The response and adaptation of COX-2, PGI-2 and TXA-2 on diabetic wistar rats to progressive resistance training

Cardiovascular diseases are the main reason of mortality in diabetic patients which include microvascular and macrovascular injuries. Chronic inflammation conditions in diabetes are associated with Cyclooxigenase 2 enzyme (COX-2) expression. The major metabolites of this enzyme which play an important role in cardiovascular homeostasis are Prostocyclin 2 (PGI-2) and Tromboxane (TXA-2). The present study investigates the response and adaptation of COX-2, PGI-2 and TXA-2 on diabetic wistar rats to progressive resistance training. in an experimental study 49 wistar rats were purchased from Pasteur institute of Iran and divided into acute resistance exercise (n=10), acute control (n=10), prolonged resistance exercise (n=12) and prolonged control(n=12) groups. The prolonged resistance exercise protocol included 8 weeks (3 sessions per weeks) of 10 sets of ascending from ladder and free weights were attached to rats’ tails (this overload is determined by maximum capacity of carrying free weights). The animals were sacrificed 48 hours after the last session of training program and sample blood was taken. After the left ventricle was drained, COX-2, PGI-2 and TXA-2 were measured; the data were analyzed by t-test via spss16 software. The results of independent t-test show no significant difference between PGI-2 level of heart in acute resistance exercise and control group (p=0.693) and prolonged resistance exercise and control group (p=0.103). Also, there were no significant difference between TXA- 2 level of heart in acute resistance exercise and control group (p=0.134) and prolonged resistance exercise and control group (p=0.103). In this study there were no significant difference in COX-2 level of heart between acute resistance training and its control group (p=0.349), but in prolonged resistance exercise group this value was significant (p=0.02). It appears that resistance exercise doesn’t have any significant effect on inflammatory, stimulatory and inhibitory factors of microvascular and macrovascular in diabetic patients.