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"Latar belakang: Latihan fisik anaerobik adalah latihan fisik yang dilakukan dalam waktu singkat dengan intensitas tinggi dan dapat merangsang apoptosis pada kardiomiosit ventrikel kiri. Penelitian ini bertujuan untuk menganalisis ekspresi apoptosis kardiomiosit pasca latihan serta pasca henti latih latihan fisik anaerobik. Metode : Identifikasi Caspase-3 dilakukan dengan cara pulasan imunohistokimia dan analisis kuantitatif persentase Caspase-3 yang dilakukan pada kelompok kontrol 4,8,12 dan 16 minggu, kelompok perlakuan latihan fisik anaerobik 4 dan 12 minggu serta henti latih 4 minggu pasca latihan (minggu ke 8 dan 16). Hasil: Analisis data menunjukkan peningkatan persentase caspase-3 pada kelompok latihan fisik anaerobik 4 dan 12 minggu dengan p=0,027. Penurunan persentase capase-3 pasca henti latih yang bermakna juga ditemukan antara kelompok latihan fisik anaerobik 4 minggu dengan kelompok henti latih 4 minggu (p=0,0001) dan antara kelompok latihan anaerobik 12 minggu dengan kelompok henti latih 16 minggu (p=0,0001).

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Introduction : Anaerobic physical exercise is a high intensity physical exercise performed in a short time. This exercise can stimulate apoptosis in left ventricular cardiomyocytes. The aims of this study is to analyze the expression of cardiomyocyte apoptosis after anaerobic exercise and detraining.

Methods : Caspase-3 expression is identified by immunohistochemistry labeling and quantitative analysis of the percentage of Caspase-3 in the control group 4,8,12 and 16 weeks, groups with 4 and 12 weeks of anaerobic physical exercise, and groups after 4 weeks of detraining ( week 8 and 16).

Conclucion: Data analyses showed a significant increase in the percentage of caspase-3 in the 4 and 12 weeks anaerobic physical exercise groups with p = 0.027. The percentage of Capase-3 after detraining showed a significant decline between the groups of 4 weeks of anaerobic physical exercise and detraining with p = 0.0001 and between groups of 12 weeks of anaerobic exercise and detraining with p = 0, 0001."

"Latar belakang: Latihan fisik anaerobik yang lama (latihan fisik ketahanan/endurance dengan intensitas berat yang melebihi kapasitas aerobik) mengakibatkan remodeling morfologi dan sistem konduksi listrik jantung. Connexin 43 (Cx43) adalah protein penyusun gap junction pada diskus interkalaris kardiomiosit ventrikel, yang bertanggung jawab atas konduksi listrik jantung. Penelitian ini bertujuan untuk menganalisis pola distribusi dan ekspresi Cx43 kardiomiosit pasca-latihan serta pasca-henti-latih fisik anaerobik.Metode: Identifikasi Cx43 dilakukan dengan cara pulasan imunohistokimia dan analisis kuantitatif luas area ekspresi Cx43 dilakukan pada kelompok kontrol (K4M, K8M, K12M dan K16Minggu) dan perlakuan latihan fisik (AN4M, AN12M) serta henti-latih (AN4MD, AN12MD).Hasil: Analisis data menunjukkan peningkatan luas area ekspresi Cx43 (pixel) pada kelompok pasca-latihan fisik (K4M: 77006±7513 dan AN4M: 116932±5552, p<0,001; K12M: 51727±2209 dan AN12M: 123781±6019, p<0,001), yang disertai oleh peningkatan proporsi lateralisasi ekspresi Cx43 (persentase area lateralisasi: K4M: 11,34±0,8% dan AN4M: 25,11±1%, p<0,001; K12M: 11,32±0,37% dan AN12M: 30,36±2,2%, p<0,001). Kelompok pascahenti-latih menunjukkan regresi luas area ekspresi Cx43 (AN12M: 123781±6019 dan AN12MD: 93908±9348, p<0,005) dan persentase area lateralisasi (AN12M: 30,36±2,2% dan AN12MD: 21,2±1,1%, p<0,001).Kesimpulan: Peningkatan ekspresi Cx43 (yang dipredominansi oleh peningkatan lateralisasi) kardiomiosit ventrikel kiri jantung tikus pasca-latihan fisik anaerobik merupakan suatu proses adaptasi fisiologis dan bersifat sementara.

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Introduction: Long-term non-resistance anaerobic exercise (excessive endurance training that exceed aerobic capacity) causes remodeling of cardiac morphology and conduction system. Major gap junction protein expressed on ventricular cardiomyocyte, connexin 43 (Cx43) is an important determinant of cardiac conduction system. The aims of this study are to analyse Cx43 expression and distribution on cardiomyocyte post-anaerobic exercise and detraining.Methods: Cx43 expression is identified by immunohistochemistry labeling and quantitative analyses on Cx43 areas are conducted on 4 and 12 weeks postanaerobic exercise rats (AN4M, AN12M) along with 4 weeks of detraining groups (AN4MD, AN12MD) and time-matched sedentary control groups (K4M, K8M, K12M dan K16M).Results: Data analyses show an increased Cx43 area expression (pixel) on postanaerobic exercise groups (K4M: 77006±7513 vs. AN4M: 116932±5552, p<0,001 and K12M: 51727±2209 vs. AN12M: 123781±6019, p<0,001), and characterized by marked increased on lateralization (K4M: 11,34±0,8% vs. AN4M: 25,11±1%, p<0,001 and K12M: 11,32±0,37% vs. AN12M: 30,36±2,2%, p<0,001). Detraining groups show regression on Cx43 area expression (AN12M: 123781±6019 vs. AN12MD: 93908±9348, p<0,005) and lateralization (AN12M: 30,36±2,2% vs. AN12MD: 21,2±1,1%, p<0,001).Conclucion: Increased Cx43 expression (predominated by lateralization) of left ventricular cardiomyocyte post-anaerobic exercise is a physiological adaptation and reversible upon detraining."

"Latar Belakang : Beberapa penelitian terbaru memperlihatkan bahwa apoptosis terjadi pada beberapa keadaan jantung patologis seperti pada keadaan kerusakan ?iskemia-reperfusi?, infark miokardium dan gagal jantung. Di sisi lain terdapat penelitian yang memperlihatkan bahwa latihan fisik dapat menurunkan apoptosis kardiomiosit. Dari beberapa jenis latihan fisik, latihan fisik aerobik merupakan latihan yang paling dianjurkan karena diyakini efektif dalam mencegah dan bahkan sebagai terapi rehabilitasi pada penyakit kardiovaskular. Keadaan henti latih pasca latihan fisik ternyata dapat mengembalikan seluruh atau sebagian adaptasi yang sudah terbentuk setelah latihan fisik. Tujuan : Penelitian ini bertujuan ingin melihat bagaimana pengaruh latihan fisik aerobik dan henti-latih terhadap apoptosis kardiomiosit ventrikel kiri dengan menggunakan protein caspase-3 sebagai parameter apoptosis. Desain : Penelitian ini menggunakan studi eksperimental in vivo pada tikus Metode : identifikasi protein caspase-3 pada jaringan ventrikel kiri jantung tikus dengan pemeriksaan pulasan imunohistokimia pada 8 kelompok tikus ( kelompok kontrol 4 minggu (K4M), kontrol 8 minggu (K4MD), kontrol 12 minggu (K12M), kontrol 16 minggu (K12MD) dan kelompok perlakuan latihan aerobik 4 minggu (AR4M), perlakuan latihan aerobik 12 minggu (AR12M), perlakuan latihan aerobik 4 minggu diikuti dengan henti-latih 4 minggu (AR4MD) serta kelompok latihan aerobik 12 minggu diikuti dengan henti-latih 4 minggu(AR12MD)). Hasil : Analisis data menunjukan peningkatan persentase ekspresi caspase-3 kelompok pasca latihan fisik aerobik (K4M 6,40%1,78 dan AR4M 65,38%2,54, p<0,001; K12M 5,72%0,88 dan AR12M 41,81%3,21, p<0,001; K4MD 8,64%±3,59 dan AR4MD 66,55%±1,88; K12MD 7,35%±2,06 dan AR12MD 46,78%±2,45, p<0,001). Kecenderungan Peningkatan persentase ekspresi caspase-3 kelompok pasca henti latih (AR4M 65,38%2,54 dan AR4MD 66,55%1,88%, p=1,000; AR12M 41,81%3,21dan AR12MD 46,78%±2,45, p=0,230). Ekspresi caspase 3 kelompok latihan aerobik 4 minggu lebih tinggi dibanding kelompok latihan aerobik 12 minggu (AR4M 65,38%2,54 dan AR12M 41,81%3,21, p<0,001). Kesimpulan : latihan fisik aerobik tidak menurunkan apoptosis kardiomiosit ventrikel kiri jantung tikus dan program henti latih tidak meningkatkan apoptosis kardiomiosit ventrikel kiri jantung tikus.

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Background: Recent studies showed that apoptosis occurs in several pathological heart condition as in myocardial ischemia-reperfusion injury, myocardial infarction and heart failure. It has been also research showing that physical exercise can reduce apoptosis on cardiomyocyte. Of some kind of physical exercise, aerobic exercise is an exercise that is most recommended because it is believed to be effective in preventing and even as a rehabilitation therapy on cardiovascular disease. Detraining was able to restore all or part of adaptation that has been formed after the exercise.

Objective: This study aimed to see the effect of aerobic exercise and detraining on left ventricular cardiomyocyte apoptosis using caspase-3 protein as a parameter of apoptosis. Design: This study used an experimental in vivo study on rats.

Methods: Caspase-3 protein in rat cardiac left ventricular tissue is identified by immunohistochemistry staining conducted on 4 sedentary control group ( 4 weeks control group (K4M), 8 weeks control group (K4MD), 12 weeks control group (K12M), 16 weeks control (K12MD)) and 4 treatment groups ( 4 & 12 weeks post aerobic exercise group (AR4M, AR12M) and 4&12 weeks post aerobic exercise followed by 4 weeks detraining (AR4MD,AR12MD)).

Results: Analysis of the data shows an increase percentage of caspase-3 expression on post-aerobic exercise group (K4M 6,40%1,78 and AR4M 65,38%2,54, p<0,001; K12M 5,72%0,88 and AR12M 41,81%3,21, p<0,001; K4MD 8,64%±3,59 and AR4MD 66,55%±1,88; K12MD 7,35%±2,06 and AR12MD 46,78%±2,45, p<0,001) The data also shows tendency an increase percentage of caspase-3 expression on detraining group (AR4M 65,38%2,54 and AR4MD 66,55%1,88%, p=1,000; AR12M 41,81%3,21 and AR12MD 46,78%±2,45, p=0,230). Percentage of caspase-3 expression on post-4 weeks aerobic exercise group is higher than post-12 weeks aerobic exercise (AR4M 65,38%2,54 and AR12M 41,81%3,21, p<0,001).

Conclusion: Aerobic physical exercise does not decrease left ventricular cardiomyocyte apoptosis and does not improve left ventricular cardiomyocyte apoptosis."

"Latar belakang : Overtraining berdampak buruk terhadap kesehatan karena dapat menyebabkan kematian mendadak pada atlet muda. Berdasarkan data epidemiologi ditemukan bahwa kejadian kematian mendadak (suddent cardiac death) pada atlet muda, penyebab paling banyak adalah gangguan kardiovaskular. Tubuh melakukan adaptasi terhadap beban berlebih, berupa remodelling (morfologi dan elektrofisiologi). Remodeling elektrofisiologis yaitu perubahan pada gap junction, berupa perubahan ekspresi Cx43 yang yang mengakibatkan gangguan penghantaran konduksi listrik. Selama latihan fisik dapat terbentuk ROS yang akan menginduksi permeabilitas mitokondria sehingga terjadi kebocoran sitokrom c, selanjutnya akan mengaktifkan kaskade apoptosis.Metode : Penelitian ini dilakukan pada 6 jaringan kardiomiosit tikus Wistar kelompok kontrol dan overtraining. Ekspresi Cx43 dan caspase-3 diamati melalui pulasan imunohistokimia dan diukur dengan image J.Hasil : Hasil penelitian ini menunjukkan peningkatan bermakna pada ekspresi Cx43 total overtraining (43644.57±27711.03) dibandingkan kelompok kontrol (13002.37±3705.41). Tidak ditemukan perbedaan bermakna ekspresi caspase-3 pada kedua kelompok meskipun diperoleh hasil lebih tinggi pada kelompok overtraining (14.15%±10.54%) dibandingkan kelompok kontrol (2,63%±3.56%).Kesimpulan : Overtraining meningkatkan ekspresi Cx43 total tetapi tidak terbukti meningkatkan caspase-3 pada kardiomiosit ventrikel kiri tikus.

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Background: overtraining has bad effect for health, overtraining can cause sudden death in young athlete, reports of sudden death incidences in young athlete claim that cardiovascular disease is the cause. The heart can face the excess load by remodeling as it?s adaptation mechanism. There is 2 type remodeling, morphology and electrophysiology. Remodeling electrophysiology is a change on Cx43 expression which can interfere the heart?s electrical conduction. Free radical which formed from physical exercise can induce mitochondrial permeability that lead leakage of cytochrome c, so that so that activate the apoptosis cascade.

Methods: This study conducted on 12 Wistar rat?s cardiomyocytes tissue that divided into control and overtraining group. Cx43 expression and caspase-3 was observed through immunohistochemical staining and measured by image J.

Results: There was significant increase in the expression of Cx43 total overtraining (43644.57 ± 27711.03) compared to the control group (13002.37 ± 3705.41). Found no significant differences in the expression of caspase-3 in both groups although the result was higher in the group of overtraining (14,15% ± 10,54%) compared to the control group (2,63% ± 3,56%).

Conclusion: Overtraining increase total Cx43 expression but not proven to increase caspase-3 in the rat left ventricular cardiomyocytes."

"Latar belakang: Latihan fisik aerobik adalah latihan fisik yang dilakukan secara teratur dan berkesinambungan sedangkan latihan fisik yang dilakukan dengan peningkatan durasi dan kecepatan secara bertahap termasuk dalam aerobik Overtraining. Penelitian ini bertujuan untuk menganalisa hipertrofi pada otot ventrikel jantung kiri tikus pasca latihan fisik aerobik serta pasca latihan fisik aerobik overtraining. Metode: Identifikasi morphologi kardiomiosit ventrikel kiri jantung tikus menggunakan pewarnaan hematoksilin eosin, sedangkan untuk jaringan fibrosis dengan pewarnaan Masson?s Trichrome. Identifikasi tersebut dilakukan pada kelompok kontrol, dan kelompok perlakuan aerobik dan overtraining yang dilakukan selama 11 minggu. Hasil: Analisis data menunjukkan terjadi hipertrofi yang ditandai dengan adanya peningkatan panjang (p=0,017), lebar (p=0,037) pada kelompok aerobik dibandingkan dengan kelompok overtraining. Peningkatan jaringan fibrosis pada kelompok overtraining dengan p= 0,00.

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Introduction : Aerobic exercise is physical exercise done regularly and continuously while physical exercise done by increasing the duration and speed gradually included in the aerobic Overtraining. This study aims to analyze hypertrophy in the left ventricle of the heart muscle of mice after aerobic exercise and aerobic exercise post overtraining.

Methods : Left ventricular cardiomyocyte morphology rat heart is identified by hematoxylin eosin staining, whereas for fibrotic tissue with Masson's Trichrome staining. Such identification is performed in the control group and the treatment group performed aerobic and overtraining for 11 weeks.

Conclucion: Analysis of the data showed that hypertrophy is characterized by an increase in length (p = 0.017), width (p = 0.037) in the aerobic group compared with the group of overtraining. Increased tissue fibrosis in the overtraining group with p = 0,00."

"Anaerobic physical exercise is a high intensity physical exercise is a high intensity physical exercise performed in a short time. This exercise can stimulate apoptosis in left ventricular cardiomyocytes after anaerobic exercise and detraining. Thirty two wistar rats ratus novergicus 250-350 grams (8-10 weeks old) were divided into the following groups (n=4) and given anaerobic physical exercise four and 12 weeks (group Exc-4, Exc-12-D). The control groups were only observed in the same period (group CTL-4, CTL-12, CTL-4-D, CTL-12-D). At he end of observation, the rats were sacrificed and examination of the expression of caspace-3 as an indicator of apoptasis was done using immunohistochemical staining. Data were analyzed with ANOVA test. An increase in expression of caspase-3 in the group Exc-4 (72.03%) compared to the CTL-4 (27.22%), (P<0,001); AND Exc-12 (79.30%) compared to the CTL-12 (30.53%) (p=0.027). Detraining process showed a significant decline capase-3 expression (31.12% in exc-4-D and 30.44% in the exc-12-D) Anaerobi physical exercise can increase apoptosis in rat left ventricle cardiomyocyte characterized by increase expression of of caspase-3. Detraining can improve heart condition characterized by decreased expression of caspase-3"

"Latar belakang: Penyakit kardiovaskular sangat umum ditemukan dan berakibat fatal pada pasien dengan usia lanjut. Disfungsi sistolik ventrikel kiri yang asimptomatik atau subklinis sering kali mendahului penyakit ini. Deteksi dini terhadap disfungsi sistolik ventrikel kiri dapat mengurangi morbiditas dan mortalitas akibat penyakit kardiovaskular. Salah satu metode deteksi dini adalah dengan penilaian global longitudinal strain (GLS). Tujuan: Tujuan dari penelitian ini adalah untuk mengetahui nilai rerata GLS pada pasien usia lanjut dengan frailty maupun non frailty dan mengetahui faktor-faktor yang berhubungan.Metode: Penelitian potong lintang dilakukan pada pasien usia lanjut diatas 60 tahun di poliklinik geriatri dan kardiologi Ilmu Penyakit Dalam RSCM. Data diperoleh dari wawancara, rekam medik dan pemeriksaan ekokardiografi transtorakal. Variabel penelitian berupa usia, frailty, hipertensi, penyakit jantung koroner, dislipidemia, dan diabetes melitus dianalisis sebagai determinan penurunan GLS. Analisis univariat terhadap masing-masing variabel. Analisis bivariat menggunakan uji chi kuadrat dengan tingkat signifikan p<0,25 dan interval kepercayaan (IK) sebesar 95%. Analisis multivariat menggunakan uji regresi logistik.Hasil: Sebanyak 194 subjek yang memenuhi kriteria pemilihan diikutkan dalam penelitian, rerata usia 66 tahun dengan 118 (60,8%) di antaranya perempuan. Penelitian ini mendapatkan beberapa determinan yang memiliki nilai p<0,25 yaitu frailty, hipertensi, dislipidemia, dan diabetes melitus dengan hasil analisis multivariat, frailty memiliki OR sebesar 2,002 (95% IK 1,042-3,925), dan diabetes melitus memiliki OR sebesar 2,278 (95% IK 1,033-5,025).Simpulan : Nilai median GLS pada usia lanjut secara umum adalah sebesar -21,6% (minimal -5,3% sampai dengan maksimal -29,9%). Faktor yang mempengaruhi penurunan GLS adalah frailty dan diabetes melitus.

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Background: Cardiovascular disease is very common and can be fatal in elderly patients. It is often preceded by asymptomatic or subclinical left ventricular systolic dysfunction (LVSD). Early detection of LVSD can reduce morbidity and mortality due to cardiovascular disease. One method used in the early detection of LVSD is an assessment of global longitudinal strain (GLS).Objective: To determine the mean value of GLS and GLS-related factors.Methods: This cross-sectional study was conducted among elderly patients aged > 60 years in the geriatric and cardiology polyclinic, Internal Medicine, CMH Hospital. Data were obtained from interviews, medical records, and transthoracic echocardiography examination. The variables of age, frailty, hypertension, coronary artery disease, dyslipidemia, and diabetes mellitus were analyzed as the determinants of a decrease in GLS. Univariate analysis was conducted for each variable. Bivariate analysis was conducted using the chi-square test with a significance level of p<0.25 and confidence interval (CI) of 95%, and multivariate analysis used a logistic regression test.Results: A total of 194 patients were admitted according to the study criteria, with a mean age of 66 years. The proportion of women was 60.8%. The study revealed that the determinants with p<0.25 are frailty, hypertension, dyslipidemia, and diabetes mellitus, with multivariate analysis frailty having an OR of 2.002 (95% CI 1.042-3.925) and diabetes mellitus having an OR of 2.278 (95% CI 1.033-5.025).Conclusions : The median value of GLS in elderly is -21,6% (minimum value -5,3% and maximum value 29,9%). The factors that influence the decrease of GLS are frailty and diabetes mellitus."

"Latar belakang. Latihan fisik yang dijalankan secara teratur dengan intensitas dan durasi tertentu akan merangsang remodeling jantung sebagai usaha untuk mempertahankan fungsi ventrikel terhadap peningkatan beban biomekanik pada jantung. Diperkirakan bahwa latihan fisik jangka panjang menimbulkan remodeling jantung menyerupai hipertrofi kardiomiopati, berupa hipertrofi miosit dengan kekacauan tatanan miosit, fibrosis, apoptosis dan ko-lokalisasi gap junction. Tujuan penelitian. Mengetahui dampak latihan fisik jangka panjang dan henti-latih pada remodeling kardiomiosit. Metode penelitian. Penelitian eksperimental in vivo pada tikus Wistar ini dilakukan di Departemen Biokimia dan Biologi Molekuler, Laboratorium Imunohistologi Departemen Patologi Anatomi dan Bagian Fisiologi, FKUI. Latihan fisik dengan intensitas dan jangka waktu latihan yang berbeda, serta henti latih setelah periode latihan diterapkan pada tikus Wistar jantan dewasa muda. Dilakukan analisis terhadap perubahan morfologi kardiomiosit, fibrosis, apoptosis (ekspresi Caspase-3, Bax dan Bcl-2), gap junction (ekspresi Connexin43) dan pola EKG. Perubahan morfologi kardiomiosit diamati menggunakan pulasan Hematoxylin Eosin, fibrosis diamati menggunakan pulasan Masson?s Trichrome, sedangkan ekspresi Caspase-3, Bax, Bcl-2 dan Connexin43 diamati melalui pulasan imunohistokimia. Rekaman EKG dilakukan dengan filter 100 Hz, pada kecepatan kertas 50 mm/detik dan kepekaan 1 mV = 20 mm. Hasil dan pembahasan. Hasil penelitian ini menunjukkan bahwa latihan aerobik dan anaerobik menimbulkan hipertrofi eksentrik dengan peningkatan fibrosis dan apoptosis serta ko-lokalisasi gap junction ke arah lateral membran. Perubahan kardiomiosit, peningkatan fibrosis dan apoptosis lebih nyata pada latihan anaerobik dibandingkan latihan aerobik. Pola EKG menunjang adanya pembesaran ventrikel akibat latihan aerobik dan anaerobik disertai gangguan repolarisasi yang nyata terutama pada latihan anaerobik. Henti latih tidak mengembalikan morfologi miosit, apoptosis dan lokalisasi gap junction ke keadaan semula. Pola EKG setelah periode henti latih pada latihan aerobik tetap menunjukkan adanya hipertrofi ventrikel tanpa gangguan penghataran impuls yang berarti, namun pada latihan anaerobik tetap didapatkan gangguan repolarisasi berupa pemanjangan interval QTc yang bermakna. Kesimpulan. Remodeling kardiomiosit akibat latihan fisik jangka panjang tidak menyerupai struktur hipertrofi kardiomiopati, namun disertai peningkatan apoptosis, kolokalisasi Cx43 dan gangguan penghantaran impuls. Henti-latih tidak memulihkan remodeling jantung maupun gangguan penghantaran impuls listrik.

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Background. Regular physical exercise with certain intensity and duration stimulates remodeling of the heart as an effort to preserve ventricular function against an increased biomechanical load. It is postulated that long-term exercise induces cardiac remodeling that resemble cardiomyopathy hypertrophy marked by cardiomyocyte disarray, fibrosis, apoptosis and co-localization of gap junction. Research objective. To study the effect of long-term physical exercise and detraining on cardiomyocyte remodeling.

Methodology. This in vivo experimental study was conducted at the Departement of Biochemistry and Molecular Biology, Immunohistology Laboratory of Departement of Pathological Anatomy and Departement of Physiology FMUI. Physical exercise with different intensity and periods of training was performed in groups of young adult male Wistar rats, followed by a period of detraining. Analysis of cardiomyocyte morphological changes, fibrosis, apoptosis (expression of Caspase-3, Bax and Bcl-2), gap junctions (expression Connexin43) and ECG pattern was conducted. Changes in cardiomyocyte morphology was observed using Haematoxylin Eosin staining, fibrosis was observed using Masson's Trichrome staining, whereas the expression of Caspase-3, Bax, Bcl-2 and Connexin43 was observed through immunohistochemical staining. ECG recording was done with a filter of 100 Hz, the paper speed of 50 mm/sec and the sensitivity of 1 mV = 20 mm.

Results and discussion. The results showed that aerobic and anaerobic exercises cause the development of eccentric hypertrophy, with increased fibrosis and apoptosis as well as co-localization of gap junction to the lateral site of the membrane. Cardiomyocyte remodeling, fibrosis and apoptosis were more prominent in anaerobic compared to aerobic exercise group. The ECG pattern supports enlargement of the ventricles due to aerobic and anaerobic exercises with noticeable repolarization disturbances, especially in the anaerobic group. Detraining did not return myocyte morphology, apoptosis and localization of gap junctions to its basic state. The ECG pattern after a period of detraining following aerobic exercise supports the existence of ventricular hypertrophy without significant disturbances in impulse conduction, however repolarization disturbances in the form of significant prolongation of QTc interval persist in the group with anaerobic exercise.

Conclusion. Cardiomyocyte remodeling due to long-term physical exercise did not resemble cardiomyopathy hypertrophy structure, although increased apoptosis, colocalization of Cx43 and distrbances in impuls conduction were observed. Detraining did not restore cardiac remodeling and disturbances in electrical impulse conduction."

"Pendahuluan: Berdasarkan intensitas, durasi, dan bagaimana energi untuk kerja otot dihasilkan, latihan fisik dibagi menjadi latihan fisik aerobik dan anaerobik. Beberapa penelitian menunjukkan adanya hubungan antara latihan fisik dengan perubahan panjang telomer sel darah putih SDP , dan sel otot jantung. Pemendekan telomer SDP sering dihubungkan dengan penyakit kronik tidak menular, salah satunya penyakit kardiovaskular. Di Indonesia belum ada penelitian yang membandingkan pengaruh latihan fisik aerobik dan anaerobik terhadap perubahan panjang telomer SDP dan sel otot jantungTujuan: Membandingkan efek latihan fisik aerobik dan anaerobik terhadap perubahan panjang telomer SDP dan sel otot jantungMetode: Penelitian ini menggunakan 24 tikus putih jantan berusia 11-13 bulan, berat rata-rata 300 gram. Dibagi secara acak dalam 3 kelompok: 1 kontrol; 2 latihan fisik aerobik; 3 latihan fisik anaerobik. Latihan fisik dilakukan 5 kali/minggu selama 4 dan 12 minggu. Perhitungan panjang telomer relatif menggunakan Real-Time PCR.Hasil: Secara signifikan terdapat perbedaan panjang telomer relatif SDP kelompok aerobik 4 minggu dan 12 minggu dibanding kontrol 4 minggu p=0,012 dan p=0,009 . Tidak terdapat perbedaan bermakna kelompok anaerobik 4 dan 12 minggu dibanding kontrol 4 minggu p=0,208 dan p=0,141 . Tidak terdapat perbedaan bermakna panjang telomer relatif sel otot jantung kelompok aerobik maupun anaerobik dibanding kontrol.Kesimpulan: Latihan fisik aerobik memberikan efek lebih baik dibanding anaerobik dalam perubahan panjang telomer SDP. Sedangkan latihan fisik aerobik maupun anaerobik tidak mempengaruhi perubahan panjang telomer sel otot jantung.Kata Kunci: Latihan fisik aerobik, latihan fisik anaerobik, telomer, sel darah putih, sel otot jantung

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Introduction Aerobic and anaerobic physical exercise are two types of physical exercise that differ based on the intensity, interval, and type of muscle fibers incorporated. Telomere length TL of leukocyte, a measure of replicative senescence, decreases with aging. Recent evidence supports that telomere length of leukocytes may be inversely correlated with the risk of several age related diseases. In Indonesia, there has been no specific research to find out the effect of aerobic and anaerobic physical exercise on changes in telomere length of leukocyte and cardiomyocyte.Methods This study was conducted on 24 male white rats Rattus norvegicus 250 300 grams age 11 13 months, randomly allocated into 3 groups 1 control 2 aerobic physical exercise APE and 3 anaerobic physical exercise AnPE . Physical exercise was performed 5 times a week, for 4 and 12 weeks. Measurement of relative telomere length using Real Time PCR.Result Relative leukocyte TL was found significantly longer in 4 and 12 weeks APE group compared to 4 week control p 0,012 and p 0,009 . Relative leukocyte TL was found not significantly different between 4 and 12 weeks AnPE group compared 4 weeks control group p 0,208 and p 0,141 . Cardiomyocyte relative telomere length APE and AnPE are no significantly better compare to control group.Conclusion Leukocyte TL is preserved in group of APE.Keywords Aerobic physical exercise, anaerobic physical exercise, telomere length, leukocyte, cardiomyocyte."

"ABSTRAKLatar belakang: latihan fisik aerobik teratur dapat menyebabkan perubahan morfometrik, peningkatan ukuran miosit dengan peningkatan ekspresi connexin43 (Cx43) tanpa lateralisasi, serta peningkatan deposisi matriks ekstraseluler. Latihan fisik sebaiknya dimulai sejak masa anak-anak, guna mencapai kesehatan kardiovaskular di masa dewasa.Metode: Tikus usia juvenile dan dewasa muda dibagi secara acak dalam 7 kelompok, yaitu: kelompok latihan fisik onset juvenile durasi 4 minggu dan kontrol, kelompok latihan fisik onset juvenile durasi 8 minggu dan kontrol, kelompok latihan fisik onset juvenile durasi 12 minggu, kelompok latihan fisik onset usia dewasa muda durasi 8 minggu dan kontrol. Latihan fisik disesuaikan dengan usia tikus dan dipertahankan pada kecepatan 20 m/menit selama 20 menit intermitten, 5x seminggu. Analisis morfometrik jantung, peningkatan ukuran miosit, deposisi matriks ekstraseluler, serta ekspresi serta distribusi Cx43.Hasil: Tikus terlatih (5, 8, dan 12 minggu) pada kedua kelompok usia menunjukkan nilai berat jantung, berat ventrikel kiri, diameter rongga ventrikel, ketebalan otot jantung yang lebih tinggi dibandingkan dengan kelompok kontrolnya. Peningkatan ukuran panjang miosit juga meningkat kelompok latihan dibanding kontrol. Deposisi matriks ekstraseluler meningkat pada kelompok latihan dibandingkan kontrol. Ekspresi Cx43 juga meningkat pada sisi lateral.Kesimpulan: Latihan fisik aerobik dapat meningkatkan ukuran jantung dengan peningkatan ukuran sel, peningkatan deposisi matriks ekstraseluler, peningkatan Cx43 pada sisi lateral. Peningkatan matriks ekstraseluler dan peningkatan lateralisasi menunjukkan peningkatan risiko aritmia.

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ABSTRACT

Background: Regular aerobic exercise can improve morphometric changes, an increase in the size of myocytes with increased expression of connexin43 (Cx43) without lateralization, and increase extracellular matrix deposition. Exercise should be started since childhood, in order to achieve cardiovascular health in adulthood.

Methods: Juvenile and young adult Rats randomly divided into 7 groups: juvenile onset 4 weeks exercise duration and control group, juvenile onset 8 weeks exercise duration and control group, exercise juvenile onset 12 weeks exercise duration, young adult onset 8 weeks exercise duration and control group. Physical exercise adapted to the age of rats and maintained at speed of 20 m/minute for 20 minutes intermittent, 5 times a week. Morphometric analysis of the heart, increase the size of myocytes, extracellular matrix deposition, expression and distribution of Cx43.

Results: Trained rats (5, 8, and 12 weeks) in both age groups showed values of heart weight, left ventricle weight, ventricular cavity diameter, heart muscle thickness is higher than control group. Increased length of myocytes also increased in exercise group compared to the control. Increased deposition of extracellular matrix in exercise group than control. Cx43 expression was also increased in the lateral side.

Conclusions: Aerobic exercise can increase the size of the heart with increased cell size, increased extracellular matrix, increased Cx43 lateralization. Increased extracellular matrix deposition and increased lateralization showed an increased risk of arrhythmia."