Slow HR recovery (HRR) from a graded exercise treadmill test (GXT) is a marker of impaired parasympathetic reactivation that is associated with elevated mortality. Our objective was to test whether demographic, behavioral, or CHD risk factors during young adulthood were associated with the development of slow HRR.
Participants from the Coronary Artery Risk Development in Young Adults study underwent symptom-limited maximal GXT using a modified Balke protocol at baseline (1985–1986) and 20-yr follow-up (2005–2006) examinations. HRR was calculated as the difference between peak HR and HR 2 min after cessation of the GXT. Slow HRR was defined as 2-min HRR <22 beats·min−1.
In 2730 participants who did not have slow HRR at baseline, mean ± SD HRR was 44 ± 11 beats·min−1 at baseline and declined to 40 ± 12 beats·min−1 in 2005–2006; slow HRR developed in 5% (n = 135) of the sample by 2005–2006. Female sex, black race, fewer years of education, obesity, cigarette smoking, higher depressive symptoms, higher fasting glucose, hypertension, metabolic syndrome, and physical inactivity and low fitness were each associated with incident slow HRR. In a multivariable model, higher body mass index, larger waist, low education, fasting glucose, and current smoking remained significantly associated with incident slow HRR. Increasing body mass index (per SD higher) during follow-up and incident hypertension, diabetes, and metabolic syndrome (in the subsets of participants who were free from those conditions at baseline) were each associated with significantly elevated odds of incident slow HRR.
On average, HRR declines with aging; however, the odds of having slow HRR in early middle age is significantly associated with traditional CHD risk factors.
1Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL; 2Kaiser Permanente Division of Research, Oakland, CA; 3Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN; 4Department of Nutrition, Faculty of Medicine, University of Oslo, Oslo, NORWAY; and 5Division of Preventive Medicine, Department of Medicine, University of Alabama, Birmingham, AL
Address for correspondence: Mercedes R. Carnethon, Ph.D., Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, 680 N. Lake Shore Drive, Suite 1400, Chicago, IL 60611; E-mail: firstname.lastname@example.org.
Submitted for publication May 2011.
Accepted for publication June 2011.