Efeitos do treinamento físico e do sedentarismo sobre a resposta cardiovascular ao estresse emocional agudo: participação do hipotálamo dorsomedial

Abstract

The urban world has two great challenges to homeostasis. First, sedentary behavior, which is considered the main impact factor on global health; and second, emotional stress, which is considered an important risk factor for the development of cardiovascular diseases, such as hypertension, cardiac arrhythmias and myocardial infarction. Studies have suggested that sedentary lifestyle exacerbates cardiovascular responses to a stressful situation and that physical exercise seems to attenuate as autonomic and cardiovascular responses to acute stress. However, the remaining mechanisms still remain unknown. The dorsomedial hypothalamus (DMH) is pointed as the key nucleus that controls the autonomic and cardiovascular responses to emotional stress. The objective of this work was to evaluate the effects of sedentary behavior and physical training on the autonomic and cardiovascular response to acute emotional stress and on the desired properties of neurons in the dorsomedial hypothalamus. The ethical protocol: 278/2017 (CEUA- UFMG). Six-week-old Wistar rats were used during eight weeks of aerobic physical training with an intensity of 50 to 60% of the maximum capacity, one hour a day, five times a week called the trained group (TRAIN). The sedentary group (SEDEN) was exposed to a treadmill for five minutes at a speed of 0.8 m/min, five times a week. Our results show that sedentary behavior changed several standard parameters (adiposity index - SEDEN: 2.8 ± 0.26 vs TREIN: 2.1 ± 0.16%; baseline sympathetic activity - SEDEN: 134 ± 5 vs TREIN: 107 ± 9 spike / min; resting heart rate - SEDEN: 382 ± 14 vs TREIN: 342 ± 7 bpm) and resulted in an exacerbation of the cardiovascular response to acute emotional stress. Disinhibition of DMH with microinjection of the GABAA antagonist bicuculline resulted in greater changes in heart rate (HR - ∆HR SEDEN: 107 ± 26 vs TREIN: 38 ± 14 bpm) and renal sympathetic nerve (ASNR - ∆ASNR SEDEN : : 96 ± 16 vs TREIN: 42 ± 10%) of sedentary animals. The stimulation of DMH NMDA receptors in awake animals clearly resulted in greater pressor response (∆PAM SEDEN: 13 ± 2 vs TREIN: 4 ± 2 mmHg) and tachycardia (∆FC SEDEN: 127 ± 23 vs TREIN: 50 ± 13 bpm ) no sedentary group. Blocking NMDA receptors in anesthetized animals resulted in increase in ASNR in trained animals (ASNR SEDEN: 1 ± 7 vs TREIN: 67 ± 21%). Our results confirm and extend previous findings showing that sedentary lifestyle alters important parameters for homeostasis and enhances the cardiovascular response associated with stress. Part of this effect appears to be altered in the GABA-Glutamate balance in DMH damage to alterations in autonomic reactivity and autonomic tone. Thus, the present study highlighted that sedentary lifestyle can be a facilitator of the development of cardiovascular diseases, including those associated with stress, and that neurochemical changes in DMH are part of the mechanisms involved.