Federal University of São Paulo (UNIFESP), Department of Medicine, Discipline of Nephrology, São Paulo, SP.
Federal University of São Paulo (UNIFESP, Department of Physiology, Discipline of Nutrition Physiology, São Paulo, SP.
Life Sci. 2016 May 1;152:156-64. doi: 10.1016/j.lfs.2016.03.040. Epub 2016 Mar 26.
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.
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.
高强度阻力训练（RT）可引起改善生理功能的适应性变化。然而，高强度、大容量和/或高频率可能导致损伤和其他健康问题，如不良的心脏效应。本研究的目的是评估 RT 对左心室蛋白质组的影响，并确定该方案引起的有害适应性变化所涉及的途径。雄性 Wistar 大鼠随机分为 2 组：训练（T）组和安静（S）组。T 组的动物接受 6 周的训练，然后所有动物被处死并分离左心室进行分析。我们鉴定了 955 种蛋白质，其中 93 种被认为是有意义的；36 种仅在 T 组中表达，4 种在 S 组中表达。基于定量分析，与 S 组相比，T 组有 42 种蛋白质表达上调，11 种蛋白质表达下调。使用基因本体论来关联这些蛋白质所涉及的生物学过程，我们得出结论，RT 方案促进了类似于心力衰竭初始阶段所发现的变化，但我们也观察到保护性蛋白质的表达同时增加，这表明激活了避免左心室重大损伤和延迟病理性肥大发生的途径。
我们的研究表明，高强度 RT 方案改变了左心室蛋白质组，改变了心脏组织的代谢特征，并诱导了对抗心脏损伤的蛋白质的表达。我们假设这些适应性变化是为了防止心脏功能障碍的发生。尽管意义重大，但仍需要确定这些适应性变化是否足以进一步保持左心室功能并发挥心脏保护作用，以及该谱是否会向适应性不良和心力衰竭转变。
