ISSN: 2161-0940
Camila Torres
Skeletal muscle fatigue represents a reversible reduction in force generating capacity that develops during prolonged or high intensity muscular activity [1]. It serves as a protective physiological mechanism that limits excessive tissue damage while preserving cellular integrity. Rather than resulting from a single cause, fatigue reflects the interaction of multiple biochemical and physiological processes occurring within skeletal muscle fibers and the nervous system. One of the earliest contributors to muscle fatigue is metabolic disturbance. During repeated muscle contraction, Adenosine Triphosphate (ATP) is rapidly consumed to support cross bridge cycling and ion transport. Although ATP concentrations remain relatively stable under most physiological conditions, the accumulation of inorganic Phosphate (Pi), Hydrogen ions (H), Adenosine Diphosphate (ADP) and other metabolic byproducts impairs contractile protein interactions and calcium sensitivity, reducing force production [2]. These metabolic changes
Published Date: 2025-06-02; Received Date: 2025-05-02