Last Word on Point:Counterpoint: The major limitation to exercise performance in COPD is <i>1</i>) inadequate energy supply to the respiratory and locomotor muscles, <i>2</i>) lower limb muscle dysfunction, <i>3</i>) dynamic hyperinflation

POINT-COUNTERPOINTLast Word on Point:Counterpoint: The major limitation to exercise performance in COPD is 1) inadequate energy supply to the respiratory and locomotor muscles, 2) lower limb muscle dysfunction, 3) dynamic hyperinflationDenis O'Donnell, and Katherine WebbDenis O'Donnell, and Katherine WebbPublished Online:01 Aug 2008https://doi.org/10.1152/japplphysiol.90739.2008MoreSectionsPDF (31 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations to the editor: The clear and resounding conclusion of the correspondents who weighed in on this debate is that exercise limitation in COPD is multifactorial. Protagonists who advance a single dominant mechanism of activity limitation in this phenotypically heterogeneous population do so at their peril. My esteemed colleagues, Drs. Maltais/Debigaré and Macklem/Aliverti must accept (however grudgingly!) that a mechanical limitation to ventilation is an important and partially reversible contributor to poor exercise performance in COPD. In fact, Maltais was lead investigator in a multicenter study that demonstrated that exercise improvement following bronchodilator treatment in COPD was partially explained by reduced lung hyperinflation (5); similarly, Macklem is a pioneer in the development of innovative endoscopic methods of lung volume reduction in advanced COPD (4). In the same confessional vein, our own group has more than a passing interest in peripheral muscle dysfunction in COPD (2).We were so intrigued by Aliverti and Macklems' hypothesis that excessive expiratory muscle activity limits exercise, we decided to test it formally in a recent study (3). We conducted mechanical measurements during symptom-limited cycle exercise in 16 patients with moderate to severe COPD (FEV1 = 48%predicted). In our preliminary analysis: intolerable dyspnea was the main exercise-limiting symptom; dynamic pulmonary hyperinflation from rest-to-peak exercise was 0.83 liters, end-inspiratory lung volume reached 93% of total lung capacity at a low peak ventilation; peak inspiratory pleural pressures reached 29% of maximal inspiratory pressures; and end-expiratory gastric pressures increased smoothly throughout exercise in all patients to reach a peak of 19% of maximal gastric pressure. We found no evidence of abdominal muscle derecruitment even in those with the most advanced disease and could find no correlation between the magnitude of expiratory muscle force generation and perceived dyspnea intensity (described mainly as inspiratory difficulty).In considering integrated mechanisms of exercise limitation, we cannot lose sight of the reality that disabling dyspnea is the primary preoccupation of the COPD patient. Our knowledge of the mechanisms of this symptom remains woefully deficient and effective management will remain an elusive goal unless research in this area develops substantially beyond its current deplorable state. In the meantime, the caregiver can at least derive some reassurance from the fact that modern long-acting bronchodilators achieve sustained pharmacological lung volume reduction with attendant improvements in activity-related dyspnea and exercise tolerance (5). A remaining challenge is to convert this newfound increase in functional capacity into longer term improvements in functional status. To do this we must reverse inactivity-related, global skeletal muscle deconditioning with structured multimodality exercise training. This, however, is particularly difficult to achieve in patients with critical ventilatory limitation and severe exertional dyspnea. New approaches that reduce the rate of dynamic pulmonary hyperinflation during exercise beyond that achieved by maximal bronchodilation [i.e., hyperoxia, heliox and ventilation-feedback methods (1)] deserve further scrutiny as potential adjuncts to exercise training in such patients.As we pursue increasingly sophisticated models of exercise limitation in COPD we should be careful not to neglect the fundamental reality—When you can't breathe nothing else matters!REFERENCES1 Collins EG, Langbein WE, Fehr L, O'Connell S, Jelinek C, Hagarty E, Edwards L, Reda D, Tobin MJ, Laghi F. Can ventilation-feedback training augment exercise tolerance in patients with chronic obstructive pulmonary disease? Am J Respir Crit Care Med 177: 844–852, 2008.Crossref | PubMed | ISI | Google Scholar2 Green H, Burnett M, Duhamel T, D'Arsigny C, O'Donnell DE, Webb KA, Ouyang J. Abnormal sarcoplasmic reticulum Ca2+-sequestering properties in skeletal muscle in chronic obstructive pulmonary disease. Am J Physiol Cell Physiol [published ahead of print on May 28, 2008]; doi:10.1152/ajpcell.00224.2008.Link | ISI | Google Scholar3 Laveneziana P, Webb KA, Ofir D, Wadell K, O'Donnell DE. Expiratory muscle recruitment patterns during constant-work-rate and incremental cycle exercise in moderate to severe COPD patients (abstract). Am J Respir Crit Care Med 177(supplement): A1000, 2008.Google Scholar4 Macklem PT. Collateral ventilation. N Engl J Med 298: 49–50, 1978.Crossref | ISI | Google Scholar5 Maltais F, Hamilton A, Marciniuk D, Hernandez P, Sciurba FC, Richter K, Kesten S, O'Donnell DE. Improvements in symptom-limited exercise performance over 8 h with once-daily tiotropium in patients with COPD. Chest 128: 1168–1178, 2005.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByImpaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exerciseJoshua R. Smith, Bruce D. Johnson, and Thomas P. Olson13 September 2019 | Journal of Applied Physiology, Vol. 127, No. 3Hemodynamic effects of high intensity interval training in COPD patients exhibiting exercise-induced dynamic hyperinflationRespiratory Physiology & Neurobiology, Vol. 217Exercise and COPD: Therapeutic Responses, Disease-Related Outcomes, and Activity-Promotion Strategies13 March 2015 | The Physician and Sportsmedicine, Vol. 41, No. 1The respiratory musclesOn- and off-exercise kinetics of cardiac output in response to cycling and walking in COPD patients with GOLD Stages I–IVRespiratory Physiology & Neurobiology, Vol. 181, No. 3Too rapid increase and too much breathlessness are distinct indices of exertional dyspnea in COPDRespiratory Physiology & Neurobiology, Vol. 176, No. 1-2BPCO et inflammation : mise au point d’un groupe d’experts. Les phénotypes en lien avec l’inflammationRevue des Maladies Respiratoires, Vol. 28, No. 2 More from this issue > Volume 105Issue 2August 2008Pages 765-765 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.90739.2008PubMed18678631History Published online 1 August 2008 Published in print 1 August 2008 Metrics

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