Kinetics and steady-state of VO2 responses to arm exercise in trained spinal cord injury humans

Cross-sectional study comparing trained spinal cord injured (SCI) subjects (lesion level: L1 - T6) with healthy young subjects (CONT).

To investigate the kinetics of response in oxygen uptake (VO(2)) in human upper-body skeletal muscles, nine trained SCI subjects underwent submaximal supine arm exercises.

The SCI subjects underwent an incremental arm exercise test until exhaustion. The days after this first round of testing, breath-by-breath VO(2) and beat-by-beat heart rate (HR) on- and off-kinetics were determined during three repetitions of constant exercise at 50% of VO(2peak). The overall time course of response was determined from the half time (t(1/2)). Increased capillary blood lactate production (delta[La]b) at the onset of exercise was defined as the difference between at rest and at the end of exercise. Cardiac output (Q) was measured using the acetylene rebreathing method during the steady state of exercise. In accordance with the Fick principle, the difference in arterial-venous O(2) content (Ca-vO(2)) was defined as VO(2)/Q.

During the steady state of the submaximal arm exercise, a more significant increase in the steady state of Q was obtained in the CONT subjects than in the trained SCI subjects: respectively, 14.9+/-1.4 l/min versus (12.7+/-0.8 l/min). There was no difference in the steady state of VO(2) between the two groups; as a result, SCI subjects had the greater Ca-v(2). Meanwhile, VO(2) on- and off-kinetics became much faster in the trained SCI subjects than in the CONT subjects. In addition, t(1/2) HR on-kinetics was not significantly different between the SCI and CONT groups. Increased Delta[La]b was closely related to larger t(1/2) VO(2) on-kinetics (r = 0.624, P < 0.05).

It is concluded that the acceleration of VO(2) on- and off-kinetics in the trained SCI subjects was observed even though there was no difference in HR on- and off-kinetics between the SCI and CONT groups and a lower steady state of Q in the trained SCI subjects. VO(2) kinetics would therefore be the limiting factor in oxidative phosphorylation in the upper skeletal muscles, thereby providing a lower lactic O(2)-deficit (ie delta[La]b).