Association of circulating angiotensin converting enzyme activity with respiratory muscle function in infants

<p>Abstract</p> <p>Background</p> <p>Angiotensin converting enzyme (ACE) gene contains a polymorphism, consisting of either the presence (I) or absence (D) of a 287 base pair fragment. Deletion (D) is associated with increased circulating ACE (cACE) activity. It has been suggested that the D-allele of ACE genotype is associated with power-oriented performance and that cACE activity is correlated with muscle strength. Respiratory muscle function may be similarly influenced. Respiratory muscle strength in infants can be assessed specifically by measurement of the maximum inspiratory pressure during crying (Pi_max). Pressure-time index of the respiratory muscles (PTImus) is a non-invasive method, which assesses the load to capacity ratio of the respiratory muscles.</p> <p>The objective of this study was to determine whether increased cACE activity in infants could be related to greater respiratory muscle strength and to investigate the potential association of cACE with PTImus measurements as well as the association of ACE genotypes with cACE activity and respiratory muscle strength in this population.</p> <p>Methods</p> <p>Serum ACE activity was assayed by using a UV-kinetic method. ACE genotyping was performed by polymerase chain reaction amplification, using DNA from peripheral blood. PTImus was calculated as (Pi_mean/Pi_max) × (Ti/Ttot), where Pi_meanwas the mean inspiratory pressure estimated from airway pressure, generated 100 milliseconds after an occlusion (P_0.1), Pi_maxwas the maximum inspiratory pressure and Ti/Ttot was the ratio of the inspiratory time to the total respiratory cycle time. Pi_maxwas the largest pressure generated during brief airway occlusions performed at the end of a spontaneous crying effort.</p> <p>Results</p> <p>A hundred and ten infants were studied. Infants with D/D genotype had significantly higher serum ACE activity than infants with I/I or I/D genotypes. cACE activity was significantly related to Pi_maxand inversely related to PTImus. No association between ACE genotypes and Pdi_maxmeasurements was found.</p> <p>Conclusions</p> <p>These results suggest that a relation in cACE activity and respiratory muscle function may exist in infants. In addition, an association between ACE genotypes and cACE activity, but not respiratory muscle strength, was demonstrated.</p

Effects of endurance training on the breathing pattern of professional cyclists

The aim of this longitudinal study was to clarify the changes induced by endurance training on the breathing pattern of 13 professional cyclists (age±SD: 24±2 years; V̇O2 max ∼75 ml · kg-1 · min-1) during the three periods (rest, precompetition, and competition) of a sports season. Both the volume and the intensity of training were quantified during these periods. In each session (corresponding to each of the three periods) all subjects performed (1) a pulmonary function test (to measure forced vital capacity [FVC], peak expiratory flow [PEF], and maximal voluntary ventilation [MVV]), and (2) a ramp test until exhaustion on a cycle ergometer (workload increases of 25 W · min-1). The following variables were recorded every 100 W until the end of the tests: pulmonary ventilation (V̇E, in / · min-1 BTPS), tidal volume (VT, in IBTPS), breathing frequency (fb, in breaths · min-1), ventilatory equivalents for oxygen (V̇E · V̇O2 -1) and carbon dioxide (V̇E · V̇CO2 -1), inspiratory (TI) and expiratory (TE) times (s), ratio of TI to total respiratory duration or inspiratory "duty cycle" (TI/TTOT), and mean inspiratory flow rate (VT/TI, in /· s-1). The results showed no changes in any of these variables (p>0.05) between the three periods of study, despite significant changes in training loads (i.e., increases in the volume and/or intensity of training throughout the season). These findings suggest that endurance conditioning does not alter the breathing pattern of professional cyclists during an incremental exercise test.Sin financiación1.077 JCR (2001) Q3, 54/74 PhysiologyUE