Abstract
We examined the effect of exercise training (Ex) without (Ex 0%) or with a 3% workload (Ex 3%) on different cardiac and renal parameters in renovascular hypertensive (2K1C) male Fisher rats weighing 150-200 g. Ex was performed for 5 weeks, 1 h/day, 5 days/week. Ex 0% or Ex 3% induced similar attenuation of baseline mean arterial pressure (MAP, 119 ± 5 mmHg in 2K1C Ex 0%, N = 6, and 118 ± 5 mmHg in 2K1C Ex 3%, N = 11, vs 99 ± 4 mmHg in sham sedentary (Sham Sed) controls, N = 10) and heart rate (HR, bpm) (383 ± 13 in 2K1C Ex 0%, N = 6, and 390 ± 14 in 2K1C Ex 3%, N = 11 vs 371 ± 11 in Sham Sed, N = 10,). Ex 0%, but not Ex 3%, improved baroreflex bradycardia (0.26 ± 0.06 ms/mmHg, N = 6, vs 0.09 ± 0.03 ms/mmHg in 2K1C Sed, N = 11). Morphometric evaluation suggested concentric left ventricle hypertrophy in sedentary 2K1C rats. Ex 0% prevented concentric cardiac hypertrophy, increased cardiomyocyte diameter and decreased cardiac vasculature thickness in 2K1C rats. In contrast, in 2K1C, Ex 3% reduced the concentric remodeling and prevented the increase in cardiac vasculature wall thickness, decreased the cardiomyocyte diameter and increased collagen deposition. Renal morphometric analysis showed that Ex 3% induced an increase in vasculature wall thickness and collagen deposition in the left kidney of 2K1C rats. These data suggest that Ex 0% has more beneficial effects than Ex 3% in renovascular hypertensive rats.
Highlights
Accumulating evidence shows that overactivity of the sympathetic nervous system and renin-angiotensin system (RAS) plays a crucial role in the development and maintenance of hypertension [1]
Mean arterial pressure (MAP) and heart rate (HR) measurements Figure 1 shows the MAP levels of Sham and 2K1C Sed rats and rats subjected to exercise training (Ex) during the 5 weeks after surgery
Ex 0% and Ex 3% attenuated the increase in MAP in 2K1C rats, beginning at the fourth week
Summary
Accumulating evidence shows that overactivity of the sympathetic nervous system and renin-angiotensin system (RAS) plays a crucial role in the development and maintenance of hypertension [1]. Cardiac hypertrophy is an important process of adaptation to an increased workload in response to a physiological (exercise training) or pathological (hypertension) stimulus. The compensatory hemodynamic overload response results in increased cardiac mass, presenting as ventricular hypertrophy. The parallel addition of sarcomeres causes an increase in myocyte width, which in turn increases the thickness of the wall. This remodeling results in concentric hypertrophy, which occurs in hypertensive states and in exercise training that requires isometric skeletal muscle contraction [2,3]. Isotonic exercise engenders myocyte lengthening through replication of sarcomeres in series, and an increase in ventricular volume, resulting in eccentric hypertrophy [3,4]
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