Lactate is a metabolic substrate that sustains extraocular muscle function

Area of Science:

• Exercise Physiology
• Skeletal Muscle Metabolism

Background:

• Lactic acid is traditionally viewed as a fatigue-inducing end product of glycolysis.
• The lactate dehydrogenase (LDH) enzyme catalyzes a reversible reaction, allowing lactate oxidation to pyruvate for energy production.

Purpose of the Study:

• To test the hypothesis that lactate sustains contractile function in rat extraocular muscles during high activity.
• To investigate the role of lactate as an energy substrate in extraocular muscles compared to extensor digitorum longus (EDL) muscles.

Main Methods:

• In vitro assessment of contractile function, LDH isoform expression, and total LDH activity in rat extraocular and EDL muscles.
• Pharmacological manipulation using cinnamate (lactate transport blocker) and exogenous lactate administration to evaluate fatigue resistance.

Main Results:

• Cinnamate significantly accelerated fatigue in extraocular muscles, reducing endurance and residual force.
• Exogenous lactate increased fatigability in EDL muscles but not in extraocular muscles when used alone.
• The combination of exogenous lactate and cinnamate led to faster fatigue in extraocular muscles.
• Extraocular muscles exhibited lower LDH-A and LDH-C isoform expression and reduced total LDH activity compared to EDL muscles.

Conclusions:

• Lactate plays a crucial role in sustaining the contractile performance of extraocular muscles.
• Extraocular muscles utilize lactate as an energy substrate, differentiating them from EDL muscles in metabolic adaptation to activity.