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(Stroke. 2008;39:3102.)
© 2008 American Heart Association, Inc.

Research Letters

Cardiac Reserve and Pulmonary Gas Exchange Kinetics in Patients With Stroke

Corey R. Tomczak, MSc; Anwar Jelani, MD; Robert G. Haennel, PhD; Mark J. Haykowsky, PhD; Robert Welsh, MD Patricia J. Manns, PhD

From the Faculty of Rehabilitation Medicine (C.R.T., R.G.H., M.J.H., P.J.M.) and the Division of Cardiology, Faculty of Medicine (A.J., M.J.H., R.W.), University of Alberta, Edmonton, Alberta, Canada.

Correspondence to Patricia J. Manns, PhD, 1–30 Corbett Hall, Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada, T6G 2G4. E-mail trish.manns{at}ualberta.ca

Background and Purpose— Cardiovascular and pulmonary factors contributing to impaired peak oxygen uptake (O₂) in patients with stroke (SP) are not well known. We assessed cardiovascular function, pulmonary gas exchange, and ventilation in SP and healthy age, gender, and activity-matched control subjects.

Methods— Ten hemiparetic SP and 10 control subjects were enrolled. Subjects completed cycle ergometry testing to assess peak and reserve O₂, carbon dioxide production, ventilation (tidal volume; breathing frequency; minute ventilation), and cardiac output. O₂, carbon dioxide production, and minute ventilation were measured throughout peak exercise recovery (off-kinetics) and at exercise onset (on-kinetics) along with heart rate during low-level exercise.

Results— Peak O₂ was 43% lower (P<0.001) in SP secondary to reduced peak and reserve cardiac output and minute ventilation. The impaired cardiac output reserve (P<0.001) was due to a 34% lower heart rate reserve (P=0.001). The impaired minute ventilation reserve (P=0.013) was due to a 41% lower tidal volume reserve (P=0.009). Stroke volume and breathing frequency reserve were preserved. O₂ off-kinetics were 29% slower in SP (P<0.001) and related to peak O₂ (R=–0.72, P<0.001) and peak cardiac output (R=–0.75, P<0.001) for the study group. Additionally, carbon dioxide production (P=0.016) and minute ventilation (P=0.023) off-kinetics were prolonged in SP. O₂ on-kinetics were 29% slower (P=0.031) during low-level exercise in SP.

Conclusions— The impaired peak O₂ in SP is secondary to a decline in peak and reserve cardiac output and ventilation. Prolonged O₂ kinetics in SP are associated in part with deconditioning and may be mediated by reduced O₂ availability and/or the rate of muscle O₂ use.

Key Words: cardiac output • exercise • oxygen uptake kinetics • stroke