A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr ;36 5 The volunteers underwent anamnesis for the collection of clinical data, the evaluation of anthropometric measurements and subsequently the evaluation of lung volume and capacity by spirometry.
Each volunteer attended the lab once and evaluations were carried out in a single day by researchers previously trained for the experimental procedure. During the anthropometric evaluation, the volunteers remained in the orthostatic position without shoes or heavy clothing. A computerized spirometer with a flow sensor, calibrated daily, was used to measure lung function Microquark; Cosmed, Roma, Italy.
The volunteers remained seated and used a nasal clip during the realization of slow vital capacity SVC and forced vital capacity FVC maneuvers, in accordance with the guidelines of the American Thoracic Society 14 and norms for the tests of lung function. Pereira CAC. Directives for pulmonary function tests. J Pneumol ; 28 3 The maneuvers were performed until three acceptable and two reproducible curves were achieved, without exceeding eight attempts. The values are expressed in liters and percentage of predicted, according to the equations established for the Brazilian population.
J Pneumol ;18 1 The BioEstat version 5. To verify the normality of the data the Kolgomorov-Smirnov normality test was used. For intragroup and intergroup comparison of age, anthropometric characteristics and the spirometric variable values, the Student t and Mann-Whitney tests were used. For analysis of the correlation of body mass, BMI and age with spirometric variables, the Pearson and the Spearman correlations were used.
Table 1 shows the data of the age and anthropometric characteristics of the study volunteers divided into groups. Table 2 shows the lung capacity and volumes of the study volunteers. In intragroup analysis, it was observed that VC suffered a decline over the years, irrespective of the level of obesity.
In terms of intergroup analysis, it was evident that irrespective of age, the morbidly obese presented a decline in lung function when compared to the obese.
Table 3 shows the effect of age, body mass and BMI on lung function. Therefore, the greater the age, the lower the spirometric variable values, while VC and IRV values increased with body weight. Fabron et al. The decrease in SVC due to aging was also observed by Matsudo et al. Matsudo SMM. FEV 1 is a variable of interest when studying lung function and is considered to be a reproducible measure as it is effort-independent. According to the ATS, 14 Standardization of Spirometry.
Eur Respir J ; The reduction in FEV 1 in the elderly may signify obstructive changes, which can be explained by a decrease in elastic lung retractility, a reduction in chest wall compliance and a reduction in the strength of the respiratory muscles, leading to the progressive decline in lung function over time.
The aging respiratory system. Clin Geriatr Med ;1 1 Physiological changes in respiratory function associated with ageing. Eur Respir J ;13 1 With respect to the decrease in respiratory muscle strength, Santos et al.
Rev Bras Geriatr Gerontol ;16 3 In a study aimed at evaluating the harm obesity can cause to lung function, Melo et al. J Bras Pneumol ;36 6 Anatomical changes Senile hyperinflation of the lungs is a well known entity in the medical literature.
Immunologic changes Bronchoalveolar lavage BAL fluids in healthy older subjects have consistently shown an increased proportion of neutrophils and lower percentage of macrophages compared with younger adults. Figure 1. Figure 3.
Table 2 Static lung volumes. Tidal volume TV Volume of air inspired or expired during quiet breathing Inspiratory reserve volume IRV Maximum volume of air inspired above the tidal volume Expiratory reserve volume ERV Maximum volume of air expired below the tidal volume Residual volume RV Amount of air in the lungs after maximum expiration.
Table 4 Lung function studies. Dyspnea and response to hypoxia and hypercapnia Minute ventilation, a product of volume inhaled per breath and respiratory rate over one minute, is identical in younger and older individuals. Bronchial hyper-responsiveness and age-related pulmonary receptor changes Age had a significant effect on airway reactivity and response to bronchodilator therapy.
Figure 4. Mechanism of action of beta agonist. Muscarinic receptor The data on age-related changes in pulmonary muscarinic receptor in humans is limited. Cysteinyl-Leukotriene CysLT 1 receptor The stimulation of cysteinyl-leukotriene CysLT 1 receptor located on the airway smooth muscles induces bronchoconstriction. Exercise capacity The effect of aging on exercise capacity is highly variable and depends upon individual fitness and regular physical activity.
Table 5 Ventilatory response to hypoxia and hypercapnia. Summary There is marked variation in the effect of aging on lung function. Table 6 Anatomical and physiological changes of respiratory system with aging. Figure 2. Relationship between lung volumes and lung capacities.
Table 3 Lung capacities are sum of two or more static lung volumes. Catalytic unit of adenylate cyclase: reduced activity in aged-human lymphocytes. J Clin Endocr Metab. Longitudinal changes in forced expiratory volume in one second in adults.
Am Rev Respir Dis. Aging, late-onset asthma and the beta-adrenoceptor. Pharm Therapeutics. Impaired bronchodilator response to albuterol in healthy elderly men and women.
Reference spirometric values using techniques and equipment that meets ATS recommendations. Loss of response to treatment with leukotriene receptor antagonists but not inhale corticosteroids in patients over 50 years of age. Ann Allergy Asthma Immunol.
Changes in FVC during methacholine-induced bronchoconstriction in elderly patients with asthma: bronchial hyper responsiveness and aging. Distribution of forced expiratory volume in one second and forced vital capacity in healthy, white, adult, never smokers in six U. Spirometry reference values for women and men 65 to 85 years of age. Cardiovascular Health Study. Respiratory muscle strength in the elderly. N Engl J Med. Airspace size in lungs of lifelong non-smokers: effect of age and sex.
The effect of age on methacholine response. J Allergy Clin Immunol. Physiological changes in respiratory function associated with aging. Eur Respir J. Eur Respir J Suppl.
How aging affects the normal lung. J Respir Dis. Changes in the normal maximal expiratory flow-volume curve with growth and aging. Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnea with aging in normal men.
J Clin Invest. Longitudinal effects of aging on lung function at rest and exercise in healthy active fit elderly adults. J Appl Physiol. Immune dysregulation in the aging human lung. Relationship between chest wall and pulmonary compliance with age.
Spirometric standards for health non-smoking adults. Effects of aging on ventilatory and occlusion pressure responses to hypoxia and hypercapnia. The contractile properties of the elderly human diaphragm. Reference values and prediction equations for normal lung function in a non-smoking white urban population. Diffusing capacity dependent on lung volume and age in normal subjects. Dead space ventilation in old age. Comparison of diaphragm strength between healthy adult elderly and young men.
Am J Epidemiol. Age-related changes in pulmonary muscarinic receptor binding properties. Am J Physiol. Age, period, and cohort effects on pulmonary function in a year longitudinal study.
Normative aging of the respiratory system. Clin Geriatr Med. Support Center Support Center. External link. Please review our privacy policy. The drop of P Pl also decreases the airways resistance by dilating the small airways and thus enhancing the air flow further. The sequence of events reverses during tidal expiration. As a result, air flows outside the alveoli following the pressure gradient, Fig. Tidal expiration is therefore a passive process, which needs no further muscle contraction.
During tidal breathing, whether inspiratory or expiratory, intra-airways P aw pressure is always more than P Pl. This explains why small airways are always opened, even at the end of tidal expiration. Intrapleural and alveolar pressures towards the end of inspiration a , expiration b , and forceful expiration c.
The dotted line indicates the change in thoracic dimensions during a , b and c compared with the previous phase of the respiratory cycle. If inspiration above the tidal limit is required, accessory muscles of inspiration must be activated. Thoracic cage expands more leading to higher drop in P Pl and P alv compared with tidal inspiration, which explains why more air is delivered to the alveoli compared with tidal inspiration.
Alternatively, expiration below the tidal level is an active process that requires contraction of expiratory muscles. During forceful expiration, the thoracic cage is compressed to the maximum. As demonstrated in Fig. This gradual drop in P aw is secondary to simultaneous increase in the airways resistance towards the trachea. Taking into consideration the relatively constant P Pl around the lung, each small airway can be subdivided into three segments Fig.
Static PVC of the lungs and chest wall. The lung and chest wall curve was plotted by the addition of the individual lung and chest wall curves. Development of airflow limiting segments occurs in small airways that lack cartilaginous support and explains why the lungs cannot be empty completely.
What limits airflow upon forceful expiration was previously explained by development of choke points i. This is akin to a waterfall in which height and flow upstream the river are unlikely to affect the speed of the free falling water; nevertheless, if waterfall is broader, an extra water will be displaced.
It is important to note that upon forced expiration, the increase in P alv is accompanied by gas compression within the lung. This will result in reduction of both lung volume and P el. The decrease in P el in turn attenuates the driving as well as the distending pressures at the choke points. This explains why the actual volume of forcefully expired air is always less than that measured with body plethysmograph.
Expiration after development of airflow limiting segments is effort independent. What remains in the lungs when small airways start to close is called the closing capacity CC [ 12 , 13 ]. Alternatively, RV remains in the lung when all small airways are closed. It is evident from the above description that pulmonary ventilation depends on the airways resistance offered to the airflow and expansibility compliance of the lungs and the thoracic cage. These two major determinants of pulmonary ventilation are crucial for understanding the pattern of change in static lung volume in different types of lung diseases.
The tracheobronchial tree undergoes successive dichotomizations, where the airways become narrower but more distensible as we proceed downward.
It is, therefore, difficult to apply simple laws of physics that govern fluid flow across single, non-branched, non-distensible tube system to evaluate respiratory airways resistance. For example, the lowest airways resistance resides on smallest bronchioles but not large airways.
Because bronchioles are arranged in parallel, their resistances depend on the total cross sectional area of all bronchioles rather than the radius of a single bronchiole. Airways resistance is inversely proportional to the lung volume. P Pl decreases significantly upon inspiration, which enhances distension of airways especially small bronchioles.
At higher lung volumes, attachments from the alveolar walls pull small airways apart and hence enhance the effect of P Pl on decreasing airways resistance. In contrast, airways resistance increases significantly during forceful expiration due to formation of flow limiting segments.
Compliance is a physical term used to predict the change in volume per unit change in the transmural pressure P T i. From physiological perspective, the P T for the lungs trans-pulmonary pressure , chest wall trans-chest wall pressure and respiratory system trans-respiratory pressure are calculated by subtracting P alv — P Pl , P Pl — P atm and P alv — P atm , respectively.
According to physics, if P T is equal to zero then the system is resting i. Like lung volumes, the lung compliance can be measured under static and dynamic conditions. Figure 3 shows the static pressure volume curves PVC of the lungs and the chest wall. The entire lung PVC in Fig. The lungs are never rested within the chest cage i. If removed outside the body then trans-pulmonary pressure can reach zero; however, the lung will not be empty completely, Fig. At this point the inward recoil tendency of the lungs is equal to the outward recoil tendency of the chest wall, Fig.
The PVC of the lungs can also be recorded during breathing to evaluate dynamic lung compliance. It is evident from Fig. This phenomenon is known as hysteresis and can be explained by the variations of surface tension at alveolar air-fluid interface during inspiration and expiration.
Pulmonary surfactant is a natural substance that reduces surface tension of the fluid layer lining the alveoli. During inspiration, alveolar surface tension is likely to increase because pulmonary surfactant spreads over a wider alveolar surface. The reverse occurs during expiration, where pulmonary surfactant condenses in a smaller alveolar surface. The work of breathing is usually estimated by the area under the dynamic PVC of the lungs Fig.
During inspiration, the work needed to overcome elastic forces of the chest wall, lungs parenchyma and alveolar surface tension is called elastic work of breathing. In addition, a resistive work is needed during inspiration to overcome tissue and airways resistance. In contrast to inspiration, only resistive work of breathing is required during expiration.
Under physiological condition the work needed for inspiration is more than that needed for expiration. The energy stored in the elastic lung structures during inspiration is partly consumed as expiratory resistive work and partly dissipated as heat Fig. Physiologically, the diseases that affect the respiratory system are characterized by restrictive, obstructive or combined pattern of ventilatory defects [ 14 , 15 ].
Restrictive lung diseases RLD are associated with decreased compliance of the lungs, chest wall or both. This results in rightward shift of static PVC of the lungs, chest wall or both [ 15 ]. In RLD, the rightward shift of dynamic lung compliance curves increases the elastic work of breathing required for inspiration, which is usually compensated by rapid shallow breathing [ 16 ]. Causes of RLD may be intrinsic or extrinsic to the lung parenchyma.
Examples of intrinsic causes are interstitial lung diseases, pneumonia and surfactant deficiency e. Alternatively, respiratory muscles weakness, chest deformities, cardiomegaly, hemothorax, pneumothorax, empyema, pleural effusion or thickening are examples of extrinsic causes. In obstructive lung diseases OLD , the pulmonary compliance is normal or increased especially if emphysematous lung changes co-exist. No extra-negative P Pl is needed as dynamic lung compliance curves are either not displaced or shifted leftward if emphysematous lung changes developed Fig.
The main defect in OLD is increased airways resistance, especially during expiration. Normally, expiration is a passive process as the energy needed to overcome expiratory resistive work of breathing is stored in the elastic fibers of the lung during inspiration.
Famous examples of obstructive pulmonary diseases include bronchial asthma, emphysema, chronic bronchitis and bronchiectasis. The lung volumes increase steadily from birth to adulthood. The lungs mature at the age of 20—25 years, yet only minimal changes occur in the lung volumes over the following 10 years [ 17 ]. After 35 years, aging is associated with gradual changes in the lung volumes and other pulmonary functions [ 18 ]. These changes include enhanced static lung compliance due to diminished alveolar elastic recoil and depressed chest wall compliance due to stiffening and increased outward recoil of the thoracic cage [ 19 , 20 ].
As a result of these changes in the lung and chest wall compliances, the inward recoil of the lung balances the outward recoil of the chest at higher FRC as age progress [ 12 , 13 ].
These variations in lung and chest wall compliances act synergistically to cause early closure of small airways upon forced expiration and hence explain increased RV in elder people [ 19 ]. As shown in Fig. It is also apparent from Fig. This results in a reduction of the difference between these two capacities i. Standard morphometric methods confirmed that males had larger lung size, more respiratory bronchioles and wider airways diameters compared with females with the same age and stature [ 21 , 22 ].
These anatomical lung differences between males and females explain the gender variations in static lung volumes and capacities. Males tend to have larger anthropometric measurements and are, therefore, more likely to have increased static lung volumes and capacities [ 23 ]. Tall stature is typically associated with higher static lung volumes and capacities [ 24 ].
Increased body weight is associated with lower lung volumes in obese subjects [ 25 ]. Waist-to-hip ratio could be a better predictor for fat distribution than BMI [ 27 ]. In athletes, repeated muscular exercise increases muscle mass and consequently body weight.
In such condition, the static lung volumes and capacities are expected to increase with weight [ 29 — 32 ]. Increased total body fat content, therefore, seems better than high BMI as an indicator of obesity as well as predictor for decreased static lung volumes and capacities [ 33 ]. Such variations were largely attributed to anthropometric differences between different ethnic groups. Recently, GLI Global Lung Initiative offered spirometric prediction equations, that also considered ethnic differences, to be used worldwide [ 38 ].
Lung volumes correlate well with the level of physical activity [ 39 ], regular exercise, especially swimming and endurance training [ 32 ]. Alternatively, ascending to high altitude may decrease lung volumes probably due to increased pulmonary blood flow, pulmonary edema or premature small airways closure [ 40 ]. Alterations in lung volumes associated with high altitude are usually temporal and resolve after returning to the sea level [ 41 ].
The position of the subject is important while measuring lung volumes and capacities [ 42 ]. Compared with the standing position, the effect of gravity on abdominal viscera is less at sitting position and least if lying supine [ 43 ].
The supine position, therefore, compromises diaphragmatic movement and chest wall recoil during breathing. The measurement of the lung volumes is not an easy task and requires cooperative patients and qualified technicians. Special attention should be given to the accuracy of the method used for estimation of the static lung volumes and capacities. Plethysmography was claimed to overestimate while dilutional techniques may underestimate the true measurements of the lung volumes and capacities [ 5 ].
The normal lung volumes and capacities can be predicted based on gender, age, weight, height and ethnicity of the subject [ 47 ]. Although authorized spirometric reference values are available for most populations, normal ranges of lung volumes and capacities were not established in others yet.
However, the use of these cut-off points may be misleading in characterizing ventilatory defects in some pulmonary diseases if only simple spirometry is performed [ 48 , 49 ]. Simultaneous increase of RV with VC reduction is indicative of obstructive lung disease because of small airway closure or expiratory flow limitation [ 53 ]. Therefore, decreased VC readings are better interpreted in conjunction with other clinical and spirometric indicators of OLD, especially if measurements of RV and TLC are not available [ 54 ].
According to Aaron et al. This hypothesis is further supported by Vandevoorde et al. If thoracic cage expansion is restricted, rightward displacement of the chest wall static PVC takes place.
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