Andrea Capalbo

Physical activity during leisure time and primary prevention of coronary heart disease: an updated meta-analysis of cohort studies

Background A vast body of evidence during the last decades has shown the clear preventive role of physical activity in cardiovascular disease. The real magnitude of the association between physical activity during leisure time (LTPA) and primary prevention of coronary heart disease (CHD) has, however, not been completely defined. Design Meta-analysis of prospective cohort studies. Methods Studies were included if they reported relative risks and their corresponding 95% confidence intervals (CI), for categories of LTPA in relation to CHD. The LTPA categories of the selected studies were grouped into three levels of intensity: high, moderate and low. The high level of physical activity was determined, to obtain a level of intensity attainable by the general population. Results Data were available for 26 studies, incorporating 513472 individuals (20666 CHD events), followed up for 4–25 years. Under a random-effects model, the overall analysis showed that individuals who reported performing a high level of LTPA had significant protection against CHD [relative risk 0.73 (95% CI 0.66–0.80), P < 0.00001]. A similar significant protection against CHD, for individuals who practised a moderate level of LTPA, has been also demonstrated [relative risk 0.88 (95% CI 0.83–0.93), P < 0.0001]. Conclusions The current meta-analysis reports significant protection against the occurrence of CHD resulting from moderate-to-high levels of physical activity. These results strengthen the recommendations of guidelines that indicate the protective effect against cardiovascular disease of physical activity profiles that are attainable by ordinary people.

Leisure time but not occupational physical activity significantly affects cardiovascular risk factors in an adult population

Background  A large number of studies have demonstrated that regular physical activity during leisure time (LTPA) accounts for a significant protection against cardiovascular diseases (CVD). On the other hand, conflicting findings on the beneficial effects of occupational physical activity (OPA) have been reported. The aim of this study is to evaluate the possible influence of different amounts of LTPA and OPA on circulating levels of several parameters associated with an increased risk of CVD.

RAS genes influence exercise-induced left ventricular hypertrophy : an elite athletes study

PURPOSE The association of ACE I/D polymorphism with changes in LV mass in response to physical training has been observed, but no association has been found with AT1R A1166C polymorphism. We investigated the ACE I/D, AT1R A1166C, and AT1R CA microsatellite polymorphisms genotype distribution in elite athletes and whether the presence of AT1R C1166 variant, in addition to ACE D allele affects the training-induced LV mass alterations in elite trained athletes. METHODS The study population comprised 28 healthy players recruited from an Italian elite male soccer team and 155 healthy male subjects. LV mass, LV mass adjusted for body surface area, septal thickness, posterior wall, end-diastolic and end-systolic ventricular dimension, and ejection fraction were determined by echocardiography in pretrained period, at rest and 7 months later during the training. All subjects were genotyped for ACE I/D, AT1R A1166C, and CA microsatellite polymorphisms. RESULTS Training induced an LV mass increase in all but six athletes. The percentage of athletes in whom an increase of LV mass was found after training was statistically different in relation to the ACE D allele: no increase was observed in three of 24 D allele carriers and in three of four II genotype players (Fishers exact test, P = 0.02). As AT1R is concerned, no increase was observed in 4 of 15 C allele carriers and in 2 of 13 AA genotype athletes (Fishers exact test, P > 0.05). The contemporary presence of ACE D and AT1R C allele did not affect the changes after training. No difference has been observed in the CA microsatellite marker allele frequencies between athletes and controls (P = 0.46). CONCLUSION In this study, we provide the evidence that soccer play does not select athletes on genotype basis. Training-induced LV mass changes in male elite athletes are significantly associated with the presence of ACE D allele, but not of AT1R C allele.

Relationship between exercise capacity, endothelial progenitor cells and cytochemokines in patients undergoing cardiac rehabilitation

No data are available about the possible role of endothelial progenitor cells (EPCs), cytochemokines and N-terminal pro-brain natriuretic peptide (NT-proBNP) in determining a different response to short period of cardiologic rehabilitation (CR), as measured by the improvement of exercise capacity. In a population of 86 cardiac surgery patients, we evaluated the numbers of EPCs, pro- and anti-inflammatory cytokines (IL-6, IL-8, IL-10, IL-1ra), hs-C-reactive protein (CRP), vascular endothelial growth factor (VEGF) and NT-proBNP before (T1), and after 15 days of CR (T2). EPCs were measured by flow cytometry, and the exercise capacity was measured at T1 and T2 by using the six-minute walk test (6MWT). At T2, a significant increase of 6MWT (p<0.0001) was detected. No significant increase of EPCs was observed, while a significant (at least p<0.05) decrease in cytochemokines, CRP and NT-ProBNP levels was evidenced. By analyzing the median improvement of 6MWT, only patients with a median improvement > or = 23% showed a significant (p<0.05) increase of EPCs at T2, with significant correlations between EPCs, VEGF and IL-10. On the contrary, in patients with a median improvement <23% a negative correlation between CRP and EPCs was observed. Finally, CD34+/KDR+ EPCs showed significant correlation with IL-8 at T1. In conclusion, a short period of CR intervention determines a different pattern of modifications for EPCs in relation to the improvement of exercise capacity.

Gene expression profile of rat left ventricles reveals persisting changes following chronic mild exercise protocol: implications for cardioprotection

BackgroundEpidemiological studies showed that physical exercise, specifically moderate lifelong training, is protective against cardiovascular morbidity and mortality. Most experimental work has focused into the effects and molecular mechanisms underlying intense, rather than mild exercise, by exploring the acute effect of training. Our study aims at investigating the cardioprotective effect of mild chronic exercise training and the gene expression profile changes at 48 hrs after the exercise cessation. Rats were trained at mild intensity on a treadmill: 25 m/min, 10%incline, 1 h/day, 3 days/week, 10 weeks; about 60% of the maximum aerobic power. By Affymetrix technology, we investigated the gene expression profile induced by exercise training in the left ventricle (LV) of trained (n = 10) and control (n = 10) rats. Cardioprotection was investigated by ischemia/reperfusion experiments (n = 10 trained vs. n = 10 control rats).ResultsMild exercise did not induce cardiac hypertrophy and was cardioprotective as demonstrated by the decreased infarct size (p = 0.02) after ischemia/reperfusion experiments in trained with respect to control rats. Ten genes and 2 gene sets (two pathways) resulted altered in LV of exercised animals with respect to controls. We validated by real-time PCR the increased expression of four genes: similar to C11orf17 protein (RGD1306959), caveolin 3, enolase 3, and hypoxia inducible factor 1 alpha. Moreover, caveolin 3 protein levels were higher in exercised than control rats by immunohistochemistry and Western Blot analysis. Interestingly, the predicted gene similar to C11orf17 protein (RGD1306959) was significantly increased by exercise. This gene has a high homology with the human C11orf17 (alias: protein kinase-A interacting protein 1 or breast cancer associated gene 3). This is the first evidence that this gene is involved in the response to the exercise training.ConclusionOur data indicated that few, but significant, genes characterize the gene expression profile of the rat LV, when examined 48 hrs since the last training section and that mild exercise training determines cardioprotection without the induction of hypertrophy.

ACE I/D polymorphism and cardiac adaptations in adolescent athletes

PURPOSE The aim of this cross-sectional study was to determine whether there is a correlation between left ventricular hypertrophy (LVH) and angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism in adolescent athletes. METHODS Seventy-five competitive soccer players (aged 15 +/- 1.2 yr) and 52 untrained control subjects (aged 15 +/- 1.6 yr) were examined with echocardiography (echo) and bioelectrical impedance analysis. The ACE genotype of all subjects was determined by PCR and correlated with left ventricular mass (LVM) indices. RESULTS Allele frequencies were comparable between athletes and controls. Body surface area (BSA), fat-free mass (FFM), and all mean echo measurements were significantly greater in athletes than in controls. LVM and LVM indices for both BSA and FFM were all significantly greater in athletes than in controls (LVM 195.3 +/- 32 g vs 165.3 +/- 37.6 g; LVM/BSA 115.5 +/- 18.9 g x mq(-1) vs 95 +/- 18.2 g x mq(-1); LVM/FFM 3.5 +/- 0.5 vs 3 +/- 0.54, P < 0.001 for the three variables). Left ventricular hypertrophy was found in 17 (23%) athletes. There was no correlation between ACE I/D polymorphism and athletes with LVH as the II and DD genotype frequencies were identical (41%). However, in athletes with LVH, the presence of the D allele was associated with a greater LVM index than compared to homozygous II genotype (LVM = 145 +/- 7.6 g x mq(-1) in DD+ID group vs 135 +/- 2.9 g x mq(-1) in II group, P = 0.008). CONCLUSIONS The results of the study show that significant changes occur in cardiac morphology and function in adolescent athletes. Interestingly, the ACE I/D polymorphism was associated with the degree of cardiac hypertrophy but not with the occurrence of LVH itself.

Physical activity and circulating endothelial progenitor cells: an intervention study

Eur J Clin Invest 2012; 42 (9): 927–932