Influence of body composition and physical fitness on arterial stiffness after marathon running.

BACKGROUND AND AIMS: Participation in exhaustive endurance sports competitions continues to be popular. Questions about the cardiovascular side effects of prolonged excessive exercise persist. Our study aimed to elucidate the acute effects of marathon running on arterial stiffness (AST) and to detect the role of body composition, fitness status, and inflammation. METHODS: Body composition was investigated in lean and obese recreational runners taking part in a marathon race. Fitness levels were determined in advance by a symptom-limited treadmill test to obtain the individual anaerobic threshold. Carotid to femoral pulse wave velocity (PWV), systolic and diastolic blood pressures (BP), and inflammatory markers (TNF-ɑ, IL-6, hsCRP) were measured before 2 hours and 24 hours after a marathon race. RESULTS: A total of 47 male runners with a wide range of body mass index (BMI) and fitness levels took part in the study. Baseline PWV was independent of body composition. Marathon running induced an acute PWV drop from 8.5 m/s to 7.9 m/s within the first two hours after the race (P < 0.05). Body composition and not physical fitness predicted the PWV differences postmarathon (P > 0.05). Changes in BP, heart rate, or inflammatory markers were not associated with PWV postmarathon. CONCLUSIONS: Though not evident at baseline, marathon running was associated with a reduced attenuation of central arterial stiffness in overweight and obese runners. The reduced responsiveness and attenuation of PWV with higher BMI, independent of hemodynamic changes and systemic inflammation, may represent masked vascular dysfunction in overweight and obese runners.

Immunomodulatory effects of aerobic training in obesity.

INTRODUCTION: Physical inactivity and obesity are independent risk factors for atherosclerosis. We analyzed the immunomodulatory capacity of 10-week intensified exercise training (ET) in obese and lean athletes. Markers of the innate immune response were investigated in obese (ONE: ET≤40 km/week) and lean athletes (LNE: ET≤40 km/week and LE: ET≥55 km/week). METHODS: Circulating dendritic cells (DC) were analyzed by flow-cytometry for BDCA-1/-2-expression. TLR-2/-4/-7 and MyD88 were analyzed by RT-PCR and Western blot. Circulating oxLDL levels were analyzed by ELISA. RESULTS: BDCA-1 expression at baseline was lower in ONE compared to both other groups (ONE 0.15%; LNE 0.27%; LE 0.33%; P < .05), but significantly increased in ONE after training (+50%; P < .05). In contrast, BDCA-2 expression at baseline was higher in ONE (ONE 0.25%; LNE 0.11%; LE 0.09%; P < .05) and decreased in ONE after the 10-week training period (-27%; P < .05). Gene activations of TLR-4 and TLR-7 with corresponding protein increase were found for all three groups (P < .01/P < .05) compared to pre training. A reduction of oxLDL levels was seen in ONE (-61%; P < .05). CONCLUSIONS: Intensified exercise induces an increase of BDCA-1+ DCs and TLR-4/-7 in obese athletes. We hereby describe new immune modulatory effects, which-through regular aerobic exercise-modulate innate immunity and pro-inflammatory cytokines in obesity.

Magnetic resonance imaging of myocardial injury and ventricular torsion after marathon running.

Recent reports provide indirect evidence of myocardial injury and ventricular dysfunction after prolonged exercise. However, existing data is conflicting and lacks direct verification of functional myocardial alterations by CMR [cardiac MR (magnetic resonance)]. The present study sought to examine structural myocardial damage and modification of LV (left ventricular) wall motion by CMR imaging directly after a marathon. Analysis of cTnT (cardiac troponin T) and NT-proBNP (N-terminal pro-brain natriuretic peptide) serum levels, echocardiography [pulsed-wave and TD (tissue Doppler)] and CMR were performed before and after amateur marathon races in 28 healthy males aged 41 ± 5 years. CMR included LGE (late gadolinium enhancement) and myocardial tagging to assess myocardial injury and ventricular motion patterns. Echocardiography indicated alterations of diastolic filling [decrease in E/A (early transmitral diastolic filling velocity/late transmitral diastolic filling velocity) ratio and E' (tissue Doppler early transmitral diastolic filling velocity)] postmarathon. All participants had a significant increase in NT-proBNP and/or cTnT levels. However, we found no evidence of LV LGE. MR tagging demonstrated unaltered radial shortening, circumferential and longitudinal strain. Myocardial rotation analysis, however, revealed an increase of maximal torsion by 18.3% (13.1 ± 3.8 to 15.5 ± 3.6 °; P=0.002) and maximal torsion velocity by 35% (6.8 ± 1.6 to 9.2 ± 2.5 °·s-1; P<0.001). Apical rotation velocity during diastolic filling was increased by 1.23 ± 0.33 °·s-1 after marathon (P<0.001) in a multivariate analysis adjusted for heart rate, whereas peak untwist rate showed no relevant changes. Although marathon running leads to a transient increase of cardiac biomarkers, no detectable myocardial necrosis was observed as evidenced by LGE MRI (MR imaging). Endurance exercise induces an augmented systolic wringing motion of the myocardium and increased diastolic filling velocities. The stress of marathon running seems to be better described as a burden of myocardial overstimulation rather than cardiac injury.