1. Six men exercised at 600 kp m/min on a cycle ergometer. After a control period they hyperventilated at about twice the control level of ventilation. Capillary blood samples were taken for lactate estimations at the end of both 6 min periods.
2. Hyperventilation resulting in a fall in end-tidal Pco2 of 12·0 mmHg was associated with rise in blood lactate concentration of 1·07 mm/l.
3. It is concluded that the increase in blood lactate concentration attributable to hyperventilation is comparatively small in exercise tests involving short periods of moderately severe exertion.
4. In an additional subject exercising similarly, hyperventilation without a fall in Pco2 (‘normocapnic’ hyperventilation) was achieved by adding 3·8% CO2 to the inspired air. Subsequent hyperventilation while breathing air resulted in a fall in end-tidal Pco2 of 19·5 mmHg (‘hypocapnic’ hyperventilation) and a rise in blood lactate concentration of 1·21 mm/l. Parallel changes in pyruvate concentration occurred suggesting that lactate production had increased. Neither the origin nor the mechanism of this increase could be ascertained; however, it appeared unlikely to be due to increased anaerobic metabolism of the respiratory muscles as normocapnic hyperventilation was associated with virtually no change in blood lactate and pyruvate concentrations.