title: Endothelial (dys)function: the target of physical exercise for prevention and treatment of cardiovascular disease.
abstract: OBJECTIVE
  Endothelial dysfunction has been recognized as the early event and the common feature of chronic disorders associated with increased risk for atherosclerotic heart diseases. While the beneficial effects of aerobic, moderate-intensity exercise on endothelial function are very well assessed, an intriguing doubt exists about the effects of long-term high-intensity physical activity. The aim of the present study was to compare recent findings of our group concerning homocysteine levels in athletes to available data in literature in order to clarify the meaning of such apparent metabolic paradox.
  
  
  METHODS
  The studied population included 185 athletes: 180 healthy age and sex matched subjects served as control group. The assessed variables included homocysteine, folate, vitamin B12, total and HDL cholesterol, LDH, CPK and IL-6. Results were compared to available data in literature.
  
  
  RESULTS
  The prevalence of hyperhomocysteinemia (>15 µmol/L) in athletes and controls was 55% and 15%, respectively. In the studied population, no correlation was found between homocysteine and all the other investigated variables.
  
  
  CONCLUSIONS
  The present results suggest that intensive physical training could induce a pathological increase of homocysteine levels. With this regard, it has been suggested that the observed increases of cardio-vascular risk factors in athletes could represent an adaptative feature marker of muscle demand but would not actually lead to endothelial damage. This remains, however, a speculative hypothesis and further analysis are needed in order to clarify the clinical significance of those observations in order to better preserve the athletes immediate and future health.
authors.affiliation: Department of Health Sciences, University of Rome Foro Italico, Rome, Italy. fabio.pigozzi@iusm.it
authors.forename: F
authors.initials: F
authors.lastname: Pigozzi
authors.forename: M
authors.initials: M
authors.lastname: Rizzo
authors.forename: F
authors.initials: F
authors.lastname: Fagnani
authors.forename: A
authors.initials: A
authors.lastname: Parisi
authors.forename: A
authors.initials: A
authors.lastname: Spataro
authors.forename: M
authors.initials: M
authors.lastname: Casasco
authors.forename: P
authors.initials: P
authors.lastname: Borrione
mesh_terms: D002318:Cardiovascular Diseases / Q000503:physiopathology / Q000517:prevention & control*; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology; D006710:Homocysteine / Q000097:blood; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology
chemical_list: D006710:Homocysteine; D009569:Nitric Oxide