Acute H(2)S intoxication produces an increase in ventilation followed by a fatal central apnea. The sites of mediation of H(2)S induced hyperpnea and apnea have been investigated since the early 20th century in various animal models. Hyperpnea is mediated by the arterial chemoreceptors, an effect that can be reproduced by injecting a solution of H(2)S at very high concentrations (high millimolar range), while the fatal apnea, which typically occurs above 1000 ppm in humans, appears to result from the cessation of the activity of the medullary respiratory neurons. More recently, moderate levels of exogenous H(2)S (20-80 ppm) have been shown to reduce, within minutes, the metabolic rate, akin to hypoxia-induced hypometabolism. This response appears to be specific to small sized mammals. The pathway through which low levels of inhaled H(2)S could exert such a powerful effect may be very relevant to the physiological mechanisms controlling non-ATP "metabolic" production. Finally, endogenous H(2)S, produced from cysteine, has been proposed to transduce the effects of hypoxia in the carotid bodies. H(2)S remains a mysterious gas: it is labile, difficult/impossible to properly measure in vivo, its oxidation can take place in most tissues including the blood, and it can affect multiple cellular pathways. The demarcation between effects reflecting a putative physiological function and those related to H(2)S poisoning remains however to be established.