Hypertension, or high blood pressure, affects nearly one in three adults in the United States, according to the U.S. Centers for Disease Control and Prevention, putting them at risk for stroke and heart failure. Medical recommendations to those with hypertension often include diet and exercise.
However, when some with hypertension engage in strenuous exercise, sympathetic nerve activity can rise to dangerously high levels, causing marked increases in arterial pressure and heart rate, increasing the probability of adverse cardiovascular events such as heart attacks, and stroke. In effect, in some people the very activity recommended to combat high blood pressure could end up killing them - and medical experts don't know why.
A Wayne State University School of Medicine researcher has secured a new four-year $2,035,448 grant (1R01HL126706-01) from the National Institutes of Health to study the mechanisms that mediate dangerously high levels of blood pressure experienced by hypertensive subjects engaging in strenuous exercise.
Exercise in hypertensive patients often produces significant increases in sympathetic nerve activity, which can constrict even the coronary circulation, Donal O'Leary, Ph.D., professor of Physiology and director of Cardiovascular Research, explained.
The mechanisms mediating abnormal cardiovascular responses to exercise in hypertension are unknown. Studies have demonstrated that activation of the metabolically sensitive nerves within active skeletal muscle can product significant increases in sympathetic nerve activity, called the muscle metaboreflex. Impaired cardiac function in hypertensive patients may lead to decreased skeletal muscle blood flow during exercise, resulting in excessive activation of the muscle metaboreflex. The mechanisms of the muscle metaboreflex are dependent upon the arterial baroreflex, the mechanism by which the body regulates blood pressure, including transmission of nerve impulses to the brain in response to changes in blood pressure. Dr. O'Leary said that while there is evidence hypertension impairs the baroreflex function while a person is at rest, researchers don't yet know whether exercise further alters the baroreflex function in hypertension.
Dr. O'Leary's study, "Mechanisms Mediating Enhanced Sympatho-Activation During Exercise in Hypertension," will focus on determining the role of the muscle metaboreflex in mediating the altered cardiovascular response to exercise, and the involvement of the arterial baroreflex in buffering these responses. His laboratory is uniquely poised to address this issue. During the last two decades, Dr. O'Leary has developed a highly innovative and technically complex instrumented animal model that allows continuous beat-by-beat monitoring of systemic hemodynamic parameters and multiple indices of ventricular function to assess the strength and mechanisms of cardiovascular reflexes at rest and during dynamic exercise.
The results, he said, may aid in the prescription of exercise regimes tailored for hypertensive patients without pushing them to the threat of cardiovascular failure or stroke, and increase understanding of the impact of hypertension on neural control of circulation "during one of the greatest challenges to cardiovascular control - whole body strenuous dynamic exercise."