Trained athletes on low-carbohydrate or ketogenic diets have lower blood lactate levels during high-intensity exercise compared to those on higher-carbohydrate diets, due to reduced breakdown of...
Mechanism
Synthesis from 1 study
When athletes eat very little carbohydrate, their muscles run out of stored sugar, so they can't break down sugar quickly during hard exercise. This means less lactic acid is made. Other changes help them stay powerful in short bursts, but they don't reduce lactate—the lack of sugar does.
Most probable mechanism
When the body runs low on stored sugar in muscles, it cannot break down sugar quickly for energy during hard exercise, so it makes less lactic acid as a result.
Dietary carbohydrate restriction lowers plasma glucose and insulin, suppressing glycogen synthesis and promoting ongoing glycogen breakdown.
Intramuscular glycogen stores decline due to continued training and insufficient dietary replenishment.
Reduced glycogen availability limits substrate for glycolytic enzymes, attenuating the rate of glycolytic ATP production.
Diminished glycolytic flux reduces pyruvate production, decreasing the substrate available for lactate dehydrogenase to convert into lactate.
Lower lactate production results in reduced blood lactate concentration during high-intensity exercise.
Less supported by current evidence, but not ruled out
During very short bursts of maximum effort, muscles use a different energy system that does not rely on sugar, so power output stays high even when sugar stores are low.
Short-duration maximal efforts rely primarily on ATP resynthesis from phosphocreatine breakdown.
Phosphocreatine breakdown generates ATP without requiring glycolysis or oxygen, making it independent of glycogen availability.
Phosphocreatine stores remain sufficient to support maximal power output during brief efforts despite low glycogen.
After hard efforts, the body uses fat for energy more efficiently, which helps restore the quick-energy system faster between bursts.
Chronic carbohydrate restriction increases mitochondrial density and upregulates enzymes that oxidize fatty acids.
Increased fat oxidation generates more ATP through oxidative phosphorylation during recovery periods.
Higher ATP availability accelerates phosphocreatine resynthesis via creatine kinase, restoring energy capacity for subsequent efforts.
When sugar stores in specific parts of muscle cells drop too low, the signal to contract becomes weaker, reducing force during repeated efforts.
Glycogen is depleted in inter- and intra-myofibrillar compartments of fast-twitch muscle fibers.
Low glycogen in these compartments reduces the efficiency of calcium release from the sarcoplasmic reticulum during muscle activation.
Reduced calcium availability decreases cross-bridge cycling rate and force production in fast-twitch fibers.
Evidence from Studies
Supporting (1)
Community contributions welcome
Effects of Low-Carbohydrate and Ketogenic Diets on Anaerobic Performance in Competitive Athletes: A Systematic Review and Meta-Analysis
Contradicting (0)
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