Key result
Two weeks of detraining did not abolish the exercise-induced attenuation in mean arterial pressure in hypertensive rats, but failed to completely preserve improvements in cardiac hypertrophy and diastolic function.
Why the study?
Does physical detraining reverse the beneficial effects of exercise on blood pressure, cardiac function, and brain inflammation in Angiotensin II-induced hypertensive rats?
Does physical detraining reverse the beneficial effects of exercise on blood pressure, cardiac function, and brain inflammation in Angiotensin II-induced hypertensive rats?
Absolute Event Rate: 151.2% vs 173%
p-value: p=<0.05
In a hypertensive rat model, two weeks of physical detraining maintains the blood pressure-lowering benefits of exercise but leads to a partial reversal of improvements in cardiac hypertrophy, diastolic function, and brain anti-inflammatory cytokines.
AIMS: This study sought to investigate the effects of physical detraining on blood pressure (BP) and cardiac morphology and function in hypertension, and on pro- and anti-inflammatory cytokines (PICs and AIC) and oxidative stress within the brain of hypertensive rats. METHODS AND RESULTS: Hypertension was induced in male Sprague-Dawley rats by delivering AngiotensinII for 42 days using implanted osmotic minipumps. Rats were randomized into sedentary, trained, and detrained groups. Trained rats underwent moderate-intensity exercise (ExT) for 42 days, whereas, detrained groups underwent 28 days of exercise followed by 14 days of detraining. BP and cardiac function were evaluated by radio-telemetry and echocardiography, respectively. At the end, the paraventricular nucleus (PVN) was analyzed by Real-time RT-PCR and Western blot. ExT in AngII-infused rats caused delayed progression of hypertension, reduced cardiac hypertrophy, and improved diastolic function. These results were associated with significantly reduced PICs, increased AIC (interleukin (IL)-10), and attenuated oxidative stress in the PVN. Detraining did not abolish the exercise-induced attenuation in MAP in hypertensive rats; however, detraining failed to completely preserve exercise-mediated improvement in cardiac hypertrophy and function. Additionally, detraining did not reverse exercise-induced improvement in PICs in the PVN of hypertensive rats; however, the improvements in IL-10 were abolished. CONCLUSION: These results indicate that although 2 weeks of detraining is not long enough to completely abolish the beneficial effects of regular exercise, continuing cessation of exercise may lead to detrimental effects.
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Agarwal et al. (2012) studied Hypertension (n=90). Exercise and detraining vs. Sedentary control was evaluated on Mean arterial pressure (MAP) in mmHg (p=<0.05). Two weeks of detraining did not abolish the exercise-induced attenuation in mean arterial pressure in hypertensive rats, but failed to completely preserve improvements in cardiac hypertrophy and diastolic function.
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