Chest
Volume 81, Issue 1, January 1982, Pages 6-10
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Clinical Investigations
Mechanisms of Oxygen Effects on Exercise in Patients with Chronic Obstructive Pulmonary Disease

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Administration of supplemental oxygen significantly improved exercise tolerance in patients with chronic obstructive pulmonary disease. This was achieved by a reduction of ventilatory requirements for the same work load, such that limiting ventilatory capacity was not achieved until later in incremental work. Breathing supplemental oxygen produced lower levels of lactate, but relief of anaerobiasis did not contribute to ventilatory changes, since potential acid-base alterations were balanced by concomitant retention of carbon dioxide.

Section snippets

Materials and Methods

We studied a group of nine patients with COPD who volunteered and gave informed consent. There were eight men and one woman. The characteristics of the patients are shown in Table 1. All had severe obstructive pulmonary disease with a forced expiratory volume in one second (FEV1) less than 48 percent of the predicted value. All had severely impaired functional capacity (class 4, American Medical Association's classification of respiratory impairment8); ie, they experienced shortness of breath

Results

All of the patients except one demonstrated an increase in the duration of exercise tolerated when breathing the 30 percent oxygen mixture (Fig 1). The maximum ventilation achieved at the breaking point of exercise was strikingly similar for each patient whether breathing air or supplemental oxygen, and no significant difference in this measurement was found between the two exercise runs. Considering the group as a whole, total work (as measured by total consumption of oxygen) increased an

Discussion

Our findings confirm previous reports which describe the improved exercise tolerance in persons with severe COPD during breathing of supplemental oxygen. This was achieved mainly by maintaining the uptake of oxygen from the enriched alveolar gas at a lower total ventilation. The reduction in ventilation seemed to be related to hypoxic drive, because ventilation correlated well with SaO2. This is consistent with the observation in normal subjects that the magnitude of ventilation per unit of

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