Aim: 

The cardiovascular benefits of regular physical exercise have been well documented, but exercise also acts as a trigger of sudden death and acute myocardial infarction in susceptible individuals. It seems consensual that acute prolonged exercise induces loss of cardiac homeostasis seen for instance in changed levels of oxidative stress, damage and apoptosis. An important aspect that has not been considered extensively comprises the notion that inflammatory processes are involved in the exercise-induced myocardial stress reaction.

Methods: 

Wistar male rats, divided into four groups (Control, Control/Melatonin, Exercise and Exercise/Melatonin) who conducted an exercise protocol on treadmill (25 m / min, 10% incline, 1 hour) and were sacrificed at 2 hours of the completion of the exercise. 30 minutes before starting the exercise, melatonin was injected intraperitoneally at a dose of 1 mg/kg body weight, control rats were treated with an equal volume of saline.

Results: 

Myeloperoxidase activity, indicative of the migration of neutrophils is increased from 153.43% (versus controls) with the protocol of exercise after 2 hours of completion, and with the treatment of melatonin decreased 55.59% (versus exercise). The protocol used for exercise promotes a significant increase in pro-inflammatory cytokines, TNF-a, IL-1b and IL-6 (92.18%, 167.09% and 1834.5% compared with controls), in the heart muscle at 2 h after completion of the exercise. Values in rats treated with melatonin decreased of 46.4%, 53.9% and 55.5% (respectively) compared with exercised animals.

Conclusion: 

The administration of melatonin before exercise prevents the increase in inflammatory activity, and decreases the responses of pro-inflammatory cytokines TNF-a, IL-1b and IL-6 following exhaustive exercise.