Author + information
- Received December 7, 2011
- Revision received February 3, 2012
- Accepted February 6, 2012
- Published online July 10, 2012.
- Mark J. Haykowsky, PhD⁎,
- Peter H. Brubaker, PhD†,
- Kathryn P. Stewart, RDMS‡,
- Timothy M. Morgan, PhD§,
- Joel Eggebeen, MS‡ and
- Dalane W. Kitzman, MD‡,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Dalane W. Kitzman, Wake Forest University, Section on Cardiology, Medical Center Boulevard, Winston-Salem, North Carolina 27157
Objectives The purpose of this study was to evaluate the mechanisms for improved exercise capacity after endurance exercise training (ET) in elderly patients with heart failure and preserved ejection fraction (HFPEF).
Background Exercise intolerance, measured objectively by reduced peak oxygen consumption (VO2), is the primary chronic symptom in HFPEF and is improved by ET. However, the mechanisms are unknown.
Methods Forty stable, compensated HFPEF outpatients (mean age 69 ± 6 years) were examined at baseline and after 4 months of ET (n = 22) or attention control (n = 18). The VO2 and its determinants were assessed during rest and peak upright cycle exercise.
Results After ET, peak VO2 in those patients was higher than in control patients (16.3 ± 2.6 ml/kg/min vs. 13.1 ± 3.4 ml/kg/min; p = 0.002). That was associated with higher peak heart rate (139 ± 16 beats/min vs. 131 ± 20 beats/min; p = 0.03), but no difference in peak end-diastolic volume (77 ± 18 ml vs. 77 ± 17 ml; p = 0.51), stroke volume (48 ± 9 ml vs. 46 ± 9 ml; p = 0.83), or cardiac output (6.6 ± 1.3 l/min vs. 5.9 ± 1.5 l/min; p = 0.32). However, estimated peak arterial-venous oxygen difference was significantly higher in ET patients (19.8 ± 4.0 ml/dl vs. 17.3 ± 3.7 ml/dl; p = 0.03). The effect of ET on cardiac output was responsible for only 16% of the improvement in peak VO2.
Conclusions In elderly stable compensated HFPEF patients, peak arterial-venous oxygen difference was higher after ET and was the primary contributor to improved peak VO2. This finding suggests that peripheral mechanisms (improved microvascular and/or skeletal muscle function) contribute to the improved exercise capacity after ET in HFPEF. (Prospective Aerobic Reconditioning Intervention Study [PARIS]; NCT01113840)
This study was supported by the following research grants: National Institutes of Health (NIH) Grants R37 AG18915 and RO1AG12257; the Claude D. Pepper Older Americans Independence Center of Wake Forest University NIH Grant P30AG21332; and the General Clinical Research Center of Wake Forest University School of Medicine Grant MO1RR07122. Dr. Kitzman is a consultant to Novartis; Relyosa; Boston Scientific; Abbott; and Gilead; and declares a minor (<$10,000) potential conflict of interest as a consultant for Boston Scientific Corporation. All other authors have reported they have no relationships relevant to the contents of this paper to disclose.
- Received December 7, 2011.
- Revision received February 3, 2012.
- Accepted February 6, 2012.
- American College of Cardiology Foundation