Why vital capacity increases during exercise

Muscle-strengthening activities like weight-lifting or Pilates build core strength, improving your posture, and toning your breathing muscles. Breathing exercises in particular can strengthen your diaphragm and train your body to breathe more deeply and more effectively. People living with lung disease can and should get regular exercise for all the same reasons as everyone else. Your lungs and heart stay stronger, you are better able to perform the tasks of daily living and you feel better in mind and body.

But if you already are dealing shortness of breath, it can be intimidating to think about increasing your physical activity. It is important to work with your healthcare team to make a fitness plan that works for you. This November your donation goes even further to improve lung health and defeat lung cancer. Double Your Gift. Your tax-deductible donation funds lung disease and lung cancer research, new treatments, lung health education, and more.

Join over , people who receive the latest news about lung health, including COVID, research, air quality, inspiring stories and resources. Thank you! You will now receive email updates from the American Lung Association. Lo Mauro, A. Pedotti, and P. Beck, L. Olson et al. Guenette, J. Witt, D. McKenzie, J. Road, and A. O'Donnell, M. Lam, and K. View at: Google Scholar S. McClaran, C. Harms, D. View at: Google Scholar D. O'Donnell, J. Guenette, F. Maltais, and K. Di Marco, J.

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This review intends to update the reader with the physiological basis, clinical significance and interpretative approaches of the standard static lung volumes and capacities. Figure 1 gives a schematic summary of the standard lung volumes and capacities [ 1 — 3 ]. The procedures used for measurement of RV, FRC and TLC are based on radiological, plethysmographic or dilutional techniques helium dilution and nitrogen washout methods [ 4 ]. However, body plethysmography and dilutional techniques may under-and overestimate lung volumes and capacities, respectively [ 5 ].

Standard lung volumes and capacities from a spirometer trace. The solid black and gray arrows indicate lung volumes and capacities respectively. Towards the end of tidal expiration, the lungs tend to recoil inward while the chest wall tends to recoil outwards. These two opposing forces lead to a negative pressure within the potential space between the parietal and visceral pleurae.

The negative intrapleural pressure P Pl is one of the important factors that keep the patency of small airways, which lack cartilaginous support. The rhythmic contraction of inspiratory muscles causes cyclic changes in the dimensions of the thoracic cage and consequently comparable cyclic fluctuation of P Pl. As a result, air flows into the alveoli. 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.

They are often used to measure the efficacy of an intervention and can be considered comparative cross-sectional. For this study, 72 male subjects were randomly selected by simple random sampling technique SRS. Measurements of respiratory indices were taken three times in the pre- and post-exercise phases of each session, and their mean values were used for analysis.

Subjects were asked not to change their habitual physical activity during the study and not to take any nutritional supplements. Each session began with a warmup period of five minutes. For the session itself, running time started at five minutes, and this interval was increased by ten minutes every three sessions, up to a maximum of 25 minutes.

Subjects had to remain in the straight sitting or standing position throughout the test, and a nose clip was tightly attached to the nostrils, allowing no air to escape during the test. FVC Maneuver: Each subject was asked to inhale completely and rapidly, pausing less than one second at total lung capacity TLC , and then exhale as quickly and completely as possible, expelling all the air.

MVV maneuver: Subjects were tested in the sitting position while wearing a nose clip. They were instructed to breathe as rapidly and deeply as possible for 12 seconds after obtaining at least three resting tidal breaths with an airtight seal around the mouthpiece.

Statistical analysis was conducted using SPSS software version The Wilcoxon test, a nonparametric analysis paired t-test , was done to determine changes pre- to post-test. Table 1 shows the mean of the anthropometric characteristics of the 72 subjects. The mean age was Table 2 shows the baseline spirometry data of predicted values for the 72 subjects.

The mean predicted FVC was 4. The mean pre-exercise FVC was 3. Post-exercise mean FVC after 5, 15, and 25 minutes was 3. The post-exercise mean FEV 1 after 5, 15, and 25 minutes was 3. Table 3 B shows the baseline spirometry data of MVV before and after exercise at different intensities.