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Smoking is a major risk factor for cardiovascular morbidity and mortality, and is considered to be the leading preventable cause of death in the world. Cigarette smoke contains more than 4000 chemical substances, including nicotine and carbon monoxide (CO) that can have harmful effects on cardiovascular function. These basic ingredients of tobacco smoke cause an increase in oxidative stress, endothelial damage and dysfunction, and are associated with significantly higher serum concentrations of total cholesterol and triglycerides, and lower levels of the cardioprotective high-density lipoprotein. By causing intravascular inflammation, smoking promotes the development of atherosclerosis and cardiovascular disease. The purpose of this article is to provide a brief description of the effects of smoking, and in particular the effects of nicotine and CO, on cardiovascular function. Nicotine deregulates cardiac autonomic function, boosts sympathetic activity, increases heart rate (HR) at rest, while blunting HR elevation during progressive exercise and lowering the maximum HR that can be achieved. At the same time, the smoking-generated CO binds with haemoglobin and myoglobin, reduces arterial O2 blood saturation, compromises the efficiency of respiratory enzymes, and causes dysfunction of the O2 production, transportation and delivery system, especially during exercise, substantially reducing the functional capacity and the performance of the circulatory system.