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Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients

¹Cardiovascular Therapeutic Exercise Laboratory, Faculty of Rehabilitation Medicine, and ²Division of Cardiology, University of Alberta, Edmonton, Alberta; ³Cardiovascular Physiology and Rehabilitation Laboratory, Experimental Medicine, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia

Submitted 5 July 2007 ; accepted in final form 21 August 2007

We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean ± SE; age: 53 ± 3 years; years posttransplant: 6 ± 4) and five age- and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (O_2p), heart rate (HR), stroke volume (SV), cardiac output (), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve O_2p, , and systemic arterial-venous oxygen difference (a-vO_2diff) were 23–52% lower (P < 0.05) in HTR. The reduced and a-vO_2diff reserves were associated with lower HR and HHb reserves, respectively. The phase II O_2p time delay was greater (HTR: 38 ± 2 vs. CON: 25 ± 1 s, P < 0.05), while time constants for phase II O_2p (HTR: 54 ± 8 vs. CON: 31 ± 3 s), (HTR: 66 ± 8 vs. CON: 28 ± 4 s), and HHb (HTR: 27 ± 5 vs. CON: 13 ± 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 ± 21 s) vs. CON (21 ± 2 s, P < 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 ± 8 s vs. CON 31 ± 6 s). The lower peak O_2p and prolonged O_2p kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.

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