Hydrogen ion buffering capacity in skeletal muscle

Hydrogen ion buffering capacity in skeletal muscle refers to the tissue’s ability to attenuate decreases in pH during high-intensity exercise via multiple intracellular (e.g., proteins, carnosine, phosphates) and extracellular (e.g., bicarbonate in blood) chemical buffers, as well as by membrane transport systems such as the sodium–hydrogen exchanger (NHE), sodium–bicarbonate co-transporter (NBC), and monocarboxylate transporters (MCTs) which extrude protons from muscle fibers. Enhanced buffering capacity can delay muscle fatigue by protecting enzymes and contractile proteins from acidosis-induced dysfunction, and is influenced by training status, muscle fiber type, nutritional interventions (e.g., beta-alanine, bicarbonate), and genetics[1][2][3][4][5][6][7][9].

Other names

Muscle buffering capacitySkeletal muscle buffer capacityH⁺ buffering in muscleIntramuscular acid–base buffering

Extracellular alkalosis (bicarbonate/citrate supplements) increases extracellular buffering, enhances H⁺ efflux from muscle, and delays acidosis/fatigue[5][9]. Beta-alanine increases muscle carnosine, augmenting intracellular pH buffering[9].