RESUMO
We aimed to investigate the effects of high doses of nandrolone decanoate and resistance training (RT) on the proteomic profile of the left ventricle (LV) of rats, using a label-free quantitative approach. Male rats were randomized into four groups: untrained vehicle (UTV), trained vehicle (TV), untrained nandrolone (UTN), and trained nandrolone (TN). Rats were familiarized with the exercise training protocol (jump exercise) for one week. Jump-exercise was performed five days a week for 6 weeks, with 30 s of inter-set rest intervals. Nandrolone was administrated for 6 weeks (5 mg/kg, twice a week, via intramuscular). Systolic and diastolic arterial pressure and heart rate were measured 48 h post-training. LV was isolated and collagen content was measured. The expression of cardiac proteins was analyzed by ultra-efficiency liquid chromatography with mass spectrometry high / low collision energy (UPLC/MSE). Nandrolone and RT led to cardiac hypertrophy, even though high doses of nandrolone counteracted the RT-induced arterial pressures lowering. Nandrolone also affected the proteome profile negatively in LV of rats, including critical proteins related to biological processes (metabolism, oxidative stress, inflammation), structural function and membrane transporters. Our findings show physiological relevance since high doses of nandrolone induced detrimental effects on the proteome profile of heart tissue and hemodynamic parameters of rats. Furthermore, as nandrolone abuse has become increasingly common among recreational athletes and casual fitness enthusiasts, we consider that our findings have clinical relevance as well.
Assuntos
NandrolonaRESUMO
High-intensity resistance training (RT) induces adaptations that improve physiological function. However, high intensity, volume and/or frequency may lead to injury and other health issues such as adverse cardiac effects. The aim of this study was to evaluate the effect of RT on left ventricle proteome, and to identify the pathways involved on the harmful adaptations induced by this protocol. Male Wistar rats were randomized into 2 groups: Trained (T) and Sedentary (S). Animals from T group were trained for 6weeks, and then all the animals were sacrificed and left ventricle was isolated for analysis. We identified 955 proteins, and 93 proteins were considered; 36 were expressed exclusively in T group, and 4 in S group. Based on quantitative analysis, 42 proteins were found overexpressed and 11 underexpressed in T group compared with S group. Using the Gene Ontology to relate the biological processes in which these proteins are involved, we conclude that RT protocol promotes changes similar to those found in the initial phase of heart failure, but we also observed a concomitant increased expression of protective proteins, suggesting the activation of pathways to avoid major damages on left ventricle and delay the onset of pathological hypertrophy. STATEMENT OF SIGNIFICANCE OF THE STUDY: Our study shows that high-intensity RT protocol changes left ventricle proteome, modifying metabolic profile of heart tissue and inducing the expression of proteins that acts against cardiac injury. We hypothesize that these adaptations occur to prevent the onset of cardiac dysfunction. Despite highly significant, it remains to be determined whether these adaptations are sufficient to further keep left ventricle function and exert cardioprotection, and whether this panel will be shifted towards maladaptation, and heart failure.
