Abstract

Conflicting data exist on the relevance of marathon (M) and half marathon (HM) running for health. The number of non-professional athletes finishing M and HM events is steadily growing. In order to investigate molecular changes occurring in amateur athletes, we enrolled 70 non-professional runners finishing a single M (34) or HM (36) event at baseline, the finish line and during recovery, and 30 controls. The measurement of the Receptor for Advanced Glycation Endproducts, Interleukin 1 receptor antagonist, ST2 and cytokeratin 18 was combined with molecules measured during clinical routine. Results were analyzed in the light of blood cell analysis, lactate measurements, correction for changes in plasma volume and body composition assessments. There were intrinsic differences in body mass index, abdominal body fat percentage and training time between M and HM runners. C-reactive protein changes in M and HM runners. While soluble RAGE, AGEs and ST2 increased immediately after the race in HM runners, HMGB1 increased in HM and M after the race and declined to baseline after a recovery period. We give insights into the regulation of various molecules involved in physical stress reactions and their possible implications for the cardiovascular system or renal function.

Highlights

  • We found statistically significant differences in BMI, abdominal girth and body fat percentage, when marathoners, half-marathoners and sedentary controls were compared

  • We found a significant increase of Soluble RAGE (sRAGE) after running a half marathon (HM) (HM_baseline vs. HM_peak, p = 0.004), which returned to baseline after 2 to 7 days of recovery

  • The fractional total CK18 and the fractional caspase-cleaved CK18 excretion remained unchanged in M and HM runners. This is the first study investigating serum concentrations of sRAGE, endogenous secretory RAGE (esRAGE), high mobility group box 1 (HMGB1), advanced glycation endproducts (AGEs), Interleukin 1 receptor antagonist (IL1-RA), suppression of tumorigenicity 2 (ST2), IL33 and caspase-cleaved CK18 in recreational runners participating in a M or HM in parallel to routine laboratory examinations, lactate measurements and assessment of anthropometrical parameters

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Summary

Introduction

Chronic endurance training seems to have protective effects on the telomere length and might decelerate the biological aging process, participation in M races may lead to telomere shortening caused by oxidative DNA damage[7] and benefits of running are hampered by “overdosing” of exercise. These conflicting results raise the question whether a single stressfull event such as running a long-distance run can lead to activation of cell-stress specific molecular programs that are activated during illness and disease. There is no published literature focusing on the effects of a single endurance event on serum concentrations of sRAGE, esRAGE and RAGE ligands in amateur runners

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