Physical Training Protects Against Release of Pro‐Inflammatory Cytokines and Prevents Alterations in Cardiac Autonomic Modulation in NA Experimental Model of COPD
Authors: MIRANDA MUNIQUE TOSTES FERREIRA , CARVALHO JORGE LUÍS COSTA , FIALHO ANA KAROLINA SÁ , IRIGOYEN MARIA CLÁUDIA , CASALI KARINA RABELLO , AIMBIRE FLÁVIO TOSTES FERREIRA 
Published: June 2021

Respiratory chronic diseases are one of the most important causes of morbidity and mortality, and Chronic Obstructive Pulmonary Disease (COPD) stands out between the others. This disease is caracterized by a limitation to airflow, which is not completely reversible, beside importants systemics effects, like damages in cardiac autonomic modulation and an overreacted inflammatory cells associated with an increased secretion of cytokines. Physical training (PT) has been well‐marked as an important therapeutic tool. However, the influence of PT in the development of this disease is not completely described, especially as a preventive method. Thus, the aim of this study was to evaluate the impact of an PT in the inflammatory profile and autonomic modulation before the establishment of COPD. Experiments were executed in 2 steps. First, 28 mice C57Bl/6 were divided in 4 groups: G1(control, n=7); G2 (COPD, n=7); G3 (PT, n=7); and G4 (COPD+PT, n=7) to analise cellularity and the levels of TNF‐alfa, IL‐6, IL‐10, TGF‐beta, CXCL‐1 and CCL2. Then, 28 mice were divided into the same groups to analise the autonomic aspects. G1 were kept without intervention for 4 weeks, while G3 and G4 were trained in a treadmill for the same period (5 days/week, 1 hour/day). G2 and G4 (at the end of the PT) passed by the COPD induction, which were caracterized by 3 days with cigarette smoke (CS) exposion and the administration of an intranasal dose of LPS at the third day. 24 hours latter, mice were euthanized and the samples were collected. Animals that provided hemodynamics data had their carotid artery cannulated in the last day of the protocol, and 24 hours latter signals were registered. Inflammatory aspects showed that the model of CS+LPS was efficient to increase total and differential cellularity in the Bronchoalveolar Lavage Fluid, and, at the same time, PT decreased the same aspects. Pro‐inflammatory cytokines levels were also increased in COPD group. In the other hand, PT significantly prevented their increase in trained animals. TGF‐beta had their level increased in trained group, showing its “tissue‐protective” feature. About the hemodynamics aspects, the proposed model of COPD induction showed an increase in the sympathetic cardiac modulation and in the sympathovagal inbalance, while there was a decrease in the parasympathetic cardiac modulation. In COPD group, artherial pressure variability was also increased. PT was efficient to increase protective parameters, like parasympathetic cardiac modulation and arterial pressure variability, while it decreased sympathetic cardiac modulation and suited sympathovagal inbalance. In conclusion, aerobic PT was able to prevent a greater release of pro‐inflammatory cytokines and regulate the presence of protective molecules, like TGF‐beta. Also, PT acts like a protective tool to suit hemodynamics parameters, increasing positive aspects related to cardiac vagal tonus and decreasing the influence of sympathetic system.

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.