Journal: Experimental Physiology
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Abbreviation
Exp Physiol
Publisher
Wiley-Blackwell
8 results
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Publications 1 - 8 of 8
- One bout of vibration exercise with vascular occlusion activates satellite cellsItem type: Journal Article
Experimental PhysiologyAguayo, David; Müller, Sandro M.; Boutellier, Urs; et al. (2016) - Increased blood-oxygen binding affinity in Tibetan and Han Chinese residents at 4200 mItem type: Journal Article
Experimental PhysiologySimonson, T.S.; Wei, G.; Wagner, H.E.; et al. (2014) - Spinal opioid receptor-sensitive muscle afferents contribute to the fatigue-induced increase in intracortical inhibition in healthy humansItem type: Journal Article
Experimental PhysiologyHilty, Lea; Lutz, Kai; Maurer, Konrad; et al. (2011) - Blood flow distribution to the respiratory muscles – physiology versus statisticsItem type: Other Journal Item
Experimental PhysiologyBeltrami, Fernando Gabe (2021) - Cerebral oxygenation in highlanders with and without high-altitude pulmonary hypertensionItem type: Journal Article
Experimental PhysiologyFurian, Michael; Latshang, T. D.; Aeschbacher, S. S.; et al. (2015) - Effect of inspiratory muscle fatigue on exercise performance taking into account the fatigue-induced excess respiratory driveItem type: Journal Article
Experimental PhysiologyWüthrich, Thomas U.; Notter, Dominic A.; Spengler, Christina M. (2013) - Myocardial infarction does not affect circulating hematopoietic stem and progenitor cell self-renewal ability in a rat modelItem type: Journal Article
Experimental PhysiologyKröpfl, Julia M.; Spengler, Christina M.; Frobert, A.; et al. (2018) - Circulating Gal-3 and sST2 are associated with acute exercise-induced sustained endothelial activation: Possible relevance for fibrosis development?Item type: Journal Article
Experimental PhysiologyKröpfl, Julia M.; Beltrami, Fernando G.; Gruber, Hans-Jürgen; et al. (2023)Long-term, intense endurance exercise training can occasionally induce endothelial micro-damage and cardiac fibrosis. The underlying mechanisms are incompletely understood. Twenty healthy, well-trained male participants (10 runners and 10 cyclists) performed a strenuous high-intensity interval training (HIIT) session matched by age, height, weight and maximal oxygen consumption. We assessed the acute exercise response of novel cardiac biomarkers of fibrosis [e.g., galectin-3 (Gal-3) and soluble suppression of tumorigenicity 2 (sST2)] per exercise modality and their relationship with haemodynamic contributors, such as preload, afterload and cardiac contractility index (CTi), in addition to endothelial damage by sustained activation and shedding of endothelial cells (ECs). Serum Gal-3 and sST2 concentrations were investigated by enzyme-linked immunosorbent assays; haemodynamics were analysed via impedance plethysmography and circulating ECs by flow cytometry. The Gal-3 and sST2 concentrations and ECs were elevated after exercise (P < 0.001), without interaction between exercise modalities. Circulating Gal-3 and sST2 concentrations both showed a positive relationship with ECs (rᵣₘ = 0.68, P = 0.001 and rᵣₘ = 0.57, P = 0.010, respectively, both n = 18). The EC association with Gal-3 was significant only in cyclists, but equally strong for both modalities. Gal-3 was also related to exercise-induced CTi (rᵣₘ = 0.57, P = 0.011, n = 18). Cardiac wall stress is increased after an acute HIIT session but does not differ between exercise modalities. Exercise-released Gal-3 from cardiac macrophages could very probably drive systemic endothelial damage, based on an enhanced CTi. The importance of acute exercise-induced vascular resistances and cardiac contractility for the release of fibrotic biomarkers and any long-term pathological endothelial adaptation should be investigated further, also relative to the exercise modality.
Publications 1 - 8 of 8