Cardiopulmonary reflex and blood pressure response after swimming and treadmill exercise in hypertensive rats.

Cardiopulmonary sensitivity was evaluated after exercise training through swimming and running in spontaneously hypertensive rats (SHR) that were divided into three groups: (a) run exercise; (b) swim exercise; and (c) sedentary. For 8 wks, the run exercise was performed on a treadmill while the swim exercise was performed by swimming. Cardiopulmonary reflex was evaluated by chemical and mechanical pathways through the injections of phenylbiguanide (PBG) (5.0 mg?kg-1) and volume expansion with isotonic saline (0.75% of body weight), respectively. Both types of exercise training decreased systolic blood pressure (SBP) compared to the sedentary group. The swim trained group reduced SBP faster than the run trained group. The sensitivity of the chemically activated endings of the cardiopulmonary reflex was increased in both exercise-trained groups for hypotensive response. The exercise training groups had higher levels of urine output after acute volume expansion. The production of urine showed that swimming and treadmill training were more efficient than the sedentary group. These results indicate that: (a) exercise improved cardiopulmonary reflex sensitivity; and (b) swim training led to a faster SBP reduction and a more sensitive reflex response to pressure stimuli

Swimming exercise demonstrates advantages over running exercise in reducing proteinuria and glomerulosclerosis in spontaneously hypertensive rats.

Experimental studies in animal models have described the benefits of physical exercise (PE) to kidney diseases associated with hypertension. Land- and water-based exercises induce different responses in renal function. Our aim was to evaluate the renal alterations induced by different environments of PE in spontaneously hypertensive rats (SHRs). The SHRs were divided into sedentary (S), swimming exercise (SE), and running exercise (RE) groups, and were trained for 8 weeks under similar intensities (60 min/day). Arterial pressure (AP) and heart rate (HR) were recorded. The renal function was evaluated through urinary volume at each week of training; sodium and potassium excretions, plasma and urinary osmolarities, glomerular filtration rate (GFR), levels of proteinuria, and renal damage were determined. SE and RE rats presented reduced mean AP, systolic blood pressure, and HR in comparison with S group. SE and RE rats showed higher urine osmolarity compared with S. SE rats showed higher free water clearance (P < 0.01), lower urinary density (P < 0.0001), and increased weekly urine volume (P < 0.05) in comparison with RE and S groups. GFR was increased in both SE and RE rats. The proteinuria of SE (7.0 ? 0.8 mg/24 h) rats was decreased at the 8th week of the PE in comparison with RE (9.6 ? 0.8 mg/24 h) and S (9.8 ? 0.5 mg/24 h) groups. The glomerulosclerosis was reduced in SE rats (P < 0.02). SE produced different response in renal function in comparison with RE, in which only swimming-trained rats had better profile for proteinuria and glomerulosclerosis

Eccentric overload muscle damage is attenuated by a novel angiotensin- (1-7) treatment.

The development of new strategies to attenuate exercise-induced muscle damage may be helpful for training regimens. The aim of this study was to determine whether a oral formulation of angiotensin Ang-(1-7)[HP?CD/Ang-(1-7)] is effective to reduce pain, and muscle damage markers after eccentric-overload exercise. HP?CD (Placebo) and HP?CD/Ang-(1-7) (Ang-(1-7) group were treated for 7 days (one capsule/day). The pain was measured by visual analogue scale, maximal strength (MS) using force platform. Blood samples were collected for cytokines and creatine kinase (CK) analysis. The Ang-(1-7)-treated group reported less pain immediately (3.46? 0.64 vs. placebo 3.80? 0.77 cm) and 24h after exercise (3.07?0.71 vs. 3.73?0.58cm placebo) and higher MS at 24h (24?12N) and 48h (30?15N) vs. placebo (-8 ? 9 N and -10 ? 9 N). The CK for Ang-(1-7) (0.5 ? 0.1 and 0.9?0.2 U/L) were lower at 48 and 72h vs. placebo (fold changes of 1.7?0.5 and 1.5?0.3 U/L). The TNF-? level was lower in the treated group post-exercise (38 ? 2.5 pg/ml) vs. placebo (45 ? 2.9 pg/ml) but no significant changes were observed for IL-6 and IL-10. Our data indicate that treatment with Ang-(1-7) may attenuate pain, some of the muscle damage markers and improves performance following eccentric exercise

Acute volume expansion decreased baroreflex response after swimming but not after running exercise training in hypertensive rats.

Background: Physical training (ET) is important to restore the reflex sensitivity involved in controlling blood pressure in various diseases. Recent investigations have demonstrated an interaction between cardiopulmonar baroreceptors and arterial baroreflex during dynamic exercise.Objective: Considering that acute and chronic hemodynamic responses to swimming (SW) are different from the race (RUN), the objective of this study was to evaluate the effect of SW and RUN on baroreflex response before and after acute volume expansion in spontaneously hypertensive rats (SHR).Methods: SHR were divided into three groups: RUN, SW and sedentary (SED) groups. After training, the mean arterial pressure (MAP) and heart rate (HR) were recorded. Baroreflex response was assessed before and after acute volume expansion.Results: Both ET conditions reduced basal levels of HR and MAP. The first volume of injected isotonic saline solution (1.25% of body weight) produced a greater decrease in HR for the SW group (?105.8 ? 8.7 bpm) compared to RUN groups (?68 ? 5.2 bpm) and SED(?49.8 ? 7.2 bpm). Both training modalities increase the baroreflex response in relation to the SED group, but after the total volume expansion, the SW group presented attenuated response (0.7 ? 0.1 ?PIms/mmHg) compared to RUN (1.5 ? 0.17 PIms/mmHg) and was not different from SED group (0.8 ? 0.2 mPIms/mmHg). Conclusion: The results show that the swim-trained group has a different baroreflex response to that observed by the run-trained group after the activation of the load receptors by saline expansion

Lifetime overproduction of circulating angiotensin?(1?7) in rats attenuates the increase in skeletal muscle damage biomarkers after exhaustive exercise.

Angiotensin?(1?7) (Ang?[1?7]) can modulate glucose metabolism and protect against muscular damage. The aim of this study was to investigate the influence of lifetime increase of circulating levels of Ang?(1?7) at exhaustive swimming exercise (ESE). Sprague?Dawley (SD) and transgenic rats TGR(A1?7)3292 (TR) which overproduce Ang?(1?7) (2.5?fold increase) were submitted to ESE. The data showed no differences in time to exhaustion (SD: 4.90 ? 1.37 h vs. TR: 5.15 ? 1.15 h), creatine kinase, and transforming growth factor beta (TGF-?). Lactate dehydrogenase (SD: 219.9 ? 12.04 U/L vs. TR: 143.9 ? 35.21 U/L) and ??actinin (SD: 336.7 ? 104.5 U/L vs. TR: 224.6 ? 82.45 U/L) values were significantly lower in TR. There was a significant decrease in the range of blood glucose levels (SD: ?41.4 ? 28.32 mg/dl vs. TR: ?13.08 ? 39.63 mg/dl) in SD rats. Muscle (SD: 0.06 ? 0.02 mg/g vs. TR: 0.13 ? 0.01 mg/g) and hepatic glycogen (SD: 0.66 ? 0.36 mg/g vs. TG: 2.24 ? 1.85 mg/g) in TR were higher. The TR presented attenuation of the increase in skeletal muscle damage biomarkers and of the changes in glucose metabolism after ESE