<p>Type 2 Inflammatory Biomarker Response After Exercise Challenge Testing</p>

Abstract

Introduction: Exercise-induced bronchoconstriction is due to osmotic stimulus of the airway epithelium and leads to a cascade of biomarker release from several inflammatory cells. Several type 2 (T2) mediators have been linked to exercise-induced bronchoconstriction, but the T2 response per se has not been described during exercise. The aim of this study was therefore to investigate T2 biomarkers in plasma and urine from subjects with asthma and healthy controls before and after an exercise challenge. Methods: Twenty-two subjects with mild asthma and 18 healthy controls performed an exercise challenge test on a treadmill, and fractional exhaled NO (FeNO) was measured at baseline. Blood and urine samples were collected repeatedly during 60 min after the test and Interleukin-13 (IL-13), thymus and activation-related chemokine (TARC), periostin and leukotrienes were measured. Results: Asthmatics and controls showed similar levels of IL-13, TARC, periostin and Cys-LT in plasma at baseline, and there were no differences in baseline levels between subjects with a negative and positive exercise challenge. After exercise, there was an overall increase in interleukin-13 (IL-13) in plasma in all subjects (p<0.001), with a peak at 10 min after the exercise challenge in both the asthmatic and control group. An increase in TARC in plasma was also seen (p<0.001), but only in the control subjects. In contrast, Cys-LT in plasma showed an overall decrease in all subjects (p<0.001), while periostin in plasma did not change. In conjunction with plasma, the level of IL-13 was increased in urine 30 min after the exercise challenge (p=0.002) and decreased again at 60 min (p=0.004). Similarly, leukotriene E 4 (LTE 4) was increased in urine samples, with a peak at 60 min and most pronounced in asthmatic subjects (p<0.001) but was seen also in controls (p=0.008). Discussion: In conclusion, circulating levels of IL-13 are increased after exercise to the same extent in asthmatics and healthy control subjects, which indicates a physiological rather than a pathophysiological response. Also, the levels of TARC and leukotrienes were affected after exercise.

Effect of 2 weeks rest-pause on oxidative stress and inflammation in female basketball players

“…In addition, in the period of immediate preparation for the competition, when the athletes were subjected to the greatest training loads, an increase in IL-10 was shown with no changes in its concentration during the rest period from training. Research results indicate that physical exercise causes a significant increase in IL-13 in non-training people (Tufvesson et al (2020) 43 and Alizadeh et al (2019) 44 ), on the other hand, Zamani et al (2014) 45 showed no significant differences in the concentration of IL-13 in elite wrestlers 24 h after training and in the control group. Observed effect of intense physical exercise on anti-inflammatory cytokines in our study may indicate a high effort tolerability and undisturbed activity of the immune system reacting with rapid activation of anti-inflammatory processes (anti-inflammatory effect of exercise).…”

Effort-induced bronchospasm in athletes: modern views on pathogenesis and diagnosis in high-school teenagers

“…Thus, the described mechanisms contribute to disrupting the balance between anti-and proinflammatory mediators. Increased physical activity causes systemic endocrine and immune process activation promoting inflammatory process activation [38,41]. It should be noted that most modern authors point to the lack of significant differences between the EIB pathogenesis in adult athletes and high-school teenagers actively involved in sports [9].…”

A breathing mask attenuates acute airway responses to exercise in sub-zero environment in healthy subjects

“…Endurance athletes also show increased airway inflammation (Bonsignore et al 2003 ), even though cold exposure per se has limited influence on systemic immune function. An exercise challenge has been shown to increase the levels of the type 2 inflammatory biomarker interleukin-13 in plasma (Tufvesson et al 2020 ). Competitive swimmers, another population with an increased risk of “sports asthma” (Couto et al 2015 ), show signs of increased airway oxidative stress (Morissette et al 2016 ).…”