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 (ATmax) at low water temperatures. In study 1, ATmax, 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 degrees C water and room air (AIR). In study 2, six males were measured during non-apnoeic face immersion in 0, 10 and 33 degrees C water for ventilation (VE), respiratory exchange ratio (RER), HR and oxygen consumption (VO2), as well for end-tidal partial pressures of oxygen (PET,O2) and carbon dioxide (PET,CO2). Results indicated that the ATmax of 30.7 s (S.D. 7.1 s) at 0 degrees C (P < 0.001) and 48.2 s (S.D. 16.0 s) at 10 degrees C (P < 0.05) were significantly shorter than that of 58 s in AIR or 33 degrees C. During apnoea at 0, 10, 20 and 33 degrees C, both the deceleration of HR (P < 0.05) and peripheral vasoconstriction (P < 0.05), as well as the peak HR at 0 degrees C (P = 0.002) were significantly greater than in AIR. At 0 degrees C in comparison with 33 degrees C, non-apnoeic face immersions gave peaks in (P = 0.039), RER (P = 0.025), (P = 0.032) and HR (P = 0.011), as well as lower minimum values for (P = 0.033) and HR (P = 0.002). With as the covariate, ANCOVA showed that remained significantly greater (P = 0.003) at lower water temperatures. In conclusion, during face immersion at 10 degrees 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.