No abstract

The aim of the study was to determine whether facilitation of reentry by potassium-channel openers is related to dispersion of refractoriness and/or modification of anisotropic properties of ventricular myocardium. The dispersion of ventricular effective refractory period (VERP), longitudinal and transverse ventricular conduction velocities (θL and θT, respectively), and wavelength [λ = VERP × θ(L or T)] were studied in Langendorff-perfused left ventricular epicardium in 20 rabbits during infusion of incremental doses of levcromakalim or nicorandil. Dispersion of refractoriness was assessed using standard deviation of VERP mean (SD-VERP), dispersion index (DI; SD-VERP/mean VERP), and maximum dispersion (Dmax = VERPmax − VERPmin). Ventricular conduction velocities and anisotropic ratio were not modified, whatever the dose used. VERP and λ were significantly shortened at high concentrations of levcromakalim and nicorandil. At these doses, SD-VERP, DI, and Dmax were increased significantly. Analysis of ventricular tachycardia induction, performed using a high-resolution ventricular mapping system, confirmed that heterogeneity and shortening of VERP were factors inducing functional conduction block. Our data suggest that, in rabbit left ventricular epicardium, functional conduction block facilitating the occurrence of reentry could be initiated by shortening and, especially, by dispersion of refractoriness during infusion of potassium-channel openers.

Endogenous nitric oxide (NO) is an important mediator of vasodilatation, bronchodilatation and lung inflammation. We hypothesised that the exhaled NO level may be modified in some endurance-trained athletes during and after intense exercise. Nine athletes with exercise-induced hypoxaemia (EIH), 12 athletes without EIH and 10 untrained subjects exercised for 15 min at 90% maximal oxygen consumption (VO(2)max). Exhaled NO was measured during exercise, and after 1 h and 22 h of recovery. Exhaled NO concentration ( C(NO)) decreased significantly during exercise in all subjects and returned to basal values after 1 h of recovery with no further modification. Exhaled NO output (V(NO)) rose significantly during exercise, rapidly dropped down following exercise and was similar to resting values after 1 h and 22 h of recovery. The results also showed that C(NO) and V(NO) were significantly lower in the athletes with EIH in comparison with the untrained subjects (V(NO) was 5.32 +/- 0.77 nmol/min versus 3.61 +/- 0.72 nmol/min at rest, 18.52 +/- 1.50 nmol/min versus 15.00 +/- 2.06 nmol/min during heavy exercise, and 5.52 +/- 1.04 nmol/min versus 3.79 +/- 0.76 nmol/min after 22 h recovery, in untrained subjects and EIH athletes, respectively). These findings do not confirm the hypothesis of pulmonary inflammation associated with EIH. However, potential NO epithelial down-regulation may occur and contribute to the development of gas exchange abnormality in some endurance-trained athletes.

Objective: To identify in a follow up study airway changes occurring during the course of a sport season in healthy endurance athletes training in a Mediterranean region. Methods: Respiratory pattern and function were analysed in 13 healthy endurance trained athletes, either during a maximal exercise test, or at rest and during recovery through respiratory manoeuvres (spirometry and closing volume tests). The exercise test was conducted on three different occasions: during basic endurance training and then during the precompetition and competitive periods. Results: During the competitive period, a slight but non-clinically significant decrease was found in forced vital capacity (23.5%, p = 0.0001) and an increase in slope of phase III (+25%, p = 0.0029), both at rest and after exercise. No concomitant reduction in expiratory flow rates was noticed. During maximal exercise there was a tachypnoeic shift over the course of the year (mean (SEM) breathing frequency and tidal volume were respectively 50 (2) cycles/min and 3.13 (0.09) litres during basic endurance training v 55 (3) cycles/min and 2.98 (0.10) litres during the competitive period; p,0.05). Conclusions: This study does not provide significant evidence of lung function impairment in healthy Mediterranean athletes after one year of endurance training.