Running effects on cognition and plasticity (ReCaP): study protocol of a longitudinal examination of multimodal adaptations of marathon running.

Regular moderate physical activity (PA) has been linked to beneficial adaptations in various somatic diseases (e.g. cancer, endocrinological disorders) and a reduction in all-cause mortality from several cardiovascular and neuropsychiatric diseases. This study was designed to investigate acute and prolonged exercise-induced cardio- and neurophysiological responses in endurance runners competing in the Munich Marathon. ReCaP (Running effects on Cognition and Plasticity) is a multimodal and longitudinal experimental study. This study included 100 participants (20-60 years). Six laboratory visits were included during the 3-month period before and the 3-month period after the Munich marathon. The multimodal assessment included laboratory measurements, cardiac and cranial imaging (MRI scans, ultrasound/echocardiography) and neurophysiological methods (EEG and TMS/tDCS), and vessel-analysis (e.g. retinal vessels and wave-reflection analyses) and neurocognitive measurements. The ReCaP study was designed to examine novel exercise-induced cardio- and neurophysiological responses to marathon running at the behavioral, functional and morphological levels. This study will expand our understanding of exercise-induced adaptations and will lead to more individually tailored therapeutic options.

Comparative electroencephalography analysis: Marathon runners during tapering versus sedentary controls reveals no significant differences.

INTRODUCTION: Previous studies described various adaptive neuroplastic brain changes associated with physical activity (PA). EEG studies focused mostly on effects during or shortly after short bouts of exercise. This is the first study to investigate the capability of EEG to display PA-induced long-lasting plasticity in runners compared to a sedentary control group. METHODS: Thirty trained runners and 30 age- and sex-matched sedentary controls (SC) were included as a subpopulation of the ReCaP (Running effects on Cognition and Plasticity) study. PA was measured with the International Physical Activity Questionnaire (IPAQ). Resting-state EEG of the runners was recorded in the tapering phase of the training for the Munich marathon 2017. Power spectrum analyses were conducted using standardized low-resolution electromagnetic tomography (sLORETA) and included the following frequency bands: delta: 1.5-6 Hz, theta: 6.5-8.0 Hz, alpha1: 8.5-10 Hz, alpha2: 10.5-12.0 Hz, beta1: 12.5-18.0 Hz, beta2: 18.5-21.0 Hz, beta3: 21.5-30.0 Hz, and total power (1.5-30 Hz). RESULTS: PA (IPAQ) and BMI differed significantly between the groups. The other included demographic parameters were comparable. Statistical nonparametric mapping showed no significant power differences in EEG between the groups. DISCUSSION: Heterogeneity in study protocols, especially in time intervals between exercise cessation and EEG recordings and juxtaposition of acute exercise-induced effects on EEG in previous studies, could be possible reasons for the differences in results. Future studies should record EEG at different time points after exercise cessation and in a broader spectrum of exercise intensities and forms to further explore the capability of EEG in displaying long-term exercise-induced plasticity.

Evidence for an exercise induced increase of TNF-α and IL-6 in marathon runners.

Regular physical activity of moderate intensity improves cardiovascular risk factors including low-grade inflammation. However, acute vigorous exercise such as marathon running results in marked increases of circulating pro-inflammatory markers. Up to now, the origin of this pro-inflammatory boost is still debated equivocally. We analyzed the change of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leptin from pre- to immediately post-race in 15 male runners (age 43 ± 10.9 years and body mass index 24.5 ± 2.7 kg/m(2) ) both on the protein level in the plasma and on the messenger ribonucleic acid (mRNA) level in blood mononuclear cells (BMNC). We observed a significant increase of IL-6 (prerace 2.08 ± 0.10 ng/L and postrace 40.14 ± 24.85 ng/L, P < 0.001) and TNF-α (prerace 8.14 ± 1.38 ng/L and postrace 12.40 ± 3.15 ng/L, P < 0.001) and a decrease of leptin (prerace 1.64 ± 2.64 µg/L and postrace 0.80 ± 1.70 µg/L, P = 0.04) serum levels after the marathon race. Furthermore, TNF-α, IL-6, and leptin were expressed (mRNA level) in BMNC. However no significant differences in mRNA levels were seen before and after the run in these cells. We found an up-regulation of TNF-α and IL-6 in the plasma during vigorous exercise. This increase is not attributable to BMNC. We assume a local production in, or release from, exercised tissues.

Marathon running improves mood and negative affect.

BACKGROUND: Physical activity has beneficial effects on depression, as well as on other mental and somatic diseases. The amount of recommended exercise is still under discussion. We investigated whether marathon runners (MA) exhibit less or more depressive symptoms and negative affects compared to sedentary controls (SC) and how their mood changes in the context of marathon training and marathon running. METHODS: We included 100 amateur marathon runners and 46 age- and gender matched sedentary controls in the ReCaP (Running effects on Cognition and Plasticity) study. Questionnaires contained Beck Depression Inventory (BDI), Hamilton Depression Scale (HAMD), Oxford Happiness Questionnaire (OHQ), Visual Analogue Scale (VAS), Positive And Negative Affect Schedule (PANAS), Global Assessment of Functioning (GAF). SC were evaluated one time at baseline, MA six times during the six months study period. RESULTS: Compared to SC, marathon runners (281.80 ± 131.44 running min/week) exhibited less depressive symptoms, more positive affects (PANAS-PA) and a higher level of functioning (GAF). Within the marathon group, negative affect (PANAS-NA) decreased and general mood states (VAS) further improved throughout the study period with a maximum 24 h after the marathon. DISCUSSION: MA had less depressive symptoms and a higher level of functioning compared to SC. Higher amounts than the recommended duration of 150 min/week aerobic training (WHO/ACSM) and the participation in a marathon seem to even further improve negative affect. These findings give new insight into the relationship between exercise and mood parameters. They can be implemented in future preventive strategies for depressive symptoms.

Influence of High Polyphenol Beverage on Stress-Induced Platelet Activation.

OBJECTIVES: Platelets are playing a crucial role in acute cardiovascular events. We investigated if physical stress activates platelets and whether this activation can be inhibited by a polyphenol-enriched diet. METHODS: Blood samples were taken from a total of 103 athletes three weeks before, one day before, immediately as well as 24 hours and 72 hours after a marathon run. Participants were randomized, double-blinded and divided into two groups. One group received a polyphenol-rich beverage the other the same beverage without polyphenols. Besides analysis of platelet counts and impedance-aggregometric-measurement of platelet activity, soluble P-selectin and Endothelin-A measurements were performed. RESULTS: In the control group, runners showed a 2.2-fold increased platelet aggregation directly after completing a marathon and within the following three days when compared with baseline values (p<0.01). In accordance, significant increases in sP-selectin (57.52ng/ml vs. 94.86ng/ml;p<0.01) were detectable. In contrast, for the group consuming a beverage with increased polyphenol content (upper quartile of study beverage intake) we did not find any increase of platelet aggregation. DISCUSSION: Physical stress causes a significant increase in platelet activity. Our results demonstrate that a diet enriched in polyphenols is capable of preventing platelet activation. These findings might indicate a diminished cardiovascular stress-reaction following pre-exposition to polyphenol-enriched diet.

Acute and chronic effects of marathon running on the retinal microcirculation.

OBJECTIVE: Previous studies indicate an association between marathon running and premature atherosclerosis. Retinal vessel diameter alterations, in particular narrower arterioles and wider venules, reflect early stages of atherosclerosis, but the influence of marathon on the retinal microcirculation is unknown. METHODS: Retinal vessel diameters were measured in 85 male runners (age 31-60 years; previous marathons 0-56) and in 45 age-matched healthy controls using a static vessel analyzer. In runners, diameters were also measured immediately and 24h after a marathon. Cardiovascular risk profiles, clinical chemistry and, in a subgroup of 46 runners, peripheral arterial wave reflections were also assessed. RESULTS: Runners had larger arterioles (median 196 µm (IQR 25) vs. 190(25); p = 0.068) and smaller venules (222(25) vs. 224(18); p = 0.063) than controls, resulting in a significantly increased arteriolar-to-venular ratio (AVR; 0.89(0.08) vs. 0.85(0.07); p < 0.001). In runners, retinal vessel diameters were not associated with body mass index, blood pressure, smoking, lipids or training history, and no differences were observed between the lowest (0.71-0.84) and highest (0.95-1.06) AVR quintiles. The marathon run induced a significant increase of AVR (0.91 (0.09); p = 0.007) due to larger arteriolar than venular dilatations, correlating weakly to race duration (r = 0.32; p = 0.003) and to a lower increase in leucocytes (r = -0.35; p = 0.001). Vessel diameters normalized 24h after the race. Augmentation index and pulse pressure decreased significantly after the race, but no associations with retinal vessel diameters were observed. CONCLUSION: Marathon running is not associated with an impairment of the retinal microcirculation. These findings contrast previous reports on atherosclerotic alterations of peripheral vessels.