In two studies, the cold shock and diving responses were investigated after human face immersion without prior hyperventilation to explore the mechanism(s) accounting for reductions in maximal apnoeic times (AT max ) at low water temperatures. In study 1, AT max , heart rate (HR) and cutaneous blood cell velocity were measured in 13 non-apnoea-trained males during apnoeic face immersion in 0, 10, 20 and 33• C water and room air (AIR). In study 2, six males were measured during non-apnoeic face immersion in 0, 10 and 33• C water for ventilation (V E ), respiratory exchange ratio (RER), HR and oxygen consumption (V O 2 ), as well for end-tidal partial pressures of oxygen (P ET,O 2 ) and carbon dioxide (P ET,CO 2 ). Results indicated that the AT max of 30.7 s (S.D. 7.1 s) at 0• C (P < 0.001) and 48.2 s (S.D. 16.0 s) at 10 • C (P < 0.05) were significantly shorter than that of ∼58 s in AIR or 33• C. During apnoea at 0, 10, 20 and 33 • C, both the deceleration of HR (P < 0.05) and peripheral vasoconstriction (P < 0.05), as well as the peak HR at 0• C (P = 0.002) were significantly greater than in AIR. At 0 • C in comparison with 33• C, non-apnoeic face immersions gave peaks inV E (P = 0.039), RER (P = 0.025), P ET,O 2 (P = 0.032) and HR (P = 0.011), as well as lower minimum values for P ET,CO 2 (P = 0.033) and HR (P = 0.002). WithV O 2 as the covariate, ANCOVA showed thatV E remained significantly greater (P = 0.003) at lower water temperatures. In conclusion, during face immersion at 10• C and below, there is a non-metabolic, neurally mediated cold shock-like response that shortens apnoea, stimulates ventilation and predominates over the oxygen conserving effects of the dive response.