HIIT sensitizes the arterial baroreflex by activating GSH-Px and downregulating calcium channel

High-intensity intermittent training (HIIT) is an emerging strategy for controlling blood pressure (BP) requiring intermittent exercise. However, few studies were focused on clinical test or related mechanisms. Here we compared the detailed aspects of HIIT on rat blood pressure control and explored its possible molecular mechanisms.

Thirty-six spontaneous hypertensive rats (SHR) were recruited to complete 8 weeks of different training pattern using treadmill. Measurements of BP, bradycardia reflex, tachycardia reflex, plasma oxidative stress biomarkers and protein expression were acquired at the end of training.

After the 8-week training, HIIT can significantly downregulate the rest heart rate (HR) and blood pressure of SHR. The bradycardia reflex induced by phenylephrine and tachycardia response to sodium nitroprusside (SNP) were both improved in the HIIT group compared with control group. By testing the plasma metabolites, we found no statistically alteration on levels of malondialdehyde (MDA) or superoxide dismutase (SOD). However, HIIT increased the plasma glutathione peroxidase (GSH-Px) activity. Besides, HIIT attenuated the vasoconstriction induced by norepinephrine while has little effect on potassium chloride stimulation. Similarly, the sensitivity of vasorelaxation induced by SNP was upregulated after HIIT. Finally, we identified a decrease of of calcium channel CaV 1.2 on blood vessel in HIIT group.

HIIT provides a better control of BP and higher sensitivity to vasorelaxation, which may be related to higher GSH-Px activity and lower CaV 1.2 expression.