Purpose: To estimate the independent relationships of running intensity with antihypertensive, LDL-cholesterol-lowering, and antidiabetic medication use when adjusted for running volume (km·d−1).
Methods: Self-reported medication use was compared cross-sectionally to running pace (m·s−1 during usual run) in 25,552 male and 29,148 female National Runners' Health Study participants.
Results: The men ran a mean ± SD of 5.2 ± 3.1 km·d−1 at 3.3 ± 0.5 m·s−1 (8.3 ± 1.4 min·mile−1) and the women 4.7 ± 2.9 km·wk−1 at 3.0 ± 0.4 m·s−1 (9.2 ± 1.8 min·mile−1). When adjusted for kilometers per day, each meter-per-second increment in intensity in men and women reduced the odds for antihypertensive drug use by 54% and 46%, respectively, reduced the odds for LDL-cholesterol-lowering medication use by 55% and 48%, respectively, and reduced the odds for antidiabetic medication use by 50% and 75%, respectively (all P < 0.0001). Compared with men who ran slower than 10 min·mile−1, the odds for medication use in those who ran or exceeded a 7-min·mile−1 pace were 72% less for antihypertensive, 78% less for LDL-cholesterol lowering, and 67% less for antidiabetic medications (the corresponding odds reductions in women were 61%, 64%, and 87%, respectively, for 8 min·mile−1 or faster versus slower than 11 min·mile−1). Although usual running pace correlated significantly with a 10-km performance (male, r = 0.55; females, r = 0.49), usual pace remained significantly related to lower use of all three medications in men and antihypertension and antidiabetic medications in women when adjusted for a 10-km performance.
Conclusions: Although these results do not prove causality, they show that exercise intensity is inversely associated with the prevalence of hypertension, hypercholesterolemia, and diabetes independent of exercise volume and cardiorespiratory fitness (10-km performance), suggesting that the more vigorous the exercise, the healthier the health benefits.
Donner Laboratory, Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA
Address for correspondence: Paul T. Williams, Ph.D., Donner Laboratory, Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA 94720; E-mail: email@example.com.
Submitted for publication February 2008.
Accepted for publication April 2008.