1. The acute ventilatory response to a brief period of hypoxia (AHVR) was measured in six subjects (a) at rest, (b) during electrically induced leg exercise (EEL), (c) during voluntary leg exercise at an external work rate matched to electrical exercise (EV1) and (d) during voluntary leg exercise at an internal work rate (i.e. metabolic rate) matched to electrical exercise (EV2). The end-tidal P-O2 during hypoxia was 50 mmHg and the end-tidal P-CO2 was held constant at 1-2 mmHg above resting values throughout each of these four protocols. 2. EEL was produced by surface electrode stimulation of the quadriceps muscles so as to cause the legs to extend at the knee and lift a set of weights via a pulley system. During EV1, each subject lifted the same weight through the same height and at the same frequency as during his EEL protocol. During EV2, the weight, the height through which it was lifted and the frequency of voluntary contractions were altered to produce a similar O-2 consumption and CO2 production as during EEL. 3. In each subject, end-tidal P-CO2 values showed no change between the four protocols, and in three subjects in whom they were measured, arterial P-CO2 values were also similar between the protocols. Venous lactate levels did not increase after EEL or EV2. 4. The AHVR during EEL (14.1 +/- 1.42 l min(-1); mean+/-S.E.M) was significantly increased (Student's paired t test) compared with rest 7.55 +/- 1.10 l min(-1); P < 0.003). The AHVR during EV2 was very similar to that during EEL(13.6 +/- 1.35 l min(-1)). The AHVR during EV1 was significantly increased compared with rest (9.62 +/- 0.88 l min(-1); P < 0.002) but significantly lower than during both EEL (P < 0.004) and EV2 (P < 0.008). 5. These results suggest that the increase in the acute ventilatory response to hypoxia which normally occurs during exercise in man can also occur in the absence of a drive to exercise from the cortex.