Efeito do treinamento físico sobre a função do canal de cálcio tipo L miocárdio de ratos obesos induzidos por dieta hiperlipídica insaturada

Abstract

Studies indicate that obesity for 15 weeks promotes myocardial dysfunction associated with changes in the function of L-type Ca2+ channel, main responsible for Ca2+ influx into the cytosol and trigger the activation of transit of intracellular Ca2+ . Studies propose that exercise training provides increased sensibility of myofilaments to Ca2+ and improves the function of proteins involved in myocardial transient of Ca2+, including the L-type Ca2+ channels. The study aim was to evaluate the effect of exercise training on myocardial L-type Ca2+ channel activity in obese rats induced by unsaturated high-fat diet. Male Wistar were used. Initially, they were divided in control (C; n = 40) and obese (Ob; n = 40) groups. The C rats received a standard diet and Ob cycle of unsaturated high-fat diets. After processes of induction (5 weeks) and exposure (15 weeks) obesity, mice were redistributed in more two groups (20 weeks). Thus, the study was composed of the following experimental groups: control (C; n = 12), subjected to control exercise training (CEx; n = 14), obese (Ob; n = 10) and obese subjected to exercise training (ObEx; n = 11). The nutritional and metabolic profiles, blood pressure, cardiac morphological characteristics and myocardial function of the animals were assessed. The exercise decreased body weight (Ob: 622 ± 48; ObEx: 553 ± 47 g; p<0.01), body fat (Ob: 57 ± 3.1; ObEx: 29.4 ± 3.0 g; p<0.01) and the adiposity index (Ob: 9.2 ± 0.5; ObEx: 5.3 ± 0.5 g; p<0.01). The Ob group presented values of total heart, right ventricle and their relations with tibia increased in comparison to C group. The same result was visualized in ObEx group in relation to CEx. The papillary muscles of animals showed similar behavior at baseline and after maneuvers of post-rest contraction and elevation of Ca+2 extracelular. After inhibition of myocardial L-type Ca2+ channel activity by diltiazem, the values of studied variables was similar. In conclusion, obesity promotes cardiac morphological adaptations without impairments in myocardial function and L-type Ca2+ channels activity (% inhibition of DT: C: 86,9% ± 6,27; Ob: 87,0% ± 6,54; CEx: 87,5% ± 5,3 e ObEx: 90,6% ± 3,95). In conclusion, obesity promotes cardiac morphological adaptations without impairments in myocardial function and L-type Ca2+ channel activity. Furthermore, exercise training, in spite of modifying body composition, does not alter morphological and functional characteristics of the heart, as well as, does not promotes adaptations on L-type Ca2+ channel function.