Background and Aim: Heart transplant recipients (HTR) have slower pulmonary oxygen uptake (VO2p) kinetics that is due, in part, to impaired cardiac output (Q) kinetics. A limitation of prior studies examining VO2p kinetics in HTR was the primary focus on large muscle mass (cycling) exercise. The effects that small muscle mass (unilateral knee extension, UKE) exercise has on cardiovascular and gas exchange kinetics have not been studied. The purpose of this investigation was to examine VO2p, Q, and muscle deoxygenation (HHb) kinetics during UKE exercise in HTR and healthy age and activity-matched controls (CON).
Methods: Four clinically stable HTR (53 +/- 6 years) and 5 CON (53 +/- 7 years) performed 2 exercise tests on separate days. On the first day, an incremental UKE test was performed during which time expired gas analysis was acquired to measure peak VO2p. On the second day, a square-wave moderate-intensity UKE protocol from a 0-Wt kicking baseline (3-minute duration) to approximately 50% of peak power output steady state (5-minute duration) was performed 4 times during which time continuous VO2p, heart rate (HR), stroke volume (SV, impedance cardiography), and HHb (near infrared spectroscopy, Hamamatsu, NIRO 300) was obtained. Exercise repetitions were time aligned and averaged and VO2p, HR, SV, Q, and HHb kinetics were quantified using nonlinear regression. Specifically, [tau] (seconds) for VO2p, Q, SV, and HHb represented the time to achieve a 63% change from baseline. Furthermore, the HR 1/2 time (the time to 50% change of total response) was also calculated. Data were analyzed using independent t tests and the alpha level was set at P < .05.
Results: VO2p (HTR, [tau]: 58 +/- 20 vs CON, [tau]: 30 +/- 8 seconds, see the figure), Q (HTR, [tau]: 66 +/- 18 vs CON, [tau]: 29 +/- 14 seconds), and HHb kinetics (HTR, [tau]: 27 +/- 10 vs CON, [tau]: 13 +/- 6 seconds) were significantly slower in HTR than in CON. Furthermore, the prolonged Q kinetics were secondary to slower HR kinetics (HTR: 113 +/- 47 vs CON: 21 +/- 3 seconds, P +/- .05) as SV kinetics were not different between HTR (40 +/- 17 seconds) and CON (32 +/- 13 seconds).
Conclusion: The prolonged VO2p kinetics in HTR versus CON during UKE are due to slower Q and HHb kinetics. Moreover, the slower Q kinetics are secondary to the blunted HR kinetics as SV kinetics were not different between groups. During small muscle mass exercise, abnormalities in oxygen delivery and utilization result in slower VO2p kinetics in HTR.