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Artykuły w czasopismach na temat „Physiological hypertrophy”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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1

Williams, Vaughan E. M. "Ventricular Hypertrophy — Physiological Mechanisms". Journal of Cardiovascular Pharmacology 8, Supplement 3 (1986): S12—S16. http://dx.doi.org/10.1097/00005344-198608003-00004.

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JACOB, R., M. VOGT i H. RUPP. "Physiological and pathological hypertrophy*". Journal of Molecular and Cellular Cardiology 18 (1986): 35. http://dx.doi.org/10.1016/s0022-2828(86)80135-3.

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Kang, Peter M., Patrick Yue, Zhilin Liu, Oleg Tarnavski, Natalya Bodyak i Seigo Izumo. "Alterations in apoptosis regulatory factors during hypertrophy and heart failure". American Journal of Physiology-Heart and Circulatory Physiology 287, nr 1 (lipiec 2004): H72—H80. http://dx.doi.org/10.1152/ajpheart.00556.2003.

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Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made hypertrophic by a pathological stimulus show increased sensitivity to apoptosis. Examination of the molecular changes associated with these distinct types of hypertrophy revealed changes in Bcl-2 family members and caspases favoring survival during physiological hypertrophy. However, in pathological hypertrophy, there were more diffuse proapoptotic changes, including changes in Fas, the Bcl-2 protein family, and caspases. Therefore, we speculate that this increased sensitivity to apoptotic stimulation along with proapoptotic changes in the apoptosis program may contribute to the development of heart failure seen in pathological cardiac hypertrophy.

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Nosenko, N. M., D. V. Shchehlov, M. Yu Mamonova i Ya E. Kudelskyi. "Left ventricular hypertrophy: differential diagnosis". Endovascular Neuroradiology 30, nr 4 (11.03.2020): 49–58. http://dx.doi.org/10.26683/2304-9359-2019-4(30)-49-58.

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There are some imaging methods for the diagnosis of left ventricular hypertrophy. Such as echocardiography, computed tomography, magnetic resonance imaging. These methods help to identify changes at different stages, evaluate the prognosis, stratify the risk and differential diagnosis.The left ventricle hypertrophy is a condition that may be due to physiological adaptation due to overload. For example, in patients with arterial hypertension, in athletes, and so on. Left ventricle hypertrophy may also be associated with a change in the actual structure: for example, with hypertrophic cardiomyopathy.Signs of left ventricle hypertrophy by echocardiography are a very significant predictor of mortality in patients with arterial hypertension in the general population. The presence of left ventricle hypertrophy by echocardiography is a high cardiovascular risk for the patient.It is important to diagnose diseases with a high risk of sudden cardiac death on time. One of these diseases is hypertrophic cardiomyopathy. A clinical diagnosis of hypertrophic cardiomyopathy is impossible without visualization. Therefore, the European Association of Cardiovascular Imaging recommends a multimodal approach in examining patients with hypertrophic cardiomyopathy.Сomputed tomography, echocardiography, and magnetic resonance imaging are used to diagnose which patient’s hypertrophy is pathological or physiological. The choice of which method to use depends on the diagnostic task, and also on the specific advantages and disadvantages of the method. Different visualization methods should be considered complementary, not competing. It is also important to choose a particular imaging technique given its diagnostic value, availability, benefits, risks and costs.

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Luckey, Stephen W., Chris D. Haines, John P. Konhilas, Elizabeth D. Luczak, Antke Messmer-Kratzsch i Leslie A. Leinwand. "Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy". Experimental Biology and Medicine 242, nr 18 (13.09.2017): 1820–30. http://dx.doi.org/10.1177/1535370217731503.

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A number of signaling pathways underlying pathological cardiac hypertrophy have been identified. However, few studies have probed the functional significance of these signaling pathways in the context of exercise or physiological pathways. Exercise studies were performed on females from six different genetic mouse models that have been shown to exhibit alterations in pathological cardiac adaptation and hypertrophy. These include mice expressing constitutively active glycogen synthase kinase-3β (GSK-3βS9A), an inhibitor of CaMK II (AC3-I), both GSK-3βS9A and AC3-I (GSK-3βS9A/AC3-I), constitutively active Akt (myrAkt), mice deficient in MAPK/ERK kinase kinase-1 (MEKK1−/−), and mice deficient in cyclin D2 (cyclin D2−/−). Voluntary wheel running performance was similar to NTG littermates for five of the mouse lines. Exercise induced significant cardiac growth in all mouse models except the cyclin D2−/− mice. Cardiac function was not impacted in the cyclin D2−/− mice and studies using a phospho-antibody array identified six proteins with increased phosphorylation (greater than 150%) and nine proteins with decreased phosphorylation (greater than 33% decrease) in the hearts of exercised cyclin D2−/− mice compared to exercised NTG littermate controls. Our results demonstrate that unlike the other hypertrophic signaling molecules tested here, cyclin D2 is an important regulator of both pathologic and physiological hypertrophy. Impact statement This research is relevant as the hypertrophic signaling pathways tested here have only been characterized for their role in pathological hypertrophy, and not in the context of exercise or physiological hypertrophy. By using the same transgenic mouse lines utilized in previous studies, our findings provide a novel and important understanding for the role of these signaling pathways in physiological hypertrophy. We found that alterations in the signaling pathways tested here had no impact on exercise performance. Exercise induced cardiac growth in all of the transgenic mice except for the mice deficient in cyclin D2. In the cyclin D2 null mice, cardiac function was not impacted even though the hypertrophic response was blunted and a number of signaling pathways are differentially regulated by exercise. These data provide the field with an understanding that cyclin D2 is a key mediator of physiological hypertrophy.

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6

Watson, Peter A., Jane E. B. Reusch, Sylvia A. McCune, Leslie A. Leinwand, Stephen W. Luckey, John P. Konhilas, David A. Brown i in. "Restoration of CREB function is linked to completion and stabilization of adaptive cardiac hypertrophy in response to exercise". American Journal of Physiology-Heart and Circulatory Physiology 293, nr 1 (lipiec 2007): H246—H259. http://dx.doi.org/10.1152/ajpheart.00734.2006.

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Potential regulation of two factors linked to physiological outcomes with left ventricular (LV) hypertrophy, resistance to apoptosis, and matching of metabolic capacity, by the transcription factor cyclic-nucleotide regulatory element binding protein (CREB), was examined in the two models of physiological LV hypertrophy: involuntary treadmill running of female Sprague-Dawley rats and voluntary exercise wheel running in female C57Bl/6 mice. Comparative studies were performed in the models of pathological LV hypertrophy and failure: the spontaneously hypertension heart failure (SHHF) rat and the hypertrophic cardiomyopathy (HCM) transgenic mouse, a model of familial idiopathic cardiomyopathy. Activating CREB serine-133 phosphorylation was decreased early in remodeling in response to both physiological (decreased 50–80%) and pathological (decreased 60–80%) hypertrophic stimuli. Restoration of LV CREB phosphorylation occurred concurrent with completion of physiological hypertrophy (94% of sedentary control), but remained decreased (by 90%) during pathological hypertrophy. In all models of hypertrophy, CREB phosphorylation/activation demonstrated strong positive correlations with 1) expression of the anti-apoptotic protein bcl-2 (a CREB-dependent gene) and subsequent reductions in the activation of caspase 9 and caspase 3; 2) expression of peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1; a major regulator of mitochondrial content and respiratory capacity), and 3) LV mitochondrial respiratory rates and mitochondrial protein content. Exercise-induced increases in LV mitochondrial respiratory capacity were commensurate with increases observed in LV mass, as previously reported in the literature. Exercise training of SHHF rats and HCM mice in LV failure improved cardiac phenotype, increased CREB activation (31 and 118%, respectively), increased bcl-2 content, improved apoptotic status, and enhanced PGC-1 content and mitochondrial gene expression. Adenovirus-mediated expression of constitutively active CREB in neonatal rat cardiac recapitulated exercise-induced upregulation of PGC-1 content and mitochondrial oxidative gene expression. These data support a model wherein CREB contributes to physiological hypertrophy by enhancing expression of genes important for efficient oxidative capacity and resistance to apoptosis.

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7

Pluncevic Gligoroska, Jasmina, Sanja Manchevska, Sunchica Petrovska i Beti Dejanova. "PHYSIOLOGICAL MECHANISMS OF MUSCLE HYPERTROPHY". Research in Physical Education, Sport and Health 11, nr 1 (2022): 153–60. http://dx.doi.org/10.46733/pesh22111153pg.

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8

Patel, Ruchi, Rebecca H. Ritchie, Claire L. Curl, Lea M. Delbridge i Igor R. Wendt. "Testosterone modulates physiological cardiac hypertrophy". Journal of Molecular and Cellular Cardiology 42, nr 6 (czerwiec 2007): S139. http://dx.doi.org/10.1016/j.yjmcc.2007.03.383.

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9

Shimizu, Ippei, i Tohru Minamino. "Physiological and pathological cardiac hypertrophy". Journal of Molecular and Cellular Cardiology 97 (sierpień 2016): 245–62. http://dx.doi.org/10.1016/j.yjmcc.2016.06.001.

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10

Kavazis, Andreas N. "Pathological vs. physiological cardiac hypertrophy". Journal of Physiology 593, nr 17 (1.09.2015): 3767. http://dx.doi.org/10.1113/jp271161.

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11

Pelozin, Bruno R. A., Ursula P. R. Soci, João L. P. Gomes, Edilamar M. Oliveira i Tiago Fernandes. "mTOR signaling-related microRNAs as cardiac hypertrophy modulators in high-volume endurance training". Journal of Applied Physiology 132, nr 1 (1.01.2022): 126–39. http://dx.doi.org/10.1152/japplphysiol.00881.2020.

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Physiological hypertrophic growth of the heart as a compensatory response to exercise training (ET) is coupled with recent progress in dissecting the microRNA (miRNA)-mediated molecular basis of hypertrophy. Aerobic ET seems to reduce miRNA-16-5p and increase miRNA-26a-5p expression in a volume-dependent mode, activating protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathways, and likely produces an enhanced left ventricular hypertrophy (LVH) in high-volume endurance training. New insight into these mechanisms can be useful in understanding physiological LVH and how it might be harnessed as a therapeutic application.

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12

Morita, Kozo, Takeshi Miyamoto, Nobuyuki Fujita, Yoshiaki Kubota, Keisuke Ito, Keiyo Takubo, Kana Miyamoto i in. "Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification". Journal of Experimental Medicine 204, nr 7 (18.06.2007): 1613–23. http://dx.doi.org/10.1084/jem.20062525.

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Chondrocyte hypertrophy during endochondral ossification is a well-controlled process in which proliferating chondrocytes stop proliferating and differentiate into hypertrophic chondrocytes, which then undergo apoptosis. Chondrocyte hypertrophy induces angiogenesis and mineralization. This step is crucial for the longitudinal growth and development of long bones, but what triggers the process is unknown. Reactive oxygen species (ROS) have been implicated in cellular damage; however, the physiological role of ROS in chondrogenesis is not well characterized. We demonstrate that increasing ROS levels induce chondrocyte hypertrophy. Elevated ROS levels are detected in hypertrophic chondrocytes. In vivo and in vitro treatment with N-acetyl cysteine, which enhances endogenous antioxidant levels and protects cells from oxidative stress, inhibits chondrocyte hypertrophy. In ataxia telangiectasia mutated (Atm)–deficient (Atm−/−) mice, ROS levels were elevated in chondrocytes of growth plates, accompanied by a proliferation defect and stimulation of chondrocyte hypertrophy. Decreased proliferation and excessive hypertrophy in Atm−/− mice were also rescued by antioxidant treatment. These findings indicate that ROS levels regulate inhibition of proliferation and modulate initiation of the hypertrophic changes in chondrocytes.

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13

Nemoto, Shino, Zelin Sheng i Anning Lin. "Opposing Effects of Jun Kinase and p38 Mitogen-Activated Protein Kinases on Cardiomyocyte Hypertrophy". Molecular and Cellular Biology 18, nr 6 (1.06.1998): 3518–26. http://dx.doi.org/10.1128/mcb.18.6.3518.

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ABSTRACT c-Jun N-terminal protein kinase (JNK) and p38, two distinct members of the mitogen-activated protein (MAP) kinase family, regulate gene expression in response to various extracellular stimuli, yet their physiological functions are not completely understood. In this report we show that JNK and p38 exerted opposing effects on the development of myocyte hypertrophy, which is an adaptive physiological process characterized by expression of embryonic genes and unique morphological changes. In rat neonatal ventricular myocytes, both JNK and p38 were stimulated by hypertrophic agonists like endothelin-1, phenylephrine, and leukemia inhibitory factor. Expression of MAP kinase kinase 6b (EE), a constitutive activator of p38, stimulated the expression of atrial natriuretic factor (ANF), which is a genetic marker of in vivo cardiac hypertrophy. Activation of p38 was required for ANF expression induced by the hypertrophic agonists. Furthermore, a specific p38 inhibitor, SB202190, significantly changed hypertrophic morphology induced by the agonists. Surprisingly, activation of JNK led to inhibition of ANF expression induced by MEK kinase 1 (MEKK1) and the hypertrophic agonists. MEKK1-induced ANF expression was also negatively regulated by expression of c-Jun. Our results demonstrate that p38 mediates, but JNK suppresses, the development of myocyte hypertrophy.

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14

Buss, Sebastian J., Johannes H. Riffel, Pratima Malekar, Marco Hagenmueller, Christina Asel, Min Zhang, Celine Weiss, Hugo A. Katus i Stefan E. Hardt. "Chronic Akt blockade aggravates pathological hypertrophy and inhibits physiological hypertrophy". American Journal of Physiology-Heart and Circulatory Physiology 302, nr 2 (styczeń 2012): H420—H430. http://dx.doi.org/10.1152/ajpheart.00211.2011.

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The attenuation of adverse myocardial remodeling and pathological left ventricular (LV) hypertrophy is one of the hallmarks for improving the prognosis after myocardial infarction (MI). The protein kinase Akt plays a central role in regulating cardiac hypertrophy, but the in vivo effects of chronic pharmacological inhibition of Akt are unknown. We investigated the effect of chronic Akt blockade with deguelin on the development of pathological [MI and aortic banding (AB)] and physiological (controlled treadmill running) hypertrophy. Primary cardiomyocyte cultures were incubated with 10 μmol deguelin for 48 h, and Wistar rats were treated orally with deguelin (4.0 mg·kg−1·day−1) for 4 wk starting 1 day after the induction of MI or AB. Exercise-trained animals received deguelin for 4 wk during the training period. In vitro, we observed reduced phosphorylation of Akt and glycogen synthase kinase (GSK)-3β after an incubation with deguelin, whereas MAPK signaling was not significantly affected. In vivo, treatment with deguelin led to attenuated phosphorylation of Akt and GSK-3β 4 wk after MI. These animals showed significantly increased heart weights and impaired LV function with increased end-diastolic diameters (12.0 ± 0.3 vs. 11.1 ± 0.3 mm, P < 0.05), end-diastolic volumes (439 ± 8 vs. 388 ± 18 μl, P < 0.05), and cardiomyocyte sizes (+20%, P < 0.05) compared with MI animals receiving vehicle treatment. Furthermore, activation of Ca2+/calmodulin-dependent kinase II in deguelin-treated MI animals was increased compared with the vehicle-treated group. Four wk after AB, we observed an augmentation of pathological hypertrophy in the deguelin-treated group with a significant increase in heart weights and cardiomyocyte sizes (>20%, P < 0.05). In contrast, the development of physiological hypertrophy was inhibited by deguelin treatment in exercise-trained animals. In conclusion, chronic Akt blockade with deguelin aggravates adverse myocardial remodeling and antagonizes physiological hypertrophy.

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15

Ozaki, Hayao, Takashi Abe, Alan E. Mikesky, Akihiro Sakamoto, Shuichi Machida i Hisashi Naito. "Physiological stimuli necessary for muscle hypertrophy". Journal of Physical Fitness and Sports Medicine 4, nr 1 (2015): 43–51. http://dx.doi.org/10.7600/jpfsm.4.43.

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Catalucci, Daniele. "Physiological myocardial hypertrophy: how and why?" Frontiers in Bioscience 13, nr 13 (2008): 312. http://dx.doi.org/10.2741/2681.

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Nader, Gustavo A. "Physiological Genomics of Skeletal Muscle Hypertrophy". Medicine & Science in Sports & Exercise 38, Supplement (maj 2006): 47. http://dx.doi.org/10.1249/00005768-200605001-00171.

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Nader, Gustavo A. "Physiological Genomics of Skeletal Muscle Hypertrophy". Medicine & Science in Sports & Exercise 38, Supplement (maj 2006): 47. http://dx.doi.org/10.1249/00005768-200605001-00312.

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Schoepe, Maria, Andrea Schrepper, Michael Schwarzer, Paulo Amorim, Friedrich W. Mohr i Torsten Doenst. "DOES EXERCISE ALWAYS CAUSE PHYSIOLOGICAL HYPERTROPHY?" Journal of the American College of Cardiology 55, nr 10 (marzec 2010): A80.E750. http://dx.doi.org/10.1016/s0735-1097(10)60751-6.

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Riedl, Moritz, Christina Witzmann, Matthias Koch, Siegmund Lang, Maximilian Kerschbaum, Florian Baumann, Werner Krutsch, Denitsa Docheva, Volker Alt i Christian Pfeifer. "Attenuation of Hypertrophy in Human MSCs via Treatment with a Retinoic Acid Receptor Inverse Agonist". International Journal of Molecular Sciences 21, nr 4 (20.02.2020): 1444. http://dx.doi.org/10.3390/ijms21041444.

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In vitro chondrogenically differentiated mesenchymal stem cells (MSCs) have a tendency to undergo hypertrophy, mirroring the fate of transient “chondrocytes” in the growth plate. As hypertrophy would result in ossification, this fact limits their use in cartilage tissue engineering applications. During limb development, retinoic acid receptor (RAR) signaling exerts an important influence on cell fate of mesenchymal progenitors. While retinoids foster hypertrophy, suppression of RAR signaling seems to be required for chondrogenic differentiation. Therefore, we hypothesized that treatment of chondrogenically differentiating hMSCs with the RAR inverse agonist, BMS204,493 (further named BMS), would attenuate hypertrophy. We induced hypertrophy in chondrogenic precultured MSC pellets by the addition of bone morphogenetic protein 4. Direct activation of the RAR pathway by application of the physiological RAR agonist retinoic acid (RA) further enhanced the hypertrophic phenotype. However, BMS treatment reduced hypertrophic conversion in hMSCs, shown by decreased cell size, number of hypertrophic cells, and collagen type X deposition in histological analyses. BMS effects were dependent on the time point of application and strongest after early treatment during chondrogenic precultivation. The possibility of modifing hypertrophic cartilage via attenuation of RAR signaling by BMS could be helpful in producing stable engineered tissue for cartilage regeneration.

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21

Oldfield, Christopher J., Todd A. Duhamel i Naranjan S. Dhalla. "Mechanisms for the transition from physiological to pathological cardiac hypertrophy". Canadian Journal of Physiology and Pharmacology 98, nr 2 (luty 2020): 74–84. http://dx.doi.org/10.1139/cjpp-2019-0566.

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The heart is capable of responding to stressful situations by increasing muscle mass, which is broadly defined as cardiac hypertrophy. This phenomenon minimizes ventricular wall stress for the heart undergoing a greater than normal workload. At initial stages, cardiac hypertrophy is associated with normal or enhanced cardiac function and is considered to be adaptive or physiological; however, at later stages, if the stimulus is not removed, it is associated with contractile dysfunction and is termed as pathological cardiac hypertrophy. It is during physiological cardiac hypertrophy where the function of subcellular organelles, including the sarcolemma, sarcoplasmic reticulum, mitochondria, and myofibrils, may be upregulated, while pathological cardiac hypertrophy is associated with downregulation of these subcellular activities. The transition of physiological cardiac hypertrophy to pathological cardiac hypertrophy may be due to the reduction in blood supply to hypertrophied myocardium as a consequence of reduced capillary density. Oxidative stress, inflammatory processes, Ca2+-handling abnormalities, and apoptosis in cardiomyocytes are suggested to play a critical role in the depression of contractile function during the development of pathological hypertrophy.

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Kong, Sek Won, Natalya Bodyak, Patrick Yue, Zhilin Liu, Jeffrey Brown, Seigo Izumo i Peter M. Kang. "Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats". Physiological Genomics 21, nr 1 (21.03.2005): 34–42. http://dx.doi.org/10.1152/physiolgenomics.00226.2004.

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Cardiac hypertrophy is a complex and nonhomogenous response to various stimuli. In this study, we used high-density oligonucleotide microarray to examine gene expression profiles during physiological hypertrophy, pathological hypertrophy, and heart failure in Dahl salt-sensitive rats. There were changes in 404/3,160 and 874/3,160 genes between physiological and pathological hypertrophy and the transition from hypertrophy to heart failure, respectively. There were increases in stress response genes (e.g., heat shock proteins) and inflammation-related genes (e.g., pancreatitis-associated protein and arachidonate 12-lipoxygenase) in pathological processes but not in physiological hypertrophy. Furthermore, atrial natriuretic factor and brain natriuretic protein showed distinctive changes that are very specific to different conditions. In addition, we used a resampling-based gene score-calculating method to define significantly altered gene clusters, based on Gene Ontology classification. It revealed significant alterations in genes involved in the apoptosis pathway during pathological hypertrophy, suggesting that the apoptosis pathway may play a role during the transition to heart failure. In addition, there were significant changes in glucose/insulin signaling, protein biosynthesis, and epidermal growth factor signaling during physiological hypertrophy but not during pathological hypertrophy.

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Iemitsu, Motoyuki, Takashi Miyauchi, Seiji Maeda, Satoshi Sakai, Tsutomu Kobayashi, Nobuharu Fujii, Hitoshi Miyazaki, Mitsuo Matsuda i Iwao Yamaguchi. "Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, nr 6 (1.12.2001): R2029—R2036. http://dx.doi.org/10.1152/ajpregu.2001.281.6.r2029.

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Pressure overload, such as hypertension, to the heart causes pathological cardiac hypertrophy, whereas chronic exercise causes physiological cardiac hypertrophy, which is defined as athletic heart. There are differences in cardiac properties between these two types of hypertrophy. We investigated whether mRNA expression of various cardiovascular regulating factors differs in rat hearts that are physiologically and pathologically hypertrophied, because we hypothesized that these two types of cardiac hypertrophy induce different molecular phenotypes. We used the spontaneously hypertensive rat (SHR group; 19 wk old) as a model of pathological hypertrophy and swim-trained rats (trained group; 19 wk old, swim training for 15 wk) as a model of physiological hypertrophy. We also used sedentary Wistar-Kyoto rats as the control group (19 wk old). Left ventricular mass index for body weight was significantly higher in SHR and trained groups than in the control group. Expression of brain natriuretic peptide, angiotensin-converting enzyme, and endothelin-1 mRNA in the heart was significantly higher in the SHR group than in control and trained groups. Expression of adrenomedullin mRNA in the heart was significantly lower in the trained group than in control and SHR groups. Expression of β1-adrenergic receptor mRNA in the heart was significantly higher in SHR and trained groups than in the control group. Expression of β1-adrenergic receptor kinase mRNA, which inhibits β1-adrenergic receptor activity, in the heart was markedly higher in the SHR group than in control and trained groups. We demonstrated for the first time that the manner of mRNA expression of various cardiovascular regulating factors in the heart differs between physiological and pathological cardiac hypertrophy.

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Zhang, Weiwei, Jiayi Liu, Zekang Wu, Guanwei Fan, Zhuo Yang i Chunhua Liu. "Notch1 Is Involved in Physiologic Cardiac Hypertrophy of Mice via the p38 Signaling Pathway after Voluntary Running". International Journal of Molecular Sciences 24, nr 4 (6.02.2023): 3212. http://dx.doi.org/10.3390/ijms24043212.

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Appropriate exercise such as voluntary wheel-running can induce physiological cardiac hypertrophy. Notch1 plays an important role in cardiac hypertrophy; however, the experimental results are inconsistent. In this experiment, we aimed to explore the role of Notch1 in physiological cardiac hypertrophy. Twenty-nine adult male mice were randomly divided into a Notch1 heterozygous deficient control (Notch1+/− CON) group, a Notch1 heterozygous deficient running (Notch1+/− RUN) group, a wild type control (WT CON) group, and a wild type running (WT RUN) group. Mice in the Notch1+/− RUN and WT RUN groups had access to voluntary wheel-running for two weeks. Next, the cardiac function of all of the mice was examined by echocardiography. The H&E staining, Masson trichrome staining, and a Western blot assay were carried out to analyze cardiac hypertrophy, cardiac fibrosis, and the expression of proteins relating to cardiac hypertrophy. After two-weeks of running, the Notch1 receptor expression was decreased in the hearts of the WT RUN group. The degree of cardiac hypertrophy in the Notch1+/− RUN mice was lower than that of their littermate control. Compared to the Notch1+/− CON group, Notch1 heterozygous deficiency could lead to a decrease in Beclin-1 expression and the ratio of LC3II/LC3I in the Notch1+/− RUN group. The results suggest that Notch1 heterozygous deficiency could partly dampen the induction of autophagy. Moreover, Notch1 deficiency may lead to the inactivation of p38 and the reduction of β-catenin expression in the Notch1+/− RUN group. In conclusion, Notch1 plays a critical role in physiologic cardiac hypertrophy through the p38 signaling pathway. Our results will help to understand the underlying mechanism of Notch1 on physiological cardiac hypertrophy.

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Yalçin, Fatih, Nagehan Kucukler, Oscar Cingolani, Blaid Mbiyangandu, Lars Sorensen, Aurelio Pinherio, M. Roselle Abraham i Theodore P. Abraham. "Evolution of ventricular hypertrophy and myocardial mechanics in physiological and pathological hypertrophy". Journal of Applied Physiology 126, nr 2 (1.02.2019): 354–62. http://dx.doi.org/10.1152/japplphysiol.00199.2016.

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Left ventricular hypertrophy (LVH) is an adaptive response to physiological or pathological stimuli, and distinguishing between the two has obvious clinical implications. However, asymmetric septal hypertrophy and preserved cardiac function are noted in early stages in both cases. We characterized the early anatomic and functional changes in a mouse model of physiological and pathological stress using serial echocardiography-based morphometry and tissue velocity imaging. Weight-matched CF-1 male mice were separated into Controls ( n = 10), treadmill Exercise 1 h daily for 5 days/wk ( n = 7), and transverse aortic constriction (TAC, n = 7). Hypertrophy was noted first in the left ventricle basal septum compared with other segments in Exercise (0.84 ± 0.02 vs. 0.79 ± 0.03 mm, P = 0.03) and TAC (0.86 ± 0.05 vs. 0.77 ± 0.04 mm, P = 0.02) at 4 and 3 wk, respectively. At 8 wk, eccentric LVH was noted in Exercise and concentric LVH in TAC. Septal E/E′ ratio increased in TAC (32.6 ± 3.7 vs. 37 ± 6.2, P = 0.002) compared with the Controls and Exercise (32.3 ± 5.2 vs. 32.8 ± 3.8 and 31.2 ± 4.9 vs. 28.2 ± 5.0, respectively, nonsignificant for both). Septal s′ decreased in TAC (21 ± 3.6 vs. 17 ± 4.2 mm/s, P = 0.04) but increased in Exercise (19.6 ± 4.1 vs. 29.2 ± 2.3 mm/s, P = 0.001) and was unchanged in Controls (20.1 ± 4.2 vs. 20.9 ± 5.1 mm/s, nonsignificant). With similar asymmetric septal hypertrophy and normal global function during the first 4–8 wk of pathological and physiological stress, there is an early marginal increase with subsequent decrease in systolic tissue velocity in pathological but early and progressive increase in physiological hypertrophy. Tissue velocities may help adjudicate between these two states when there are no overt anatomic or functional differences. NEW & NOTEWORTHY Pathological and physiological stress-induced ventricular hypertrophy have different clinical connotations but present with asymmetric septal hypertrophy and normal global function in their early stages. We observed a marginal but statistically significant decrease in systolic tissue velocity in pathological but progressive increase in velocity in physiological hypertrophy. Tissue velocity imaging could be an important tool in the management of asymmetric septal hypertrophy by adjudicating between these two etiologies when there are no overt anatomic or functional differences.

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Dobrzyn, Pawel, Aleksandra Pyrkowska, Monika K. Duda, Tomasz Bednarski, Michal Maczewski, Jozef Langfort i Agnieszka Dobrzyn. "Expression of lipogenic genes is upregulated in the heart with exercise training-induced but not pressure overload-induced left ventricular hypertrophy". American Journal of Physiology-Endocrinology and Metabolism 304, nr 12 (15.06.2013): E1348—E1358. http://dx.doi.org/10.1152/ajpendo.00603.2012.

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Cardiac hypertrophy is accompanied by molecular remodeling that affects different cellular pathways, including fatty acid (FA) utilization. In the present study, we show that cardiac lipid metabolism is differentially regulated in response to physiological (endurance training) and pathological [abdominal aortic banding (AAB)] hypertrophic stimuli. Physiological hypertrophy was accompanied by an increased expression of lipogenic genes and the activation of sterol regulatory element-binding protein-1c and Akt signaling. Additionally, FA oxidation pathways regulated by AMP-activated protein kinase (AMPK) and peroxisome proliferator activated receptor-α (PPARα) were induced in trained hearts. Cardiac lipid content was not changed by physiological stimulation, underlining balanced lipid utilization in the trained heart. Moreover, pathological hypertrophy induced the AMPK-regulated oxidative pathway, whereas PPARα and expression of its downstream targets, i.e., acyl-CoA oxidase and carnitine palmitoyltransferase I, were not affected by AAB. In contrast, pathological hypertrophy leads to cardiac triglyceride (TG) and diacylglycerol (DAG) accumulation, although the expression of lipogenic genes and the levels of FA transport proteins (CD36 and FATP) were not changed or reduced compared with the sham group. A possible explanation for this phenomenon is a decrease in lipolysis, as evidenced by the increased content of adipose triglyceride lipase inhibitor G0S2, the increased phosphorylation of hormone-sensitive lipase at Ser565, and the decreased protein levels of DAG lipase that attenuate TG and DAG contents. The increased TG and DAG accumulation observed in AAB-induced hypertrophy might have lipotoxic effects, thereby predisposing to cardiomyopathy and heart failure in the future.

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Li, Haobo, Lena E. Trager, Xiaojun Liu, Margaret H. Hastings, Chunyang Xiao, Justin Guerra, Samantha To i in. "lncExACT1 and DCHS2 Regulate Physiological and Pathological Cardiac Growth". Circulation 145, nr 16 (19.04.2022): 1218–33. http://dx.doi.org/10.1161/circulationaha.121.056850.

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Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. Methods: RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and cardiomyogenesis or transverse aortic constriction for 2 or 8 weeks to induce pathological hypertrophy or heart failure. The top lncRNA candidate was overexpressed in hearts with adeno-associated virus vectors and inhibited with antisense locked nucleic acid–GapmeRs to examine its function. Downstream effectors were identified through promoter analyses and binding assays. The functional roles of a novel downstream effector, dachsous cadherin-related 2 (DCHS2), were examined through transgenic overexpression in zebrafish and cardiac-specific deletion in Cas9-knockin mice. Results: We identified exercise-regulated cardiac lncRNAs, called lncExACTs. lncExACT1 was evolutionarily conserved and decreased in exercised hearts but increased in human and experimental heart failure. Cardiac lncExACT1 overexpression caused pathological hypertrophy and heart failure; lncExACT1 inhibition induced physiological hypertrophy and cardiomyogenesis, protecting against cardiac fibrosis and dysfunction. lncExACT1 functioned by regulating microRNA-222, calcineurin signaling, and Hippo/Yap1 signaling through DCHS2. Cardiomyocyte DCHS2 overexpression in zebrafish induced pathological hypertrophy and impaired cardiac regeneration, promoting scarring after injury. In contrast, murine DCHS2 deletion induced physiological hypertrophy and promoted cardiomyogenesis. Conclusions: These studies identify lncExACT1-DCHS2 as a novel pathway regulating cardiac hypertrophy and cardiomyogenesis. lncExACT1-DCHS2 acts as a master switch toggling the heart between physiological and pathological growth to determine functional outcomes, providing a potentially tractable therapeutic target for harnessing the beneficial effects of exercise.

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Weeks, Kate L., Yow Keat Tham, Suzan G. Yildiz, Yonali Alexander, Daniel G. Donner, Helen Kiriazis, Claudia A. Harmawan i in. "FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K". American Journal of Physiology-Heart and Circulatory Physiology 320, nr 4 (1.04.2021): H1470—H1485. http://dx.doi.org/10.1152/ajpheart.00838.2020.

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Regulators of exercise-induced physiological cardiac hypertrophy and protection are considered promising targets for the treatment of heart failure. Unlike pathological hypertrophy, the transcriptional regulation of physiological hypertrophy has remained largely elusive. To our knowledge, this is the first study to show that the transcription factor FoxO1 is a critical mediator of exercise-induced cardiac hypertrophy. Given that exercise-induced hypertrophy is protective, this finding has important implications when one is considering FoxO1 as a target for treating the diseased heart.

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Brown, Brittany F., Anita Quon, Jason R. B. Dyck i Joseph R. Casey. "Carbonic anhydrase II promotes cardiomyocyte hypertrophy". Canadian Journal of Physiology and Pharmacology 90, nr 12 (grudzień 2012): 1599–610. http://dx.doi.org/10.1139/y2012-142.

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Pathological cardiac hypertrophy, the maladaptive remodelling of the myocardium, often progresses to heart failure. The sodium–proton exchanger (NHE1) and chloride–bicarbonate exchanger (AE3) have been implicated as important in the hypertrophic cascade. Carbonic anhydrase II (CAII) provides substrates for these transporters (protons and bicarbonate, respectively). CAII physically interacts with NHE1 and AE3, enhancing their respective ion transport activities by increasing the concentration of substrate at their transport sites. Earlier studies found that a broad-spectrum carbonic anhydrase inhibitor prevented cardiomyocyte hypertrophy (CH), suggesting that carbonic anhydrase is important in the development of hypertrophy. Here we investigated whether cytosolic CAII was the CA isoform involved in hypertrophy. Neonatal rat ventricular myocytes (NRVMs) were transduced with recombinant adenoviral constructs to over-express wild-type or catalytically inactive CAII (CAII-V143Y). Over-expression of wild-type CAII in NRVMs did not affect CH development. In contrast, CAII-V143Y over-expression suppressed the response to hypertrophic stimuli, suggesting that CAII-V143Y behaves in a dominant negative fashion over endogenous CAII to suppress hypertrophy. We also examined CAII-deficient (Car2) mice, whose hearts exhibit physiological hypertrophy without any decrease in cardiac function. Moreover, cardiomyocytes from Car2 mice do not respond to prohypertrophic stimulation. Together, these findings support a role of CAII in promoting CH.

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Lv, Dongchao, Qi Sun, Yuping Deng, Jiahong Xu, Huansen Huang i Junjie Xiao. "Exercise-induced Physiological Hypertrophy: Insights from Genomics". Current Genomics 16, nr 2 (2.03.2015): 95–98. http://dx.doi.org/10.2174/1389202916999150120153618.

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Kolataj, A., Z. Reklewski, J. Dembowski, D. Tyrawska-Spychalowa i C. Dziewiecki. "Physiological aspects of muscular hypertrophy in cattle". Zeitschrift für Tierzüchtung und Züchtungsbiologie 95, nr 1-4 (26.04.2010): 222–26. http://dx.doi.org/10.1111/j.1439-0388.1978.tb01474.x.

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Kołątaj, A., A. H. Swiergiel, Cz Dziewiecki i A. M. Konecka. "Physiological aspects of muscular hypertrophy in cattle1". Zeitschrift für Tierzüchtung und Züchtungsbiologie 96, nr 1-4 (26.04.2010): 186–90. http://dx.doi.org/10.1111/j.1439-0388.1979.tb00213.x.

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Gabryelak, T., Z. Wojtkowiak, A. Kolataj i W. Leyko. "Physiological aspects of muscular hypertrophy in cattle". Zeitschrift für Tierzüchtung und Züchtungsbiologie 96, nr 1-4 (26.04.2010): 253–59. http://dx.doi.org/10.1111/j.1439-0388.1979.tb00221.x.

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KOŁATAJ, A., CZ DZIEWIȨCKI, A. S̀WIERGIEL, A. PIEKARZEWSKA i A. M. KONECKA. "Physiological aspects of muscular hypertrophy in cattle1". Zeitschrift für Tierzüchtung und Züchtungsbiologie 99, nr 1-4 (26.04.2010): 253–56. http://dx.doi.org/10.1111/j.1439-0388.1982.tb00383.x.

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Nakamura, Michinari, i Junichi Sadoshima. "Mechanisms of physiological and pathological cardiac hypertrophy". Nature Reviews Cardiology 15, nr 7 (19.04.2018): 387–407. http://dx.doi.org/10.1038/s41569-018-0007-y.

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Pretorius, Lynette, Kate L. Owen, Garry L. Jennings i Julie R. McMullen. "PROMOTING PHYSIOLOGICAL HYPERTROPHY IN THE FAILING HEART". Clinical and Experimental Pharmacology and Physiology 35, nr 4 (kwiecień 2008): 438–41. http://dx.doi.org/10.1111/j.1440-1681.2008.04893.x.

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Mone, Suzanne M., Stephen P. Sanders i Steven D. Colan. "Control Mechanisms for Physiological Hypertrophy of Pregnancy". Circulation 94, nr 4 (15.08.1996): 667–72. http://dx.doi.org/10.1161/01.cir.94.4.667.

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Whalley, Gillian A., i Robert N. Doughty. "Definition of physiological hypertrophy in ultramarathon athletes". Journal of the American College of Cardiology 44, nr 2 (lipiec 2004): 469. http://dx.doi.org/10.1016/j.jacc.2004.04.027.

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Dorn, Gerald W. "The Fuzzy Logic of Physiological Cardiac Hypertrophy". Hypertension 49, nr 5 (maj 2007): 962–70. http://dx.doi.org/10.1161/hypertensionaha.106.079426.

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Bhullar, Sukhwinder K., i Naranjan S. Dhalla. "Angiotensin II-Induced Signal Transduction Mechanisms for Cardiac Hypertrophy". Cells 11, nr 21 (22.10.2022): 3336. http://dx.doi.org/10.3390/cells11213336.

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Although acute exposure of the heart to angiotensin (Ang II) produces physiological cardiac hypertrophy and chronic exposure results in pathological hypertrophy, the signal transduction mechanisms for these effects are of complex nature. It is now evident that the hypertrophic response is mediated by the activation of Ang type 1 receptors (AT1R), whereas the activation of Ang type 2 receptors (AT2R) by Ang II and Mas receptors by Ang-(1-7) exerts antihypertrophic effects. Furthermore, AT1R-induced activation of phospholipase C for stimulating protein kinase C, influx of Ca2+ through sarcolemmal Ca2+- channels, release of Ca2+ from the sarcoplasmic reticulum, and activation of sarcolemmal NADPH oxidase 2 for altering cardiomyocytes redox status may be involved in physiological hypertrophy. On the other hand, reduction in the expression of AT2R and Mas receptors, the release of growth factors from fibroblasts for the occurrence of fibrosis, and the development of oxidative stress due to activation of mitochondria NADPH oxidase 4 as well as the depression of nuclear factor erythroid-2 activity for the occurrence of Ca2+-overload and activation of calcineurin may be involved in inducing pathological cardiac hypertrophy. These observations support the view that inhibition of AT1R or activation of AT2R and Mas receptors as well as depression of oxidative stress may prevent or reverse the Ang II-induced cardiac hypertrophy.

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Pirompol, Prapawadee, Vassana Teekabut, Wattana Weerachatyanukul, Tepmanas Bupha-Intr i Jonggonnee Wattanapermpool. "Supra-physiological dose of testosterone induces pathological cardiac hypertrophy". Journal of Endocrinology 229, nr 1 (kwiecień 2016): 13–23. http://dx.doi.org/10.1530/joe-15-0506.

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Testosterone and androgenic anabolic steroids have been misused for enhancement of physical performance despite many reports on cardiac sudden death. Although physiological level of testosterone provided many regulatory benefits to human health, including the cardiovascular function, supra-physiological levels of the hormone induce hypertrophy of the heart with unclear contractile activation. In this study, dose- and time-dependent effects of high-testosterone treatment on cardiac structure and function were evaluated. Adult male rats were divided into four groups of testosterone treatment for 0, 5, 10, and 20 mg/kg BW for 4, 8, or 12 weeks. Increases in both percentage heart:body weight ratio and cardiomyocyte cross-sectional area in representing hypertrophy of the heart were significantly shown in all testosterone-treated groups to the same degree. In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation. In contrast, pathological cardiac hypertrophy was observed in 8- and 12-week testosterone-treated groups, as indicated by suppression of myofilament activation and myocardial collagen deposition without transition of MHC isoforms. Only in 12-week testosterone-treated group, eccentric cardiac hypertrophy was demonstrated with unaltered myocardial stiffness, but significant reductions in the phosphorylation signals of ERK1/2 and mTOR. Results of our study suggest that the outcome of testosterone-induced cardiac hypertrophy is not dose dependent but is rather relied on the factor of exposure to duration in inducing maladaptive responses of the heart.

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Zang, Rongjia, Qingyun Tan, Fanrong Zeng, Dongwei Wang, Shuang Yu i Qingdong Wang. "JMJD1A Represses the Development of Cardiomyocyte Hypertrophy by Regulating the Expression of Catalase". BioMed Research International 2020 (13.05.2020): 1–14. http://dx.doi.org/10.1155/2020/5081323.

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The histone demethylase JMJD family is involved in various physiological and pathological functions. However, the roles of JMJD1A in the cardiovascular system remain unknown. Here, we studied the function of JMJD1A in cardiac hypertrophy. The mRNA and protein levels of JMJD1A were significantly downregulated in the hearts of human patients with hypertrophic cardiomyopathy and the hearts of C57BL/6 mice underwent cardiac hypertrophy induced by transverse aortic constriction (TAC) surgery or isoproterenol (ISO) infusion. In neonatal rat cardiomyocytes (NRCMs), siRNA-mediated JMJD1A knockdown facilitated ISO or angiotensin II-induced increase in cardiomyocyte size, protein synthesis, and expression of hypertrophic fetal genes, including atrial natriuretic peptide (Anp), brain natriuretic peptide (Bnp), and Myh7. By contrast, overexpression of JMJD1A with adenovirus repressed the development of ISO-induced cardiomyocyte hypertrophy. We observed that JMJD1A reduced the production of total cellular and mitochondrial levels of reactive oxygen species (ROS), which was critically involved in the effects of JMJD1A because either N-acetylcysteine or MitoTEMPO treatment blocked the effects of JMJD1A deficiency on cardiomyocyte hypertrophy. Mechanism study demonstrated that JMJD1A promoted the expression and activity of Catalase under basal condition or oxidative stress. siRNA-mediated loss of Catalase blocked the protection of JMJD1A overexpression against ISO-induced cardiomyocyte hypertrophy. These findings demonstrated that JMJD1A loss promoted cardiomyocyte hypertrophy in a Catalase and ROS-dependent manner.

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Sakamoto, Masaya, Haurhiro Toko, Yuzeng Zou, Hiroshi Akazawa, Masanori Sano, Mutsuo Harada i Issei Komuro. "Heat shock proteins are upregulated in physiological hypertrophy but not in pathological hypertrophy". Journal of Cardiac Failure 9, nr 5 (październik 2003): S40. http://dx.doi.org/10.1016/s1071-9164(03)00495-0.

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Lara-Pezzi, Enrique. "Understanding Cardiac Physiological Hypertrophy in a LncRNA Way". Journal of Cardiovascular Translational Research 15, nr 1 (luty 2022): 3–4. http://dx.doi.org/10.1007/s12265-022-10212-5.

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A. Richey, Phyllis, i Stanley P. Brown. "Pathological versus physiological left ventricular hypertrophy: A review". Journal of Sports Sciences 16, nr 2 (styczeń 1998): 129–41. http://dx.doi.org/10.1080/026404198366849.

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Abel, E. D., i T. Doenst. "Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy". Cardiovascular Research 90, nr 2 (21.01.2011): 234–42. http://dx.doi.org/10.1093/cvr/cvr015.

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Gorbenko, A. V., Yu P. Skirdenko, N. A. Nikolaev, O. V. Zamahina, S. A. Sherstyuk i A. V. Ershov. "Physiological or pathological hypertrophy of athlete’s heart syndrome". Patologiya krovoobrashcheniya i kardiokhirurgiya 24, nr 2 (3.07.2020): 16. http://dx.doi.org/10.21688/1681-3472-2020-2-16-25.

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<p>Intense physical activity increases the risk of sudden death by 10–17 fold. Some of the most important tasks of modern pathophysiology in sports medicine include searching for factors that allow an athlete’s body to adapt to loads, understanding the line between adaptation and pathology and identifying risk groups of adaptation failure. It is necessary to distinguish between hypertrophic cardiomyopathy and true myocardial hypertrophy in athletes that results from the adaptation of the cardiovascular system to intense physical exertion. In Seattle, the American Medical Society of Sports Medicine together with the European Society of Cardiology proposed standards for the interpretation of electrocardiogram in athletes and considered criteria for the detection of pathological changes. The best functional state of an athlete and the effectiveness of his/her training are noted with high autonomy and high variability of heart rate. This is reflected in rhythmocardiogram data by increases in high frequency and root mean square of successive differences in heartbeats and a decrease in the low-frequency to high-frequency ratio.<br />A promising direction in the study of markers of an athletic heart is the analysis of echocardiographic (EchoCG) images of young and professional athletes. According to EchoСG analysis, nonadaptive remodelling is the loss of the ellipsoid shape of the left ventricle in favour of a spherical one. In athletes, when assessing transmitral flow by EchoCG, a low A peak can be considered a reserve of adaptive capabilities of the heart and not a pathology. For athletes-dischargers, a concentric variant of changing the geometry of the myocardium is characteristic. Upon reaching the qualification of a candidate, master of sports<br />an eccentric change in the left ventricle cavity prevails.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</p><p><strong>Author contributions</strong><br />Conception and design: Y.P. Skirdenko <br />Drafting the article: A.V. Gorbenko, O.V. Zamahina, S.A. Sherstyuk<br />Critical revision of the article: N.A. Nikolaev<br />Final approval of the version to be published: A.V. Gorbenko, Y.P. Skirdenko, N.A. Nikolaev, O.V. Zamahina, S.A. Sherstyuk, A.V. Ershov</p>

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Ueda, Kazutaka, Haruhiro Toko i Issei Komuro. "Endothelial Cell–Derived Angiocrines Elicit Physiological Cardiomyocyte Hypertrophy". Circulation 139, nr 22 (28.05.2019): 2585–87. http://dx.doi.org/10.1161/circulationaha.119.040632.

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Dolinsky, Vernon W., Carrie-Lynn M. Soltys, Kyle J. Rogan, Anita Y. M. Chan, Jeevan Nagendran, Shaohua Wang i Jason R. B. Dyck. "Resveratrol prevents pathological but not physiological cardiac hypertrophy". Journal of Molecular Medicine 93, nr 4 (15.11.2014): 413–25. http://dx.doi.org/10.1007/s00109-014-1220-8.

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Malhotra, Aneil, i Sanjay Sharma. "Hypertrophic Cardiomyopathy in Athletes". European Cardiology Review 12, nr 2 (2017): 80. http://dx.doi.org/10.15420/ecr.2017:12:1.

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Sudden cardiac death (SCD) in a young person is a rare but tragic occurrence. The impact is widespread, particularly in the modern era of media coverage and visibility of social media. Hypertrophic cardiomyopathy (HCM) is reported historically as the most common cause of SCD in athletes younger than 35 years of age. A diagnosis of HCM may be challenging in athletes as pathological hypertrophy of the left ventricle may also mimic physiological left ventricular hypertrophy (LVH) in response to exercise. Differentiation of physiological LVH from HCM requires an array of clinical tools that rely on detecting subtle features of disease in a supposedly healthy person who represents the segment of society with the highest functional capacity. Most studies are based on comparisons of clinical tests between healthy unaffected athletes and sedentary individuals with HCM. However, data are emerging that report the clinical features of athletes with HCM. This article focuses on studies that help shed further light to aid the clinical differentiation of physiological LVH from HCM. This distinction is particularly important in a young person: a diagnosis of HCM has significant ramifications on participation in competitive sport, yet an erroneous diagnosis of physiological adaptation in a young athlete with HCM may subject them to an increased risk of SCD.

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