This study examined the acute effects of 10-ppm hydrogen sulfide (H2S) inhalation, a concentration equal to its occupational exposure limit, on the cardiovascular, metabolic, and biochemical responses in healthy volunteers. Fifteen men and 13 women completed two 30-minute exercise sessions at 50% of their maximal oxygen uptake, during which they inhaled medical air or 10 ppm H2S in a blind manner. Arterial and finger-prick blood samples were obtained before and during the final minute of exercise. Muscle biopsies were withdrawn from the right vastus lateralis immediately after exercise. Cardiorespiratory measurements were monitored using an automated metabolic cart interfaced with an electrocardiogram and blood pressure apparatus. A significant decrease in oxygen uptake (V˙O2), with a concomitant increase in blood lactate, was observed in men and women as a result of H2S exposure. No significant changes were observed in arterial blood parameters and the cardiovascular responses under these conditions. Muscle lactate, as well as the activities of lactate dehydrogenase, citrate synthase, and cytochrome oxidase, were not significantly altered by H2S exposure. However, there was a tendency for muscle lactate to increase and citrate synthase activity to decrease in both genders in the presence of H2S. It appeared that 10-ppm H2S inhalation reduced V˙O2 during exercise, most likely by inhibiting the aerobic capacity of the exercising muscle. These findings question the scientific validity of the current occupational exposure limit for H2S.