TY  - THES
AU  - Mosaferi Ziaaldini, Mohammad
TI  - Effect of endurance exercise alone and in combination with IGF-1 administration on cellular markers involved in sarcopenia
PY  - 2015
SP  - 123
DO  - 10.17624/TF.2015.02
UR  - https://m2.mtmt.hu/api/publication/2921417
ID  - 2921417
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Mosaferi Ziaaldini, Mohammad
AU  - Koltai, Erika
AU  - Csende, Zsolt
AU  - Goto, Sataro
AU  - Boldogh, Istvan
AU  - Taylor, Albert W
AU  - Radák, Zsolt
TI  - Exercise training increases anabolic and attenuates catabolic and apoptotic processes in aged skeletal muscle of male rats
JF  - EXPERIMENTAL GERONTOLOGY
J2  - EXP GERONTOL
VL  - 67
PY  - 2015
SP  - 9
EP  - 14
PG  - 6
SN  - 0531-5565
DO  - 10.1016/j.exger.2015.04.008
UR  - https://m2.mtmt.hu/api/publication/2883904
ID  - 2883904
AB  - Abstract Aging results in significant loss of mass and function of the skeletal muscle, which negatively impacts the quality of life. In this study we investigated whether aerobic exercise training has the potential to alter anabolic and catabolic pathways in the skeletal muscle. Five and twenty eight month old rats were used in the study. Aging resulted in decreased levels of follistatin/mTOR/Akt/Erk activation and increased myostatin/Murf1/2, proteasome subunits, and protein ubiquitination levels. In addition, TNF-α, reactive oxygen species (ROS), p53, and Bax levels were increased while Bcl-2 levels were decreased in the skeletal muscle of aged rats. Six weeks of exercise training at 60% of VO2max reversed the age-associated activation of catabolic and apoptotic pathways and increased anabolic signaling. The results suggest that the age-associated loss of muscle mass and cachexia could be due to the orchestrated down-regulation of anabolic and up-regulation of catabolic and pro-apoptotic processes. These metabolic changes can be attenuated by exercise training.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Torma, Ferenc Gergely
AU  - Koltai, Erika
AU  - Nagy, E
AU  - Mosaferi Ziaaldini, Mohammad
AU  - Pósa, Anikó
AU  - Koch, LG
AU  - Britton, SL
AU  - Boldogh, I
AU  - Radák, Zsolt
TI  - Exercise increases markers of spermatogenesis in rats selectively bred for low running capacity
JF  - PLOS ONE
J2  - PLOS ONE
VL  - 9
PY  - 2014
IS  - 12
PG  - 11
SN  - 1932-6203
DO  - 10.1371/journal.pone.0114075
UR  - https://m2.mtmt.hu/api/publication/2796664
ID  - 2796664
AB  - The oxidative stress effect of exercise training on testis function is under debate. In the present study we used a unique rat model system developed by artificial selection for low and high intrinsic running capacity (LCR and HCR, respectively) to evaluate the effects of exercise training on apoptosis and spermatogenesis in testis. Twenty-four 13-month-old male rats were assigned to four groups: control LCR (LCR-C), trained LCR (LCR-T), control HCR (HCR-C), and trained HCR (HCR-T). Ten key proteins connecting aerobic exercise capacity and general testes function were assessed, including those that are vital for mitochondrial biogenesis. The VO2 max of LCR-C group was about 30% lower than that of HCR-C rats, and the SIRT1 levels were also significantly lower than HCR-C. Twelve weeks of training significantly increased maximal oxygen consumption in LCR by nearly 40% whereas HCR remained unchanged. LCR-T had significantly higher levels of peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1alpha), decreased levels of reactive oxygen species and increased acetylated p53 compared to LCR-C, while training produced no significant changes for these measures in HCR rats. BAX and Blc-2 were not different among all four groups. The levels of outer dense fibers -1 (Odf-1), a marker of spermatogenesis, increased in LCR-T rats, but decreased in HCR-TR rats. Moreover, exercise training increased the levels of lactate dehydrogenase C (LDHC) only in LCR rats. These data suggest that rats with low inborn exercise capacity can increase whole body oxygen consumption and running exercise capacity with endurance training and, in turn, increase spermatogenesis function via reduction in ROS and heightened activity of p53 in testes.
LA  - English
DB  - MTMT
ER  -