Since the discovery of the O2 and CO2 respiratory chemoreceptors there has been a long debate as to their relative contributions to eupnea and the ventilatory responses to hypoxia and hypercapnia. Recent evidence suggests that attempting to assign relative contributions to the central and peripheral chemoreceptors may not be a useful approach (e.g., Teppema & Dahan, 2010; Smith et al., 2010) if the two sets of chemoreceptors interact in other than a simply additive way and are thus capable of modulating the responsiveness of one another. This means that neural signals arising from stimuli at both sets of chemoreceptors have the potential to interact; indeed, such interdependence is a pre‐condition for hypo‐ or hyperadditive interaction (Adams & Severns, 1982). In this pro/con debate three potential interaction modes are discussed: hypoadditive, additive and hyperadditive. The literature reports a broad spectrum of results and opinions between the extremes of hypo‐ and hyperaddition (reviewed in Teppema & Dahan, 2010; Blain et al., 2010; Smith et al., 2010). Here we focus on recent evidence that supports a hyperadditive or multiplicative (synergistic) interaction; we will not discuss the well‐known O2‐CO2 interaction at the level of the carotid bodies (Fitzgerald & Parks, 1971; Lahiri & DeLaney, 1975). This article is protected by copyright. All rights reserved.