The contribution of respiratory muscle work to the development of the O₂ consumption (O₂) slow component is a point of controversy because it has been shown that the increased ventilation in hypoxia is not associated with a concomitant increase in O₂ slow component. The first purpose of this study was thus to test the hypothesis of a direct relationship between respiratory muscle work and O₂ slow component by manipulating inspiratory resistance. Because the conditions for a O₂ slow component specific to respiratory muscle can be reached during intense exercise, the second purpose was to determine whether respiratory muscles behave like limb muscles during heavy exercise. Ten trained subjects performed two 8-min constant-load heavy cycling exercises with and without a threshold valve in random order. O₂ was measured breath by breath by using a fast gas exchange analyzer, and the O₂ response was modeled after removal of the cardiodynamic phase by using two monoexponential functions. As anticipated, when total work was slightly increased with loaded inspiratory resistance, slight increases in base O₂, the primary phase amplitude, and peak O₂ were noted (14.2%, P < 0.01; 3.5%, P > 0.05; and 8.3%, P < 0.01, respectively). The bootstrap method revealed small coefficients of variation for the model parameter, including the slow-component amplitude and delay (15 and 19%, respectively), indicating an accurate determination for this critical parameter. The amplitude of the O₂ slow component displayed a 27% increase from 8.1 ± 3.6 to 10.3 ± 3.4 ml · min¹ · kg¹ (P < 0.01) with the addition of inspiratory resistance. Taken together, this increase and the lack of any differences in minute volume and ventilatory parameters between the two experimental conditions suggest the occurrence of a O₂ slow component specific to the respiratory muscles in loaded condition.