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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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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DOI: https://doi.org/10.1007/s00421-014-3031-6