Key result
Exercise training in mice with heart failure significantly reduced urinary norepinephrine excretion (360.7 vs 666.8 ng/24 h; P=0.03) and upregulated Nrf2 and NQO-1 expression.
Why the study?
The link between exercise training and antioxidant enzyme expression in the brain of animals with chronic heart failure was not clear.
Does exercise training upregulate Nrf2 protein in the RVLM and reduce sympathetic function in mice with heart failure?
Population
Mice with CHF and sham controls
Comparison
Exercise training vs sedentary condition in sham and CHF mice
Design
Animal experimental study
Follow-up
8 wk
Authors
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Supports Nrf2-mediated sympathetic attenuation in experimental HF; leaves open human translation and clinical relevance.
Does exercise training upregulate Nrf2 protein in the RVLM and reduce sympathetic function in mice with heart failure?
Absolute Event Rate: 360.7% vs 666.8%
p-value: p=0.03
Exercise training in heart failure mice upregulates the antioxidant transcription factor Nrf2 in the RVLM, which correlates with reduced sympathetic outflow.
Wafi et al. (2019) studied Chronic heart failure. Exercise training vs. Sedentary was evaluated on Urinary norepinephrine (NE) excretion (p=0.03). Exercise training in mice with heart failure significantly reduced urinary norepinephrine excretion (360.7 vs 666.8 ng/24 h; P=0.03) and upregulated Nrf2 and NQO-1 expression.
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