Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ.kg-1 (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats.min-1 (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol.l-1 (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg.ml-1. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg.ml-1 vs 116.0 (SEM 13.5) pg.ml-1 and 200.0 (SEM 23.0) pg.ml-1 vs 206.5 (SEM 25.9) pg.ml-1, respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.
We tested the hypothesis that the awake ventilatory response to hypoxia and hypercapnia may contribute to the variability of respiratory effort developed in response to upper airway obstruction in obstructive sleep apnea syndrome. The polygraphic recordings of 38 patients diagnosed as having obstructive sleep apnea on the basis of an apnea+hypopnea index greater than 10 were examined. All subjects received hypoxic and hypercapnic ventilatory tests the day before the nocturnal polysomnography. Thirty apneas during non-rapid eye movement (NREM) sleep and at least 10 apneas during rapid eye movement sleep were analyzed. For each considered apnea, we measured esophageal pressure (Pes) swings during the first three breaths preceding apnea and during the first three and last three occluded efforts occurring during the apnea. We considered as indices of respiratory effort the overall increase from the minimum to the maximum Pes (delta Pes), the rate of increase of Pes during apnea (RPes), and the maximal respiratory effort at the end of apnea (Pes max fin). In NREM sleep, all three indices of respiratory effort were correlated positively with the awake ventilatory response to hypoxia or hypercapnia and with the apnea index. No correlation was found between the indices of respiratory effort and body mass index, age, pulmonary function tests, awake blood gases, apnea duration, and apnea desaturation. In rapid eye movement sleep, none of the considered variables predicted the degree of respiratory effort. In conclusion, our results suggest that the degree of ventilatory response to upper airway occlusion in obstructive sleep apnea may be influenced by the sensitivity of central neural drive to chemical stimuli.
The survival rate of heart transplant patients has increased considerably since the development of new immunosuppressive drugs. In the long term, however, cardiac transplantation results in a high incidence of osteoporosis which represents a major functional handicap. To examine whether patients in the early stages have impaired phosphocalcic metabolism, intact parathyroid hormone (PTH 1-84), native osteocalcin, ionized Ca++ and pH were measured at rest and during muscular exercises a dynamic test used to override circadian and ultradian PTH variations. A group of 12 patients receiving the usual immunosuppressive therapy, which is mainly an association of cyclosporin and prednisolone, and 8 sedentary control subjects performed a square-wave endurance test at the same relative intensity for 30 min. No patient had previous bone disease and the period since transplantation was 12.2 +/- 2.7 months. For the transplant patients, initial PTH concentrations and responses to exercise were higher (P < 0.01) compared to the control subjects with a dramatic increase after 10 min of recovery. From higher (P < 0.001) resting concentrations, osteocalcin further increased during exercise (P < 0.01) in the heart transplant group but not in the control subjects. In both groups pH showed the same time-course with a rapid fall during exercise (P < 0.05) and Ca++ concentrations increased during the exercise period. (P < 0.01 for patients; P < 0.05 for controls) with a significant fall in both groups after 10 min of recovery (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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