Exercise Hypertension occurs when cells cant relax, Hopkins researchers find
So-called "exercise hypertension," an abnormally high spike in blood pressure experienced by generally healthy people during a workout, is a known risk factor for permanent and serious high blood pressure at rest. But who gets it, and why, has been largely unknown.
Now, Johns Hopkins scientists say they have reason to believe that the problem is rooted in the failure of cells that line the blood vessels to allow the arteries to expand to accommodate increased blood flow during exertion.
"Our study shows that this impaired ability of the endothelial cells, which control large blood vessel relaxation, is a potential cause of exercise hypertension," says Kerry J. Stewart, Ed.D., lead study author and director of clinical exercise physiology at Hopkins. "Because as many as 90 percent of adults are at risk for developing high blood pressure, knowing this may point to a cellular target for preventive therapies."
Normally during exercise, blood pressure increases to push the flow of oxygen-rich blood throughout the body. However, in some individuals, the response to exercise is exaggerated. Instead of reaching a systolic (upper number) blood pressure of around 200 mmHg at maximal exercise, they spike at 250 mmHg or higher.
For the study, published in the April issue of the American Journal of Hypertension, the investigators evaluated 38 men and 44 women ages 55 to 75 who had untreated mild hypertension but were otherwise healthy. Their blood pressures at rest ranged from 130 to 159 mmHg systolic (the upper number) and 85 to 99 mmHg diastolic (the lower number).
To measure endothelial function, the researchers first used ultrasound to measure the size of a large artery in the arm. Next they put a tight blood pressure cuff on one of the subjects arms for five minutes to stop blood flow to the arm, then deflated the cuff, causing a surge of blood flow. They then repeated the artery size measurement, comparing it to the resting measure of the artery. The ability of the blood vessels to expand under these conditions is an indicator of endothelial function.
In a second test, they examined blood vessel stiffness -- a marker of early heart disease -- by using ultrasound to measure how fast blood traveled from arteries in the subjects necks to their legs with each heart beat. Because stiff blood vessels do not absorb any of the pressure behind the blood flow, the faster the blood travels, the more stiff the vessel is. They compared these readings with blood pressure measures taken at rest and while the participants walked to maximal effort on a treadmill.
In their analysis, researchers found that higher blood pressures in response to exercise were associated with poorer blood vessel expansion in the arm following the cuff test, suggesting that the endothelial cells failed to dilate enough to handle the extra blood flow. There was no correlation between the stiffness of blood vessel walls or resting blood pressure with increased blood pressure during exercise.
Impaired endothelial function is not solely related to high blood pressure, Stewart adds. It also is associated with aging, menopause, high cholesterol, smoking and diabetes, and may be a common process for developing heart disease among all of these risk factors.
"Its too early to recommend that people have exercise tests just to measure their blood pressures," Stewart says. "However, careful attention should be paid to exercise blood pressure if measured as part of a medical evaluation, or during a workout at a gym, since it may be a warning that your resting blood pressure may also increase."
The study was supported by the National Institutes of Health and the Johns Hopkins Bayview General Clinical Research Center. Study coauthors were Jidong Sung, Harry Silber, Jerome Fleg, Mark Kelemen, Katherine Turner, Anita Bacher, Devon Dobrosielski, James DeRegis, Edward Shapiro, and Pamela Ouyang.
Stewart, Kerry et al., "Exaggerated Exercise Blood Pressure is Related to Impaired Endothelial Vasodilator Function," American Journal of Hypertension, April 2004;17(4):314-320.
Joanna Downer | EurekAlert!