William G. Reddan

Effects of acute through life-long hypoxic exposure on exercise pulmonary gas exchange.

Abstract The adequacy, efficiency and control of pulmonary gas exchange during exercise was compared among groups who were exposed for various durations of time to moderate hypoxia (3100 m altitude, P i O2 100 mm Hg. These groups included native lowlanders during acute, shortterm (4 to 45 days) and long-term (1–16 yr) exposure and native highlanders of 1 to 3 generations exposure. The working sojourner depended almost entirely on his ventilatory adaptation for maintaining adequate pulmonary and systemic O2 transport at 3100 m. Exercise D lco , VC, (A-a) DO2 and Hb concentration were unchanged from acute through 21 days exposure, although (A-a) DO2 widened after 45 days at 3100 m. In contrast to the sojourner, the resident of 3100 m hypoventilated during exercise and maintained PaCO2 at or above resting levels. He depended on a high O2 carrying capacity and most importantly on an increased D lco and Vc and narrowed (A-a) D o2 for his enhanced systemic O2 delivery during work. No differences in the pulmonary response to work were found among long-term and native residents of 3100 m. Hence, the highlander avoided the high levels of ventilatory work and exertional dyspnea experienced by the sojourner without compromising systemic O2 delivery.

Control of exercise hyperpnea under varying durations of exposure to moderate hypoxia

Abstract Ventilation and arterial acid-base status at rest and during steady-state work at P i O 2 100, 145 and 250 mm Hg, were studied in: (1) lowlanders at sea level and after 4, 21 and 45 days sojourn at 3100 m altitude; (2) lowlanders residing for 2–15 years at 3100 m; and (3) native altitude residents. The total ventilatory changes at rest and work in the sojourner between ambient conditions at 250 and 3100 m altitudes were attributed: (a) to (acute) hypoxia alone, particularly during moderate to severe exercise; and (b) to the secondary effects of altitude sojourn which accounted for most of the final levels of hyperventilation achieved under all conditions of rest and work, and were complete after 4 days sojourn. Because of: (a) the absence of a significant respiratory alkalosis in response to acute hypoxia at rest, and (b) the normal ventilatory acclimatization to altitude in a lowlander subject who was non-responsive to hypercapnic-hypoxic stimuli combinations, it was reasoned that current theories based on a restoration of CSF [H + ] were not sufficient to explain the hyperventilation obtained upon sojourn to 3100 m. In residents of 3100 m: (a) Exercise e was significantly lower, Pa CO 2 higher (PIo2100), and the Δe with removal of hypoxemia less than in the sojourner at 3100 m, but similar to the sojourners results obtained during acute hypoxic exposure at sea-level; and (b) native residents and resident low-landers were similar in all respects. Sojourner-resident differences in hypoxic exercise hyperpnea at 3100 m were attributed primarily to the acquired hyper-responsiveness in the sojourner and to a lesser extent to some degree of subnormal ventilatory chemosensitivity in the resident.

Exercise training in patients with COPD.

Exercise is a useful therapeutic intervention for many COPD patients. The progressive stress test is the single most important means of clinical evaluation, although a thorough physical examination and preexercise ECG are also mandatory. The exercise program is prescribed according to duration of exercise and the maximal load reached by the patient during testing. As tolerance builds, exercise time, speed, and grade level are increased. Patients who exercise routinely should be watched carefully for problems, such as hypoxia, hypertension, abnormal right-sided cardiac function, and air tapping. Supplemental oxygen is required for those who are hypoxic.