Experimental Physiology

Journal: Experimental Physiology

Abbreviation

Exp Physiol

Publisher

Wiley-Blackwell

ISSN

0958-0670
1469-445X

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Publications 1 - 8 of 8

One bout of vibration exercise with vascular occlusion activates satellite cells
Aguayo, David; Müller, Sandro M.; Boutellier, Urs; et al. (2016)
Experimental Physiology
Increased blood-oxygen binding affinity in Tibetan and Han Chinese residents at 4200 m
Simonson, T.S.; Wei, G.; Wagner, H.E.; et al. (2014)
Experimental Physiology
Spinal opioid receptor-sensitive muscle afferents contribute to the fatigue-induced increase in intracortical inhibition in healthy humans
Hilty, Lea; Lutz, Kai; Maurer, Konrad; et al. (2011)
Experimental Physiology
Blood flow distribution to the respiratory muscles – physiology versus statistics
Beltrami, Fernando Gabe (2021)
Experimental Physiology
Cerebral oxygenation in highlanders with and without high-altitude pulmonary hypertension
Furian, Michael; Latshang, T. D.; Aeschbacher, S. S.; et al. (2015)
Experimental Physiology
Effect of inspiratory muscle fatigue on exercise performance taking into account the fatigue-induced excess respiratory drive
Wüthrich, Thomas U.; Notter, Dominic A.; Spengler, Christina M. (2013)
Experimental Physiology
Myocardial infarction does not affect circulating hematopoietic stem and progenitor cell self-renewal ability in a rat model
Kröpfl, Julia M.; Spengler, Christina M.; Frobert, A.; et al. (2018)
Experimental Physiology
Circulating Gal-3 and sST2 are associated with acute exercise-induced sustained endothelial activation: Possible relevance for fibrosis development?
Kröpfl, Julia M.; Beltrami, Fernando G.; Gruber, Hans-Jürgen; et al. (2023)
Experimental Physiology
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

Journal: Experimental Physiology

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