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 requires further examination. We used sodium bicarbonate (NaHCO 3 ) 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 -2 ; 42.18±8.56 mL‧kg -1 ‧min -1 ) completed two identical high-intensity interval training sessions following ingestion of NaHCO 3 (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 post-exercise. Free-living energy intake (electronic food diaries) was measured the day before, of, and after each experimental session. In BICARB, blood lactate was greater post-exercise (p<0.002, d>0.70) though acylated ghrelin was similar (p=0.075, =0.206) at all time-points post-exercise (p>0.034, d<0.22). NPY (p=0.006, >0.509) and AgRP (p<0.001, >0.488) had main effects of time increasing following exercise and returning to baseline, with no differences between sessions (NPY: p=0.0.192, =0.149; AgRP: p=0.422, =0.060). α-MSH had no main effect of time (p=0.573, =0.063) or session (p=0.269, =0.110). Appetite perceptions were similar during BICARB and PLACEBO (p=0.007, d=0.28) increasing in both sessions post-exercise (p<0.088, d>0.57). Energy intake had a main effect of day (p=0.025, =0.825), where the experimental session day was greater than the day before (p=0.010, d=0.59) with no other differences between days (p>0.260, d<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.