Acute exercise-induced glycocalyx shedding does not differ between exercise modalities, but is associated with total antioxidative capacity.

Affiliation

Kröpfl JM(1), Beltrami FG(1), Rehm M(2), Gruber HJ(3), Stelzer I(4), Spengler CM(5).
Author information:
(1)Exercise Physiology Lab, Institute of Human Movement Sciences and Sport, ETH Zurich, Switzerland.
(2)Department of Anaesthesiology, Ludwig-Maximilians-University Munich, Germany.
(3)Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Austria.
(4)Institute of Medical and Chemical Laboratory Diagnostics, LKH Hochsteiermark, Austria.
(5)Exercise Physiology Lab, Institute of Human Movement Sciences and Sport, ETH Zurich, Switzerland; Zurich Center for Integrative Human Physiology
(ZIHP), University of Zurich, Switzerland. Electronic address: [Email]

Abstract

OBJECTIVES: Regular physical exercise is known to protect endothelial integrity. It has been proposed that acute exercise-induced changes of the (anti-)oxidative system influence early (glycocalyx shedding) and sustained endothelial activation (shedding of endothelial cells, ECs) as well as endothelial-cell repair by circulating hematopoietic stem and progenitor cells (HPCs). However, results are not conclusive and data in trained participants performing different exercise modalities is lacking. DESIGN: Eighteen healthy, well-trained participants (9 runners, 9 cyclists; age: 29.7 ± 4.2 yrs) performed a strenuous acute exercise session consisting of 4 bouts of 4-min high-intensity with decreasing power profile and 3-min low-intensity in-between. METHODS: Average power/speed of intense phases was 85% of the peak achieved in a previous incremental test. Before and shortly after exercise, total oxidative and antioxidative capacities (TAC), shedding of syndecan-1, heparan sulfate, hyaluronan, ECs, and circulating HPCs were investigated. RESULTS: TAC decreased from 1.81 ± 0.42 nmol/L to 1.47 ± 0.23 nmol/L post-exercise (p = 0.010) only in runners. Exercise-induced early and sustained endothelial activation were enhanced post-exercise- syndecan-1: 103.2 ± 63.3 ng/mL to 111.3 ± 71.3 ng/mL, heparan sulfate: from 2637.9 ± 800.1 ng/mL to 3197.1 ± 1416.3 ng/mL, both p < 0.05; hyaluronan: 84.3 ± 21.8 ng/mL to 121.4 ± 29.4 ng/mL, ECs: from 6.6 ± 4.5 cells/μL to 9.5 ± 6.2 cells/μL, both p < 0.01; results were not different between exercise modalities and negatively related to TAC concentrations post-exercise. HPC proportions and self-renewal ability were negatively, while EC concentrations were positively associated with circulating hyaluronan concentrations. CONCLUSIONS: These results highlight the importance of the antioxidative system to prevent the endothelium from acute exercise-induced vascular injury - independent of exercise modality - in well-trained participants. Endothelial-cell repair is associated with hyluronan signaling, possibly a similar mechanism as in wound repair.