Greater lactate accumulation does not alter peripheral concentrations of key appetite-regulating neuropeptides.

The potential mechanisms involved in lactate's role in exercise-induced appetite suppression require further examination. We used sodium bicarbonate (NaHCO) supplementation in a double-blind, placebo-controlled, randomized crossover design to explore lactate's role on neuropeptide Y (NPY), agouti-related peptide (AgRP), and alpha-melanocyte-stimulating hormone (α-MSH) concentrations. Twelve adults (7 males; 24.2 ± 3.4 kg·m; 42.18 ± 8.56 mL·kg·min) completed two identical high-intensity interval training sessions following ingestion of NaHCO (BICARB) or sodium chloride (PLACEBO) pre-exercise. Blood lactate, acylated ghrelin, NPY, AgRP, α-MSH, and appetite perceptions were measured pre-exercise, 0-, 30-, 60-, and 90-min postexercise. Free-living energy intake (electronic food diaries) was measured the day before, of, and after each experimental session. In BICARB, blood lactate was greater postexercise ( < 0.002, > 0.70), though acylated ghrelin was similar ( = 0.075, [Formula: see text] = 0.206) at all time points postexercise ( > 0.034, < 0.22). NPY ( = 0.006, [Formula: see text] > 0.509) and AgRP ( < 0.001, [Formula: see text] > 0.488) had main effects of time increasing following exercise and returning to baseline, with no differences between sessions (NPY: = 0.0.192, [Formula: see text] = 0.149; AgRP: = 0.422, [Formula: see text] = 0.060). α-MSH had no main effect of time ( = 0.573, [Formula: see text] = 0.063) or session ( = 0.269, [Formula: see text] = 0.110). Appetite perceptions were similar during BICARB and PLACEBO ( = 0.007, = 0.28), increasing in both sessions postexercise ( < 0.088, > 0.57). Energy intake had a main effect of day ( = 0.025, [Formula: see text] = 0.825), where the experimental session day was greater than the day before ( = 0.010, = 0.59) with no other differences between days ( > 0.260, < 0.38). The lower accumulation of lactate than our previous work did not generate exercise-induced appetite suppression as there were no differences in acylated ghrelin, appetite perceptions, or peripheral concentrations of neuropeptides. Current evidence supports lactate's role in exercise-induced appetite suppression. Here, we demonstrate a smaller degree of lactate accumulation with sodium bicarbonate ingestion and HIIT than our previous work and no subsequent suppression of acylated ghrelin concentrations, subjective appetite perceptions, or peripheral concentrations of neuropeptides. These results suggest either changes in central appetite-regulating neuropeptides are not reflected peripherally or the smaller magnitude of lactate accumulation did not generate exercise-induced appetite suppression as seen previously.