Aims
Regular exercise is recommended in postmenopausal women to prevent the development of heart disease, but mechanism underlying the protection is not completely understood. Many studies have suggested that exercise training notably mediated whole body immune and inflammatory functions. Whether exercise training prevents cardiac dysfunction after deprivation of female sex hormones by inhibiting cardiac immune activation is therefore interesting. Main
Methods
Nine-week treadmill running program was introduced in sham-operated and ovariectomized rats. In addition, chronic angiotensin II infusion was further challenged to activate pathological cardiac remodeling. Cardiac remodeling in associated with the density and degranulation of cardiac mast cells was then evaluated. Key findings: With exogenous angiotensin II-induced hypertension, cardiac hypertrophy with myocardial fibrosis was shown similarly in both sham-operated controls and ovariectomized rats. Although exercise training did not prevent cardiac hypertrophy, myocardial fibrosis was abolished by exercise. While ovariectomy increased both cardiac mast cell density and degranulation percentage, angiotensin II infusion only enhanced mast cell density. Exercise training could not decrease the density of mast cells, but it did normalize the percentage of degranulation in all groups. Correlation analysis suggested that cardiac mast cell activation is inversely associated with cardiomyocyte hypertrophy due to exercise training but is directly correlated to cardiac hypertrophy by angiotensin II infusion. Significance: Exercise training could attenuate cardiac mast cell hyperactivation induced by either deprivation of female sex hormones or excessive angiotensin II. Additionally, cardiac mast cells could be a solution in the distinction between physiological and pathological hypertrophic development.
Significance
Exercise training could attenuate cardiac mast cell hyperactivation induced by either deprivation of female sex hormones or excessive angiotensin II. Additionally, cardiac mast cells could be a solution in the distinction between physiological and pathological hypertrophic development.