Cardiorespiratory mechanisms underlying the impaired oxygen uptake kinetics at exercise onset after stroke.

Abstract

Oxygen uptake (V˙O2) kinetics at the onset of exercise is slower in patients with stroke than in healthy adults. However, little is known about the cardiorespiratory mechanisms underlying the impaired V˙O2 kinetics. This study aimed to investigate the relative effect of impaired oxygen delivery and utilisation on V˙O2 kinetics at the onset of submaximal exercise in patients with stroke by comparing the time constants of cardiac output (τCO) and V˙O2 (τV˙O2). In addition, we aimed to examine the association between the kinetics of cardiorespiratory variables and functional outcomes. We included 21 patients with stroke (15 males, mean [SD] age 58.7 [9.5] years, mean days post-stroke 67.9 [30.9]). A submaximal constant-load exercise test was performed to measure τV˙O2, τCO, and the time constant of arterialvenous oxygen difference (τAVO2diff). The ratio of τCO to τV˙O2 was calculated to assess the matching of oxygen delivery and consumption. Fugl-Meyer lower-extremity motor scores, comfortable gait speeds, and Functional Independence Measure motor scores were used as functional variables. Mean (SD) τAVO2diff was markedly shorter than τV˙O2 and τCO (26.1 [7.1] vs. 38.7 [10.2] and 46.6 [23.2 s], P<0.05), with no significant difference between τV˙O2 and τCO (P=0.444). The greater ratio of τCO to τV˙O2 was related to poorer motor function (rho=-0.484, P=0.026) and slower comfortable gait speed (r=-0.482, P=0.027). An increase in CO was slower than that in AVO2diff in patients with stroke. Therefore, V˙O2 kinetics in patients with stroke appears to be affected by a delayed increase in CO rather than AVO2diff. Furthermore, these patients with motor and gait impairments may have a poor matching of oxygen delivery and consumption during exercise onset.