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Mohammad Rahman Rahimi

Mohammad Rahman Rahimi

Academic rank: Associate Professor
ORCID: 0000-0002-4302-1472
Education: PhD.
ScopusId: 35103291100
HIndex: 20/00
Faculty: Faculty of Humanities and Social Sciences
Address: Department of Exercise Physiology, University of Kurdistan, 66177-15175 , Sanandaj, Iran
Phone: 2259

Research

Title
The apoptotic response to resistance exercise with different intensities in athletes
Type
JournalPaper
Keywords
Resistance training - Apoptosis - Caspases
Year
2011
Journal MEDICINA DELLO SPORT
DOI
Researchers Saeed Sadeghi Boroujerdi ، Mohammad Rahman Rahimi

Abstract

Aim. Apoptosis is programmed cell death which plays an essential role in development and homeostasis of mature tissues in order to remove unwanted, mutant and dangers cells by intrinsic pathway. The purpose of this study was to investigate the effects of RE with 80 and 65% of one repetition maximum (1RM) loads on apoptosis response in resistance trained men. Methods. Nine resistance trained college-age men (age: 22.37±1.99 years; weight: 71.32±5.57 kg; at least 1 year of RE experience) performed two RE protocols on two randomized separate sessions that include 4 sets of the bench press, leg press, sited bar shoulder press, arm curls and lat pull down exercises using either low intensity (65% of 1RM) or high intensity (80% of 1RM). Blood draws occurred at pre-exercise, immediately post and 3h post exercise for measurement of serum p53, caspase-3 and caspase-9, and plasma IGF-1 and lactate concentration. Urine samples were also taken at the time of blood samples collection for measurement urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) excretion. Results. The concentration of 8-OHdG at 3 h after RE was significantly higher than pre-exercise, in both RE protocols, and there was no significant difference in oxidative DNA damage between two protocols. Serum p53 concentrations were significantly grater at RE protocol with 65% of 1RM load than 80% of 1RM load post and 3h post exercise. However, no difference in p53 concentrations was seen at post and 3 h post exercises in both RE sessions. No difference in caspase-9 and caspse-3 concentrations was seen between two RE protocols at any time. Serum IGF-1 concentrations were significantly higher at immediately post of RE with 65% of 1RM load compared with 80% of 1RM load. Bloodlactate concentrations significantly increased at post exercise for 2 protocols, but no significant protocols differences were observed. Conclusion. These data suggest that acute RE increases oxidative DNA damage, but does not affect tumor suppressor p53 pro