Delayed Rebound of Glycemia During Recovery Following Short-Duration High-Intensity Exercise: Are There Lactate and Glucose Metabolism Interactions?

Laurent A Messonnier; Benjamin Chatel; Chi-An W Emhoff; Léo Blervaque; Samuel Oyono-Enguéllé

doi:10.3389/fnut.2021.734152

Delayed Rebound of Glycemia During Recovery Following Short-Duration High-Intensity Exercise: Are There Lactate and Glucose Metabolism Interactions?

Front Nutr. 2021 Nov 11:8:734152. doi: 10.3389/fnut.2021.734152. eCollection 2021.

Authors

Laurent A Messonnier¹, Benjamin Chatel², Chi-An W Emhoff³, Léo Blervaque¹, Samuel Oyono-Enguéllé⁴

Affiliations

¹ Laboratoire Interuniversitaire de Biologie de la Motricité, Université Savoie Mont Blanc, Chambéry, France.
² Cellmade Laboratories, Le Bourget-du-Lac, France.
³ Department of Kinesiology, Saint Mary's College of California, Moraga, CA, United States.
⁴ Laboratoire de Physiologie de la Faculté de Médecine, Université Yaoundé 1, Yaoundé, Cameroon.

Abstract

Lactate constitutes the primary gluconeogenic precursor in healthy humans at rest and during low-intensity exercise. Data on the interactions between lactate and glucose metabolisms during recovery after short-duration high-intensity exercise are sparse. The aim of the present study was to describe blood glucose ([glucose]_b) and lactate ([lactate]_b) concentration curves during recovery following short-duration high-intensity exercise. Fifteen healthy Cameroonian subjects took part in the study and performed successively (i) an incremental exercise to exhaustion to determine maximal work rate (P_max) and (ii) a 2-min 110% P_max exercise after which blood lactate and glucose concentrations were measured during the 80-min passive recovery. In response to the 2-min 110% P_max exercise, [glucose]_b remained stable (from 4.93 ± 1.13 to 4.65 ± 0.74 mmol^.L^-1, NS) while [lactate]_b increased (from 1.35 ± 0.36 to 7.87 ± 1.66 mmol^.L^-1, p < 0.0001). During recovery, blood lactate concentrations displayed the classic biphasic curve while blood glucose concentrations displayed a singular shape including a delayed and transitory rebound of glycemia. This rebound began at 27.7 ± 6.2 min and peaked at 6.78 ± 0.53 mmol^.L^-1 at 56.3 ± 9.7 min into recovery. The area under the curve (AUC) of [lactate]_b during the rebound of glycemia was positively correlated with the peak value of glycemia and the AUC of [glucose]_b during the rebound. In conclusion, the delayed rebound of glycemia observed in the present study was associated with lactate availability during this period.

Keywords: gluconeogenesis; glucose; lactate; liver; recovery.