Abstract
Objective To investigate effects of two different high intensity training modes on angiotensin Ⅱ (AT Ⅱ) and ATIR in serum and kidney of rats, and also to investigate its pathogenesis. Methods Two different high intensity training modes were: the once-only exhausting training mode and the load accumulation training mode. (1) In the first training mode, rats were randomly divided into the control group (group A), training group 1 (group B1) and training group 2 (group B2). Animals in group B1 and B2 were made to take on the once-only exhausting running exercises on treadmill. Urine data and concentration of angiotensin Ⅱ in serum and kidney, and the expression of AT1R in kidney were determined with immunohistochemistry upon termination of training and 24 hours after training. (2) In the second training mode, rats were randomly divided into control group 1 (group C1), the moderate intensity training group (group D1), control group 2 (group C2) and the high intensity training group (group D2). Rats in group D1 were forced to take on progressively moderate intensity running exercises on treadmill for 4 weeks. Rats in group D2 were forced to take on progressively high intensity running exercises on treadmill for 8 weeks. Various data of group C1 and D1 were determined at the end of the fourth week, and data of group C2 and D2 were also measured at the end of the eighth week. Results (1) In the exhausting training mode group, chemical data,such as urine protein, urease, concentration of angiotensin Ⅱ in serum and kidney, and the expression of AT1R in group B1 all ncreased significantly right after training (P<0.05) , when compared with those of group A. Twenty-four hours later, all the data of group B2 decreased to some extent, when a comparison was made with those of group BI, but were still higher than those of the control group (P<0.05). (2) In the load accumulation training mode, chemical data, such as urine protein, urease and concentration of angiotensin Ⅱ in serum and kidney elevated obviously in group D1 at week 4, when compared with those of control group 1 (C1), whereas the expression of AT1R decreased obviously (P <0.05). When the high intensity training came to the end of week 8, all the data of group D2 were higher than those of group C2 (P < 0.05). The relationship between the concentration of angiotensin Ⅱ in kidney and urine protein was obviously closer than that of angiotensin Ⅱ in serum. Conclusions Different training modes and intensity could induce changes to various degrees in concentration of angiotensin Ⅱ and the expression of AT1R, and might be positively correlated with urinary albumin. These effects might be of importance in pathogenesis of renal injury caused by high intensity training. Key words: Exercise injury; Kidney; Angiotensin; AT1R
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