Swimming training improves cardiovascular autonomic dysfunctions and prevents renal damage in rats fed a high‐sodium diet from weaning.

New Findings: What is the central question of this study?How does swimming exercise training impact hydro‐electrolytic balance, renal function, sympathetic contribution to resting blood pressure and cerebrospinal fluid (CSF) [Na+] in rats fed a high‐sodium diet from weaning?What is the main finding and its importance?An exercise‐dependent reduction in blood pressure was associated with decreased CSF [Na+], sympathetically driven vasomotor tonus and renal fibrosis indicating that the anti‐hypertensive effects of swimming training in rats fed a high‐sodium diet might involve neurogenic mechanisms regulated by sodium levels in the CSF rather than changes in blood volume. High sodium intake is an important factor associated with hypertension. High‐sodium intake with exercise training can modify homeostatic hydro‐electrolytic balance, but the effects of this association are mostly unknown. In this study, we sought to investigate the effects of swimming training (ST) on cerebrospinal fluid (CSF) Na+ concentration, sympathetic drive, blood pressure (BP) and renal function of rats fed a 0.9% Na+ (equivalent to 2% NaCl) diet with free access to water for 22 weeks after weaning. Male Wistar rats were assigned to two cohorts: (1) fed standard diet (SD) and (2) fed high‐sodium (HS) diet. Each cohort was further divided into trained and sedentary groups. ST normalised BP levels of HS rats as well as the higher sympathetically related pressor activity assessed by pharmacological blockade of ganglionic transmission (hexamethonium). ST preserved the renal function and attenuated the glomerular shrinkage elicited by HS. No change in blood volume was found among the groups. CSF [Na+] levels were higher in sedentary HS rats but were reduced by ST. Our findings showed that ST effectively normalised BP of HS rats, independent of its effects on hydro‐electrolytic balance, which might involve neurogenic mechanisms regulated by Na+ levels in the CSF as well as renal protection. [ABSTRACT FROM AUTHOR]