Author(s): YOU, S., YANG, W., Institution: CHA UNIVERSITY, GRADUATE SCHOOL, Country: KOREA, SOUTH, Abstract-ID: 522

INTRODUCTION:
Low-intensity exercise (LIE) is traditionally regarded as a metabolically unchallenging domain dominated by fat oxidation and minimal carbohydrate involvement. However, blood lactate and glucose concentrations during the early stages of lactate threshold testing in well-trained athletes exhibit a consistent reduction in both parameters. This phenomenon cannot be fully explained by substrate preference alone. Therefore, this literature review aimed to describe capillary blood glucose and lactate-related mechanisms during LIE as a metabolic recovery-sensitive regulation. Recovery-sensitive metabolic regulation refers to coordinated metabolic control mechanisms that are preferentially engaged under recovery-dominant, low-intensity exercise conditions.
METHODS:
This literature study was conducted using online databases based on Scopus, PubMed (Medline) and Web of Science. Original articles and reviews in the English language published in scientific journals were included. A total of 167 articles were screened from the abovementioned databases. 30 papers were excluded due to unavailable full-text articles and the absence of specific data relating to blood glucose and lactate without exercise intensities. Finally, 115 articles were screened for eligibility.
RESULTS:
Decreased lactate and glucose reflects coordinated hepatic–muscle substrate exchange, redistribution of blood flow and enzymatic bias towards gluconeogenesis under conditions of high fatty acid availability. During LIE, resting and exercise-derived lactate is preferentially transported to the liver and kidney via the bloodstream. Lactate availability and predominant fat-derived energy induce effective glucose production via gluconeogenesis due to allosteric regulation. At the molecular level, fatty acid-derived acetyl-CoA accumulation promotes allosteric inhibition of pyruvate dehydrogenase while activating pyruvate carboxylase and phosphoenolpyruvate carboxykinase. This thereby redirects pyruvate flux from oxidation and towards gluconeogenic and anaplerotic pathways. These enzymatic activations are reinforced by hormonal and redox-dependent mitochondrial control which collectively suppresses glycolytic reliance despite ongoing glucose turnover.
CONCLUSION:
The concept of alterations in blood lactate–glucose levels during LIE was introduced as an integrated biomarker of aerobic base, capturing metabolic flexibility, substrate partitioning and systemic resilience. This framework extends conventional first lactate threshold interpretation by emphasising the use of LIE as a diagnostic into recovery ability with implications for endurance and intermittent sports. This review provides a refined interpretation of LIE metabolism and highlights its relevance for performance monitoring and training diagnostics for individualised exercise prescription.