Key result
Treadmill exercise lowers SBP ~18 mmHg and boosts cardioprotective BDNF expression in SHR.
Why the study?
The mechanisms by which exercise increases BDNF expression to benefit hypertension and associated cognitive impairment were unknown.
Does 5 weeks of moderate-intensity treadmill exercise training reduce blood pressure and restore hippocampal and cardiac BDNF/TrkB signaling via FNDC5 upregulation in spontaneously hypertensive rats?
Does 5 weeks of moderate-intensity treadmill exercise training reduce blood pressure and restore hippocampal and cardiac BDNF/TrkB signaling via FNDC5 upregulation in spontaneously hypertensive rats?
In a rodent model of genetic hypertension, endurance exercise lowers blood pressure, increases cardiac BDNF protein, and normalizes hippocampal dentate gyrus BDNF expression alongside increased skeletal muscle (but not central or cardiac) FNDC5 protein.
Answers are grounded in this paper and cite their sources.
Does not support clinical adoption; leaves open translation of exercise-BDNF/FNDC5 effects from hypertensive rats to humans.
Increased sympathetic activity contributes to the development of cardiovascular diseases such as hypertension. Exercise training lowers sympathetic activity and is beneficial for the prevention and treatment of hypertension and associated cognitive impairment. Increased BDNF expression in skeletal muscle, heart, and brain may contribute to these actions of exercise, but the mechanisms by which this occurs are unknown. We postulated that hypertension is associated with decreased hippocampal BDNF, which can be restored by exercise-mediated upregulation of fibronectin type-II domain-containing 5 (FNDC5). Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were subjected to 5 weeks of motorized treadmill training. BDNF and FNDC5 expressions were measured in the left ventricle (LV), quadriceps, soleus muscle, and brain areas. Exercise training reduced blood pressure (BP) in both strains. BDNF and FNDC5 protein in the LV were increased in SHR, but exercise increased only BDNF protein in both strains. BDNF mRNA, but not protein, was increased in the quadriceps of SHR, and BDNF mRNA and protein were decreased by exercise in both groups. FNDC5 protein was higher in SHR in both the quadriceps and soleus muscle, whereas exercise increased FNDC5 protein only in the quadriceps in both strains. BDNF mRNA was lower in the dentate gyrus (DG) of SHR, which was normalized by exercise. BDNF mRNA expression in the DG negatively correlated with BP. No differences in FNDC5 expression were observed in the brain, suggesting that enhanced BDNF signaling may contribute to the cardiovascular and neurological benefits of exercise training, and these processes involve peripheral, but not central, FNDC5.
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Wang et al. (2019) studied Hypertension (rodent model) (n=32). Moderate-intensity motorized treadmill exercise training vs. Sedentary control (handled daily under the same conditions and exposed to the immobile treadmill for comparable times) was evaluated on Systolic blood pressure (SBP) and BDNF/FNDC5 expression in the left ventricle, skeletal muscle, and brain (dentate gyrus) (MD -18 mmHg in SHR (reported in text as 28 mmHg lower in SHR-ExT vs SHR-Sed), p=<0.05). Five weeks of treadmill exercise reduced systolic blood pressure in SHR, normalized hippocampal dentate gyrus BDNF mRNA, and increased LV BDNF and quadriceps FNDC5 protein.
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