Gabriella Amodeo

Lipid peroxidation and total antioxidant status in unprofessional athletes before and after a cardiopulmonary test.

We examined lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS) and total antioxidant status (TAS) before and after a cardiopulmonary test, in 20 sedentary controls and in 62 unprofessional male athletes subdivided into 3 subgroups. The first included subjects who practised endurance sports (14 cyclists and 9 endurance swimmers), the second subjects who practised mixed sports (6 basket players, 6 judoists, 8 water polo players) and the third group subjects who practised power sports (3 sprint runners, 4 weightlifters, 12 sprint swimmers). In the whole group of athletes an increase in TBARS and a decrease in TAS were present at baseline. Subdividing the whole group into three subgroups we observed an increase in TBARS in all and a decrease in TAS only in the endurance and mixed athletes. After the test, TBARS showed a more significant increase in controls compared to the whole group and each subgroup of athletes, while TAS increased only in the whole group and in those who practised mixed sports. In conclusion, at baseline in athletes the oxidative status shows a different behaviour compared to controls, while after the test the antioxidant protection is more marked and it may be related to an increase of antioxidant systems.

Erythrocyte deformability and nitric oxide metabolites in athletes before and after a cardiopulmonary test

Objective:To evaluate erythrocyte deformability, nitric oxide metabolites, and their modifications induced by exercise in athletes who practised different sports. Design:This evaluation was effected before and after cardiopulmonary test, using a cycloergometer. Setting:The study was performed in the Department of Internal Medicine, Cardiovascular and Renal Diseases of the University of Palermo. Participants:We enrolled 62 male athletes who practised endurance (n = 23), mixed (n = 20), and power (n = 19) sports and 20 sedentary male subjects as controls. Assessment of Risk Factors:No subject had diabetes or hypertension or dyslipidemia. Five control subjects and 14 athletes were smokers. Main Outcome Measures:Erythrocyte deformability was examined as elongation index (EI) using a diffractometer. The nitric oxide metabolites (nitrite + nitrate = NOx) were evaluated employing the Griess reagent. Results:In the whole group, an increase in EI and NOx was present. Subdividing the whole group into 3 subgroups, we noted an increase in EI and NOx only in endurance and mixed athletes. The EI before and after the cardiopulmonary test significantly decreased in the whole group and in power athletes but not in endurance and mixed athletes. Before and after the test, NOx did not significantly change in the whole group and in the 3 subgroups. Conclusions:In athletes who practised endurance and mixed sports, we observed an increase of NOx level and an increase of erythrocyte deformability. The latter did not change after an exercise test in the same subgroups, whereas it decreased in power athletes.

Relationship between elastase and total antioxidant status in young subjects with recent myocardial infarction.

In a group of young subjects with acute myocardial infarction (AMI) (68 men and 7 women; mean age 39.6+/-5.7 years) we examined the plasma concentration of elastase, the thiobarbituric acid-reactive substances (TBARS) and the total antioxidant status (TAS) at the initial stage of AMI. In this group we found an increase of elastase (p<0.001) and TBARS (p<0.001) and a decrease of TAS (p<0.001). A statistical correlation was observed in the whole group of AMI patients between plasma elastase and TAS (p<0.01) and this correlation was more statistically significant in patients with more risk factors and not in those with more involved vessels.

Persistence of high plasma elastase level in young subjects with acute myocardial infarction.

Activated granulocytes release several proteins and among these elastase plays a key-role in the development and progression of coronary heart disease (CHD). In subjects with angiographically diagnosed coronary lesions, plasma elastase was significantly increased in comparison with normal controls and also distinguished subjects with coronary complex atheromatous plaque from those with simple plaque (1,2). In the Edinburgh Artery Study (3) the group of subjects with baseline angina, during more than 5-year follow-up, showed a positive association between elastase level and risk for fatal or nonfatal cardiovascular events. Other authors (4) had previously observed an increase of peptide Bβ30-43 (a specific human granulocyte elastase-derived peptide) in subjects with unstable angina and acute myocardial infarction (AMI). Elastase was evaluated during and after cardiopulmonary resuscitation in a group of subjects with cardiac arrest subdivided according to the return or not to spontaneous circulation (5). This proteolytic enzyme, measured after arrival at the emergency department and after 30 minutes, 60 minutes, 6 hours, and 24 hours, was increased in the survivors and also at the first points of observation in the nonsurvivors. In the survivor group, elastase reached the peak after 6 and 24 hours and this trend is similar to that observed by other authors (6). Our group (7) recently evaluated plasma elastase, employing an enzyme-linked immunosorbent assay method, in a group of 49 young subjects with AMI (46 men and 3 women; mean age 38.8 ± 6.8 years; range 19–45 years). Regarding risk factors, 49% had family history of CHD, 61% were cigarette smokers, and 16% exsmokers; hypercholesterolemia was present in 26%, diabetes mellitus in 14%, and essential hypertension in 10%. Two of the three women were taking oral contraceptives. The time interval between AMI onset and the first examination (T1) was 13 ± 7 days and all the patients were reexamined three months after the first evaluation (T2). All the patients were treated with angiotensin-converting enzyme (ACE) inhibitors, statins, and platelet antiaggregation agents (aspirin or ticlopidine or clopidogrel). In this group of AMI patients, the elastase level was raised compared to control subjects, both at T1 (AMI patients: 101.60 ± 41.90 ng/mL; control subjects: 59.73 ± 17.60 ng/mL; P < .001) and at T2 (AMI patients: 91.65 ± 36.50 ng/mL; P < .001 vs control subjects). In control subjects and in AMI patients, both at T1 and T2, no relationship was found between plasma elastase and granulocyte count. These data confirm our previous findings regarding other aspects of granulocyte function in subjects with recent AMI (8). We in fact observed an abnormality in granulocyte membrane fluidity and cytosolic Ca2+ content (in particular after in vitro activation) that was still present after 12 months. An antielastase action has been observed for some calcium channel blockers (9,10), but their employment in AMI patients has not been evaluated from this point of view and is controversial because of collateral effects. In experimental models of myocardial ischemia, administration of elastase inhibitors was followed by a decrease in tissue damage (11,12).