Nine non-cold-acclimated subjects (5 female, 4 male, mean age 22.5 years) were studied to determine whether nonshivering thermogenesis contributes to cold-induced metabolic heat production during rest (50 min standing) and exercise (40 min treadmill walking) in 5 °C. Propranolol was administered orally (females, 60 mg, 1.12 mg∙kg−1; males, 80 mg, 0.96 mg∙kg−1) to block nonshivering thermogenesis. Measurements were taken at both 25 °C, 13.1 Torr (water vapor pressure; 1 Torr = 133.3 Pa) and 5 °C, 3.6 Torr, with sessions randomly assigned to be drug–neutral (DN), drug–cold (DC), placebo–neutral (PN), and placebo–cold (PC). Body core temperature was not different between any of the experimental conditions. Mean body temperature (5 °C, 32.2 ± 0.20 °C (±SEM); 25 °C, 35.3 ± 0.20 °C) and mean skin temperature (5 °C, 22.4 ± 0.70 °C; 25 °C, 31.4 ± 0.60 °C) were lower (p < 0.05) in the 5 °C than 25 °C environment (rest, exercise, drug (D), placebo (P), combined); while shivering (EMG) was higher (16.5 ± 3.9% above baseline) at 5 °C than 25 °C (15 ± 2.1% below baseline) (p < 0.05). The greater [Formula: see text] in 5 °C compared with 25 °C for the same condition is the thermoregulatory [Formula: see text]. [Formula: see text] (mL∙min−1) was lower (p < 0.05) on the D [Formula: see text] than on the P [Formula: see text] during rest and during exercise (D, 206.1 ± 63.7; P, 338.4 ± 46.7). The EMG was 21% above baseline in the DC, and 12% above baseline for PC (p > 0.05). These results suggest a nonshivering component to heat production during acute cold exposure, which can be blocked with propranolol.Key words: nonshivering thermogenesis, propranolol, β-adrenergic blockade, body temperature, exercise, shivering.