# Biochemical Responses to Experimentally Induced Short‐Term Low Energy Availability in Athletes: A Systematic Review

## TL;DR

This systematic review examines how the body's biochemistry responds to short-term low energy availability in athletes, highlighting changes in bone metabolism and hormone levels.

## Contribution

The study provides a synthesis of experimental evidence on short-term biochemical effects of low energy availability in athletes.

## Key findings

- Short-term LEA leads to increased βCTX-1 and decreased P1NP, indicating altered bone metabolism.
- Leptin levels consistently decrease, while testosterone decreases in half of the interventions.
- No consistent changes were observed in estradiol, progesterone, or iron status.

## Abstract

Low energy availability (LEA) occurs when dietary energy intake is insufficient to meet the combined demands of exercise and essential physiological functions. Problematic LEA is recognized as the primary driver of Relative Energy Deficiency in Sport (RED‐S), but the short‐term physiological consequences of LEA remain less clearly defined. Thus, this systematic review aimed to synthesize evidence from experimental studies examining the short‐term effects of experimentally induced LEA on biochemical markers in athletic populations. A systematic search was conducted in PubMed, Web of Science, and Scopus in accordance with PRISMA guidelines. Eligible studies included experimental designs, with pre–post assessments of an LEA intervention (> 24 h). Outcomes included biomarkers of bone metabolism, calcium metabolism, energy regulation, inflammation, iron status, sex hormones, and thyroid function. Thirteen studies (145 participants) were included. Approximately half of the interventions reported significant increases in βCTX‐1 and reductions in P1NP. Leptin consistently decreased following LEA, whereas IGF‐1 and T3 remained stable in most studies, and testosterone decreased in 50% of interventions. No consistent changes were observed in estradiol, progesterone, calcium metabolism, inflammatory markers, or iron status. Short‐term experimentally induced LEA elicits early endocrine and metabolic adaptations, particularly affecting bone remodeling, leptin, and testosterone. However, these responses should be interpreted in the context of the frequent coexistence of low carbohydrate availability, which may contribute to or exacerbate the observed effects. These findings emphasize the relevance of monitoring key biochemical markers during periods of potential LEA risk and underscore the need for standardized, sex‐specific protocols in future research.