To test whether the prevalence of hypertension, hypercholesterolemia, and diabetes declines with marathon participation independent of annual running mileage.
Cross-sectional associations of self-reported medication use in 62,284 male and 45,040 female participants of the National Runners' Health Study adjusted for age, diet, alcohol, and annual distance run.
By self-report, 31.7% of men and 29.1% of women ran 0.2 and 0.8 marathons per year, 8.6% of men and 4.4% of women ran between 1.0 and 1.8 marathons per year, and 3.8% of men and 1.5% of women ran an average of ≥2 marathons per year. The men's odds ratio per marathons per year run was 0.85 for antihypertensive (P < 0.0001), 0.87 for LDL-cholesterol-lowering (P = 0.002), and 0.52 for antidiabetic medication use (P < 0.0001). Compared with nonmarathoners, men who averaged 0.2-0.8 marathons per year had 13% lower odds for antihypertensive medication use, 22% lower odds for LDL-cholesterol-lowering medication use, and 67% lower odds for antidiabetic medication use. Marathon participation was also associated with lower LDL-cholesterol-lowering and antidiabetic medication use in women, but not when adjusted for annual distance run. Each additional hour required to complete their marathon had odds ratio of 1.31 and 1.22 for men's antihypertensive and LDL-cholesterol-lowering medication use and 2.01 for women's antidiabetic medication use (all P < 0.0001). Among all runners (marathoners and nonmarathoners combined), prevalence in the use of all three medications decreased in association with the length of the longest usual run, independent of total annual mileage.
Prevalence of hypertension, hypercholesterolemia, and diabetes decreases with the frequency of marathon participation independent of annual running distance. This may be due to the inclusion of longer training runs in preparation for marathons or to genetic or other innate differences between marathon and nonmarathon runners.
Life Sciences Division, Lawrence Berkeley Laboratory, Donner Laboratory, Berkeley, CA
Address for correspondence: Paul T. Williams, Ph.D., Life Sciences Division, Lawrence Berkeley Laboratory, Donner Laboratory, Berkeley, CA 94720; E-mail: firstname.lastname@example.org.
Submitted for publication March 2008.
Accepted for publication May 2008.