Brussels chicory affluent in phenolic acids could inhibit atherosclerosis; however, its effects on exercise performance and post-exercise recovery are unknown. We hypothesized that Brussels chicory could enhance exhaustive aerobic exercise performance and post-exercise recovery by promoting lactate oxidation.

Dietary supplementation with Brussels chicory may enhance short-term, progressive workload, high-intensity, exhaustive aerobic exercise performance and post-exercise recovery in humans, possibly by accelerating LDHB-mediated lactate oxidation.

This is a single-blind, randomized, placebo-controlled two-way cross-over trial involving 32 untrained college students (men 18) who consumed either Brussels chicory juice (100 g of Brussels chicory containing ~130 mg phenolic acids and 180 mL fresh milk) or placebo (180 mL fresh milk) for 7 days with a 2-week washout period. On the 7th day, participants received a short-term, progressive workload, high-intensity, exhaustive aerobic exercise with the Bruce protocol. Time to exhaustion and blood lactate were evaluated after exercise. C2C12 myotubes were treated with Brussels chicory phenolic acids (0.625-10 μM) to evaluate these effects on lactate metabolism and lactate dehydrogenase A (LDHA) and B (LDHB), two enzymes responsible for lactate biosynthesis and oxidation, respectively.

Brussels chicory consumption increased time to exhaustion by 8.3% and 12.2% for men and women participants, respectively. This administration also promoted post-exercise recovery, evidenced by a reduction in blood lactate (14.5% for men and 10.6% for women). In C2C12 myotubes, Brussels chicory protocatechuic acid and caffeic acid did not affect LHDA-mediated lactate production, whereas these compounds dose-dependently promoted LDHB-mediated lactate oxidation through an enrichment of mitochondria LDHB. Conclusions: Dietary supplementation with Brussels chicory may enhance short-term, progressive workload, high-intensity, exhaustive aerobic exercise performance and post-exercise recovery in humans, possibly by accelerating LDHB-mediated lactate oxidation.