Journal of Applied Physiology
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J Appl Physiol 88: 1228-1238, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 4, 1228-1238, April 2000

VO2 kinetics reveal a central limitation at the onset of subthreshold exercise in heart transplant recipients

Bertrand Mettauer1, Quan Ming Zhao1, Eric Epailly1, Anne Charloux1, Eliane Lampert1, Bernadette Heitz-Naegelen1, François Piquard1, Pietro E. di Prampero2, and Jean Lonsdorfer1

1 Département de Physiologie, Jeune Equipe 2105 Centre National de la Recherche Scientifique, Services des Explorations du Système Circulatoire et des Explorations Fonctionnelles Respiratoires, Hôpital Central, F-67091 Strasbourg Cedex, France; and 2 Dipartimento di Scienze e Tecnologie Biomediche, Universita di Udine, I-33100 Udine, Italy

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O2 uptake (VO2) kinetics at the onset of subthreshold exercise are slowed because of an impaired early "cardiodynamic" phase 1, rather than an abnormal subsequent "metabolic" phase 2. Thus we compared the VO2 kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 ± 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 ± 14 W; C67W group). Time-averaged heart rate, breath-by-breath VO2, and O2 pulse (O2p) data yielded monoexponential time constants of the VO2 (s) and O2p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 VO2 time constant (&tgr;<SUB>ph2 <A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB></SUB>). The VO2 time constant was higher in HTR (38.4 ± 7.5) than in C40W (22.9 ± 9.6; P <=  0.002) or C67W (30.8 ± 8.2; P <=  0.05), as was the O2p time constant, resulting from a lower phase 1 VO2 increase (287 ± 59 vs. 349 ± 66 ml/min; P <=  0.05), O2p increase (2.8 ± 0.6 vs. 3.6 ± 1.0 ml/beat; P <=  0.0001), and a longer phase 1 duration (36.7 ± 12.3 vs. 26.8 ± 6.0 s; P <=  0.05), whereas the &tgr;<SUB>ph2 <A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB></SUB> was similar in HTR and C (31.4 ± 9.6 vs. 29.9 ± 5.6 s; P = 0.85). Thus the HTR have slower subthreshold VO2 kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster &tgr;<SUB>ph2 <A><AC>V</AC><AC>˙</AC></A><SC>o</SC><SUB>2</SUB></SUB> in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.

heart transplantation; pulmonary gas exchange; oxygen consumption; heart rate


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