A physiological evaluation of professional soccer players.
(9/1040)
The purpose of this study was to evaluate the physiological functions of a professional soccer team in the North American Soccer League (NASL). Eighteen players were evaluated on cardiorespiratory function, endurance performance, body composition, blood chemistry, and motor fitness measures near the end of their competitive season. The following means were observed: age, 26 yrs; height, 176 cm; weight 75.5 kg; resting heart rate, 50 beats/min; maximum heart rate (MHR), 188 beats/min; maximum oxygen intake (VO2 max), 58.4 ml/kg-min-1; maximum ventilation (VEmax BTPS), 154 L/min; body fat, 9.59%; 12-min run, 1.86 miles; and Illinois agility run, 15.6 secs. Results on resting blood pressure, serum lipids, vital capacity, flexibility, upper body strength, and vertical jump tests were comparable to values found for the sedentary population. Comparing the results with previously collected data on professional American Football backs indicated that the soccer players were shorter; lighter in body weight; higher in VO2 max (4 ml/kg-min-1) and body fat (1.8%); and similar in MHR, VE max, and VC. The 12-min run scores were similar to the initial values observed for the 1970 Brazilian World Cup Team. The agility run results were superior to data collected from other groups. Their endurance capabilities, agility, and low percent of body fat clearly differentiate them from the sedentary population and show them to be similar to that of professional American football backs. (+info)
Respiratory mechanics in airways obstruction associated with inspiratory dyspnoea.
(10/1040)
Inspiratory muscle strength and the flow and elastic pressure opposing inspiration were measured in seven patients with severe airways obstruction who found inspiration difficult at rest. A comparison was made of measurements obtained from seven normal subjects and five patients with airways obstruction not experiencing inspiratory dyspnoea at rest. Measurements were also obtained when inspiratory dyspnoea was induced in the normal subjects by adding an inspiratory resistance or by voluntarily increasing lung volume. Compared with the controls the inspiratory muscle strength of the patients was reduced but was not significantly less than that of the patients without inspiratory dyspnoea. The pressure required to produce inspiratory flow was significantly greater when inspiratory dyspnoea was present (P = 0-01). However, there was considerable overlap in the pressures of those with and without inspiratory dyspnoea. A better relationship was obtained when muscle strength was considered. The ratio of inspiratory muscle strength to the pressure required to produce flow was 0-24 +/- 0-07 (mean +/- SD) in patient with inspiratory dyspnoea, 0-10 +/- 0-03 in patients without inspiratory dyspnoea, and 0-033 +/- 0-019 in normal subjects. There was no overlap between the two patient groups. The ratios of the normal subjects were increased when inspiratory dyspnoea was induced and, with the exception of two cases, were all above those obtained when inspiratory dyspnoea was absent. Inspiratory dyspnoea was experienced with lower ratios in the normals than in the patients with airways obstruction. (+info)
Pattern of total and regional lung function in subjects with bronchoconstriction induced by 15-me PGF2 alpha.
(11/1040)
Closing volume (single breath nitrogen test), regional ventilation and perfusion (using intravenous xenon-133), and total lung function (TLC, VC, and FEV) were measured before and after intramuscular administration of 250 mug 15-methyl prostaglandin F2alpha (15-me PGF2alpha) in 10 healthy women. The cardiac output was measured with the Minnesota impedance cardiograph model 304A and the transthoracic impedance was used as an expression of the thoracic fluid volume. The slope of the alveolar plateau on the closing volume tracing showed a 271% increase 20 minutes after the prostaglandin administration, at which time the closing volume per cent (CV%) had decreased (P less than 0-01) and the closing capacity (CC%) had increased (P less than 0-05). Vital capacity (VC) decreased (P less than 0-01), residual volume (RV) increased (P less than 0-01), and the total lung capacity (TLC) remained unchanged. The maximal decrease (9%) in FEV1 was seen after 20 minutes. All these measurements except the slope of the alveolar plateau returned to control levels after 60 minutes. The redistribution of regional ventilation was more pronounced than that of the regional pulmonary blood flow. No change was observed in cardiac output and transthoracic impedance. None of the patients experienced any dyspnoea. Our results are consistent with a more pronounced effect of prostaglandin F2alpha on the small airways (the alveolar plateau) than on the larger airways (FEV1). In cases where an increase in the slope of the alveolar plateau is observed, the closing volume per cent should not be used as a measurement of the lung disease. It is concluded that the single breath nitrogen test (N2 closing volume) is more sensitive than the conventional tests. (+info)
The immediate effect of a Boston brace on lung volumes and pulmonary compliance in mild adolescent idiopathic scoliosis.
(12/1040)
Idiopathic scoliosis (IS) is known to result in lung volume and pulmonary compliance reduction. Boston brace treatment of IS is an additional factor causing restrictive respiratory syndrome due to external chest wall compression. Nevertheless, the immediate effect of Boston bracing on the pulmonary compliance of scoliotic patients has not been studied systematically. Spirometric and plethysmographic lung volumes, static lung compliance (C(ST)(L)) and specific lung compliance (C(ST)(L)/functional residual capacity) of 15 scoliotic adolescents (14 females and 1 male, of mean age 14.1+/-1.67 years, with mean Cobb angle 24.1 degrees+/-7.88 degrees) were recorded twice, in a random sequence: once without the Boston brace (nBB) and once immediately after wearing the brace (BB). Our findings showed that bracing reduced vital capacity, residual volume, functional residual capacity (FRC), total lung capacity, and forced expiratory volume in 1s in a proportional and significant way (P < 0.001). C(ST)(L) was also significantly reduced (P < 0.001), but C(ST)(L)/FRC remained unaltered. All BB and nBB indices were highly correlated. We concluded that Boston bracing in IS patients results in an immediate, predictable, and uniform reduction of lung volumes and pulmonary compliance. The reduction of C(ST)(L) under bracing conditions was related to the decrease of lung volume; the C(ST)(L)/FRC remained unaltered. (+info)
Airway closure, atelectasis and gas exchange during general anaesthesia.
(13/1040)
Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV-ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related. (+info)
External thoracic restriction, respiratory sensation, and ventilation during exercise in men.
(14/1040)
Multiple factors may contribute to the dyspnea associated with restrictive ventilatory disease (RVD). Simple models that examine specific features of this problem are likely to provide insight into the mechanisms. Previous models of RVD utilizing elastic loads may not represent completely the impact on pulmonary and chest wall receptors derived from breathing at low thoracic volumes. The purpose of this study was to investigate the sensory consequences of breathing at low lung volumes induced by external thoracic restriction in an attempt to further elucidate the etiology of dyspnea in this setting. Ten men were studied, with and without an inelastic corset applied at residual volume (restriction resulted in mean reductions in vital capacity, functional residual capacity, residual volume, and forced expired volume in 1 s of 44, 31, 12.5, and 42%, respectively). During 10-min steady-state exercise tests (at a workload set to achieve approximately 65% maximum heart rate), restriction resulted in significant increases, compared with control, in minute ventilation (61 vs. 49 l/min), respiratory frequency (43 vs. 23 breaths/min), and visual analog scale measurements of respiratory discomfort (65 vs. 20 mm). Alveolar hyperventilation (end-tidal PCO2 = 39 vs. 44 Torr for control) and mild O2 desaturation (arterial blood O2 saturation = 93 vs. 95% for control) occurred. Hypoxemia, atelectasis, increased work and effort of breathing, or a decrease in the volume-related feedback from chest wall and/or lungs could be responsible for the increased dyspnea reported. External thoracic restriction provides a useful model to study mechanisms of dyspnea in RVD. (+info)
Compensatory alveolar growth normalizes gas-exchange function in immature dogs after pneumonectomy.
(15/1040)
To determine the extent and sources of adaptive response in gas-exchange to major lung resection during somatic maturation, immature male foxhounds underwent right pneumonectomy (R-Pnx, n = 5) or right thoracotomy without pneumonectomy (Sham, n = 6) at 2 mo of age. One year after surgery, exercise capacity and pulmonary gas-exchange were determined during treadmill exercise. Lung diffusing capacity (DL) and cardiac output were measured by a rebreathing technique. In animals after R-Pnx, maximal O2 uptake, lung volume, arterial blood gases, and DL during exercise were completely normal. Postmortem morphometric analysis 18 mo after R-Pnx (n = 3) showed a vigorous compensatory increase in alveolar septal tissue volume involving all cellular compartments of the septum compared with the control lung; as a result, alveolar-capillary surface areas and DL estimated by morphometry were restored to normal. In both groups, estimates of DL by the morphometric method agreed closely with estimates obtained by the physiological method during peak exercise. These data show that extensive lung resection in immature dogs stimulates a vigorous compensatory growth of alveolar tissue in excess of maturational lung growth, resulting in complete normalization of aerobic capacity and gas-exchange function at maturity. (+info)
Role of expiratory flow limitation in determining lung volumes and ventilation during exercise.
(16/1040)
We determined the role of expiratory flow limitation (EFL) on the ventilatory response to heavy exercise in six trained male cyclists [maximal O2 uptake = 65 +/- 8 (range 55-74) ml. kg-1. min-1] with normal lung function. Each subject completed four progressive cycle ergometer tests to exhaustion in random order: two trials while breathing N2O2 (26% O2-balance N2), one with and one without added dead space, and two trials while breathing HeO2 (26% O2-balance He), one with and one without added dead space. EFL was defined by the proximity of the tidal to the maximal flow-volume loop. With N2O2 during heavy and maximal exercise, 1) EFL was present in all six subjects during heavy [19 +/- 2% of tidal volume (VT) intersected the maximal flow-volume loop] and maximal exercise (43 +/- 8% of VT), 2) the slopes of the ventilation (DeltaVE) and peak esophageal pressure responses to added dead space (e.g., DeltaVE/DeltaPETCO2, where PETCO2 is end-tidal PCO2) were reduced relative to submaximal exercise, 3) end-expiratory lung volume (EELV) increased and end-inspiratory lung volume reached a plateau at 88-91% of total lung capacity, and 4) VT reached a plateau and then fell as work rate increased. With HeO2 (compared with N2O2) breathing during heavy and maximal exercise, 1) HeO2 increased maximal flow rates (from 20 to 38%) throughout the range of vital capacity, which reduced EFL in all subjects during tidal breathing, 2) the gains of the ventilatory and inspiratory esophageal pressure responses to added dead space increased over those during room air breathing and were similar at all exercise intensities, 3) EELV was lower and end-inspiratory lung volume remained near 90% of total lung capacity, and 4) VT was increased relative to room air breathing. We conclude that EFL or even impending EFL during heavy and maximal exercise and with added dead space in fit subjects causes EELV to increase, reduces the VT, and constrains the increase in respiratory motor output and ventilation. (+info)