ABSTRACT
Under resting conditions in healthy individuals, the respiratory muscles use little (-1.5%) of the total oxygen consumption (V02;lot) or cardiac output (Robertson et al. , 1977 a). This situation is altered, however, when the relation between respiratory muscle metabolic demand and systemic oxygen transport is perturbed. This occurs during exercise, when disease increases the impedance of the respiratory system, and when oxygen delivery is reduced (Anholm et al ., 1987; Boutellier et al., 1986; Collett et al., 1985; Oligaiti et al., 1986; Viires et al. , 1983; Robertson et al., 1977a; Cala et al., 1991). In normal subjects, respiratory muscle oxygen consumption (V~resp) increases linearly with exercise (Chemiack, 1959; Robertson et al., 1977b) because of the increased power output by the respiratory muscles. In patients with pulmonary disease, in contrast, Vo2resp at rest may account for 25% of Vo2tot (Chemiack, 1959; Field et al., 1982). Changes in resting muscle length and recruitment of postural and synergistic accessory muscles, which do not directly contribute to ventilation, furthermore, result in a progressive decrease in respiratory muscle efficiency (V~resp/work of breathing) as minute ventilation increases (Chemiack, 1959; Fritts et al., 1959; Rochester et al ., 1976). In a theoretical analysis, Riley (1954) has suggested that the degree to which such patients may increase their minute ventilation is limited by oxygen availability. That is, as ventilation increases, an ever-increasing proportion of the additional 0 2 uptake is diverted to the respiratory muscles at the expense of 0 2 available for nonrespiratory work. A point will be reached beyond which the increase in Vo~sp becomes
664 Ward and Hussain
greater than the increase in V<>7tot, and further increases in ventilation become detrimental.
