اثر تمرين ورزشي تناوبي شديد بر سطوح سرمي و بيان ژن Tfam و PGC1α در هيپوكمپ رت‌هاي نر

The effect of high-intensity exercise training on serum levels and gene expression of Tfam and PGC1α in hippocampus of male rats

ﻧﻘﺶ ﮐﻠﯿﺪي در ﺣﻔﻆ ﺗﻌﺪاد ﮐﭙﯽ و ﻓﻌﺎﻟﯿﺖ ﻧﺴﺨﻪﺑﺮداري mtDNA ﻣﯿﺘﻮﮐﻨﺪرﯾﺎﯾﯽ دارد. ﻫﺪف از ﺗﺤﻘﯿﻖ ﺣﺎﺿﺮ، ﺗﻌﯿﯿﻦ اﺛﺮ ﺗﻤﺮﯾﻦ ورزﺷﯽ ﺗﻨﺎوﺑﯽ ﺷﺪﯾﺪ (HIIT) ﺑﺮ ﻓﺎﮐﺘﻮرﻫﺎي ﺑﺎﯾﻮژﻧﺰ ﻣﯿﺘﻮﮐﻨﺪرﯾﺎﯾﯽ در ﻫﯿﭙﻮﮐﻤﭗ رتﻫﺎي ﻧﺮ ﺑﻮد. در ﺗﺤﻘﯿﻖ ﺣﺎﺿﺮ 20 ﺳﺮ رت ﻧﮋاد وﯾﺴﺘﺎر در دو ﮔﺮوه HIIT و ﮐﻨﺘﺮل ﻗﺮار ﮔﺮﻓﺘﻨﺪ. HIIT ﺑﻪ ﻣﺪت 60 دﻗﯿﻘﻪ در ﻫﺮ ﺟﻠﺴﻪ و ﺑﻪ ﻣﺪت ﭼﻬﺎر ﺟﻠﺴﻪ در ﻫﻔﺘﻪ اﻧﺠﺎم ﮔﺮﻓﺖ. ﮔﺮوه ﺗﻤﺮﯾﻦ ورزﺷﯽ، 15 وﻫﻠﮥ 4 دﻗﯿﻘﻪاي را ﺑﺎ 90 – 85 درﺻﺪ VO2max ﺑﺎ ﺳﻪ دﻗﯿﻘﻪ رﯾﮑﺎوري ﺑﺎ ﺷﺪت 70 درﺻﺪ VO2max (ﺑﯿﻦ وﻫﻠﻪﻫﺎي HIIT) اﺟﺮا ﮐﺮد. ﺳﭙﺲ، ﻧﻤﻮﻧﻪﮔﯿﺮي ﺧﻮﻧﯽ و ﺑﺎﻓﺖﺑﺮداري از ﻫﯿﭙﻮﮐﻤﭗ رتﻫﺎ اﻧﺠﺎم ﮔﺮﻓﺖ. PGC1α و Tfam ﺑﺎ اﺳﺘﻔﺎده از ﮐﯿﺖﻫﺎي ﺗﺠﺎري و ﺑﯿﺎن ژن آﻧﻬﺎ ﺑﺎ اﺳﺘﻔﺎده از روش Real-Time PCR ارزﯾﺎﺑﯽ ﺷﺪﻧﺪ. ﻧﺘﺎﯾﺞ ﺑﯿﺎﻧﮕﺮ اﻓﺰاﯾﺶ ﻣﻌﻨﺎدار VO2max و ﺳﻄﻮح ﺳﺮﻣﯽ PGC1α و Tfam ﺑﻮد (0/05

Mitochondrial transcription factor A (Tfam) has a key role in keep of copy numbers and transcription activity of mtDNA. The object of the recent study was to determine the effect of exercise training on serum levels and gene expression of mitochondrial transcription factor A and PGC1α in hippocampus of male rats. In the present study 20 Wistar rats were divided into training and control groups. Training protocol was done 60 min in each session for four sessions in each week. Training group was carried out 15 × 4 min bouts of training with 85 to 90% of VO2max that sustained with three min recovery with 70% of VO2max. PGC1α and Tfam and their gene translations were evaluated by commercial kits and Real-Time PCR method, respectively. Results illustrated that VO2max and serum levels of biomarkers of mitochondrial biogenesis were significantly increased (p<0.05). Also, PGC1α and Tfam gene translations in hippocampus were significantly increased (p<0.05). It seems that, the present three-week training protocol has competency to increase in both hippocampus and serum levels of PGC1α and Tfam in male rats. Likewise, there is a likelihood that significant increase of Tfam is due to meaningful vicissitudes of PGC1α.