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Published on: February 3, 2023
Transcriptomic signatures reveal systemic adaptations and immune modulation in response to training and competitive
Izabela Dąbrowska1, Jowita Grzędzicka-Agko1, Paula Kiełbik1
1Department of Large Animal Diseases and Clinic, Institute of Veterinary Medicine, Warsaw University of Life Sciences, Warsaw, Poland.
Background:
The molecular mechanisms underlying adaptation to physical exertion and racing stress in horses remain incompletely understood. Peripheral blood transcriptomics offers a minimally invasive method to monitor systemic responses to exercise and identify biomarkers of adaptation or overload.
Objectives:
To evaluate transcriptomic changes in peripheral blood of racehorses during different phases of training and competition and to identify molecular markers of physiological adaptation and race-induced stress.
Study Design:
Prospective transcriptomic profiling of trained racehorses across three exercise conditions.
Methods:
Forty racehorses (29 Arabian, 11 Thoroughbred) were sampled before (p0) and after (p1) exercise at three stages: initial training (T1), mid-season training (T2) and racing (R). RNA-seq was performed, followed by differential expression analysis (DESeq2) and pathway enrichment (g:Profiler, DAVID). Identified differentially expressed genes were integrated into STRING protein-protein interaction condition-exclusive subnetworks (Merge tool in Cytoscape) to compare the transcriptomes between conditions.
Results:
Distinct molecular programmes were identified at each stage. At T1, immediate-early response genes such as FOS, FOSB and HSPA6 were strongly up-regulated, reflecting acute stress and immune activation. At T2, immune-related transcripts (KLRD1, CCL4, PRF1) remained enriched, but genes linked to remodelling and adaptation, including DNAJA1, HSPH1 and CXCR4, became prominent, suggesting a shift toward recovery and regulatory processes. Post-race, chemokines such as CCL5 and stress markers (HSP90 family, JUN) were highly induced, accompanied by widespread transcriptomic divergence and down-regulation of certain immune regulators (IL18, ARHGAP44), indicating both heightened innate activation and transient immune suppression.
Main Limitations:
Transcriptomic profiling was limited to peripheral blood, which may not reflect tissue-specific responses. Only three sampling points were included, potentially overlooking transient transcriptomic changes.
Conclusions:
Transcriptomic dynamics in blood reflect the transition from early immune activation (T1), through adaptation (T2), to stress-related activation post-race (R). This approach offers promising molecular biomarkers for monitoring training adaptation and detecting physiological overload in equine athletes.
