Greater lactate accumulation following an acute bout of high-intensity exercise in males suppresses acylated ghrelin and appetite postexercise.

High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given lactate may mediate these effects, we used sodium bicarbonate (NaHCO) supplementation in a double-blind, placebo-controlled, crossover design to investigate lactate's purported role in exercise-induced appetite suppression. Eleven males completed two identical high-intensity interval training sessions (10 × 1 min cycling bouts at ~90% heart rate maximum interspersed with 1-min recovery), where they ingested either NaHCO (BICARB) or sodium chloride (NaCl) as a placebo (PLACEBO) preexercise. Blood lactate, acylated ghrelin, GLP-1, and PYY concentrations, as well as overall appetite were assessed preexercise and 0, 30, 60, and 90 min postexercise. Blood lactate was greater immediately ( < 0.001) and 30 min postexercise ( = 0.049) in the BICARB session with an increased ( = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 ( = 0.014) and 90 min postexercise ( = 0.016), with a decreased AUC ( = 0.039). The BICARB session had increased PYY ( = 0.034) with an increased AUC ( = 0.031). The BICARB session also tended ( = 0.060) to have increased GLP-1 at 30 ( = 0.003) and 60 min postexercise ( < 0.001), with an increased AUC ( = 0.030). The BICARB session tended ( = 0.059) to reduce overall appetite, although there was no difference in AUC ( = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression. We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression, given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.