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J Appl Physiol 103: 1722-1727, 2007. First published August 23, 2007; doi:10.1152/japplphysiol.00725.2007
8750-7587/07 $8.00
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Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients

Nicholas G. Jendzjowsky,1 Corey R. Tomczak,1 Richard Lawrance,2 Dylan A. Taylor,2 Wayne J. Tymchak,2 Kenneth J. Riess,1 Darren E. R. Warburton,3 and Mark J. Haykowsky1,2

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 (VO2p), heart rate (HR), stroke volume (SV), cardiac output (Q), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve VO2p, Q, and systemic arterial-venous oxygen difference (a-vO2diff) were 23–52% lower (P < 0.05) in HTR. The reduced Q and a-vO2diff reserves were associated with lower HR and HHb reserves, respectively. The phase II VO2p time delay was greater (HTR: 38 ± 2 vs. CON: 25 ± 1 s, P < 0.05), while time constants for phase II VO2p (HTR: 54 ± 8 vs. CON: 31 ± 3 s), Q (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 VO2p and prolonged VO2p 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.


Address for reprint requests and other correspondence: Mark Haykowsky, Cardiovascular Therapeutic Exercise Laboratory, 1-30 Corbett Hall, Faculty of Rehabilitation Medicine, Univ. of Alberta, Edmonton AB, Canada, T6G 2G4 (E-mail: mark.haykowsky{at}ualberta.ca)




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