Author + information
- Received July 10, 2019
- Revision received August 26, 2019
- Accepted August 28, 2019
- Published online January 27, 2020.
- Ambarish Pandey, MD, MSCSa,
- William E. Kraus, MD, PhDb,
- Peter H. Brubaker, PhDc and
- Dalane W. Kitzman, MDd,∗ ()
- aDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
- bDivision of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina
- cDepartment of Exercise and Health Science, Wake Forest University, Winston-Salem, North Carolina
- dSections on Cardiovascular Medicine and Gerontology, Wake Forest School of Medicine, Winston-Salem, North Carolina
- ↵∗Address for correspondence:
Dr. Dalane W. Kitzman, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1045.
Objectives The aim of this study was to evaluate the association between age and invasive cardiovascular hemodynamics during upright exercise among healthy adults.
Background The marked age-related decline in maximal exercise oxygen uptake (peak VO2) may contribute to the high burden of heart failure among older individuals and their greater severity of exertional symptoms. However, the mechanisms underlying this decline are not well understood.
Methods A total of 104 healthy community-dwelling volunteers age 20 to 76 years well screened for cardiovascular disease underwent exhaustive upright exercise with brachial and pulmonary artery catheters; radionuclide ventriculography; and expired gas analysis for the measurement of peak VO2, cardiac output, left ventricular stroke volume, end-diastolic volume, end-systolic volume, ejection fraction, pulmonary capillary wedge pressure, and arteriovenous oxygen difference.
Results Over a 5.5-decade age range, there was a 40% decline in peak VO2 due primarily to reduced peak exercise cardiac output; peak arteriovenous oxygen difference was unaffected by age. The lower age-related exercise cardiac output was related to lower peak exercise heart rate and stroke volume. Aging was also associated with lower peak exercise ejection fraction, indicating reduced inotropic reserve. Peak exercise end-diastolic volume was lower with aging despite similar left ventricular filling pressure, suggesting age-related reduced diastolic compliance limiting the use of the Frank-Starling mechanism to compensate for reduced chronotropic and inotropic reserves. These age relationships were unaffected by sex.
Conclusions The age-related decline in exercise capacity among healthy persons is due predominantly to cardiac mechanisms, including reduced chronotropic and inotropic reserve and possibly reduced Frank-Starling reserve. Peak exercise left ventricular filling pressure and arteriovenous oxygen difference are unchanged with healthy aging.
- cardiovascular hemodynamics
- exercise reserve
- peak exercise oxygen capacity
- pulmonary capillary filling pressure
Dr. Kitzman is supported in part by National Institute of Health grants R01AG18915, P30AG021332, and R01AG045551, and the Kermit G. Phillips Endowed Chair in Cardiovascular Medicine. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 10, 2019.
- Revision received August 26, 2019.
- Accepted August 28, 2019.
- 2020 American College of Cardiology Foundation
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