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

Abstract

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 (NaHCO₃) 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 NaHCO₃ (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 (P < 0.001) and 30 min postexercise (P = 0.049) in the BICARB session with an increased (P = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 (P = 0.014) and 90 min postexercise (P = 0.016), with a decreased AUC (P = 0.039). The BICARB session had increased PYY (P = 0.034) with an increased AUC (P = 0.031). The BICARB session also tended (P = 0.060) to have increased GLP-1 at 30 (P = 0.003) and 60 min postexercise (P < 0.001), with an increased AUC (P = 0.030). The BICARB session tended (P = 0.059) to reduce overall appetite, although there was no difference in AUC (P = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression.NEW & NOTEWORTHY 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.

Keywords: anorexigenic; appetite regulation; gut peptides; high-intensity interval training; orexigenic.

Fig. 1.

Experimental session timeline. HIIT, high-intensity interval training; VAS, visual analog scale.

Fig. 2.

A: changes in blood lactate across all time points in each experimental session. B: area under the curve (AUC) values for each experimental session. *Significantly different between sessions: A: *P < 0.05 and *B: P < 0.05.

Fig. 3.

A: changes in acylated ghrelin across all time points in each experimental session. B: area under the curve (AUC) values for each experimental session. *Significantly different between sessions: A: *P < 0.05 and *B: P < 0.05.

Fig. 4.

A: changes in PYY across all time points in each experimental session. B: area under the curve (AUC) values for each experimental session. *Significantly different between sessions: A: *P < 0.05 and *B: P < 0.05.

Fig. 5.

A: changes in GLP-1 across all time points in each experimental session. B: area under the curve (AUC) values for each experimental session. *Significantly different between sessions: B: *P < 0.05. †Significant difference approached between sessions.

Fig. 6.

A: changes in overall appetite across all time points in each experimental session. B: area under the curve (AUC) values for each experimental session. ^aSignificant increase compared with preexercise, P < 0.001. ^bSignificant increase compared with immediately postexercise, P < 0.001. ^cSignificant increase compared with 30 min postexercise, P < 0.001. †Significant difference approached between sessions.