Training-induced apoptosis in skeletal muscle.
Abstract: Apoptosis or programmed cell death is a genetically controlled response of cells to commit suicide and is associated with DNA fragmentation or laddering. The common inducers of apoptosis include Ca2+i and oxygen free radicals/oxidative stress, which are also implicated in the pathogenesis of exercise-induced myopathies. To examine training-induced apoptosis, Thoroughbred horses were subjected to 3 months training programme on a treadmill. At the end of the training programme venous blood samples were taken for a creatine kinase (CK) assay. In addition, muscle biopsy samples were obtained for a membrane lipid peroxidation measurement by malondialdehyde (MDA) assay and for apoptosis detection. Apoptosis was studied by visualising the apoptotic myocytes on the paraffin sections by the modified TUNEL method. DNA laddering was evaluated by subjecting the DNA obtained from the biopsies to 1.5% agarose gel electrophoresis. There was a significant increase (P<0.05) of protein-bound MDA, and a nonsignificant trend (P = 0.14) for the control group to have higher levels of CK compared to the trained group. Under light microscopy, percentage of the TUNEL positive cells was higher (P<0.001) in the training group. This result was corroborated with the findings of DNA fragmentation by gel electrophoresis, which showed higher ladders of DNA band at the same group. In conclusion, these results clearly demonstrate that there is training-induced apoptosis in skeletal muscle. It is probable that apoptosis allows the work/recovery/rebound/supercompensation cycle, when unaccustomed muscle cells activate programmed cell death and are replaced by new and stronger cells, which is the mechanism for training-induced increases in fitness.
Publication Date: 2002-10-31 PubMed ID: 12405700DOI: 10.1111/j.2042-3306.2002.tb05432.xGoogle Scholar: Lookup
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- Journal Article
Summary
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This research focused on understanding whether physical training induces programmed cell death (known as apoptosis) in skeletal muscle. Such apoptosis might be a mechanism for enhancing fitness because it could lead to the replacement of older muscle cells with stronger, newer ones. The researchers used thoroughbred horses and treadmills in a three-month training programme to study the phenomenon.
Methodology
- The researchers used Thoroughbred horses as the subject of the research. These horses underwent a three-month training programme on a treadmill. This provided a controlled environment to monitor any changes closely.
- At the end of the training, venous blood samples were taken for a creatine kinase (CK) assay, a test to understand muscle damage.
- Muscle biopsy samples were also obtained. These samples were used for two measurements. One was to detect the level of membrane lipid peroxidation by performing a malondialdehyde (MDA) assay. This helped understand the level of oxidative stress in the muscle cells. The second was to detect the presence of apoptotic cells.
- To detect apoptosis, the so-called TUNEL method was used. This method identifies cells where the DNA is in the process of being cut into smaller fragments, as normally happens during apoptosis.
- Finally, the DNA obtained from the biopsies was subjected to 1.5% agarose gel electrophoresis. This is a laboratory method used to visualize DNA fragmentation — a characteristic of apoptosis.
Results
- The research showed a significant increase in the levels of protein-bound MDA, indicating increasing levels of oxidative stress.
- While there was a nonsignificant trend for the control group to have higher levels of CK compared to the trained group, it doesn’t definitively prove no muscle damage in the trained group.
- Under light microscopy, the percentage of TUNEL positive cells (those going through apoptosis) was higher in the trained group. This was confirmed by checking for DNA fragmentation, which also showed higher levels of DNA fragmentation in the same group.
Conclusions
- Based on the results, the study concludes that physical training indeed induces apoptosis in skeletal muscle. The apoptosis might be a way for the body to replace older muscle cells with stronger, newer ones — a mechanism that could underlie training-induced increases in fitness.
Cite This Article
APA
Boffi FM, Cittar J, Balskus G, Muriel M, Desmaras E.
(2002).
Training-induced apoptosis in skeletal muscle.
Equine Vet J Suppl(34), 275-278.
https://doi.org/10.1111/j.2042-3306.2002.tb05432.x Publication
Researcher Affiliations
- Equine Exercise Physiology Center, Faculty of Veterinary Medical Science, The University of La Plata, Buenos Aires, Argentina.
MeSH Terms
- Animals
- Apoptosis
- Biopsy / veterinary
- Creatine Kinase / blood
- DNA Fragmentation
- Electrophoresis, Agar Gel / veterinary
- Exercise Test / veterinary
- Female
- Horses / physiology
- In Situ Nick-End Labeling / veterinary
- Lipid Peroxidation / physiology
- Male
- Malondialdehyde / metabolism
- Muscle, Skeletal / cytology
- Muscle, Skeletal / physiology
- Physical Conditioning, Animal / physiology
- Random Allocation
Citations
This article has been cited 5 times.- Ropka-Molik K, Stefaniuk-Szmukier M, Piórkowska K, Szmatoła T, Bugno-Poniewierska M. Molecular characterization of the apoptosis-related SH3RF1 and SH3RF2 genes and their association with exercise performance in Arabian horses. BMC Vet Res 2018 Aug 14;14(1):237.
- Brancaccio P, Maffulli N, Politano L, Lippi G, Limongelli FM. Persistent HyperCKemia in Athletes. Muscles Ligaments Tendons J 2011 Jan;1(1):31-5.
- Sudo M, Kano Y. Myofiber apoptosis occurs in the inflammation and regeneration phase following eccentric contractions in rats. J Physiol Sci 2009 Nov;59(6):405-12.
- Hakimi P, Yang J, Casadesus G, Massillon D, Tolentino-Silva F, Nye CK, Cabrera ME, Hagen DR, Utter CB, Baghdy Y, Johnson DH, Wilson DL, Kirwan JP, Kalhan SC, Hanson RW. Overexpression of the cytosolic form of phosphoenolpyruvate carboxykinase (GTP) in skeletal muscle repatterns energy metabolism in the mouse. J Biol Chem 2007 Nov 9;282(45):32844-55.
- Brancaccio P, Limongelli FM, Maffulli N. Monitoring of serum enzymes in sport. Br J Sports Med 2006 Feb;40(2):96-7.
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