Trial reportSkeletal muscle2026
NSAIDs trigger drug-specific response to exercise: a multi-omics systems biology analysis of a randomized crossover trial.
Trial report in Skeletal muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05512013 (The Effects of Non-steroidal Anti-inflammatory Drugs on Circulating Markers of Bone Metabolism Following Plyometric Exercise in Humans), which is not on this map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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The Effects of Non-steroidal Anti-inflammatory Drugs on Circulating Markers of Bone Metabolism Following Plyometric Exercise in Humans
Who cites it
0 citing papers in PubMed.
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-steroidal anti-inflammatory drugs (NSAIDs) are widely used by athletes and those who exercise, yet their influence on the molecular responses to exercise remains unclear. Prior studies have often focused on a limited set of molecular pathways, potentially overlooking broader regulator effects of NSAIDs on skeletal muscle signaling. Therefore, we conducted a systems biology study of skeletal muscle biopsies taken before and after exercise, in combination with NSAID consumption, using transcriptomics and metabolomics, to identify differentially enriched pathways and biofunctions.
methodsWe conducted a randomized, counterbalanced, double-masked, crossover trial (NCT05512013) in which 12 healthy adults ingested ibuprofen (IBU, 800 mg), celecoxib (CEL, 200 mg), flurbiprofen (FLU, 100 mg), or placebo (PLA) before a 10 × 10 bout of plyometric exercise. Skeletal muscle biopsies were collected before NSAID consumption and three hours post-exercise. Whole transcriptome profiling was performed using RNA-seq, and the metabolomics profile was assessed via untargeted mass spectrometry. Differential expression analysis and pathway enrichment were used to evaluate NSAID-specific effects across biological domains.
resultsFLU regulated the largest number of differentially expressed transcripts, followed by IBU and CEL. All NSAIDs activated immune-related gene networks and reversed exercise-induced lipid catabolism, with IBU enhancing adaptive immune signaling and CEL modulating both innate and adaptive pathways. Muscle remodeling pathways, including angiogenesis and cell migration, were activated across all NSAIDs, though cachexia-related genes were also upregulated. Interestingly, FLU uniquely upregulated transcripts involved in neuritogenesis.
conclusionNSAIDs trigger drug-specific molecular responses in skeletal muscle post-exercise, affecting early recovery through changes in immune, metabolic, and neuronal signaling.
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