پاﺳﺦ ﺗﻐﯿﯿﺮات ﻣﮑﺎﻧﯿﮑﯽ ﺑﻄﻦﻫﺎي ﭼﭗ و راﺳﺖ ﻋﻀﻠﮥ ﻗﻠﺐ ورزﺷﮑﺎران ﻣﺘﻌﺎﻗﺐ دو ﺷﯿﻮة ﺗﻤﺮﯾﻦ ﻣﻘﺎوﻣﺘﯽ ﺷﺪﯾﺪ

Response of Mechanical Changes in the Left and Right Ventricles of Athletes' Myocardium following Two Methods of High Intensity Resistance Training

ﭼﮑﯿﺪه اﺟﺮاي ﻓﻌﺎﻟﯿﺖﻫﺎي ﻣﻘﺎوﻣﺘﯽ ﺷﺪﯾﺪ و ﻃﻮﻻﻧﯽﻣﺪت ﺑﺮ دﯾﻮارﻫﺎي ﺑﻄﻨﯽ ﻓﺸﺎر وارد ﻣﯽﮐﻨﺪ و ﻣﯽﺗﻮاﻧﺪ ﺑﻪﺻﻮرت ﺣﺎد ﮐﺎر ﻣﮑﺎﻧﯿﮑﯽ ﺑﻄﻦﻫﺎ را ﻣﺨﺘﻞ ﺳﺎزد. از ﻃﺮﻓﯽ ﺗﺄﺛﯿﺮ اﺟﺮاي ﻓﻌﺎﻟﯿﺖﻫﺎي ﻣﻘﺎوﻣﺘﯽ ﺷﺪﯾﺪ ﺑﺮ اﺧﻼل ﺳﺎزوﮐﺎر ﻗﻠﺒﯽ ﻣﺸﺨﺺ ﻧﯿﺴﺖ؛ ﺑﻨﺎﺑﺮاﯾﻦ ﭘﮋوﻫﺶ ﺣﺎﺿﺮ ﺑﺎ ﻣﺘﻌﺎدل ﮐﺮدن ﺷﺎﺧﺺ ﺣﺠﻢ و ﺷﺪت در دو ﺷﯿﻮة ﻓﻌﺎﻟﯿﺖ ﺳﺖﻫﺎي واﻣﺎﻧﺪهﺳﺎز و ﺳﺖﻫﺎي ﺧﻮﺷﻪاي، ﭘﺎﺳﺦﻫﺎي ﻋﻤﻠﮑﺮدي ﺑﻄﻦﻫﺎي راﺳﺖ )RV( و ﭼﭗ )LV( را ﺑﺮرﺳﯽ ﻣﯽﮐﻨﺪ. 12 ورزﺷﮑﺎر ﻣﺮد ﺑﺎ ﺳﺎﺑﻘﮥ ﺗﻤﺮﯾﻨﯽ 9/33±2/99 ﺳﺎل، داوﻃﻠﺒﺎﻧﻪ دو ﻧﻮع ﭘﺮوﺗﮑﻞ ﺗﻤﺮﯾﻨﯽ ﺳﺖﻫﺎي واﻣﺎﻧﺪهﺳﺎز و ﺧﻮﺷﻪاي را ﺑﺎ ﻃﺮح ﭘﯿﺶآزﻣﻮن و ﭘﺎﯾﺶ 30 دﻗﯿﻘﻪ، 6 و 24 ﺳﺎﻋﺖ ﺑﻌﺪ را ﻣﺠﺰا اﺟﺮا ﮐﺮدﻧﺪ. ﻫﺮ دو ﻧﻮع ﭘﺮوﺗﮑﻞ ﺷﺎﻣﻞ 9 ﺣﺮﮐﺖ در داﻣﻨﮥ شدت (RM15-12) و حجم هاي تمريني برابر بود، براي ست هاي وامانده ساز در سه چرخه 12 تا 15 تكرار و ست هاي خوشه اي 9 چرخه 4 ﺗﺎ 5 ﺗﮑﺮار اﺟﺮا ﺷﺪ. در ﭘﺎﯾﺶ ﺑﻌﺪ از ﻓﻌﺎﻟﯿﺖ ﺳﺖﻫﺎي واﻣﺎﻧﺪهﺳﺎز در ﻣﻘﺎﯾﺴﻪ ﺑﺎ ﺧﻮﺷﻪاي، ﺿﺮﺑﺎن ﻗﻠﺐ ﺑﺎ اﻧﺪازة اﺛﺮ )0/87=d( و درﺻﺪ ﺗﻐﯿﯿﺮات )24%=PC(، ﺣﺠﻢ ﺿﺮﺑﻪاي )0/69=d( و )14%=PC(، ﺑﺮونده ﻗﻠﺒﯽ )2/06=d( و )35%=PC(، ﺣﺠﻢ ﭘﺎﯾﺎن ﺳﯿﺴﺘﻮﻟﯽ )0/68=d( و)10%=PC(، دﯾﺎﺳﺘﻮﻟﯽ )0/85=d( و )13 %=PC( ﺑﺎﻻ ﺑﻮد. درﺻﻮرﺗﯽﮐﻪ ﻣﺘﻮﺳﻂ ﻓﺸﺎر ﺧﻮن )0/99=d( و )10%=PC(، ﻣﻘﺎوﻣﺖ ﻋﺮوﻗﯽ ﻋﻤﻮﻣﯽ )0/91=d( و )35%=PC( ﭘﺎﯾﯿﻦ ﺑﻮد )0/05P(. ﻣﻘﺪار d=1/03) RVFAC( و )11%=PC( و d=1/38) RVGLS( و )%21=PC( در ﭘﺎﯾﺶ 30 دﻗﯿﻘﻪ ﺑﻌﺪ از ﺳﺖﻫﺎي واﻣﺎﻧﺪهﺳﺎز ﮐﺎﻫﺶ داﺷﺖ ﮐﻪ ﺑﻌﺪ از 24 ﺳﺎﻋﺖ ﺑﻪ ﺳﻄﻮح ﭘﺎﯾﻪ ﺑﺮﮔﺸﺖ )0/05

Intensive and prolonged resistance training puts pressure on the ventricular walls and can severely disrupt ventricular mechanical work. On the other hand, the effect of high intensity resistance training on cardiac mechanism disturbance is not obvious. Therefore, this study investigated right ventricular (RV) and left ventricular (LV) functional responses to two types of training (failure sets and cluster sets) with balancing intensity and volume index. 12 male athletes with training history of 9.33 ± 2.99 years voluntarily preformed two training protocols of failure sets and cluster sets separately with pretest and 30 minutes, 6 and 24 hours posttest design. Both protocols consisted of 9 movements in equal training volumes and intensity range (12-15 RM) which were performed in 3 cycles of 12-15 repetitions for failure sets and 9 cycles of 4-5 repetitions for cluster sets. At the posttest, heart rate with effect size (d=0.87) and percentage change (PC=24%), stroke volume (d=0.69) (PC=14%), cardiac output (d=2.06) (PC=35%), end systolic volume (d=0.68) (PC=10%) and end diastolic volume (d=0.85) (PC=13%) were higher after failure sets compared with cluster sets. However, mean blood pressure (d=0.99) (PC=10%) and systemic vascular resistance (d=0.91) (PC=35%) were low (P<0.05). In both training protocols, no significant changes were observed in the ejection fraction, global longitudinal strain (GLS) and (E / é) ratio (P>0.05). RVFAC (d=1.03) (PC=11%) and RVGLS (d=1.38) (PC=21%) decreased in 30 minutes after the failure sets, which returned to the baseline after 24 hours (P<0.05). RV function was severely disrupted and deteriorated after the failure sets, which was associated with increased diastolic and systolic end dimensions of the RV. The heart is trying to optimally maintain the LV function in blood pumping and ventricular injection by modifying the ventricular filling and injection procedures.