDICAL RESEARCH AND HEALTH SCIENCES}, volume = {5}, unique-id = {26517300}, issn = {2319-5886}, year = {2016}, pages = {521-528} } @article{MTMT:26476831, title = {Effects of elastic band resistance training and nutritional supplementation on muscle quality and circulating muscle growth and degradation factors of institutionalized elderly women: the Vienna Active Ageing Study (VAAS)}, url = {https://m2.mtmt.hu/api/publication/26476831}, author = {Hofmann, M and Schober-Halper, B and Oesen, S and Franzke, B and Tschan, H and Bachl, N and Strasser, E-M and Quittan, M and Wagner, K-H and Wessner, B}, doi = {10.1007/s00421-016-3344-8}, journal-iso = {EUR J APPL PHYSIOL}, journal = {EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY}, volume = {116}, unique-id = {26476831}, issn = {1439-6319}, year = {2016}, eissn = {1439-6327}, pages = {885-897} } @inproceedings{MTMT:26476826, title = {Response of BAX, Bcl-2 proteins, and SIRT1/PGC-1α mRNA expression to 8-week treadmill running in the aging rat skeletal muscle}, url = {https://m2.mtmt.hu/api/publication/26476826}, author = {Li, F-H and Yu, H-T and Xiao, L and Liu, Y-Y}, booktitle = {Oxygen Transport to Tissue XXXVIII}, doi = {10.1007/978-3-319-38810-6_38}, publisher = {Springer Netherlands}, unique-id = {26476826}, year = {2016}, pages = {283-289} } @article{MTMT:26183986, title = {Redox control of skeletal muscle atrophy}, url = {https://m2.mtmt.hu/api/publication/26183986}, author = {Powers, Scott K and Morton, Aaron B and Ahn, Bumsoo and Smuder, Ashley J}, doi = {10.1016/j.freeradbiomed.2016.02.021}, journal-iso = {FREE RADICAL BIO MED}, journal = {FREE RADICAL BIOLOGY AND MEDICINE}, volume = {98}, unique-id = {26183986}, issn = {0891-5849}, year = {2016}, eissn = {1873-4596}, pages = {208-217} } @article{MTMT:26476830, title = {Evidence for the involvement of the CXCL12 system in the adaptation of skeletal muscles to physical exercise}, url = {https://m2.mtmt.hu/api/publication/26476830}, author = {Puchert, M and Adams, V and Linke, A and Engele, J}, doi = {10.1016/j.cellsig.2016.05.019}, journal-iso = {CELL SIGNAL}, journal = {CELLULAR SIGNALLING}, volume = {28}, unique-id = {26476830}, issn = {0898-6568}, year = {2016}, eissn = {1873-3913}, pages = {1205-1215} } @mastersthesis{MTMT:26804544, title = {Skeletal muscle and cardiac adaptations to swimming -induced exercise in adult zebrafish. Adaptacions del múscul esquelètic i cardiac a l’exe rcici per natació induïda en el peix zebra adult}, url = {https://m2.mtmt.hu/api/publication/26804544}, author = {Rovira, I Berger M}, unique-id = {26804544}, year = {2016} } @article{MTMT:26476829, title = {Exercise training as a drug to treat age associated frailty}, url = {https://m2.mtmt.hu/api/publication/26476829}, author = {Viña, J and Salvador-Pascual, A and Tarazona-Santabalbina, FJ and Rodriguez-Mañas, L and Gomez-Cabrera, MC}, doi = {10.1016/j.freeradbiomed.2016.03.024}, journal-iso = {FREE RADICAL BIO MED}, journal = {FREE RADICAL BIOLOGY AND MEDICINE}, volume = {98}, unique-id = {26476829}, issn = {0891-5849}, year = {2016}, eissn = {1873-4596}, pages = {159-164} } @article{MTMT:26476828, title = {Hypertrophy-promoting effects of leucine supplementation and moderate intensity aerobic exercise in pre-senescent mice}, url = {https://m2.mtmt.hu/api/publication/26476828}, author = {Xia, Z and Cholewa, J and Zhao, Y and Yang, Y-Q and Shang, H-Y and Guimarães-Ferreira, L and Naimo, MA and Su, Q-S and Zanchi, NE}, doi = {10.3390/nu8050246}, journal-iso = {NUTRIENTS}, journal = {NUTRIENTS}, volume = {8}, unique-id = {26476828}, year = {2016}, eissn = {2072-6643} } @article{MTMT:26476832, title = {Intermittent bout exercise training down-regulates age-associated inflammation in skeletal muscles}, url = {https://m2.mtmt.hu/api/publication/26476832}, author = {Kim, J-S and Yi, H-K}, doi = {10.1016/j.exger.2015.11.001}, journal-iso = {EXP GERONTOL}, journal = {EXPERIMENTAL GERONTOLOGY}, volume = {72}, unique-id = {26476832}, issn = {0531-5565}, year = {2015}, eissn = {1873-6815}, pages = {261-268} } @mastersthesis{MTMT:34479517, title = {EFFECT OF ENDURANCE EXERCISE ALONE AND IN COMBINATION WITH IGF-1 ADMINISTRATION ON CELLULAR MARKERS INVOLVED IN SARCOPENIA}, url = {https://m2.mtmt.hu/api/publication/34479517}, author = {Ziaaldini, Mohammad Mosaferi}, unique-id = {34479517}, year = {2015} }