The Importance of Cardiopulmonary Testing in Pulmonary Diseases

        The primary aim of exercising is to improve quality of life, strength, endurance, and/or movement capabilities. Integrating a resistance and cardiovascular training program into a client’s lifestyle can improve posture, respiration, musculoskeletal strength and cardiovascular endurance, which may help improve lung function, motivation, adherence to exercising and overall quality of life. While research has shown that exercising facilitates improvements across many health factors, what isn’t exactly clear is what intensity, duration, frequency, and volume (performance baselines) are appropriate to train at when faced with a pulmonary condition. This is because standard predicted equations are based on healthy subjects.

           It is critically important to monitor and understand the impact exercise training has on lung function, skeletal muscle strength, cardiopulmonary ventilation, cardiovascular endurance, neuromuscular facilitation, and quality of life in pulmonary diseases. Subjective and/or objective test needs to be administered in order to monitor these variables. The problem however, arises in the fact that pulmonary diseases don’t present themselves the same way in each individual. There are commonalities, but there isn’t an absolute, especially in exercise capacity. This is why performance testing is important in understanding exercise capacity.

          Exercise specialists and researchers are challenged to evaluate the optimal work to rest ratio to increase exercise tolerance without sustaining higher lactate accumulation and/or cardiac and pulmonary strain in pulmonary disease.  Performance tests are great for connecting objective measures to an individual’s physical fitness. Exercise testing is imperative to understand capabilities, but not everyone will be able to use the same parameters. During exercise, oxygen consumption can increase 10 to 15 times resting values (Joyner & Casey, 2015). As exercise demand increases, respiration is exhausted due to plateau in tidal volume (V_T) expansion.  In healthy individuals, O_2- pulse parallels heart rate (HR), with heart rate having a sharper increase if deconditioning is present. There should be a linear association between the HR with oxygen consumption (VO₂) in response to exercise to a certain degree. This is a normal cardiovascular response unless cardiac or pulmonary vascular disease are also present.

           The ability for an individual to overcome inertia and create force production during a performance test is a multifactorial process. It takes many components (i.e. neurological, circulatory, metabolic, respiratory, skeletal systems etc.) to fight against gravity to generate chemical energy and shuttle it into mechanical energy. As the duration at which mechanical energy is needed there is an increase for oxygen to supply that demand. In performance tests that focus on oxygen consumption, limiting factors that are seen earlier in individuals with pulmonary diseases compared to healthy individuals are a decrease in pulmonary diffusion capacity, cardiac output, oxygen carrying capacity, and peripheral oxygen diffusion.

           Maximal heart rate is one of several standard predicted measures used in health and science application and is established based on healthy individuals. Individuals with pulmonary diseases commonly have to fight against a decreased lung function, pulmonary exacerbations, dyspnea, chronic coughing, decreased immune system, decreased maturation growth, and decreased skeletal muscle mass. All at which are not considered in standard predicted equations. The baselines and thresholds also can be considered too high to be useful for predicting exercise estimations and valid outcomes based on healthy individual outcomes. Further evidence on the impact exercise has on the pulmonary diseases is needed to create clarity and standards to quality approaches to exercise training. This is why it is important to collect cardiopulmonary metrics. This includes but not limited to VO_2max, heart rate, blood pressure, pulmonary function test, heart rate reserve or VO₂ reserve, Rate of Perceived Exertion Scale (RPE) and/or Borg Scale.  This allows the professional to establish metrics based on the individual and not on standard predicted measures for healthy individuals.

Incremental exercise increases cardiopulmonary demand. Individuals with respiratory disease have ventilation/perfusion (V_A/Q) inequality altering ventilation baseline demands. Ventilation-perfusion ratio is the amount of air that reaches the alveoli divide by the amount of blood that flows through the pulmonary capillaries in the lungs. On average there is 4 to 6 L/min liters of air entering the respiratory tract with 5 liters of blood flowing through the capillaries every minute (V/Q ratio of 0.8-1) (Lumb & Horner, 2019).

 In individuals with respiratory disease, O² conduction and exchange is impeded because of chronic inflammation, chronic infections, airway obstructions, necrotic tissue, leading to faster increase in hypoxemia and hypercapnia. As a result, cardiopulmonary exercise testing in individuals with respiratory disease have shown to have lower than expected peak work rate and a VO_2peak that is below the age-predicted norms (Parazzi et al. 2015). The initial stages of exercise testing tend to have a normal value, but as time under stress increases there is a faster decline compared to healthy individuals. The result of overventilation within compensatory areas of the lungs, minute ventilation (V_E) and carbon dioxide production (VCO₂) which normally declines and becomes negative in healthy individuals, increases and stays constant with individuals with respiratory disease (V_E/VCO₂). The disproportion between V_A/Q is all interdependent on the severity of the respiratory disease.  Cardiopulmonary exercise testing in individuals with a respiratory disease has shown to have lower than expected peak work rate and a VO_2peak that is below the age-predicted norms.

            In healthy lungs, gas exchange is directed and distributed throughout the alveoli within the lungs. Gas exchange in respiratory disease is impeded because of, but not limited to, chronic inflammation, chronic infections, airway obstructions, and lung necrosis.  This causes gas exchange abnormalities arising from alveolar and capillary damage. At rest, a healthy individual’s physiological dead space to tidal volume ratio (V_D/V_T) is estimated to be 0.30-0.40 and declines to ≤ 0.20 during exercise. In respiratory disease, V_D/V_T tends to be elevated at rest and doesn’t decline at rest like healthy individuals. With an increase in the ventilatory CO₂ and a lower ventilatory reserve, dyspnea and muscle fatigue set in earlier. Thin et. al. (2004) looked at airway dead-space during exercise in patients who had been diagnosed with cystic fibrosis and compared them to normal healthy subjects. Six patients who had been free of acute pulmonary exacerbations for two months, went through a four-stage exercise protocol that looked at submaximal steady-state ventilation. The exercise protocol progressively increased each stage from rest, up to the 40W. The last and final stage was determined based on the participants third stage ventilator responses at 40W. Bipolar electrocardiogram and ear lobe pulse oximetry were recorded throughout testing.  At rest, there wasn’t a difference in ventilator dead-space in the CF group compared to healthy individuals. During exercise however, there was a higher respiratory frequency in the CF group compared to healthy subjects causing a disproportional ratio of airway dead-space to ventilation compared to healthy individuals. The increase in unproductive ventilation increases ventilation to maintain normal PaCO₂ and PaO_2. This results in increased V_E/VCO₂ and V_E/VO₂ and fail to decrease V_D/V_T at rest and during exercise. Thin et. al. (2004) study the results showed that patients with cystic fibrosis have to work harder to sustain adequate gas exchange resulting in elevated airway dead-space and decreased utilization of airway ventilation.

         Understanding the full health history and using testing measures that are appropriate to the individual are the best approach to creating individualized performance outcomes. Using the standard predicted equations to determine intensity, duration, frequency, and/or volume can be misleading in respiratory disease. Individualizing the metrics by using performance testing can help quantify the outcomes and information to help produce proper results. If you want to truly make an impact on an individual’s ability to exercise, test what matters and understand the general guidelines created, but do not see them as an absolute metric to exercise performance in pulmonary conditions Not everyone’s exercise capacity is the same, so not everyone should be measured under the same standard equations.

References

Joyner, M. J., & Casey, D. P. (2015). Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiological Reviews, 95(2), 549–601.

 Lumb, A. B. & Horner, D. (2^nd ed.). (2019). Pharmacology and Physiology for Anesthesia. Elsevier Inc.

 Parazzi, P. L., Marson, F. A., Ribeiro, M. A., de Almeida, C. C., Martins, L. C., Paschoal, I. A., Toro, A. A., Schivinski, C. I., & Ribeiro, J. D. (2015). Ventilatory abnormalities in patients with cystic fibrosis undergoing the submaximal treadmill exercise test. BMC  Pulmonary Medicine, 15, 63.

Thin, A., Dodd, J., Gallagher, C., Fitzgerald, M., & Mcloughlin, P. (2004). Effects of respiratory rate on airway deadspace ventilation during exercise in cystic fibrosis. Respiratory Medicine, (98), 1063-1070

For more exercises check out our YouTube Channel: Cystic Fibrosis Fitness Institute 

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