Previous studies have shown that cognitive deficits precede the classical motor symptoms seen in Parkinson's disease (PD) and that physical exercise may exert beneficial effects on PD. We have recently verified that the monoamine-depleting drug reserpine – at doses that do not modify motor function – impairs memory processes in rats. Here, we evaluated the potential of physical exercise to improve cognitive and motor deficits induced by reserpine. Adult Wistar rats were assigned to six groups: (1) untrained-vehicle; (2) untrained-reserpine; (3) running wheel (RW)-vehicle; (4) RW-reserpine; (5) treadmill-vehicle; and (6) treadmill-reserpine. Exercise groups were given free nocturnal access to RW or continuous treadmill exercise (20–25min/day) for 5 days/week over 4 weeks. The animals were injected subcutaneously with reserpine (1.0 or 5.0mg/kg) or vehicle 48h after the end of physical program, and 24h later they were tested in a battery of behavioral paradigms. RW and treadmill improved the motor deficits induced by a high reserpine dose (5.0mg/kg), as evaluated in the rotarod and open-field tests. Moreover, untrained rats treated with a low reserpine dose (1.0mg/kg) presented short-term social memory deficits (without motor or olfactory disturbance) that were selectively improved by the exercise training. Our results reinforce the potential of low to moderate physical exercise as a useful tool in the prevention of motor and cognitive impairments associated to CNS monoaminergic depletion.