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Artykuły w czasopismach na temat "Physiological hypertrophy"
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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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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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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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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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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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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.
Pełny tekst źródłaRozprawy doktorskie na temat "Physiological hypertrophy"
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Crampton, Matthew S., i n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy". Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.
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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
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Crampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Pełny tekst źródłaStreszczenie:
Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
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Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy". Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.
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Abstract :Cardiac hypertrophy has been identified as the most important independent risk factor
for cardiovascular-related morbidity and mortality and is therefore regarded as
a pathological condition. Despite this, beneficial physiological forms also appear to
exist, such as in response to exercise, leading to maintained or improved cardiac
function. The aim of this thesis was to examine two distinct rodent models, an endurance
run-trained rat, and the DOCA-salt hypertensive rat, representing physiological
and pathological hypertrophy, respectively, in order to develop a better understanding
of the molecular changes associated with each condition. The thesis also examined
the effect of dietary supplementation of L-arginine to the pathological model,
a treatment that has been shown to ameliorate/prevent many of the cardiovascular
impairments. Studies examined selected candidate genes (qRT-PCR), including conventional
biomarkers of hypertrophy and exploratory analysis of adenosine-related
genes (given adenosine’s established regulatory and protective role in the heart, yet
minimally studied in cardiac hypertrophy), and explored global transcriptomic shifts
via microarrays. The hypothesis of this work was that cardiac hypertrophy lies on
a continuum, with similarities existing at the cardiac transcriptional level between
early (adaptive) stages of pathological hypertrophy (DOCA-salt rat) and later stages
of physiological hypertrophy (endurance run-trained rat).
Examination of ten biomarkers of hypertrophy (ANF, BNP, -MHC, -MHC, cardiac
-actin, skeletal -actin, SERCA2, PPAR, Coll I and III) revealed that the pathological
model displayed alterations in the expression of many of these molecules in
line with the literature. These changes were not observed in the physiological model.
This therefore reinforces the value of conventional biomarkers in delineating pathological
vs. physiological hypertrophies, and reveals fundamental differences in genesis
of these two forms of hypertrophy.
The adenosine system (receptors and purine handling molecules) was altered in
the pathological hypertrophy model as evidenced by the modulation of genes corresponding
to A3AR, Ada, and Adk, with a potential shift from purine salvage towards
degradation of adenosine to inosine. Furthermore, this study represents the
first report of altered regulation of the nucleoside transporter ENT3 in a pathological
condition. None of these changes were seen in the physiological model with only
modulation of the A2aAR evident.
Examination of the transcriptional response to physiological hypertrophy revealed
that short (6 week) and long (12 week) training programmes resulted in different profiles,
likely reflecting progression of the hypertrophy process. The short programme
stimulated genes associated with the mitochondria, oxidoreductase, receptor binding
and coenzymemetabolismand repressed the expression of transcripts associated with
phosphorylation, catalytic activity, defence/immunity and energy pathways. Thus,
initial changes observed are primarily of a metabolic and signalling nature. In contrast,
the longer programme resulted in shifts in protein handling and synthesis, and
genes involved in structural molecule activity, nucleotide binding and cellular homeostasis.
These patterns support a progression with time from initial metabolic adaptations
to longer term shifts in protein phenotype and structural adaptations, consistent
with longer term changes in heart structure.
Similarly, the pathologicalmodel displayed different time-dependent gene expression
profiles. Overall, the pattern of changewith early (2week) treatment is suggestive
of changes in intracellular signalling and increasing transcriptional capacity with the
later changes (at 4 weeks) indicative of structural adaptations (intra- and extracellularly)
togetherwith an inflammation response. Genes coding for calciumhandling, ion
channels, and gap junctions were altered throughout themodel andmay contribute to
electrical conduction defects and cardiac dysfunction. The adrenergic signalling pathway
was modulated as associated signalling molecules were down-regulated. The
study revealed many expected and novel changes, of which further study should focus
on: calcium regulation, metabolic regulation, gap junctions, and (as might be exii
pected) signalling via the adrenergic pathway, insulin-like growth factor, PI3K, and
Jak/STAT.
L-Arginine modulated biomarker expression in pathological hypertrophy, with
stimulation of PPAR and SERCA2 with little or no effect on the adenosine-related
genes. L-Arginine affected the overall transcriptional response to DOCA-salt treatment,
stimulating genes involved in cell growth andmaintenance, nerve transmission,
heparin and glycosaminoglycan binding, peptide binding and protein targeting, as
well as the repression of genes related to apoptosis (favouring a pro-apoptotic state),
intracellular organisation and biogenesis, and enzyme inhibitor activity. The beneficial
effects of L-arginine in the setting of pathological hypertrophy may be due to
modulation of metabolism, improving calcium handling and overall enhancing cellular
functioning.
This work demonstrates that cardiac hypertrophy is clearly different at the transcriptional
level depending upon the aetiology. This repudiated the hypothesis of the
thesis that cardiac hypertrophy lies on a continuum with similarities existing at the
cardiac transcriptional level between early (adaptive) stages of pathological hypertrophy
and later stages of physiological hypertrophy. Whilst some of the data was in accordance
with current knowledge of these states, novel changes were also discovered,
contributing to our understanding of the molecular aspects of cardiac hypertrophy.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
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McMahon, Gerard. "The physiological and biomechanical bases of muscular hypertrophy/atrophy". Thesis, Manchester Metropolitan University, 2013. http://e-space.mmu.ac.uk/314030/.
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Introduction: The aims of the current investigations were to modulate muscle-tendon complex (MTC - vastus lateralis [VL] & patella tendon [PT]) adaptations through mechanical stress and strain. Groups performed resistance training (8 weeks) with the MTC placed in a shortened (SL) or a lengthened position (LL) with internal loading standardised. A third group trained over an entire ROM (LX) with the external loading matched to that in SL. MTC response to detraining (4 weeks) was also measured. A control, untrained group was measured during this 12-week period. Methods: Measurements using ultrasonography, dynamometry, electromyography and dual energy absorptiometry were made at baseline (week 0), post-training (week 8), detraining 1 (week 10) and detaining 2 (week 12). VL measurements included volume, cross-sectional area (CSA), and architecture. PT properties included stiffness and Young’s Modulus. Quadriceps MTC function was measured by isometric maximal voluntary contractions (MVC) over a range of joint –angles. Circulating levels of a growth factor (IGF-I) and cytokines (TGF-β1, TNF-α) were measured using enzyme-linked immuno-sorbant assay. Main Results: VL volume, CSA, fascicle length, PT stiffness, modulus, quadriceps MVCs and IGF-I (LL only) were significantly greater (p<0.05) in both LL and LX groups compared to SL post-training. During detraining, CSA, fascicle length, stiffness, modulus, IGF-I (LL only) remained significantly elevated in the LL and LX groups compared to SL. There was no significant change in the control group in any measurement during the study period (p>0.05). Conclusion: Training with the MTC in a lengthened position is more effective for inducing (and retaining) enhanced training MTC adaptations, owing to internal mechanical and physiological stress in this position. This loading method should therefore be incorporated into a structured resistance training program for a range of populations such as athletic, recreationally active, clinical or elderly individuals.
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Sculthorpe, Nicholas. "Left ventricular long axis dynamics in pathological and physiological left ventricular hypertrophy". Thesis, University of South Wales, 2002. https://pure.southwales.ac.uk/en/studentthesis/left-ventricular-long-axis-dynamics-in-pathological-and-physiological-left-ventricular-hypertrophy(eeeb9f18-b0d5-433b-b261-2907df223717).html.
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Sub-endocardial fibres line the inner surface of both ventricles and are responsible for longitudinal oscillations of the mitral annulus, such oscillations may be measured using tissue Doppler echocardiography (IDE). During systole the annulus descends and during early diastole (ETDE) and atrial systole (ATDE) itascends. This thesis examined whether changes in the velocity of the annulus ineach of these phases of oscillation, measured using tissue Dopplerechocardiography (TDE), could determine the nature of increases in left ventricular size (pathological or physiological). Study one examined differences at rest in longitudinal velocities between individuals with hypertrophic cardiomyopathy (HCM), hypertension (HT), weightlifters, runners and controls, (n = 15 all groups) and all groups were aged between 20 - 36 years. The results demonstrated that both pathological groups had systolic and ETDE velocities significantly lower than groups with physiological hypertrophy (weightlifters or runners) or controls p < 0.05. AIDE however was not significantly different between groups. Additionally runners also demonstrated a significantly higher ETDE than either weightlifters or controls (p < 0.05). Binomial logistic regression identified longitudinal systolic velocity < 9 cm s" 1 and ETDE velocity < 11 cm s" 1 as the best combination of variables to predict pathological increases in heart size. Study two examined older subjects in order to determine whether the criteria set out in study one were applicable to senior athletes. The subject groups were the same as in study one however all subjects were aged between 36-55. In this case systolic annular velocity was significantly lower in groups with pathological LVH but ETDE < 9 cm s" 1 was a better differentiator. Binomial logistic regression identified ETDE < 9 cm s" 1 and a mitral E / A ratio < 1 as the best combination of variables to predict pathological LVH. Study three examined the age related changes in long axis function using the pooled data from studies one and two. This demonstrated that in the pathological LVH groups only ETDE / ATDE ratio was significantly correlated with age (r = - 0.5 p < 0.05) suggesting that there appears to be no summation of the effects of pathology and age on mitral annular velocities. The control groups demonstrated a significant age related reduction in all long axis variables (systolic velocity r = - 0.7 p < 0.05; ETDE r = - 0.6 p < 0.01; ATDE r = 0.5 p < 0.05; ETD E / ATDE r = - 0.5 p< 0.01). Weightlifters however did not demonstrate an age related decline in either systolic or diastolic annular velocities. Runners had no age related decline in systolic annular velocities, and whilst they had an age dependent fall in ETDE ( r = - 0.62 p < 0.05) the older runners ETDE were still significantly faster (p < 0.05) than that seen in control subjects. Study four investigated relationship between mitral annular velocity and VOiruK in runners, weightlifters and controls. These results demonstrated peak exercise E TDE strongly correlated to VO^PEAK (r = 0.8 p < 0.01). ConclusionsTaken together these data suggest that longitudinal velocities of the mitral annulus may be useful in determining the nature of increases in heart size, in addition the increased performance of endurance - trained athletes is due in part to functional changes of the long axis.
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Kim, Jeong-Su. "The relationship of growth factor and muscle soreness to muscle hypertrophy". Virtual Press, 1998. http://liblink.bsu.edu/uhtbin/catkey/1101585.
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The purpose of the present study was to examine the relationship between exercise induced muscle damage and growth factors during two different modes of exercise. Nine healthy untrained male subjects participated in this study and performed two separate single bouts of isokinetic concentric (Con) and eccentric (Ecc) leg extension exercise on the CYBEX NORMT°". The workload was maintained at 75% of 1 RM for each trial, respectively. The maximum sets of 10 repetitions were performed during the Con trial, and the number was also duplicated during the Ecc trial, with 40 seconds of rest between sets. Serum levels of hGH, creatine kinase (CK), and lactic acid were measured, and the CK level was used to determine the degree of muscle tissue damage. A muscle soreness questionnaire was provided to the subjects to assess the degree of quadriceps muscle soreness following each trial. The EMG activity of the rectus femoris and vastus medialis muscles was recorded during each trial. The results of the present study demonstrated no significant differences in hGH output and CK activity between the exercise trials, although there was a significant different lactic acid response (P < 0.05). However, the Con trial produced significant increases (P < 0.05) in hGH and CK levels above the resting value at the post-exercise times. In fact, the 75% Con trial conducted in this study induced an increase in hGH release (peak: 8.23 ± 3.21 ng/ml) that was 2 X higher than a 120% Ecc trial (peak: 3.8 ± 1.2 ng/mI) of the prior study. The results of the present study demonstrate that a single bout of Con resistance exercise at the same intensity (75% of 1 RM), angular velocity, and ROM as a single bout of Ecc exercise can produce greater increases in hGH output and CK response than its Ecc counterpart. This finding does not support the previous results from this laboratory, showing that Ecc exercise is a stronger promoter of hGH output. However, it suggests that the amount of work performed is an important factor for hGH release because the exercise volume applied in the present study was greater than that of the prior study. The CK response of the subjects in this study, as well as the previous work indicate that hGH output is also dependent on exercise that elicits muscle damage. Therefore, the results of the present study suggest that the mode of exercise, Con vs. Ecc, is not as important as the stress placed on the exercising muscle in order to induce optimal muscle hypertrophy.School of Physical Education
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Arthur, Gavin Donald. "Calcium activated neutral protease : defining a physiological role in the development of cardiac hypertrophy". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0027/NQ48598.pdf.
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Pugh, Jamie K. "Physiological responses to concurrent resistance exercise and high-intensity interval training : implications for muscle hypertrophy". Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/25092.
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Wansapura, Arshani N. "The role of alpha Na,K-ATPase isoforms in mediating cardiac hypertrophy in response to endogenous cardiotonic steroids". University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1282577884.
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Kirby, Tyler. "GLOBAL-SCALE ANALYSIS OF THE DYNAMIC TRANSCRIPTIONAL ADAPTATIONS WITHIN SKELETAL MUSCLE DURING HYPERTROPHIC GROWTH". UKnowledge, 2015. http://uknowledge.uky.edu/physiology_etds/22.
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Skeletal muscle possesses remarkable plasticity in responses to altered mechanical load. An established murine model used to increase mechanical load on a muscle is the surgical removal of the gastrocnemius and soleus muscles, thereby placing a functional overload on the plantaris muscle. As a consequence, there is hypertrophic growth of the plantaris muscle. We used this model to study the molecular mechanisms regulating skeletal muscle hypertrophy.
Aged skeletal muscle demonstrates blunted hypertrophic growth in response to functional overload. We hypothesized that an alteration in gene expression would contribute to the blunted hypertrophic response observed with aging. However, the difference in gene expression was modest, with cluster analysis showing a similar pattern of expression between the two groups. Despite ribosomal protein gene expression being higher in the aged group, ribosome biogenesis was significantly lower in aged compared with young skeletal muscle in response to the hypertrophic stimulus (50% versus 2.5-fold, respectively). The failure to fully up-regulate pre-47S ribosomal RNA (rRNA) expression in old skeletal muscle undergoing hypertrophy indicated ribosomal DNA transcription by RNA polymerase I was impaired. Contrary to our hypothesis, the findings of the study suggest that impaired ribosome biogenesis was a primary factor underlying the blunted hypertrophic response observed in old skeletal muscle rather than dramatic differences in gene expression.
As it appears ribosomal biogenesis may limit muscle hypertrophy, we assessed the dynamic changes in global transcriptional output during muscle hypertrophy, as the majority of global transcription is dedicated to ribosome biogenesis during periods of rapid growth. Metabolic labeling of nascent RNA using 5-ethynyl uridine permitted the assessment of cell type specific changes in global transcription and how this transcription is distributed within the myofiber. Using this approach, we demonstrate that myofibers are the most transcriptionally active cell-type in skeletal muscle, and furthermore, myonuclei are able to dramatically upregulate global transcription during muscle hypertrophy. Interestingly, the myonuclear accretion that occurs with hypertrophy actually results in lower transcriptional output across nuclei within the muscle fiber relative to sham conditions. These findings argue against the notion that nuclear accretion in skeletal muscle is necessary to increase the transcriptional capacity of the cell in order to support a growth response.
Książki na temat "Physiological hypertrophy"
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The effect of training volume on strength and hypertrophy of the quadriceps and hamstring muscles. 1994.
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Zoccali, Carmine, Davide Bolignano i Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.
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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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Left ventricle size in weight lifters using anabolic steroids. 1988.
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Left ventricle size in weight lifters using anabolic steroids. 1986.
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Myocardial structure and function differences between steroid using and non-steroid using elite powerlifters and endurance athletes. 1989.
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Myocardial structure and function differences between steroid using and non-steroid using elite powerlifters and endurance athletes. 1992.
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The effects of age and exercise training on size and composition of rat left main coronary artery. 1988.
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The effects of age and exercise training on size and composition of rat left main coronary artery. 1988.
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The effect of habitual physical activity on left ventricular end diastolic diameter and left ventricular posterior wall thickness: In postmenopausal women as measured by M-mode echocardiography. 1987.
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The effect of habitual physical activity on left ventricular end diastolic diameter and left ventricular posterior wall thickness: In postmenopausal women as measured by M-mode echocardiography. 1987.
Znajdź pełny tekst źródłaCzęści książek na temat "Physiological hypertrophy"
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Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis i in. "Physiological Cardiac Hypertrophy". W Encyclopedia of Exercise Medicine in Health and Disease, 711. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2877.
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Kalmar, Jayne M., Brigid M. Lynch, Christine M. Friedenreich, Lee W. Jones, A. N. Bosch, Alessandro Blandino, Elisabetta Toso i in. "Cardiac Hypertrophy, Physiological". W Encyclopedia of Exercise Medicine in Health and Disease, 171–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_39.
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Cuspidi, Cesare, Laura Lonati, Lorena Sampieri, Gastone Leonetti i Alberto Zanchetti. "Physiological Versus Pathological Hypertrophy". W Advances in Experimental Medicine and Biology, 145–58. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5385-4_16.
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Jacob, R., M. Vogt i H. Rupp. "Physiological and Pathological Hypertrophy". W Developments in Cardiovascular Medicine, 39–56. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2051-7_2.
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Pluim, B. M., A. van der Laarse i E. E. van der Wall. "The Athlete’s Heart: A Physiological or a Pathological Phenomenon?" W Left Ventricular Hypertrophy, 85–106. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_7.
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Malhotra, Aneil, i Sanjay Sharma. "Distinguishing Physiological Left Ventricular Hypertrophy from Hypertrophic Cardiomyopathy in Athletes". W IOC Manual of Sports Cardiology, 439–48. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119046899.ch40.
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Wang, Lijun, Jiaqi Wang, Guoping Li i Junjie Xiao. "Non-coding RNAs in Physiological Cardiac Hypertrophy". W Advances in Experimental Medicine and Biology, 149–61. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1671-9_8.
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Merello, Giacomo, Luna Cavigli i Flavio D’Ascenzi. "Physiological Versus Pathological Left Ventricular Hypertrophy in the Hypertensive Athlete". W Exercise, Sports and Hypertension, 101–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07958-0_7.
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Laks, Michael M. "Potential Role of Catecholamines in the Production of Physiological and Pathological Hypertrophy". W Developments in Cardiovascular Medicine, 57–72. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2051-7_3.
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Laks, M. M. "The Effects of Chronic Infusion of Norepinephrine on Cardiac Structure, Function and Biochemistry — Physiological vs. Pathological Hypertrophy". W Developments in Cardiovascular Medicine, 14–30. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2621-2_2.
Pełny tekst źródłaStreszczenia konferencji na temat "Physiological hypertrophy"
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Hyekyeong Kwon, Jang-Soo Chun, Zee-Yong Park i Dong-Yu Kim. "Poster title (mass spectrometric protein profiling analyses of pathological and physiological hypertrophy cardiac muscle tissues)". W 2012 IEEE 2nd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2012. http://dx.doi.org/10.1109/iccabs.2012.6182652.
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Baicu, Catalin F., i Michael R. Zile. "Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells". W ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23158.
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Abstract Pathological processes which cause diastolic congestive heart failure (CHF), such as pressure overload hypertrophy (POH), produce abnormalities in the material properties of cardiac muscle cells (cardiomyocytes) and may selectively alter its elastic stiffness, viscosity, or both. Previous methods used to characterize these cardiomyocyte viscoelastic properties were constrained by specific biological and engineering limitations, which prevented testing in conditions that mimic normal physiology. The current study proposes an uniaxial variable-rate stretching method, in which isolated cardiomyocytes embedded in a three-dimensional gel matrix were subjected to stretch. Physiological Ca++ (2.5 mM) and rapid stretch rates up to 100 μm/sec provided experimental conditions parallel to in vivo physiology. The proposed method identified and individually quantified both cellular stiffness and viscosity, and showed that POH increased both elastic and viscous cardiomyocyte diastolic properties.
Raporty organizacyjne na temat "Physiological hypertrophy"
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Yahav, Shlomo, John McMurtry i Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.
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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Yahav, Shlomo, John Brake i Orna Halevy. Pre-natal Epigenetic Adaptation to Improve Thermotolerance Acquisition and Performance of Fast-growing Meat-type Chickens. United States Department of Agriculture, wrzesień 2009. http://dx.doi.org/10.32747/2009.7592120.bard.
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: The necessity to improve broiler thermotolerance and performance led to the following hypothesis: (a) thethermoregulatory-response threshold for heat production can be altered by thermal manipulation (TM) during incubation so as to improve the acquisition of thermotolerance in the post-hatch broiler;and (b) TM during embryogenesis will improve myoblast proliferation during the embryonic and post-hatch periods with subsequent enhanced muscle growth and meat production. The original objectives of this study were as follow: 1. to assess the timing, temperature, duration, and turning frequency required for optimal TM during embryogenesis; 2. to evaluate the effect of TM during embryogenesis on thermoregulation (heat production and heat dissipation) during four phases: (1) embryogenesis, (2) at hatch, (3) during growth, and (4) during heat challenge near marketing age; 3. to investigate the stimulatory effect of thermotolerance on hormones that regulate thermogenesis and stress (T₄, T₃, corticosterone, glucagon); 4. to determine the effect of TM on performance (BW gain, feed intake, feed efficiency, carcass yield, breast muscle yield) of broiler chickens; and 5. to study the effect of TM during embryogenesis on skeletal muscle growth, including myoblast proliferation and fiber development, in the embryo and post-hatch chicks.This study has achieved all the original objectives. Only the plasma glucagon concentration (objective 3) was not measured as a result of technical obstacles. Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” In order to sustain or even improve broiler performance, TM during the period of embryogenesis when satellite cell population normally expand should increase absolute pectoralis muscle weight in broilers post-hatch. Major conclusions: Intermittent TM (39.5°C for 12 h/day) during embryogenesis when the thyroid and adrenal axis was developing and maturing (E7 to E16 inclusive) had a long lasting thermoregulatory effect that improved thermotolerance of broiler chickens exposed to acute thermal stress at market age by lowering their functional Tb set point, thus lowering metabolic rate at hatch, improving sensible heat loss, and significantly decreasing the level of stress. Increased machine ventilation rate was required during TM so as to supply the oxygen required for the periods of increased embryonic development. Enhancing embryonic development was found to be accomplished by a combination of pre-incubation heating of embryos for 12 h at 30°C, followed by increasing incubation temperature to 38°C during the first 3 days of incubation. It was further facilitated by increasing turning frequency of the eggs to 48 or 96 times daily. TM during critical phases of muscle development in the late-term chick embryo (E16 to E18) for 3 or 6 hours (39.5°C) had an immediate stimulatory effect on myoblast proliferation that lasted for up to two weeks post-hatch; this was followed by increased hypertrophy at later ages. The various incubation temperatures and TM durations focused on the fine-tuning of muscle development and growth processes during late-term embryogenesis as well as in post-hatch chickens.