The contribution of respiratory muscle work to the development of the VO₂ slow component is a point of controversy since it has been shown that the increased ventilation in hypoxia is not associated with a concomitant increase in VO₂ slow component. The first purpose of this study was thus to test the hypothesis of a direct relationship between respiratory muscle work and VO₂ slow component by manipulating inspiratory resistance. Since the conditions for a VO₂ slow component specific to respiratory muscle can be reached during intense exercise, the second purpose was to determine whether the 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. VO₂ was measured breath-by-breath using a fast gas exchange analyzer, and the O₂ uptake response was modeled after removal of the cardiodynamic phase by using two mono-exponential functions. As anticipated, when total work was slightly increased with loaded inspiratory resistance, slight increases in VO_{2 base}, the primary phase amplitude and VO_{2 peak} 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 VO₂ slow component displayed a 27% increase from 8.1 ± 3.6 to 10.3 ± 3.4 ml^.min^-1.kg^-1 (P < 0.01) with the addition of inspiratory resistance. Taken together, this increase and the lack of any differences in V_E and ventilatory parameters between the two experimental conditions suggest the occurrence of a VO₂ slow component specific to the respiratory muscles in loaded condition.