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Dr. Levine is Professor of Medicine, at MCP Hahneman University, Adjunct Professor of Medicine at the University of Pennsylvania School of Medicine, and Attending Physician in medicine at the Philadelphia VA Medical Center.
Correspondence to: Sanford Levine, MD, FCCP, Professor of Medicine, Department of Veterans Affairs Medical Center, University and Woodland Aves, Philadelphia, PA 19104; e-mail: sdlevine@mail.med.upenn.edu
At the present time, the diagnosis of a ventilatory limitation to exercise is based on the breathing reserve concept, ie, how close the peak exercise ventilation (VE) approaches the maximum voluntary ventilation (MVV) or some estimate of the MVV (typically the FEV1 multiplied by 35 or 40). Therefore, a small or no breathing reserve indicates a VE limitation to muscular exercise (VE limit), whereas a large breathing reserve rules out a VE limit. At a given intensity of external work, the four major causes of an increased VE—and therefore, a decreased breathing reserve—are some combination of the following: (1) arterial hypoxemia; (2) arterial acidosis effected by increases in lactate concentration; (3) anxiety and phobias regarding exercise and/or sensations related to it; and (4) inefficiency in performing a particular type of exercise.1 Many investigators have demonstrated that the administration of supplemental oxygen during exercise will decrease VE at a given exercise intensity and thereby increase the breathing reserve. Similarly, comprehensive pulmonary rehabilitation programs containing an exercise training component will decrease the arterial lactate concentration, anxiety, and inefficient limb muscle use at any given intensity of exercise, and thereby decrease the VE and increase the breathing reserve at that exercise intensity. In summary, the major strength of the breathing reserve concept is its direct therapeutic applications, whereas a problem is that this analysis provides us no mechanistic insight into the physiologic mechanisms underlying a VE limit.
In a review article in this issue of CHEST (see page 488), Johnson et al point out the utility of the exercise tidal flow-volume loop (ETFVL) in elucidating mechanisms underlying VE limit. Briefly, these authors depict exercise breaths as ETFVL and align these loops within the maximum flow-volume loop (MFVL). Assuming a proper alignment of the ETFVL within the MFVL, these authors point out that this analysis allows one to quantitate the amount of expiratory flow limitation, to measure changes in both end-expiratory lung volume and end-inspiratory lung volume, and to calculate a theoretical maximum exercise VE based on measured inspiratory and expiratory flow-rates over the range of the measured tidal volumes referenced to the MFVL. The combination of the analysis presented by Johnson et al coupled with our current knowledge of respiratory muscle physiology allows us to diagnose the particular mechanism(s) accounting for VE limitation. Additionally, recent papers by Belman et al2 and O'Donell and coworkers3 and others suggest that measurements of this type will be useful in gaining further understanding of the psychophysics underlying the sensation(s) of shortness of breath (ie, dyspnea) during exercise.
All of the material presented in the paper by Johnson et al has previously been published. Why then should this review article be accompanied by a solicited editorial? I believe that the answer is "timeliness." Prior to recent developments in instrumentation for measuring airflow and the use of more powerful microprocessors with improved graphics capabilities for cardiopulmonary exercise testing (CPET) laboratories, this type of approach would have required an inordinate allocation of health-care resources (ie, too much physician and technician time). However, within the next several years, this new equipment will replace older models in most CPET laboratories; therefore, this type of analysis will be deemed "cost-effective." While this technology-driven change can be most useful to clinicians engaged in the practice of cardiopulmonary medicine and surgery, the reader should understand that the analysis advocated by Johnson et al requires physicians and/or exercise physiologists who have experience with these type of measurements (including esophageal pressure) during CPET.
Last, I turn to the relationship between the measurements advocated by Johnson et al and those proposed by Wasserman et al.4 Over the past 3 decades, these latter authors have presented methodologies for using ventilatory and pulmonary gas exchange measurements during exercise to assess cardiopulmonary function and tissue respiration.4 The bottom line is that the methods advocated by Wasserman et al and Johnson et al are not mutually exclusive; in fact, they represent complementary approaches. Indeed, the relative importance of the two approaches will depend on the specific question(s) being asked.
References
This article has been cited by other articles:
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  T. E. Dolmage and R. S. Goldstein Repeatability of Inspiratory Capacity During Incremental Exercise in Patients With Severe COPD Chest, March 1, 2002; 121(3): 708 - 714. [Abstract] [Full Text] [PDF]
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