Low energy availability, the gut microbiome, and bone health in athletes: a mechanistic narrative review based on athlete evidence and clinical analogues.

Low energy availability (LEA) is a central aetiological factor in Relative Energy Deficiency in Sport (REDs) and is frequently associated with impaired skeletal health in athletic populations, although skeletal responses can be heterogeneous. However, athletes with apparently similar energetic and training exposures can differ in bone mineral density, bone turnover and bone stress injury risk, indicating that additional physiological mediators may modify the skeletal response to under-fuelling. The gut microbiome has emerged as a plausible candidate because microbial metabolites, intestinal barrier integrity, immune signalling and endocrine pathways can influence bone remodelling. Direct studies integrating energy availability, gut microbiome profiling and bone outcomes in athletes are currently lacking. This narrative review therefore synthesises athlete evidence for the LEA-bone relationship and uses clinical and preclinical analogues of chronic energy deficiency to develop a testable gut-bone framework for sport. The accumulated evidence from athletes primarily supports the direct LEA-bone relationship, whereas the candidate gut-bone microbiome component remains a biologically plausible hypothesis based on clinical and preclinical models. Specifically, evidence from athletes supports LEA and REDs risk as contributors to lower bone mineral density, altered bone microarchitecture, suppressed bone formation markers and bone stress injury risk, although findings vary by sex, sport type, skeletal loading, assessment method and timing. Evidence from anorexia nervosa and other undernutrition models suggests that energy deficiency can be accompanied by altered microbial diversity, depletion of short-chain fatty acid-producing taxa, lower short-chain fatty acid availability, impaired barrier function and low-grade inflammation. Mechanistically, short-chain fatty acids, endotoxin-mediated inflammation, insulin-osteocalcin signalling, bile acid pathways and amino acid metabolites may intersect with canonical REDs endocrine disturbances to influence bone remodelling. The available evidence does not establish a causal gut-mediated pathway in athletes, but it supports a biologically plausible model that should be tested in prospective athlete cohorts using integrated assessments of energy availability, diet, training load, microbiome composition and function, endocrine status, bone turnover and bone structure.