Circulating Antimicrobial Peptides as Biomarkers of Inflammation and Airway Dysfunction After Marathon Running
Marie-Therese Lingitz, Hannes Kühtreiber, Lisa Auer, Michael Mildner, Claus G. Krenn, Clemens Aigner, Bernhard Moser, Christine Bekos, Hendrik Jan Ankersmit
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Simple Summary
Endurance sports like marathon running are becoming increasingly popular, but they exert intense strain on the body. This physical stress can temporarily weaken the immune system and affect the lungs, occasionally causing breathing problems after exercise. Our study investigated whether specific substances circulating in the blood - antimicrobial peptides, which help the body fight off infections - change after endurance exercise and if they are linked to breathing issues occurring thereafter.
We measured these markers in long-distance runners before, immediately after, and several days after races. We also compared these levels with those of people who do not regularly perform endurance exercise. We found that several of these markers increased after running, particularly in runners who showed signs of airway narrowing, which can make breathing harder. These changes mostly returned to normal after a few days.
This suggests a heightened immune activation during and immediately after prolonged running and may play a role in temporary breathing difficulties. Understanding these changes could help identify athletes at risk and improve how we support respiratory health during intense physical activity. Our findings could lead to better training plans and recovery strategies for runners and other endurance athletes.
Abstract
Marathon running exerts physical stress and may lead to transient immune dysregulation, increasing susceptibility to airway inflammation and exercise-induced bronchoconstriction (EIB). This study investigated systemic levels of antimicrobial peptides in athletes and their association with EIB.
Serum concentrations of angiogenin, human beta-defensin 2 (hBD-2), major basic protein (MBP), S100A8, and S100A8/A9 were measured in 34 marathoners and 36 half-marathoners at baseline, immediately after the race, and seven days post-race using enzyme-linked immunosorbent assays and compared with 30 sedentary controls. Lung function was assessed by spirometry to identify bronchoconstriction.
Levels of hBD-2 and S100A8/A9 were significantly elevated post-race in runners compared to baseline and controls, returning to baseline during recovery. During recovery, S100A8 levels remained slightly elevated in marathoners with EIB. Similarly, human beta-defensin 2 was modestly increased in runners who developed bronchoconstriction. Notably, S100A8 levels correlated negatively with lung function parameters, including forced expiratory volume and mid- expiratory flows.
These findings suggest that endurance running induces systemic inflammatory responses and modulates innate immune peptides, particularly in individuals prone to bronchoconstriction. These peptides may serve as biomarkers of respiratory stress and help guide personalized strategies in endurance sports.
Link | PDF (Preprint: Preprints.org) [Open Access]
Marie-Therese Lingitz, Hannes Kühtreiber, Lisa Auer, Michael Mildner, Claus G. Krenn, Clemens Aigner, Bernhard Moser, Christine Bekos, Hendrik Jan Ankersmit
[Line breaks added]
Simple Summary
Endurance sports like marathon running are becoming increasingly popular, but they exert intense strain on the body. This physical stress can temporarily weaken the immune system and affect the lungs, occasionally causing breathing problems after exercise. Our study investigated whether specific substances circulating in the blood - antimicrobial peptides, which help the body fight off infections - change after endurance exercise and if they are linked to breathing issues occurring thereafter.
We measured these markers in long-distance runners before, immediately after, and several days after races. We also compared these levels with those of people who do not regularly perform endurance exercise. We found that several of these markers increased after running, particularly in runners who showed signs of airway narrowing, which can make breathing harder. These changes mostly returned to normal after a few days.
This suggests a heightened immune activation during and immediately after prolonged running and may play a role in temporary breathing difficulties. Understanding these changes could help identify athletes at risk and improve how we support respiratory health during intense physical activity. Our findings could lead to better training plans and recovery strategies for runners and other endurance athletes.
Abstract
Marathon running exerts physical stress and may lead to transient immune dysregulation, increasing susceptibility to airway inflammation and exercise-induced bronchoconstriction (EIB). This study investigated systemic levels of antimicrobial peptides in athletes and their association with EIB.
Serum concentrations of angiogenin, human beta-defensin 2 (hBD-2), major basic protein (MBP), S100A8, and S100A8/A9 were measured in 34 marathoners and 36 half-marathoners at baseline, immediately after the race, and seven days post-race using enzyme-linked immunosorbent assays and compared with 30 sedentary controls. Lung function was assessed by spirometry to identify bronchoconstriction.
Levels of hBD-2 and S100A8/A9 were significantly elevated post-race in runners compared to baseline and controls, returning to baseline during recovery. During recovery, S100A8 levels remained slightly elevated in marathoners with EIB. Similarly, human beta-defensin 2 was modestly increased in runners who developed bronchoconstriction. Notably, S100A8 levels correlated negatively with lung function parameters, including forced expiratory volume and mid- expiratory flows.
These findings suggest that endurance running induces systemic inflammatory responses and modulates innate immune peptides, particularly in individuals prone to bronchoconstriction. These peptides may serve as biomarkers of respiratory stress and help guide personalized strategies in endurance sports.
Link | PDF (Preprint: Preprints.org) [Open Access]
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