Key result
Acute HIIT linked to ~38% higher galectin-3 alongside sustained endothelial activation in athletes.
Why the study?
Long-term, intense endurance exercise training can occasionally induce endothelial micro-damage and cardiac fibrosis, but the underlying mechanisms are incompletely understood.
Does acute high-intensity interval training increase circulating cardiac biomarkers of fibrosis (Gal-3, sST2) and sustained endothelial activation in healthy, well-trained male athletes?
Observational (n=20)
No
Does acute high-intensity interval training increase circulating cardiac biomarkers of fibrosis (Gal-3, sST2) and sustained endothelial activation in healthy, well-trained male athletes?
Acute high-intensity exercise temporarily elevates biomarkers of cardiac wall stress and endothelial activation, providing mechanistic insight into possible exercise-induced fibrosis pathways.
Acute HIIT may transiently elevate fibrosis biomarkers in athletes; leaves open links to chronic remodeling and should not yet change practice.
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 ( r rm = 0.68, P = 0.001 and r rm = 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 ( r rm = 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.
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Kröpfl et al. (2023) conducted an observational in Healthy, well-trained endurance athletes (n=20). High-intensity interval training (HIIT) vs. Baseline (pre-exercise) was evaluated on Serum galectin-3 (Gal-3) concentration post-exercise (p=<0.001). Acute high-intensity interval training significantly increased circulating galectin-3 (from 4.11 to 5.66 ng/mL) and sST2 in healthy male athletes, associating with sustained endothelial activation.
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