Elsevier

Molecular Metabolism

Volume 9, March 2018, Pages 114-130
Molecular Metabolism

Original Article
Ghrelin mediates exercise endurance and the feeding response post-exercise

https://doi.org/10.1016/j.molmet.2018.01.006Get rights and content
Under a Creative Commons license
open access

Highlights

  • High intensity exercise transiently increases plasma ghrelin.

  • Without ghrelin action on its receptors (growth hormone secretagogue receptors), exercise markedly reduces food intake.

  • An intact ghrelin system enhances exercise endurance.

Abstract

Objective

Exercise training has several well-established health benefits, including many related to body weight, appetite control, and blood glucose homeostasis. However, the molecular mechanisms and, in particular, the hormonal systems that mediate and integrate these beneficial effects are poorly understood. In the current study, we aimed to investigate the role of the hormone ghrelin and its receptor, the growth hormone secretagogue receptor (GHSR; ghrelin receptor), in mediating the effects of exercise on food intake and blood glucose following exercise as well as in regulating exercise endurance capacity.

Methods

We used two mouse models of treadmill running to characterize the changes in plasma ghrelin with exercise. We also assessed the role of the ghrelin system to influence food intake and blood glucose after exercise, exercise endurance, and parameters potentially linked to responses to exercise. Mice lacking GHSRs (GHSR-null mice) and wild-type littermates were studied.

Results

An acute bout of exercise transiently elevated plasma acyl-ghrelin. Without the action of this increased ghrelin on GHSRs (as in GHSR-null mice), high intensity interval exercise markedly reduced food intake compared to control mice. The effect of exercise to acutely raise blood glucose remained unmodified in GHSR-null mice. Exercise-induced increases in plasma ghrelin positively correlated with endurance capacity, and time to exhaustion was reduced in GHSR-null mice as compared to wild-type littermates. In an effort to mechanistically explain their reduced exercise endurance, exercised GHSR-null mice exhibited an abrogated sympathoadrenal response, lower overall insulin-like growth factor-1 levels, and altered glycogen utilization.

Conclusions

Exercise transiently increases plasma ghrelin. GHSR-null mice exhibit decreased food intake following high intensity interval exercise and decreased endurance when submitted to an exercise endurance protocol. These data suggest that an intact ghrelin system limits the capacity of exercise to restrict food intake following exercise, although it enhances exercise endurance.

Keywords

GHSR
Ghrelin
Exercise
Treadmill
Endurance
Food intake

Abbreviations

ACC
acetyl coA carboxylase
AMP 5′
adenosine monophosphate
AMPK
AMP-activated protein kinase
CNS
central nervous system
COX IV
cytochrome c oxidase subunit 4
G6P
glucose-6-phosphatase
GH
growth hormone
GHSR
growth hormone secretagogue receptor
HIIE
high intensity interval exercise
HNF4α
hepatocyte nuclear factor 4α
IGF-1
insulin-like growth factor-1
IGFBP-1
insulin-like growth factor binding protein-1
PC
pyruvate carboxylase
PCG1α
peroxisome proliferator-activated receptor gamma coactivator 1α
PEPCK
phosphoenolpyruvate carboxykinase
PYGL
glycogen phosphorylase, liver
RT-PCR
reverse transcriptase-polymerase chain reaction
VMH
ventromedial hypothalamus

Cited by (0)

5

Bharath K. Mani and Carlos M. Castorena contributed equally to this work.