Key result
Acute aerobic exercise similarly increased aortic stiffness and cerebrovascular pulsatility in adults with treated hypertension and matched adults without hypertension (P < 0.05).
Why the study?
Does acute aerobic exercise affect arterial stiffness and cerebrovascular pulsatility differently in adults with treated hypertension compared to those without?
Does acute aerobic exercise affect arterial stiffness and cerebrovascular pulsatility differently in adults with treated hypertension compared to those without?
p-value: p=<0.05
Adults with treated hypertension experience similar increases in aortic stiffness and cerebrovascular hemodynamic pulsatility during early recovery from acute aerobic exercise as normotensive adults.
Similar acute vascular responses to exercise in treated hypertension; leaves open differential chronic cerebrovascular effects.
OBJECTIVES: Stiffer central arteries, as seen in hypertension (HTN), foster transmission of pulsatile hemodynamics into fragile cerebral vessels. Aerobic exercise is recommended for adults with HTN, but its effects on arterial stiffness and pulsatility in this group are unclear. This study sought to investigate the effect of acute aerobic exercise on arterial stiffness and cerebrovascular pulsatility in 30 adults with treated HTN and 30 age, sex, and BMI-matched adults without HTN (56 ± 6 years, BMI 28.2 ± 2.9 kg/m; 28 women). METHODS: Patients underwent hemodynamic measures before/after 30-min cycling (≈55% peak oxygen consumption). Aortic stiffness was measured using carotid-femoral pulse wave velocity, and carotid artery stiffness was assessed with β-stiffness via ultrasound. Aortic/carotid pulse pressure (aortic via radial generalized transfer function) was measured by tonometry and calibrated to brachial mean pressure and diastolic pressure. Carotid/middle cerebral artery (MCA) blood velocity pulsatility indices were measured using Doppler. Carotid wave intensity analysis was used to derive forward wave intensity (W1). RESULTS: Exercise impacted hemodynamics similarly in HTN compared to no-HTN. Carotid-femoral pulse wave velocity, MCA pulsatility index, carotid pulsatility index, and W1 increased similarly after exercise in both groups (P < 0.05). Carotid pulse pressure and β-stiffness were unaltered after exercise. Postexercise changes in W1 were positively associated with carotid pulsatility index, which was further associated with MCA pulsatility index. CONCLUSIONS: These data suggest adults with treated HTN experience similar increases in aortic stiffness and cerebrovascular hemodynamic pulsatility during early recovery from acute aerobic exercise as their counterparts without HTN.
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Lefferts et al. (2018) studied Hypertension (n=60). Acute aerobic exercise vs. Adults without hypertension was evaluated on Arterial stiffness and cerebrovascular pulsatility (p=<0.05). Acute aerobic exercise similarly increased aortic stiffness and cerebrovascular pulsatility in adults with treated hypertension and matched adults without hypertension (P < 0.05).
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