Background: Erythropoietin (EPO) is a glycoprotein hormone produced primarily by the kidney when there is a decrease in circulating oxygen level and your main function is to regulate
erythropoiesis. Analog of EPO invaded the backstage of sporting high performance scenario, especially in aerobic modalities, because it acts on the heart, circulation, aerobic endurance, leading to an
increased tissue oxygenation, decreasing the feeling of fatigue and an ergogenic function. Furthermore, it is known that EPO has actions in non-hematopoietic tissues with anti-apoptotic function,
anti-inflammatory, cell proliferation and differentiation. Thus, this study aimed to evaluate the effects of chronic administration of EPO combined with exercise training on cardiac and renal tissue
Methods: The animals were divided into four groups: sedentary control group (SCG, n=10), trained control group (TCG, n=8), sedentary EPO group (SEG, n=10) and trained EPO group (TEG,
n=8). 50IU/kg EPO were administered (subcutaneously) and was performed swimming training (increasing volume and intensity). After eight weeks of protocol we evaluated the baseline heart rate (HR) and
blood pressure (BP), cardiac hypertrophy (relative cardiac mass and diameter of cardiomyocytes) and cardiac and renal fibrosis (slides stained with picrosirius). For all the results we used a
significance level of p≤0,05.
Results: The animals of the SEG and TEG showed increased levels hematocrit compared with their respective control groups (SEG: 51,79±2,23%; TEG: 53,35±2,19%; SCG: 40,10±1,70%; TCG:
36,71±2,46%), as been expected. The animals of the TCG exhibited rest bradycardia compared to SCG (TCG: 309,28±9,95 bpm vs SCG: 348,80±12,56 bpm) and the EPO has triggered an increase in systolic
blood pressure in the sedentary group compared with the SCG (SEG: 126,69±4,31 mmHg vs SCG: 113±3,76 mmHg), which was not observed in diastolic. The TCG showed higher heart relative mass (TCG:
0,0042±0,0003g vs SCG:0,0037±0,0001g), an estimative of cardiac hypertrophy. SEG presented a higher diameter of cardiomyocytes as compared to the SCG (SEG: 4,98±0,04µm vs SCG: 4,16 ±0,04µm). Both
groups receiving EPO had fibrosis on heart compared with control groups (SEG: 30,15±0,71%; TEG: 39,74±1,03%; SCG: 18,63±0,70%; TCG: 18,08±0,64%). The same result was found in kidney (SEG: 15,83±0,58%;
TEG: 30,64±0,46%; SCG: 5,75±0,70%; TCG: 9,61±0,59%).
Conclusions: These results suggest that the chronic administration of EPO can cause a pathologic hypertrophy, cardiac and renal fibrosis. In this case unfortunately, the exercise
training by swimming was ineffective in reversing these damages.