Charles G. Gallagher

Exercise and chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease have abnormal respiratory mechanics, respiratory muscle function, gas exchange, and cardiovascular function during exercise. Their impaired exercise tolerance is at least partly due to altered respiratory mechanics, but factors that increase ventilation during exercise indirectly contribute to exercise limitation. Clinical exercise testing is a very important tool in the assessment of exercise capacity, assessment of factors that contribute to exercise limitation, and differential diagnosis of cardiopulmonary disease.

Lack of importance of respiratory muscle load in ventilatory regulation during heavy exercise in humans.

1. Seven active subjects (24 +/‐ 1 years; maximal oxygen uptake (VO2,max), 3.77 +/‐ 0.2 l min‐1; mean +/‐ S.E.M.) performed constant work rate heavy exercise (CWHE, approximately 80% of maximal incremental work rate) to exhaustion on 2 days, one with (unload) and one without (control) respiratory muscle unloading. 2. With unloading, a special device applied flow‐proportional mouth pressure assist (positive with inspiratory (I), negative with expiratory (E) flows) throughout each breath. No pressure assist occurred during control CWHE. To confirm unloading, respiratory muscle pressures (Pmus) were derived (n = 5) from measured pleural pressure and chest wall elastic and resistive pressures. 3. Other than minor differences in early exercise, the temporal course of minute ventilation (VE) was similar in both tests as exercise progressed. The fall in estimated mean alveolar CO2 (PA,CO2) throughout CWHE was identical in both tests. There were no significant differences (ANOVA) in VE, tidal volume, frequency, oxygen consumption rate (VO2), heart rate or PA,CO2, between unload and control CWHE, at matched times (at 50% of control duration and at the end of exercise). Unloading reduced Pmus significantly throughout CWHE; at 50% control duration, peak Pmus,I and Pmus,E fell by 24 and 41%, respectively, with unloading, as did mean Pmus,I and Pmus,E (21 and 44%). 4. The lack of any significant changes in VE, PA,CO2 or breathing pattern, despite a marked reduction in respiratory muscle load throughout CWHE, indicates that the load on the respiratory muscles has only a minor role in the regulation of ventilation during heavy exercise. 5. The absence of improvement in CWHE duration (control, 11.4 +/‐ 1.2 min; unload, 12.6 +/‐ 2.1 min, n.s.) with unloading implies that respiratory muscle function does not limit endurance exercise performance during cycling in healthy humans.

Differential ventilatory control during constant work rate and incremental exercise

The purpose of this study was to determine whether the tachypneic breathing pattern of constant work rate, heavy exercise (CWE) is unique to CWE or whether it represents the usual pattern of the respiratory control system at high levels of ventilation (VI). We compared breathing pattern in ten healthy subjects (age 20-29 years) during CWE and maximal incremental exercise (MIE) on a bicycle ergometer. Work rate was constant at 76% of maximum work rate in CWE and progressively increased by 25 watts/minute until exhaustion during MIE. Breathing pattern was examined at matched levels of VI equivalent to 80% and about 100% of maximum VI during CWE (97.1 and 121.4 L.min-1, respectively). Exercise duration (mean+standard deviation) was 13 +/- 6 and 12 +/- 1 min during CWE and MIE, respectively (P = NS). Tidal volume (VT) fell by an average of 0.20 L towards the end of CWE, but was maintained relatively high and constant towards the end of MIE. At high, but not lower, matched levels of VI breathing pattern during CWE was significantly more rapid and shallow than that during MIE. The tachypnoea of CWE did not correlate with the progressive rise in VI, oxygen uptake or cardiac frequency during CWE. We conclude that (1) CWE is associated with a tachypneic influence that is absent or less during incremental exercise; this tachypnea is most marked at the end of CWE. (2) The tachypnoea of CWE is not part of a generalized rate accelerating process during CWE. The mechanism(s) underlying the tachypnoea are unclear but it may be related to inspiratory muscle fatigue, pulmonary oedema, and/or altered respiratory mechanics.

CLINICAL EXERCISE TESTING IN CHRONIC AIRFLOW LIMITATION

Exercise testing has become an essential tool in the management of patients with CAL. In addition to its ability to assess exercise limitation objectively, it has usefulness in detecting the presence or absence of associated disease processes, in assessing the response to therapies, in allowing assessment of the importance of psychological factors in exercise limitation, and in guiding prescription for exercise rehabilitation programs. Although much is known about the clinical usefulness of exercise testing in this disease, and much has been learned about how this disease functionally impairs the exercise capacity of the patient, additional study is necessary to appreciate fully the physiologic abnormalities demonstrated by patients with CAL during exercise.