Contrary to earlier smaller trials, we observed similar improvements in exercise capacity and peripheral endothelial function following AIT and ACT in a large population of CAD patients.

The Oxygen Uptake Efficiency Slope (OUES), a new parameter derived from respiratory gas analysis, has been suggested as a submaximal index of cardiopulmonary functional reserve. We evaluated the clinical application and the effect of physical training on the OUES in patients with coronary artery disease (CAD). Maximal cycle-ergometer testing with respiratory gas analysis (breath-by-breath) was performed in 590 patients with CAD and again after three months of physical training in 425 patients. OUES was determined from the linear relation of oxygen uptake (V.O (2)) vs. the logarithm of pulmonary ventilation (V (E)) during exercise, i.e. V.O (2) = a log (10) V (E) + b, where a is the OUES. The ventilatory anaerobic threshold (VAT) and the slope of the relation of V (E) nu carbon dioxide production (V.CO (2)) (V (E)-V.CO (2) slope) were also determined. Correlation coefficients of the relation from which OUES was derived in individuals averaged 0.975 +/- 0.024 (mean +/- SD) when calculated from data up to a respiratory gas exchange ratio of 1.0. Submaximal OUES was marginally lower (5.4 +/- 7.9 %, p < 0.05) than the OUES calculated from 100 % of respiratory exercise data. Of all submaximal parameters, submaximal OUES (r = 0.837, p < 0.001) and VAT (r = 0.860, p < 0.001) correlated best with peak V.O (2), followed by V (E)-V.CO (2) slope (r = - 0.469, p < 0.001). OUES was lower in patients who underwent coronary artery bypass grafting as compared with patients after coronary angioplasty (p < 0.05). Peak V.O (2) and OUES increased significantly (p < 0.001) after training with 24 +/- 19.2 % and 20.9 +/- 19.3 %, respectively. Changes in peak V.O (2) correlated better with changes in OUES and in VAT (r = 0.61 and r = 0.55, p < 0.001, respectively) than with changes in V (E)-V.CO (2) slope (r = - 0.171, p < 0.001). The submaximal OUES is clinically useful for the quantification of exercise performance and is sensitive to physical training in patients with CAD.

Age, baseline exercise performance and training characteristics were predictive for training effects in cardiac rehabilitation. Anti-arrhythmics and ST-segment depression at baseline exercise testing were predictive for complications.

BackgroundIt is widely accepted that genetic variability might explain a large part of the observed heterogeneity in aerobic capacity and its response to training. Significant associations between polymorphisms of different genes with muscular strength, anaerobic phenotypes and body composition have been reported. Muscular endophenotypes are positively correlated with aerobic capacity, therefore, we tested the association of polymorphisms in twelve muscular related genes on aerobic capacity and its response to endurance training.Methods935 Coronary artery disease patients (CAD) who performed an incremental exercise test until exhaustion at baseline and after three months of training were included. Polymorphisms of the genes were detected using the invader assay. Genotype-phenotype association analyses were performed using ANCOVA. Different models for a genetic predisposition score (GPS) were constructed based on literature and own data and were related to baseline and response VO2 scores.ResultsCarriers of the minor allele in the R23K polymorphism of the glucocorticoid receptor gene (GR) and the ciliary neurotrophic factor gene (CNTF) had a significantly higher increase in peakVO2 after training (p < 0.05). Carriers of the minor allele (C34T) in the adenosine monophosphate deaminase (AMPD1) gene had a significantly lower relative increase (p < 0.05) in peakVO2. GPS of data driven models were significantly associated with the increase in peakVO2 after training.ConclusionsIn CAD patients, suggestive associations were found in the GR, CNTF and the AMPD1 gene with an improved change in aerobic capacity after three months of training. Additionally data driven models with a genetic predisposition score (GPS) showed a significant predictive value for the increase in peakVO2.

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Ser49Gly and haplotype combinations of Ser49Gly and Gly389Arg of the beta(1)AR gene are associated with aerobic power, but not with the response to physical training in patients with CAD included in the CAREGENE study.

It is concluded that both drugs affect endurance exercise capacity in young, normotensive men, with a tendency to a smaller reduction during bisoprolol treatment. Haemodynamic variables are unlikely to be involved in the reduction of endurance exercise capacity. The role of the reduced availability of plasma free fatty acids remains unclear.

Exercise training significantly improves exercise performance in cardiac patients with AF. AF affects exercise performance but does not impair the beneficial effects of training. Patients with chronic AF should therefore not be dissuaded from participating in exercise training after a cardiac event.