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Effects of physical activity upon the liver

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  • Published:
European Journal of Applied Physiology Aims and scope Submit manuscript

Abstract

Purpose

To review the responses of the liver to acute and chronic physical activity and to summarize relationships between physical activity and liver health.

Methods

A systematic search of HealthStar/Ovid from 1975 through June of 2013, supplemented by articles from other sources.

Results

351 of 8,010 articles identified by HealthStar/Ovid were supplemented by 92 other papers; after focussing, the review was reduced to 435 citations. Prolonged acute exercise reduces hepatic blood flow, stimulating hepatic glycogenolysis, gluconeogenesis and synthesis of some proteins; however, lipid metabolism shows little change. Glutathione depletion suggests oxidative stress. Enzymes affecting carbohydrate metabolism are up-regulated, and lipogenic enzymes are down-regulated. The main triggers are humoral, but hepatic afferent nerves, cytokines, reactive oxygen species, and changes in hepatic blood flow may all play some role. Regular aerobic exercise training improves blood glucose control during exercise by increasing glycogen stores and up-regulating enzymes involved in gluconeogenesis and carbohydrate metabolism. Resistance to oxidant stress is generally increased by training. Lipogenic enzymes are down-regulated, and lipid metabolism is augmented. Modulations of insulin, insulin-like growth factor, glucagon and interleukin-6 may trigger the adaptive responses to training. Cross-sectional and longitudinal studies show that regular exercise can reduce hepatic fat, but the effect on circulating aminotransferases is unclear and the modality and dose of physical activity optimizing health benefits need clarification.

Conclusions

Regular moderate physical activity enhances liver health. Adverse functional changes can develop if habitual activity is inadequate, and extremely prolonged competitive exercise may also be harmful, particularly under harsh environmental conditions.

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Abbreviations

ACC:

Acetyl-coa carboxylase

ADP:

Adenosine diphosphate

AKT:

Protein kinase B

ALT:

Alanine transaminase

AMP:

Adenosine monophosphate

AMPK:

Adenosine monophosphate kinase

ARFRP1:

ADP-ribosylation factor-related protein 1

AST:

Aspartate transaminase

ATP:

Adenosine triphosphate

BCKDH:

Branched-chain alpha-ketoacid dehydrogenase

cAMP:

Cyclic adenosine monophosphate

CK:

Cytokeratin

CoA:

Coenzyme A

CT:

Computerized tomography

DNA:

Desoxyribonucleic acid

eIF2:

Eukaryotic initiation factor 2

ERK:

Extracellular signal-regulated kinase

FFA:

Free fatty acid

GGT:

Gamma glutamyl transferase

GLUT-2:

Glucose-transporter-2

G protein:

Guanine-nucleotide binding protein

GTP:

Guanosine triphosphate

HAD:

Β-hydroxyacyl-dehydrogenase

HDL-c:

High-density lipoprotein cholesterol

HISS:

Hepatic insulin sensitizing substance

HMG-CoA:

Hydroxymethylglutaryl-CoA

HSP:

Heat shock protein

IGF-1:

Insulin-like growth factor-1

IGFBP:

Insulin-like growth factor binding protein

IL:

Interleukin

IMTG:

Intramyocellular triglyceride

JAK:

Janus kinase

JNK:

c-jun N-terminal kinase

LDH:

Lactate dehydrogenase

MAPK:

Mitogen-activated protein kinase

MDA:

Malondialdehyde

mRNA:

Messenger ribonucleic acid

NAFLD:

Non-alcoholic fatty liver disease

NF-κB:

Nuclear factor kappa-B

NOx:

Mononitrogen oxides

PECPK:

Phosphoenolpyruvate carboxykinase

PERK:

Protein-kinase like endoplasmic reticular kinase

SCD-1:

Stearoyl-CoA desaturase-1

sFasL:

Soluble Fas ligand

SREBP-1c:

Regulatory element-binding protein-1c

STAT:

Signal transducer and activator of transcription

TRB3:

Tribbles-related protein 3

VLDL:

Very low density lipoprotein triglycerides

\({\dot{\text{V}}}\)O2max :

Maximal oxygen intake

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Correspondence to Roy J. Shephard.

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Communicated by Nigel A.S. Taylor.

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Shephard, R.J., Johnson, N. Effects of physical activity upon the liver. Eur J Appl Physiol 115, 1–46 (2015). https://doi.org/10.1007/s00421-014-3031-6

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