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Clinical Investigations: CARDIOLOGY |

Effect of Exercise Training on Postexercise Oxygen Uptake Kinetics in Patients With Reduced Ventricular Function*

Jonathan Myers, PhD; Renato Gianrossi, MD; Juerg Schwitter, MD; Doris Wagner, MD; Paul Dubach, MD
Author and Funding Information

*From the Cardiology Divisions (Drs. Wagner and Dubach), Kantonsspital Chur, Basel, Switzerland; University Hospital(Dr. Schwitter), Zurich, Switzerland; the University of Genoa (Dr. Gianrossi), Genoa, Italy; and Palo Alto Veterans Affairs Medical Center and Stanford University (Dr. Myers), Palo Alto, CA.

Correspondence to: Jonathan Myers, PhD, Palo Alto Veterans Affairs Health Care System, Cardiology 111C, 3801 Miranda Ave, Palo Alto, CA 94304; e-mail: DRJ993@aol.com



Chest. 2001;120(4):1206-1211. doi:10.1378/chest.120.4.1206
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Background: The time required for oxygen uptake (V̇o2) to return to baseline level (recovery kinetics) is prolonged in patients with reduced ventricular function, and the degree to which it is prolonged is related to the severity of heart failure, markers of abnormal ventilation, and prognosis. In the present study, we sought to determine the effect of exercise training on V̇o2 recovery kinetics in patients with reduced ventricular function.

Methods: Twenty-four male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. V̇o2 kinetics in recovery from maximal exercise were calculated before and after the study period and expressed as the slope of a single exponential relation between V̇o2 and time during the first 3 min of recovery.

Results: Peak V̇o2 increased significantly in the exercise group (19.4 ± 3.0 mL/kg/min vs 25.1 ± 4.7 mL/kg/min, p < 0.05), whereas no change was observed in control subjects. The V̇o2 half-time in recovery was reduced slightly after the study period in both groups (108.7 ± 33.1 to 102.1 ± 50.5 s in the exercise group and 122.3 ± 68.7 to 107.5 ± 36.0 s in the control group); neither the change within or between groups was significant. The degree to which V̇o2 was prolonged in recovery was inversely related to measures of exercise capacity (peak V̇o2, watts achieved, and exercise time; r = − 0.48 to − 0.57; p < 0.01) and directly related to the peak ventilatory equivalents for oxygen (r = 0.59, p < 0.01) and carbon dioxide (r = 0.57, p < 0.01).

Conclusion: Two months of high-intensity training did not result in a faster recovery of V̇o2 in patients with reduced ventricular function. This suggests that adaptations to exercise training manifest themselves only during, but not in, recovery from exercise.

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