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Purpose: Little is known about the heart rate (HR) responses at the onset of exercise, at peak exercise, and recovery in apparently healthy men and women. The purpose of this study was to determine the prevalence of abnormal HR acceleration at the onset of exercise, define the HR acceleration profile, determine if traditional cardiovascular disease (CVD) risk factors are associated with abnormal HR acceleration, and identify whether abnormal chronotropic responses cluster with abnormal HR acceleration in an asymptomatic, self-referred, adult population. Methods: A retrospective examination of a symptom-limited maximal treadmill test was performed for participants of a university-based fitness program between 1990 and 2006. Records were analyzed for various HR responses from individuals (N=947) of both sexes who represented a broad range of age and fitness levels (mean VO2: 32.9±9.4ml∙kg-1∙min-1). Abnormal HR acceleration at minute 1 and ⅓ total exercise time was defined as a HR increase from standing rest of ≤14 and ≤28 beats respectively. Results: The prevalence of abnormal HR acceleration at minute 1 and ⅓ total exercise time was 30.6% and 31.3% respectively. The mean HR increase during the first minute and ⅓ total exercise time was 20.5 ± 10.3 and 33.7 ± 10.4 beats respectively. Abnormal accelerators had a significantly better CVD risk factor profile (lower systolic and diastolic blood pressure, BMI, total cholesterol, triglycerides, higher VO2, and higher percent of regular exercise) than normal accelerators, despite consisting of a greater percentage of current smokers. Lastly, abnormal HR acceleration showed higher prevalence with abnormal HR recovery than with chronotropic incompetence. Conclusions: In the present study cohort, a lower HR increase at the onset of exercise was associated with a better CVD risk factor profile but the same differences were not seen at ⅓ total exercise time. / School of Physical Education, Sport, and Exercise Science

Copies of author's previously published works inserted. / Bibliography: leaves 219-244. / xv, 244 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Examines the mechanisms of induction of nitrate tolerance utilizing an in vitro model (isolated bovine coronary artery rings) and an in vivo haemodynamic model (systemic haemodynamics in patients undergoing cardiac catheterization). / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1996

Thesis (Ph. D.)--University of Washington, 1989. / Vita. Includes bibliographical references.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv., 2004. / Härtill 4 uppsatser.

Thesis (M.A.)--Northern Kentucky University, 2008. / Made available through ProQuest. Publication number: AAT 1459938. ProQuest document ID:1622195111. Includes bibliographical references (p. 28-29)

Thesis (Ph. D.)--University of Wisconsin, 1938. / Typescript (carbon copy). eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (p. [i]-iii).

Thesis (M.A.)--Northern Kentucky University, 2009. / Made available through ProQuest. Publication number: AAT 1465559. ProQuest document ID: 1814562511. Includes bibliographical references (p. 38-41)

Thesis (M.S.)--Ball State University, 2009. / Title from PDF t.p. (viewed on June 07, 2010). Includes bibliographical references.