Lactic acidosis: implications for human exercise performance.

Area of Science:

• Exercise Physiology
• Skeletal Muscle Physiology
• Biochemistry

Background:

• High-intensity exercise leads to lactic acidosis, characterized by increased myoplasmic and plasma concentrations of lactate and protons.
• The precise role of acidosis in exercise-induced fatigue remains a subject of critical evaluation.

Purpose of the Study:

• To critically evaluate the contribution of lactic acidosis to fatigue during human exercise.
• To differentiate the effects of lactate concentration versus proton concentration on muscle performance.

Main Methods:

• Review and critical analysis of existing literature on exercise-induced acidosis and fatigue.
• Examination of data on muscle force, power, and intracellular/extracellular ion concentrations during exercise.
• Consideration of studies involving lactate infusion, induced acidosis, and animal muscle preparations.

Main Results:

• Elevated lactate concentrations alone have minimal detrimental effects and can be ergogenic.
• Exercise-induced intracellular acidosis, especially in fast-twitch fibers (pH ~6.2), significantly reduces maximum force, shortening velocity, and peak power.
• Acidosis and increased inorganic phosphate reduce myofilament function, while potentially offering some protection against potassium disturbances.
• Extracellular acidosis contributes to perceived exertion and fatigue sensations via muscle afferents.

Conclusions:

• Severe intracellular acidosis in fast-twitch muscle fibers is a significant contributor to force and power fatigue during intense exercise.
• The detrimental effects of acidosis on myofilament function appear to outweigh protective effects on action potentials during fatigue.
• Modulation of acid-base balance regulators supports the role of intracellular acidosis in fatigue development.