An intense physical exercise induces an inflammatory reaction as demonstrated by the delayed increase in blood of acute phase proteins and among them of C-reactive protein (CRP). There is also evidence for a diminished acute phase reaction due to regular exercise suggesting a suppression of the inflammatory response through training. With this background CRP was measured by a sensitive enzyme immunoassay under resting conditions before and after 9 months of training in 14 subjects preparing for a marathon with the aim of studying the effect of training on the base-line CRP concentration. The mean distance run per week increased significantly from 31 +/- 9 km at the beginning to 53 +/- 15 km after 8 months of training (p < 0.01). The aerobic capacity rose significantly after training as demonstrated by the increase of running velocity during a maximal treadmill test from 3.82 +/- 0.29 m/s pre-training to 4.17 +/- 0.17 m/s post-training at a blood lactate concentration of 4 mmol/L (p< 0.01). In 10 of 12 runners base-line CRP was diminished after training in spite of a continuous increase of training intensity. The CRP median fell from 1.19 mg/L before to 0.82 mg/L after training (p < 0.05). Since intense physical exercise is known to be associated with an inflammatory reaction of muscles and tendons, the CRP decrease was unexpected. In 2 subjects the CRP concentration rose markedly because of a borrelia infection and a knee injury, respectively. These values were caused by a pathological condition and were not considered for the statistical evaluation. In 10 non-training control subjects the CRP median did not change significantly during the same 9 months period. The decrease of the CRP base-line concentration after training suggests that intensive regular exercise has a systemic anti-inflammatory effect. This is of particular interest with regard to several recent reports confering on the concentration of CRP in plasma a predictive value for the risk of cardiac infarction, venous thrombosis or stroke.

These results suggest an association of combined angiotensin I-converting enzyme gene I/D polymorphism genotypes, and angiotensinogen gene M235T polymorphism genotypes with left ventricular hypertrophy due to long-term athletic training. A synergistic effect of angiotensin I-converting enzyme gene DD genotype and angiotensinogen gene TT genotype on left ventricular mass in endurance athletes appears to occur.

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In 12 moderately trained subjects reduced glutathione (GSH) and oxidized glutathione (GSSG) as well as thiobarbituric acid reactive substances (TBARS) were measured in the blood before and during the first two hours and first two days after a 2.5-h run. The participants covered between 19 and 26 km (20.8 +/- 2.5 km, mean +/- SD). The running speed was between 53 and 82% of the speed at which blood lactate concentration reached 4 mmol/L lactate (67.9 +/- 8.2%, mean +/- SD) assessed during a previously performed treadmill test. Blood samples were collected 1 h before, immediately before, immediately after, 1 and 2 h after, as well as 1 and 2 days after the run. Immediately after exercise GSH was significantly decreased (p < 0.01) and GSSG significantly increased (p < 0.01). In all subjects the ratio of GSH to GSSG showed a marked decline to 18 +/- 4% (mean +/- SD) of the pre-exercise values (p < 0.01). One hour later the mean GSH and GSSG values returned to baseline. However, there were considerable inter-individual differences. In some subjects the GSH/ GSSG ratio overshot the pre-exercise levels, in others the ratio remained low even two hours after exercise. Compared with the pre-exercise values TBARS concentrations did not change significantly at any time point after exercise. The findings suggest that after prolonged exercise in moderately trained subjects a critical shift in the blood glutathione redox status may be reached. The changes observed were generally short-lived, the duration of which may have depended on the relative importance of reactive oxygen species generation by the capillary endothelial cells and neutrophil and eosinophil granulocytes after the end of exercise.

From January 1992 until December 1994 the Cologne model of ambulant cardiac rehabilitation (ACR) in the greater area of Cologne, Germany, was performed and is still in progress. In Germany until 1992 the cardiac rehabilitation was exclusively performed stationary. The objective of the "Cologne model" was to evaluate, whether the transfer of the stationary cardiac rehabilitation programs into the ambulatory setting is achievable without deficits in efficiency, safety and overall quality. The results obtained are intended to serve for standardization and quality control of future ambulatory cardiac rehabilitation programs in Germany. From 1992 to 1994 108 patients (94 men, 14 women; 52.3 +/- 8.0 years old) with coronary artery disease (CAD) which were compatible with the criteria of the "Cologne model" (Table 1) participated in the 4-week ACR. The indications for inclusion into the ACR were in 74 cases a myocardial infarction (MI), in 34 cases CAD without MI, but with PTCA/stent-procedure (Table 3). Seven patients discontinued the ACR prematurely, 2 patients because of cardiovascular reasons. Reasons for the preference of the ambulatory over a stationary cardiac rehabilitation program were in 40.6% of the patients refusal of "hospital ambience", in 43.6% familiar or in 12.9% professional reasons. During the 4-week ACR patients participated in a mean of 72.9 +/- 6.7 hours of therapy (Table 4). As a result of the ACR exercise tolerance increased highly significantly (**) from 116.4 +/- 28.8 to 129.9 +/- 34.6 watt). This improvement was maintained at the 1- and 3-year control (128.7 +/- 35.8**) examinations (Tables 5 and 7). One year after ACR 77% of the patients stated to be physically active in ambulatory heart groups (AHG) (27.6%) or on their own (49.4%). Three years after ACR the rate of regularly physically active patients still was 59.2%. Furthermore, as a result of ACR the dietary behavior was changed significantly. There was a reduction in the consumption of lipids by 20.8%, saturated fatty acids by 30.7% and of cholesterol by 30.5%. The plasma concentrations of cholesterol decreased from 231 +/- 49.8 to 213.2 +/- 35.9 mg%**. Six (and 12) months after ACR they increased again to 225.6 +/- 39.4 mg%. Three years after ACR the mean cholesterol level was 219.1 +/- 39.3 mg%. In the high risk group (cholesterol at the initial visit > 220 mg%) cholesterol levels were reduced from 266 +/- 44 to 232 +/- 31.9 mg%**. Six and 12 months after ACR they were 239.7 +/- 35.8 mg% and 245.8 +/- 32.6 mg%, respectively, (Tables 6 and 7) and still significantly lower than before ACR, though only 19% of the patients were treated with lipid lowering agents. Three years after ACR cholesterol were 234.6 +/- 37.7 mg%** in the high-risk group. 34.2% of the patients received lipid lowering agents. Mean body weight remained unaltered over the 3-year period. Smoking behavior was not altered significantly during the 4-week ACR. However, before the cardiovascular event 67.3% of the patients had smoked cigarettes. At the beginning and at the e...