Cardiac Reserve and Pulmonary Gas Exchange Kinetics in Patients With Stroke

Background and Purpose—Cardiovascular and pulmonary factors contributing to impaired peak oxygen uptake (V u O2 )i n 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 V u O2, carbon dioxide production, ventilation (tidal volume; breathing frequency; minute ventilation), and cardiac output. V u 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 V u O2 was 43% lower (P0.001) in SP secondary to reduced peak and reserve cardiac output and minute ventilation. The impaired cardiac output reserve (P0.001) was due to a 34% lower heart rate reserve (P0.001). The impaired minute ventilation reserve (P0.013) was due to a 41% lower tidal volume reserve (P0.009). Stroke volume and breathing frequency reserve were preserved. V u O2 off-kinetics were 29% slower in SP (P0.001) and related to peak V u O2 (R0.72, P0.001) and peak cardiac output (R0.75, P0.001) for the study group. Additionally, carbon dioxide production (P0.016) and minute ventilation (P0.023) off-kinetics were prolonged in SP. V u O2 on-kinetics were 29% slower (P0.031) during low-level exercise in SP. Conclusions—The impaired peak V u O2 in SP is secondary to a decline in peak and reserve cardiac output and ventilation. Prolonged V u 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. (Stroke. 2008;39:3102-3106.)