Swimming is superior to operating in inducing physiological cardiac hypertrophy and enhancing myocardial efficiency

Bernardo, B. C., Ooi, J. Y. Y., Weeks, Ok. L., Patterson, N. L. & McMullen, J. R. Understanding key mechanisms of Exercise-Induced cardiac safety to mitigate illness: present information and rising ideas. Physiol. Rev. 98 (1), 419–475 (2018).

Google Scholar 

Nakamura, M. & Sadoshima, J. Mechanisms of physiological and pathological cardiac hypertrophy. Nat. Rev. Cardiol. 15 (7), 387–407 (2018).

Google Scholar 

Pelliccia, A., Culasso, F., Di Paolo, F. M. & Maron, B. J. Physiologic left ventricular cavity dilatation in elite athletes. Ann. Intern. Med. 130 (1), 23–31 (1999).

Google Scholar 

Hoogsteen, J. et al. Myocardial adaptation in numerous endurance sports activities: an echocardiographic research. Int. J. Cardiovasc. Imaging. 20 (1), 19–26 (2004).

Google Scholar 

Contarteze, R. V. L., Manchado, F. B., Gobatto, C. A. & De Mello, M. A. R. Stress biomarkers in rats submitted to swimming and treadmill operating workout routines. Comp. Biochem. Physiol. Mol. Integr. Physiol. 151 (3), 415–422 (2008).

Google Scholar 

Wang, Y., Wisloff, U. & Kemi, O. J. Animal fashions within the research of exercise-induced cardiac hypertrophy. Physiol. Res. 59 (5), 633–644 (2010).

Google Scholar 

Schaible, T. F. & Scheuer, J. Effects of bodily coaching by operating or swimming on ventricular efficiency of rat hearts. J. Appl. Physiol. Respir Environ. Exerc. Physiol. 46 (4), 854–860 (1979).

Google Scholar 

Yoshizaki, A. et al. Swimming coaching improves myocardial Mechanics, prevents Fibrosis, and alters expression of Ca2 + Handling proteins in older rats. J. Gerontol. Biol. Sci. Med. Sci. 73 (4), 468–474 (2018).

Google Scholar 

Serra, A. J. et al. Exercise coaching inhibits inflammatory cytokines and greater than prevents myocardial dysfunction in rats with sustained beta-adrenergic hyperactivity. J. Physiol. 588 (Pt 13), 2431–2442 (2010).

Google Scholar 

Ceci, M., Ross, J. Jr. & Condorelli, G. Molecular determinants of the physiological adaptation to emphasize within the cardiomyocyte: a deal with AKT. J. Mol. Cell. Cardiol. 37 (5), 905–912 (2004).

Google Scholar 

Kemi, O. J. et al. Activation or inactivation of cardiac Akt/mTOR signaling diverges physiological from pathological hypertrophy. J. Cell. Physiol. 214 (2), 316–321 (2008).

Google Scholar 

Catalucci, D., Latronico, M. V. & Condorelli, G. MicroRNAs management gene expression: significance for cardiac growth and pathophysiology. Ann. N Y Acad. Sci. 1123, 20–29 (2008).

Google Scholar 

Fernandes, T., Barauna, V. G., Negrao, C. E., Phillips, M. I. & Oliveira, E. M. Aerobic train coaching promotes physiological cardiac transforming involving a set of MicroRNAs. Am. J. Physiol. Heart Circ. Physiol. 309 (4), H543–H552 (2015).

Google Scholar 

Liu, X. et al. miR-222 is important for exercise-induced cardiac development and protects in opposition to pathological cardiac transforming. Cell. Metab. 21 (4), 584–595 (2015).

Google Scholar 

DeBosch, B. et al. Akt1 is required for physiological cardiac development. Circulation 113 (17), 2097–2104 (2006).

Google Scholar 

Ma, Z., Qi, J., Meng, S., Wen, B. & Zhang, J. Swimming train training-induced left ventricular hypertrophy entails MicroRNAs and synergistic regulation of the PI3K/AKT/mTOR signaling pathway. Eur. J. Appl. Physiol. 113 (10), 2473–2486 (2013).

Google Scholar 

Sanchis-Gomar, F. et al. Circulating MicroRNAs fluctuations in exercise-induced cardiac transforming: A scientific assessment. Am. J. Transl Res. 13 (12), 13298–13309 (2021).

Google Scholar 

Bodine, S. C. mTOR signaling and the molecular adaptation to resistance train. Med. Sci. Sports Exerc. 38 (11), 1950–1957 (2006).

Google Scholar 

Millet, G. P. et al. Modeling the transfers of coaching results on efficiency in elite triathletes. Int. J. Sports Med. 23 (1), 55–63 (2002).

Google Scholar 

Tanaka, H. Effects of cross-training. Transfer of coaching results on VO2max between biking, operating, and swimming. Sports Med. 18 (5), 330–339 (1994).

Google Scholar 

Jones, J. H. J. Resource ebook for the design of animal train protocols. Am. J. Vet. Res. 68 (6), 583 (2007).

Google Scholar 

Vigelso, A., Andersen, N. B. & Dela, F. The relationship between skeletal muscle mitochondrial citrate synthase exercise and complete physique oxygen uptake variations in response to train coaching. Int. J. Physiol. Pathophysiol Pharmacol. 6 (2), 84–101 (2014).

Google Scholar 

Bylund, A. C. et al. Physical coaching in man. Skeletal muscle metabolism in relation to muscle morphology and operating capability. Eur. J. Appl. Physiol. Occup. Physiol. 36 (3), 151–169 (1977).

Google Scholar 

Veiga, E. C. et al. Cardiac implications after myocardial infarction in rats beforehand present process bodily train. Arq. Bras. Cardiol. 100 (1), 37–43 (2013).

Google Scholar 

dos Santos, L., Antonio, E. L., Souza, A. F. & Tucci, P. J. Use of afterload hemodynamic stress as a sensible methodology for assessing cardiac efficiency in rats with coronary heart failure. Can. J. Physiol. Pharmacol. 88 (7), 724–732 (2010).

Google Scholar 

Kuo, P. L. et al. Myocyte form regulates lateral registry of sarcomeres and contractility. Am. J. Pathol. 181 (6), 2030–2037 (2012).

Google Scholar 

Kawai, M., Karam, T. S., Michael, J. J., Wang, L. & Chandra, M. Comparison of elementary steps of the cross-bridge cycle in rat papillary muscle fibers expressing alpha- and beta-myosin heavy chain with sinusoidal evaluation. J. Muscle Res. Cell. Motil. 37 (6), 203–214 (2016).

Google Scholar 

Locher, M. R., Razumova, M. V., Stelzer, J. E., Norman, H. S. & Moss, R. L. Effects of low-level & alpha;-myosin heavy chain expression on contractile kinetics in Porcine myocardium. Am. J. Physiol. Heart Circ. Physiol. 300 (3), H869–H878 (2011).

Google Scholar 

Sevrieva, I. R. et al. Cardiac myosin regulatory mild chain kinase modulates cardiac contractility by phosphorylating each myosin regulatory mild chain and troponin I. J. Biol. Chem. 295 (14), 4398–4410 (2020).

Google Scholar 

Toepfer, C. N., West, T. G. & Ferenczi, M. A. Revisiting Frank-Starling: regulatory mild chain phosphorylation alters the speed of pressure redevelopment (ktr) in a length-dependent style. J. Physiol. 594 (18), 5237–5254 (2016).

Google Scholar 

McNamara, J. W., Singh, R. R. & Sadayappan, S. Cardiac myosin binding protein-C phosphorylation regulates the super-relaxed state of myosin. Proc. Natl. Acad. Sci. U S A. 116 (24), 11731–11736 (2019).

Google Scholar 

Fitzsimons, D. P., Bodell, P. W. & Baldwin, Ok. M. Phosphorylation of rodent cardiac myosin mild chain 2: results of train. J. Appl. Physiol. (1985). 67 (6), 2447–2453 (1989).

Google Scholar 

Chakouri, N. et al. Stress-induced protein S-glutathionylation and phosphorylation crosstalk in cardiac sarcomeric proteins – Impact on coronary heart perform. Int. J. Cardiol. 258, 207–216 (2018).

Google Scholar 

Kemi, O. J. et al. Aerobic interval coaching enhances cardiomyocyte contractility and Ca2 + biking by phosphorylation of camkii and Thr-17 of phospholamban. J. Mol. Cell. Cardiol. 43 (3), 354–361 (2007).

Google Scholar 

Schaible, T. F. & Scheuer, J. Cardiac perform in hypertrophied hearts from chronically exercised feminine rats. J. Appl. Physiol. Respir Environ. Exerc. Physiol. 50 (6), 1140–1145 (1981).

Google Scholar 

Tang, X. Y. et al. Effects of train of various intensities on the angiogenesis, infarct therapeutic, and performance of the left ventricle in postmyocardial infarction rats. Coron. Artery Dis. 22 (7), 497–506 (2011).

Google Scholar 

Rodrigues, F. et al. Cardioprotection afforded by train coaching previous to myocardial infarction is related to autonomic perform enchancment. BMC Cardiovasc. Disord. 14, 84 (2014).

Google Scholar 

Serra, A. J. et al. Exercise coaching prevents beta-adrenergic hyperactivity-induced myocardial hypertrophy and lesions. Eur. J. Heart Fail. 10 (6), 534–539 (2008).

Google Scholar 

Lavorato, V. N. et al. Mesenchymal stem cell remedy related to endurance train coaching: results on the structural and practical transforming of infarcted rat hearts. J. Mol. Cell. Cardiol. 90, 111–119 (2016).

Google Scholar 

Lorell, B. H. & Carabello, B. A. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation 102 (4), 470–479 (2000).

Google Scholar 

Claessens, C. et al. Structural coronary heart variations in triathletes. Acta Cardiol. 54 (6), 317–325 (1999).

Google Scholar 

Fathi, M., Gharakhanlou, R. & Rezaei, R. The modifications of coronary heart miR-1 and miR-133 expressions following physiological hypertrophy as a consequence of endurance coaching. Cell. J. 22 (Suppl 1), 133–140 (2020).

Google Scholar 

Soci, U. P. et al. MicroRNAs 29 are concerned within the enchancment of ventricular compliance promoted by cardio train coaching in rats. Physiol. Genomics. 43 (11), 665–673 (2011).

Google Scholar 

Ghalehgir, S., Vakili, J., Khani, M. & Alamdari, A. The impact of eight weeks excessive depth interval coaching on the expression of cardiac miRNA-21 and miRNA-1 in Wistar male rats. J. Sport Exerc. Physiol. 15 (4), 82–92 (2022).

Google Scholar 

Yang, G. & Yang, W. Regulating the expression of exercise-induced micro-RNAs and lengthy non-coding rnas: implications for controlling cardiovascular illnesses and coronary heart failure. Front. Mol. Biosci. 12, 1587124 (2025). Published 2025 May 20.

Google Scholar 

Fernandes, T. et al. Aerobic train training-induced left ventricular hypertrophy entails regulatory MicroRNAs, decreased angiotensin-converting enzyme-angiotensin ii, and synergistic regulation of angiotensin-converting enzyme 2-angiotensin (1–7). Hypertension 58 (2), 182–189 (2011).

Google Scholar 

Liu, X., Platt, C. & Rosenzweig, A. The position of MicroRNAs within the cardiac response to train. Cold Spring Harb Perspect. Med. 7 (12), a029850 (2017).

Google Scholar 

Fernandes, T., Soci, U. P. & Oliveira, E. M. Eccentric and concentric cardiac hypertrophy induced by train coaching: MicroRNAs and molecular determinants. Braz J. Med. Biol. Res. 44 (9), 836–847 (2011).

Google Scholar 

Guimaraes, G. G. et al. Exercise induces renin-angiotensin system unbalance and excessive collagen expression within the coronary heart of Mas-deficient mice. Peptides 38 (1), 54–61 (2012).

Google Scholar 

Ma, S. & Liao, Y. Noncoding RNAs in exercise-induced cardio-protection for power coronary heart failure. EBioMedicine 46, 532–540 (2019).

Google Scholar 

Palabiyik, O. et al. Alteration in cardiac PI3K/Akt/mTOR and ERK signaling pathways with using development hormone and swimming, and the roles of miR21 and miR133. Biomed. Rep. 0 (0), 1–10 (2019).

Google Scholar 

Maehama, T. & Dixon, J. E. The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate. J. Biol. Chem. 273 (22), 13375–13378 (1998).

Google Scholar 

Weeks, Ok. L., Bernardo, B. C., Ooi, J. Y. Y., Patterson, N. L. & McMullen, J. R. The IGF1-PI3K-Akt signaling pathway in mediating Exercise-Induced cardiac hypertrophy and safety. Adv. Exp. Med. Biol. 1000, 187–210 (2017).

Google Scholar 

Tham, Y. Ok., Bernardo, B. C., Ooi, J. Y., Weeks, Ok. L. & McMullen, J. R. Pathophysiology of cardiac hypertrophy and coronary heart failure: signaling pathways and novel therapeutic targets. Arch. Toxicol. 89 (9), 1401–1438 (2015).

Google Scholar 

Wu, G., Zhang, X. & Gao, F. The epigenetic panorama of train in cardiac well being and illness. J. Sport Health Sci. 10 (6), 648–659 (2020).

Morisco, C. et al. Glycogen synthase kinase 3beta regulates GATA4 in cardiac myocytes. J. Biol. Chem. 276 (30), 28586–28597 (2001).

Google Scholar 

Ikeda, S. et al. MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes. Mol. Cell. Biol. 29 (8), 2193–2204 (2009).

Google Scholar 

Woodcock, H. V. et al. The mTORC1/4E-BP1 axis represents a vital signaling node throughout fibrogenesis. Nat. Commun. 10 (1), 6 (2019).

Google Scholar 

Zhang, J., Gao, Z. & Ye, J. Phosphorylation and degradation of S6K1 (p70S6K1) in response to persistent JNK1 activation. Biochim. Biophys. Acta. 1832 (12), 1980–1988 (2013).

Google Scholar 

McArdle, W. D. Metabolic stress of endurance swimming within the laboratory rat. J. Appl. Physiol. 22 (1), 50–54 (1967).

Google Scholar 

Wisloff, U., Helgerud, J., Kemi, O. J. & Ellingsen, O. Intensity-controlled treadmill operating in rats: VO(2 max) and cardiac hypertrophy. Am. J. Physiol. Heart Circ. Physiol. 280 (3), H1301–H1310 (2001).

Google Scholar 

Yoshizaki, A. et al. Swimming coaching improves myocardial Mechanics, prevents Fibrosis, and alters expression of Ca²⁺ dealing with proteins in older rats. J. Gerontol. Biol. Sci. Med. Sci. 73 (4), 468–474 (2018).

Google Scholar 

Souza Vieira, S. et al. Increased myocardial retention of mesenchymal stem cells Post-MI by Pre-Conditioning train coaching. Stem Cell. Rev. Rep. 16 (4), 730–741 (2020).

Google Scholar 

Manchini, M. T. et al. Low-Level laser utility within the early myocardial infarction stage has no helpful position in coronary heart failure. Front. Physiol. 8, 23 (2017).

Google Scholar 

Feliciano, R. D. S. et al. Photobiomodulation remedy on myocardial infarction in rats: transcriptional and posttranscriptional implications to cardiac transforming. Lasers Surg. Med. 53 (9), 1247–1257 (2021).

Google Scholar 

de Melo, B. L. et al. Exercise coaching attenuates proper ventricular transforming in rats with pulmonary arterial stenosis. Front. Physiol. 7, 541 (2016).

Google Scholar