Physical exercise provokes platelet desensitization in men who smoke cigarettes - involvement of sympathoadrenergic mechanisms - a study of monozygotic twin pairs discordant for smoking

Abstract

Since chronic smoking is known to be a dominant risk factor for morbidity and mortality in cardiovascular diseases related to enhanced atherogenesis and arterial thrombogenesis, the mechanisms causing these effects are of interest. The present study aims to assess the basic biochemical and haemorheological parameters among male monozygotic twinpairs, who have been discordant for smoking in average for over 20 years. Because smoking is known to cause enhanced sympathoadrenergic activation, the study was designed to further stimulate this by means of physical exercise. The platelet aggregation in vitro and serum-thromboxane B 2 (S-TxB 2) did not differ at rest, but after exercise smokers′ platelets were desensitized to all doses of adrenaline and low doses of ADP as well as collagen and the levels of S-TxB 2 were lower than among nonsmokers. This finding was supported by the decreased release of serotonin and TxB 2 during aggregation induced with adrenaline. The leucocyte counts were significantly higher among smokers at rest and haematocrit as well as platelet counts showed the same tendency. Fibrinogen tended to be be elevated among smokers after exercise and together with haematocrit levels implicated increased blood viscosity. FVIII, vWF and β-thromboglobulin did not differ. In conclusion we suggest that in smokers the significant exhaustion of platelets to in vitro stimulation might be a consequence of continuous platelet activation during physical stress. This phenomenon together with our other findings implies that the sympathoadrenergic system has a multiple role in vivo, which needs further research to elucidate the mechanisms involved in the effects of smoking on cardiovascular diseases.