The Effects of Aerobic Exercise and Detraining on Left Ventricular Cardiomyocyte Apoptosis

Authors

  • Mustika Putri Faculty of Medicine and Health Science Syarif Hidayatullah State Islamic University

https://doi.org/10.33476/jky.v24i3.276

Abstract

Apoptosis can occur in several pathological heart conditions. Physical exercise, particularly aerobic exercise may reduce apoptosis on cardiomyocytes. Detraining can restore adaptation after exercise. This study aimed to see the effect of aerobic exercise and detraining on left ventricular cardiomyocyte apoptosis using caspase-3 as the parameter.

This was an in vivo experimental study on Wistar rats Rattus Novergicus. Rats divided to 8 groups: 4 sedentary control groups: 4-week (C4), 8-week (C4D), 12-week (C12), 16-week control (C12D), and 4 aerobic exercise treatment groups: 4-week (A4) and 12-week (A12), and 4 & 12-week post aerobic exercise treatment followed by 4 weeks detraining (A4D, A12D). Caspase-3 protein in rat left ventricular tissue was identified by immunohistochemistry staining. Data were analized with ANOVA test using SPSS proggramme version 20.

Data analysis showed an increase percentage of caspase-3 expression on post-aerobic exercise (A), be compared with conntrol group (C) (A4 65,3%±2,54 vs K4 6,4%±1,78, p<0,001; A12 41,8%±3,21 vs K12 5,7%±0,88, p<0,001; A4D 66,6%±1,89 vs K4D 8,6%±3,60, p<0,001; A12D 45,1%±1,50 vs K12D 7,4%±2,06, p<0,001). Percentage of caspase-3 expression was not different on post-aerobc exercise (A), be compare with detraining group (A4D 66,6%±1,89% vs A4 65,4%±2,54, p=0,484; A12D 45,1%±1,50 vs A12 41,8%±3,21, p=0,063). Percentage of caspase-3 expression on post 4-week aerobic exercise group was higher than post12-week aerobic exercise (A4 65,4%±2,54 vs A12 41,8%±3,21, p<0,001).

In conclusion, the aerobic exercise protocol used in this study, was not found to decrease left ventricular cardiomyocyte apoptosis. Detraining did not increase left ventricular cardiomyocyte apoptosis.

References

The American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statics 2009 Update: A Report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2009; 119: e21 – e181.

Kwak HB. Effect of aging and exercise training on apoptosis in the heart. JER. 2013;9:212-19.

Giam CK, Teh KC. Ilmu kedoteran olahraga. Diterjemahkan oleh Satmoko H. Jakarta:Binarupa Aksara;1993.

Gomez Cabrera MC, Domenech E, Vina J. Moderate exercise is an antioxidant:upregulating of antioxidant genes by training. Elsevier.2007;44(2008):126-131.

Berzosa C et all. Acute exercise increase plasma total antioxidant status and antioxidant enzyme activities in untrained men. Journal of Biomeicine and Biotechnology. 2011.

Mooren FC, Volker K, editor. Molecular and celullar exercise physiology. USA:Human Kinetics;2005.

Phaneuf S, Leeuwenburgh C. Apoptosis and exercise. Med Scie Sports Exerc. 2001;33:393-396.

Dyspersyn GGD, Borgers M. Apoptosis in the heart:about programmed cell death and survival. News Physiol Sci.2001;16volume:41-47.

Mujik I, Padilla S. Detraining: loss of training-induced physiological and performance adaptations Part I.Sport Medicine. 2000;30(2):79-87.

Elmore S. Apoptosis: A review of programmed cell death. toxicol pathol. 2007;35:495-516.

Igney FH, Krammer PH. Death and anti death: tumor resistance to apoptosis. Nat Rev Cancer.2002;2:277-88.

Zeiss CJ. The apoptosis-necrosis Continuum:insight from genetically altered mice. Vet Pathol.2003;40:481-95.

Dewi N. Sari, Sutjahjo Endardjo, Dewi I.S. Santoso. Blood lactate level in Wistar rats after four and twelve week intermittent aerobic training. Medical Journal of Indonesia.2013;22(3).

Manchado FB, Gobatto CA, Contarteze RV, Papoti M, De Mello MAR. Maximal lactate steady state in running rats. JEPonline. 2005;8(4):29-35.

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Published

2017-01-26