Serum S100B level increases after running but not cycling exercise

Abstract

The objective of this study was to investigate the effect of running versus cycling exercises upon serum S100B levels and typical markers of skeletal muscle damage such as creatine kinase (CK), aspartate aminotransferase (AST) and myoglobin (Mb). Although recent work demonstrates that S100B is highly expressed and exerts functional properties in skeletal muscle, there is no previous study that tries to establish a relationship between muscle damage and serum S100B levels after exercise. We conducted a cross-sectional study on 13 male triathletes. They completed 2 submaximal exercise protocols at anaerobic threshold intensity. Running was performed on a treadmill with no inclination (RUN) and cycling (CYC) using a cycle-simulator. Three blood samples were taken before (PRE), immediately after (POST) and 1 h after exercise for CK, AST, Mb and S100B assessments. We found a significant increase in serum S100B levels and muscle damage markers in RUN POST compared with RUN PRE. Comparing groups, POST S100B, CK, AST and Mb serum levels were higher in RUN than CYC. Only in RUN, the area under the curve (AUC) of serum S100B is positively correlated with AUC of CK and Mb. Therefore, immediately after an intense exercise such as running, but not cycling, serum levels of S100B protein increase in parallel with levels of CK, AST and Mb. Additionally, the positive correlation between S100B and CK and Mb points to S100B as an acute biomarker of muscle damage after running exercise.

Response of protein S100B to playing American football, lifting weights, and treadmill running

“…Past research has also indicated that [S100B] may increase independently of head injury, as illustrated by increases in [S100B] following participation in exercise where head injury is uncommon . Findings include increased [S100B] as a result of: swimming, running, and number of jumps while playing basketball . Playing soccer has also been shown to cause increases in [S100B], of which the cause has reasonably been attributed to the number of head contacts with the ball (headers) a player experiences .…”

“…Beginning in the 21st century, S100B has been under investigation as a serum biomarker of mild traumatic brain injury in sport, specifically as an indicator of sport‐related concussion and subconcussion injury . Although serum S100B concentration ([S100B]) has been shown to increase in response to the number of contacts an athlete experiences, [S100B] has also been shown to rise in relation to exercise alone . Findings of increased [S100B] caused by marathon running, a 25‐km running race, jogging 10 km, running for 40 minutes at ventilatory threshold, sprinting for 2 minutes, and a 7600 m swimming race, paired with the presence of S100B in extracranial tissue, have cast doubt over the use of S100B as a valid biomarker of brain injury in sport …”

Biomarkers of Traumatic Brain Injury: Temporal Changes in Body Fluids

“…High S100β levels correlate with mortality and unfavorable prognosis (Mercier et al, 2013). However, S100β is not brain injury specific: its concentration increases in some other diseases and traumas (Anderson et al, 2001; Undén et al, 2005; Studer et al, 2015), as well as during intensive physical exercise (Stocchero et al, 2014). A later sampling (12–36 h after trauma) of S100β has shown enhanced prognostic value over early sampling (Thelin et al, 2013).…”

Cellular and molecular mechanisms of sarcopenia: the S100B perspective

“…97 Moreover, S100B becomes expressed in breast tumour epithelial cells under the combined action of homeobox C1 and steroid receptor coactivator, and strong associations between S100B tissue expression and reduced disease-free survival in breast cancer were reported, with elevated serum levels of S100B strongly predicting poor survival. [106][107][108] Extracellular effects of S100B are largely brought about by its interaction with RAGE (receptor for advanced glycation end products, encoded by AGER/ Ager) 109,110 ; however, at least in the case of muscle injury, S100B can activate either RAGE or the basic fibroblast growth factor (bFGF)/FGF receptor 1 (FGFR1) complex depending on its own local concentration, myoblast density, and bFGF availability. [99][100][101] Indeed, S100B is secreted constitutively by astrocytes 88 and following stimulation with catecholamines by white adipocytes, 102 and by activated macrophages.…”