From an experimental design perspective, the key hypothesis is not that the peptides duplicate each others effects, but rather that they might support different rate-limiting steps in repair, such as cell recruitment to the injury site, fibroblast function, extracellular matrix organization, angiogenesis, and the transition from inflammatory signaling to remodeling
Monitoring focuses on liver/kidney context, glucose, lipids, and muscle-stress markers when training load is relevant
discussion S72-91
Meanwhile: Systemic reviews still note that trailed human data are sparse, and most benefits remain in the preclinical promise category
Published data shows this mechanism is particularly relevant in NSAID-induced gut damage models, where NO dysregulation contributes significantly to tissue destruction