Made available in DSpace on 2015-07-22T20:50:32Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-03-30. Added 1 bitstream(s) on 2015-08-11T03:26:08Z : No. of bitstreams: 1 Publico-12662a.pdf: 1757646 bytes, checksum: 6d16ce4a1b202b49620fcd389bf661cb (MD5). Added 1 bitstream(s) on 2015-08-11T03:26:08Z : No. of bitstreams: 2 Publico-12662a.pdf: 1757646 bytes, checksum: 6d16ce4a1b202b49620fcd389bf661cb (MD5) Publico-12662b.pdf: 1556068 bytes, checksum: 9e7692a17342eb563d00b00cb4170335 (MD5) / As evidências científicas que se acumulam ao longo do tempo mostram o impacto positivo do exercício físico para a saúde humana, em especial para a saúde cerebral. Os efeitos como o aumento da atividade neurotrófica do BDNF e do IGF-1, devido ao exercício físico aeróbio, parecem influenciar os neurônios do hipocampo, e estão associados com a melhora do aprendizado e da memória espacial. No entanto, nada se sabe sobre a influência do exercício físico resistido na memória hipocampo-dependente, nem se as vias celulares associadas a essa melhora, pelo exercício físico aeróbio, seriam também ativadas pelo treinamento resistido. Objetivo: Verificar os efeitos dos exercícios físicos aeróbio e resistido na aprendizagem, na memória espacial e nas vias de sinalizações celulares BDNF/ TrKB e do IGF-1/ IGF-1R no hipocampo de ratos. Material e Métodos: ratos Wistar machos adultos foram distribuídos em quatro grupos (controle, CTRL; sham, SHAM; aeróbio, AERO; e resistido, RES), submetidos a oito semanas de treinamento aeróbio (esteira motorizada) ou treinamento resistido (escalada em escada com sobrecarga). Após a intervenção, observou-se que houve, em ambos os grupos AERO e RES, uma melhora da aprendizagem e da memória espacial (hipocampo-dependente), avaliada por meio do labirinto aquático de Morris. Além disto, o grupo AERO ativou mais a via BDNF/ TrKB/ CaMKII do que o RES. No entanto, este grupo ativou mais a via IGF-1/ IGF-1R/ AKT do que o grupo AERO. Apesar de os dois grupos terem aumentado a expressão da sinapsina e da sinaptofisina de forma semelhante. Conclusões: o treinamento aeróbio ou o resistido por oito semanas aumentou, de maneira similar, a aprendizagem e a memória espacial dos ratos. Embora os mecanismos moleculares pelo qual isso ocorreu, até certo ponto tenham sido divergentes. Isso porque, o exercício físico aeróbio ativou a via BDNF/TrKB/CaMKII e, o resistido a via IGF-1/IGF-1R/AKT, embora ambos, de maneira similar, tenham aumentado, no hipocampo, a expressão da sinapsina e da sinaptofisina. / A growing body of scientific evidence indicates that exercise has a positive impact on human health and on neurological health in particular. Effects such as increased BDNF and IGF-1 neurotrophic activity are induced by aerobic exercise and appear to influence hippocampal neurons, leading to improved spatial learning and memory. However, nothing is known about the effect of resistance exercise on hippocampus-dependent memory or whether the cellular pathways associated with aerobic exercise are also activated by resistance training. Objective: we therefore tested whether spatial learning and memory in rats is similarly enhanced by aerobic or resistance exercise and whether the cellular signals involved are similar, focusing on the BDNF/ TrKB and IGF-1/ IGF-1R pathways. Material and Methods: Adult male Wistar rats underwent eight weeks of aerobic training on a treadmill (AERO group) or resistance training on a vertical ladder (RES group); control and sham groups were also included. After the training period, both the AERO and RES groups showed improved learning and spatial memory. In addition, the BDNF/TrkB/CaMKII pathway had a higher activity in the AERO group than in the RES group. In contrast, the RES group showed greater activation of the IGF-1/IGF-1R/AKT pathway. Moreover, the two exercise groups had similar increases in synapsin and synaptophysin expression. Conclusions: We therefore conclude that, in rats, both aerobic and resistance training for eight weeks increases learning and spatial memory in a similar manner. However, the two forms of exercise seem to employ at least partially divergent mechanisms. Specifically, aerobic exercise modulates neuroplasticity selectively via the BDNF/TrkB pathway by activating CaMKII and stimulating the synthesis of synapsin and synaptophysin. In contrast, resistance training appears to increase synapsin and synaptophysin expression via the IGF-1/IGF-1R pathway. / TEDE / BV UNIFESP: Teses e dissertações

Made available in DSpace on 2014-12-17T14:13:33Z (GMT). No. of bitstreams: 1 RodrigoGSV_Tese.pdf: 3463456 bytes, checksum: 9ee4f593a4e49ca7d2840717243e4e47 (MD5) Previous issue date: 2009-05-15 / Changes introduced by cardiopulmonar and neuromuscular training on basal serum insulin-like grow factor-1 (IGF-1) and cortisol levels, functional autonomy and quality of life in elderly women The aim of this study was to compare the effects of strength and aerobic training on basal serum IGF-1 and Cortisol levels, functional autonomy (FA) and quality of life (QoL) in elderly women after 12 weeks of training. The subjects were submitted the strength training (75-85% 1-RM) with weight exercises (SG; n=12; age=66.08 ? 3,37 years; BMI=26,77 ? 3,72 kg/m2), aerobic training with aquatic exercises (AG; n=13; age=68,69 ? 4,70 years; BMI=29,19 ? 2,96 kg/m2) and control group (CG; n=10; age=68,80 ? 5,41 years; BMI=29,70 ? 2,82 kg/m2). Fasting blood was analyzed to measure basal IGF-1 and cortisol levels by chemiluminescence method. The t-Student test showed increased IGF-1 in the SG (p<0.05) for intragroup comparison. The Repeated-measure ANOVA presented increased IGF-1 (p<0.05) in the SG compared to the other two groups. There were no differences in cortisol levels. All the FA tests (GDLAM autonomy protocol) presented decreased significant in the time marked in seconds to the SG. The same results were found in the AG, except in the rise from a sitting position test. The autonomy index presented significant improvements (p<0.05) in the SG related to the AG and CG and in the AG to the CG. The SG showed increased QoL (p<0.05) (by WHOQOL-Old questionnaire) in the facet 1 (sensorial functioning) and facet 5 (death and dying). Thus, the SG obtained positive changes on IGF-1 and FA levels when compared to the AG. This suggests that strength training can indicated to decrease the effects of ageing. / O objetivo do estudo foi comparar os efeitos dos treinamentos de for?a e ?bico sobre os n?veis s?ricos basais de IGF-1 e Cortisol, autonomia funcional (AF) e qualidade de vida (QV) em mulheres idosas ap?s 12 semanas de treinamento. Os sujeitos foram submetidos a um treinamento de for?a (75-85% 1-RM) na muscula??o (GF; n=12; idade=66,08 ? 3,37 anos; IMC=26,77 ? 3,72 kg/m2), treinamento aer?bico na hidrogin?stica (GA; n=13; idade=68,69 ? 4,70 anos; IMC=29,19 ? 2,96 kg/m2) e um grupo controle (GC; n=10; idade=68,80 ? 5,41 anos; IMC=29,70 ? 2,82 kg/m2). A coletada de sangue foi feita em jejum para as an?lises dos n?veis de IGF-1 e Cortisol basal (M?todo Quimioluminesc?ncia). O teste t-Student mostrou aumento do IGF-1 no GF (p<0,05) na compara??o intragrupo. A ANOVA de medidas repetidas apresentou eleva??o do IGF-1 (p<0,05) no GF comparado aos demais grupos. Os n?veis de cortisol n?o apresentaram diferen?as. Todos os testes de AF (protocolo de autonomia GDLAM) apresentaram redu??es significativas nos tempos aferidos em segundos para o GF. Os mesmos resultados foram encontrados para o GA, exceto no teste levantar da posi??o sentada. O ?ndice de autonomia apresentou melhoras significativas (p<0,05) do GF para o GA e GC e do GA para o GC. O GF apresentou aumentos significativos (p<0,05) na QV (question?rio WHOQOLOld) nas facetas 1 (habilidade sens?rio) e 5 (morte e morrer). Assim, o GF obteve melhoras significativas nos n?veis de IGF-1 e de AF quando comparado ao GA. Isto sugere que o treinamento de for?a pode ser indicado para minimizar os efeitos delet?rios do envelhecimento

(EN) GH/IGF-1 axis components (GH, growth hormone receptor (GH-R), IGF-1, IGF-1 receptor (IGF-1R), IGF-binding proteins (IGFBPs)) participate in the control of glucose metabolism, inflammatory processes as well as cell proliferation and differentiation, including adipocytes and monocytes. The aim of the present study was to evaluate the role of local mRNA expression of GH/IGF-1 axis components in subcutaneous adipose tissue (SCAT) and peripheral monocytes (PM) in the development of insulin resistance and differences of adipose tissue mass in following groups of patients: obese females with and without type 2 diabetes mellitus and subjects with active untreated acromegaly. A total number of 66 subjects were included in the study: obese females without type 2 diabetes mellitus (OB), obese females with type 2 diabetes mellitus (T2DM), acromegalic patients (AC) and healthy lean control subjects (C). T2DM underwent 2 weeks of very-low- calorie diet (VLCD - energy content 2500 kJ/day). According to our results we suggest that decreased mRNA expression of IGF-1, IGF-1R, IGFBP-2 and IGFBP-3 in adipose tissue of T2DM subjects may contribute to changes of fat differentiation capacity and the increased IGF-1R mRNA expression in peripheral monocytes in these patients may play a role in the regulation of...

Sabe-se que o hipotireoidismo (Hipo) resulta em supressão do eixo hormônio de crescimento (GH)/ insulin-like growth factor I (IGF-I) e em atraso no desenvolvimento esquelético. Em um estudo anterior, vimos que o tratamento de ratas jovens Hipo com GC-1, um análogo da triiodotironina (T3) seletivo pela isoforma <font face=\"symbol\">b de receptor de hormônio tireoideano (TR<font face=\"symbol\">b), não teve efeito sobre o IGF-I sérico ou sobre a expressão protéica de IGF-I nas lâminas epifisiais, mas parcialmente reverteu alterações esqueléticas decorrentes do Hipo, o que sugere que: (i) o desenvolvimento esquelético requer ações do T3 mediadas pelo TR<font face=\"symbol\">a1 e TR<font face=\"symbol\">b1 (isoformas de TR expressas no osso); ou (ii) requer interações entre o eixo GH/IGF-I e o hormônio tireoideano. Neste estudo, investigamos essas hipóteses tratando ratas recém desmamadas Hipo com T3 ou GC-1 em associação ou não com o GH por 4 semanas. Os nossos achados mostram que o T3 e GH interagem para promover o desenvolvimento ósseo, mas que uma série de efeitos do T3 nesse processo independe do eixo GH/IGF-I e são mediadas pelo TR<font face=\"symbol\">a e/ou TR<font face=\"symbol\">b. / Thyroid hormone (TH) has important effects on bone development and metabolism. It is known that triiodotyronine (T3) has indirect actions in the skeleton through its influence on the production and secretion of growth hormone (GH)/ insulin-like growth factor (IGF-I) and/or other factors. On the other hand, direct actions of T3 on bone are recognized but not yet clear. Most of T3 action is mediaded by its nuclear receptors (TRs). TR<font face=\"symbol\">a1, TR<font face=\"symbol\">b1 e TR<font face=\"symbol\">b2 bind T3, while TR<font face=\"symbol\">a2 does not bind T3 and acts as an antagonist of genic transcription of TR<font face=\"symbol\">a1 and TR<font face=\"symbol\">b1. All these receptors, except TR<font face=\"symbol\">b2, are expressed in chondrocytes of growth plate, osteoblasts and osteoclastos. However, the functional roles of each TR isoformas in the bone development are incompletely understood. A few years, it is development GC-1, a synthetic analog of T3 which is selectivwe for TR<font face=\"symbol\">b1 over TR<font face=\"symbol\">a1. In recent study, we showed that treatment of hypothyroid young rats with T3 revert the IGF-I deficiency and skeleton defects caused by hypothyroidism. Since GC-1 treatment does not effects on serum levels of IGF-I or protein expression of IGF-I in the growth plate, but revert some bone alterations induced by T3 deficiency. Considering the selectivity of GC-1 for TR<font face=\"symbol\">b, these findings suggest that T3 has effects on bone development that are mediated by TR<font face=\"symbol\">b and independent of GH/IGF-I axis. On the other hand, the inability of GC-1 in completely revert the alterations of bone development suggests that the normal skeleton development require (i) T3 actions mediated by TR<font face=\"symbol\">a1 and TR<font face=\"symbol\">b1, or (ii) synergic or additive actions between GH/IGF-I axis and thyroid hormone. To investigate these hypotheses, 21 day-old hypothyroid female rats were treated with T3 or GC-1 in association or not with GH for 4 weeks. Our findings show that T3 interacts with GH to promote body growth, differentiation of growth plate hypertrofic chondrocytes, intramembranous ossification of cranial bone, and increased of bone resistance and other biomechanics parameters that contribute to the best bone quality. On the other hand, ours results suggest strongly that TH acts in bone mass acquisition, in organization of growth plate chondrocytes and endocondral ossification mainly independent of GH/IGF-I axis and via TR<font face=\"symbol\">a and/or TR<font face=\"symbol\">b.

(EN) GH/IGF-1 axis components (GH, growth hormone receptor (GH-R), IGF-1, IGF-1 receptor (IGF-1R), IGF-binding proteins (IGFBPs)) participate in the control of glucose metabolism, inflammatory processes as well as cell proliferation and differentiation, including adipocytes and monocytes. The aim of the present study was to evaluate the role of local mRNA expression of GH/IGF-1 axis components in subcutaneous adipose tissue (SCAT) and peripheral monocytes (PM) in the development of insulin resistance and differences of adipose tissue mass in following groups of patients: obese females with and without type 2 diabetes mellitus and subjects with active untreated acromegaly. A total number of 66 subjects were included in the study: obese females without type 2 diabetes mellitus (OB), obese females with type 2 diabetes mellitus (T2DM), acromegalic patients (AC) and healthy lean control subjects (C). T2DM underwent 2 weeks of very-low- calorie diet (VLCD - energy content 2500 kJ/day). According to our results we suggest that decreased mRNA expression of IGF-1, IGF-1R, IGFBP-2 and IGFBP-3 in adipose tissue of T2DM subjects may contribute to changes of fat differentiation capacity and the increased IGF-1R mRNA expression in peripheral monocytes in these patients may play a role in the regulation of...

L’Insulin-like growth factor-1 (IGF-1) est un peptide vasoconstricteur qui joue un rôle proéminent dans la progression des maladies cardiovasculaires, grâce à la génération d'espèces réactives de l'oxygène (ERO), ainsi que par l'hyperactivation des voies de signalisation qui promeuvent la croissance et l'expression aberrante des gènes. Les histones désacétylases (HDACs), par leur aptitude à modifier le statut d'acétylation des résidus lysine dans les protéines d'histones et non-histones, régulent la transcription des gènes. Des études récentes ont montré qu'une activation accrue des HDACs, notamment HDAC5, est associée à des troubles vasculaires tels que l'athérosclérose. Cependant, le rôle de l'IGF-1 dans l'activation des HDACs par phosphorylation demeure mal caractérisé. Donc, dans les études présentes, on a examiné l’effet de l’IGF-1 sur la phosphorylation de HDAC5 dans les cellules musculaires lisses vasculaires (CMLV) de type A10 et on a identifié les voies de signalisation impliquées dans ce processus. Le traitement des CMLV avec l’IGF-1 a augmenté la phosphorylation de HDAC5 sur la serine 498 de manière temps- et dose-dépendante. La pré-incubation des cellules avec l’AG1024, un inhibiteur pharmacologique du récepteur membranaire à l’IGF-1, a significativement atténué la phosphorylation d’HDAC5 induite par l'IGF-1. Par contre, le prétraitement avec l’AG1478, un inhibiteur du récepteur du facteur de croissance épidermique, n'a pas eu d'effet significatif sur les niveaux de phosphorylation d’HDAC5. En outre, le blocage pharmacologique de la voie MAP kinase avec divers inhibiteurs (PD98059, UO126, SP600125 et SB203580) n’a pas abrogé la phosphorylation d’HDAC5, cependant les inhibiteurs de la voie protéine kinase B (PKB)/PI3-K, SC-66 et wortmannine respectivement, ont complètement aboli la phosphorylation d’HDAC5 induite par l’IGF-1. Ces données ont été confirmées par des expériences d’immunofluorescence et de silençage génique de PKB par interférence d’ARN. En outre, le prétraitement des cellules avec le diphénylèneiodonium (DPI) et l’apocynine, deux inhibiteurs de la NAD(P)H oxydase, ainsi que l'antioxydant N-acétyl-cystéine (NAC), a atténué la phosphorylation de HDAC5 et de PKB par l’IGF-1. De plus, le silençage génique de Nox4, la principale NAD(P)H oxydase des CMLV, a atténué la phosphorylation d’HDAC5 induite par l’IGF-1. De plus, l’utilisation des techniques d’extraction nucléaire a indiqué que le SC-66 et le DPI inhibent l’exportation nucléaire de HDAC5 induit par IGF-1. En résumé, ces données suggèrent que l'IGF-1 induit la phosphorylation et l’exportation nucléaire de HDAC5 de façon ERO et PKB-dépendante dans les CMLV. / Insulin-like growth factor 1 (IGF-1), a potent mitogenic and vasoactive factor, has been shown to play a role in the development of cardiovascular diseases. This occurs through the generation of reactive oxygen species (ROS) as well as through the hyperactivation of mitogenic and growth promoting signaling pathways and the subsequent alteration in gene expression. Histone deacetylases (HDACs), by their ability to modify the acetylation status of the lysine residues in histone and non-histone proteins, regulate gene transcription. Recent studies have demonstrated that a heightened activation of HDACs, notably HDAC5, is associated with vascular disorders such as atherosclerosis. However, a role of IGF-1 in HDAC phosphorylation and activation has not been investigated. Therefore, in the present studies, we examined the effect of IGF-1 on the phosphorylation of HDAC5 in vascular smooth muscle cells (VSMCs) and identified the signaling pathways involved in this process. Treatment of A10 VSMCs with IGF-1 enhanced the phosphorylation of HDAC5 at serine 498 in a time and dosedependent fashion. Pretreatment of cells with AG1024, a selective pharmacological inhibitor of IGF-1R, significantly inhibited IGF-1-induced HDAC5 phosphorylation in A10 VSMCs whereas AG1478, a selective inhibitor of epidermal growth factor receptor (EGFR), did not have an inhibitory effect on the levels of phospho-HDAC5. Pharmacological blockade of the MAPK pathway with PD98059, UO126, SP600125 and SB203580 had no effect on HDAC5 phosphorylation, whereas inhibitors of the PI3K/ PKB pathways, wortmannin and SC-66 respectively, almost completely attenuated IGF- 1-induced HDAC5 phosphorylation. These findings were confirmed by immunofluorescence localization of phospho-HDAC5 and by siRNA-induced silencing of PKB. In addition, pretreatment of A10 VSMCs with Diphenyleneiodonium (DPI) and apocynin, two NAD(P)H oxidase inhibitors, as well as the antioxidant N-Acetyl-Cysteine (NAC), resulted in an attenuation of IGF-1-induced HDAC5 and PKB phosphorylation. Furthermore, siRNA-induced silencing of Nox4, the main NADPH oxidase expressed in VSMC, inhibited IGF-1 induced HDAC5 phosphorylation. Moreover, IGF-1-induced phosphorylation of HDAC5 resulted in its nuclear export, which was reversed by blockade of PKB by SC-66 or NAD(P)H oxidase inhibition by DPI. In summary, these data demonstrate that IGF-1 induces the phosphorylation and nuclear export of HDAC5 in a Nox4-derived ROS- and PKB-dependent fashion in VSMCs.

Un remodelage vasculaire anormal est à la base de la pathogenèse des maladies cardio-vasculaires (MCV) telles que l’athérosclérose et l’hypertension. Des dysfonctionnements au niveau de la migration, l’hypertrophie et la prolifération des cellules musculaires lisses vasculaires (CMLV) sont des évènements cellulaires qui jouent un rôle primordial dans le remodelage vasculaire. L’insulin-like growth factor 1 (IGF-1), puissant facteur mitogène, contribue au développement des MCV, notamment via l’activation des protéines MAPK et PI3-K/PKB, composantes clés impliquées dans les voies de croissance cellulaire. Ces molécules sont également impliquées dans la modulation de l’expression de nombreux facteurs de transcription, incluant le facteur Egr-1. Egr-1 est régulé à la hausse dans différents types de maladies vasculaires impliquant les voies de signalisation de croissance et de stress oxydant qui par ailleurs peuvent être déclenchées par l’IGF-1. Cependant, la question d’une possible modulation de l’expression d’Egr-1 dans les CMLV demeure inabordée; plus spécifiquement, la caractérisation de la voie de signalisation reliant l’action d’IGF-1 à l’expression d’Egr-1 reste à établir. Dans cette optique, l’objectif de cette étude a été d’examiner l’implication de MAPK, PKB et des dérivés réactifs de l’oxygène (DRO) dans l’expression d’Egr-1 induite par l’IGF-1 dans les CMLV. L’IGF-1 a induit une augmentation marquée du niveau protéique de l’Egr-1 en fonction du temps et de la concentration utilisés. Cette augmentation a été inhibée en fonction des doses d’agents pharmacologiques qui ciblent les voies de signalisation de MAPK, PKB et DRO. De plus, l’expression du facteur de transcription, Egr-1, en réponse de l’IGF-1, a été atténuée suite à un blocage pharmacologique des processus cellulaires responsables de la synthèse d’ARN et de synthèse protéique. Pour conclure, on a démontré que l’IGF-1 stimule l’expression d’Egr-1 via les voies de signalisation, impliquant ERK1/2/JNK, PI3K/PKB. On a également proposé que les DRO jouent un rôle important dans ce processus. Dans l’ensemble, nous avons suggéré un nouveau mécanisme par lequel l’IGF-1 promeut la prolifération et l’hypertrophie cellulaire, processus à la base des anomalies vasculaires. / Aberrant vascular remodelling underlies the pathogenesis of major cardiovascular diseases (CVD), such as atherosclerosis and hypertension. Abnormal growth, migration and proliferation of vascular smooth muscle cells (VSMC) are believed to play a critical role in vascular remodelling. IGF-1, potent mitogen, is believed to contribute to the development of CVD through the hyperactivation of proliferative and growth promoting pathways including mitogen-activated protein kinase (MAPK) and protein kinase B (PKB) pathways. It has also been implicated in modulating the expression of multiple transcription factors, including the early growth response protein-1 (Egr-1). Egr-1 upregulation has been observed in different models of vascular diseases implicating growth and redox signalling such as observed in response to IGF-1. However, modulation of Egr-1 expression by IGF-1 in VSMC, more specifically the signaling pathways involved in this process remain poorly characterized. Therefore, in the present studies, we investigated the implication of MAPK, PKB and ROS in IGF-1-induce Egr-1 expression in VSMC. IGF-1 induced a marked increase in Egr-1 protein level in a time and dose-dependent fashion. This increase was dose dependently inhibited by different pharmacological inhibitors targeting MAPK, PKB and reactive oxygen species (ROS) generation. Furthermore, pharmacological inhibitors of RNA and protein synthesis also attenuated IGF-1-induce response on Egr-1 expression. In conclusion, we showed that IGF-1 stimulates the expression of Egr-1 through ERK1/2/JNK and PI3K/PKB. We also propose that ROS generation plays an important role in this response. Overall, we propose a novel mechanism through which IGF-1 may exert its deleterious responses in vascular abnormalities.

Hormonal aspects of antler growth regulation Erika Kužmová Abstract Deer antlers are the only mammalian organ that completely regenerates and therefore they became an object of rising interest as a potential model for bone growth and development. In recent years, it has been confirmed that annual regeneration of the antler is initiated from the stem cell niche localised in the pedicle periosteum. Antlers grow to the length at the tip. Only a little is known about endocrine stimulation of antler growth and some discrepancy has arisen between in vivo and in vitro studies over the decades. As the secondary sexual character, the antler cycle timing and growth are linked to seasonal levels of testosterone. Since the levels are at their minimum during the antler growth phase, according to many mainly in vitro studies, insulin-like growth factor-1 (IGF-1) tends to be accepted as the "antler stimulating hormone". Since the conclusion about the role of IGF-1 was contradictory to previous opinions and also in contrast with our own experience, we aimed to verify the role of IGF-1 in vitro. Our ex- periments were based on existing in vivo studies demonstrating the importance of testosterone, even in its low levels, and on the hypothesis that testosterone should be the "antler stimulating hormone". We performed in vitro...

<p>Rapporten laddas upp av lärare om detta godkänns av handledare.</p>

Os hormônios de crescimento, principalmente os do eixo GH/IGF-I são responsáveis pelo crescimento tecidual e estrutural desde o nascimento. O GH produzido na hipófise é um hormônio com funções metabólicas e anabólicas e é o principal estimulador da síntese e liberação do IGF-I no fígado que tem suas ações endócrinas, parácrinas e autócrinas mediadas pelas IGFBPs. O exercício físico está intimamente ligado à função anabólica, estimulando a secreção e a ação dos hormônios do eixo GH/IGF-I.Existe a hipótese de haver um comportamento bifásico do eixo durante uma temporada de treinamento,caracterizado por uma fase catabólica, seguida de uma fase anabólica dependendo das fases do treinamento, porém vários estudos têm resultados controversos. O objetivo desse projeto foi investigar o impacto de uma temporada de treinamento em atletas de voleibol sobre o eixo GH/IGF-I e IGFBP-3 e sua relação com desempenho em testes físicos. A amostra foi composta por 10 jogadores de Voleibol categoria adulto da equipe de Franca-SP que foram analisados no início(A1), durante(A2) e ao final(A3) de 15 semanas de treinamento. Foram analisados dados antropométricos, altura de salto e potência de membros inferiores no Squat Jump (SJ), Counter Moviment Jump(CMJ)e Drop Jump 40 cm (DJ40), Índice de Força Reativa (IFR), Razão de Utilização Excêntrica (RUE) e concentrações deIGF-I e IGFBP-3. Para as análises estatísticas foram utilziadas ANOVA de medidas repetidas, Magnitude de Efeito (ES) e Probabilidade Quantitativa de Chances (QC). Os resultados mostram redução dos valores de Massa Coporal Total (MCT), Percentual de Gordura Coporal (%GC), Massa Magra (MM) e Massa Gorda (MG), com menor valor em A3, os resultados dos saltos apresentaram aumento linear com diferença estatísitca (p < 0,05) no DJ40 em A3. A sessão de treino não teve influência sobre as concentrações de IGF-I e IGFBP-3, indicando que a intensidade de disputa dessa modalide não é capaz de alterar as concentrações desses hormônios. Não foi verificada diferença estatísitca (p < 0,05) entre as coletas durante o período de treinamento, mas, as análises de ES e QC indicam tendência de aumento do IGF-I em A3. O comportamento bifásico do eixo GH/IGF-I não foi observado nesse estudo, possivelmente devido a forma de planejamento do período de treinamento, contudo, o IGF-I apresentou maiores concentrações em A3 coincidindo com os maiores resultados de altura de salto. Com esses resultados foi possível inferir que a concentração de IGF-I está correlacionada positivamente com o desempenho físico de atletas de voleibol e que a redução ou a incapacidade de aumento de IGF-I pode ser um sinal de alerta para atletas e treinadores. Ainda assim, são necessários novos estudos para investigar se o treinamento terá efeitos semelhantes durante longos períodos de treinamento, períodos de treinamento com maior intensidade, diferentes fases durante o período de preparação ou competição produzirão respostas hormonais semelhantes / Growth hormones, especially the GH/IGF-I axis is responsible for tissue and structural growth from birth. GH produced in the pituitary gland is a hormone with metabolic and anabolic functions and is the main stimulator for the synthesis and release of IGF-I in the liver that has its endocrine, paracrine and autocrine actions mediated by IGFBPs. Physical exercise is closely linked to anabolic function, stimulating the secretion and action of the hormones of the GH/IGF-I axis. There is a hypothesis of a biphasic behavior of the axis during a training season, characterized by a catabolic phase, followed by an anabolic phase depending on the training phases, but several studies have controversial results. The objective of this project was to investigate the impact of a training season on volleyball athletes on the GH/IGF-I axis and IGFBP-3 and its relation to performance in physical tests. The sample consisted of 10 adult category Volleyball players from the Franca-SP team who were analyzed at baseline (A1), during (A2) and at the end (A3) of 15 weeks of training. Anthropometric data, jump height and power of lower body in Squat Jump (SJ), Counter Movement Jump (CMJ) e Drop Jump 40 cm (DJ40), Reactive Force Index (RFI), Eccentric Usability Ratio (EUR) and IGF-I and IGFBP-3 concentrations were analyzed. Statistical analyzes were performed using repeated measures ANOVA, Effect Size test (ES) and Probability of Quantitative Chances(QC). The results show a reduction in Total Body Mass (TBM) values, Percentage of Body Fat (%BF), Lean Mass (LM) and Fat Mass (FM), with a lower value in A3, the jump results showed a linear increase with a statistical difference (p <0.05) in DJ40 in A3. The training session had no influence on the concentrations of IGF-I and IGFBP-3, indicating that the intensity of contention of this modality is not able to alter the concentrations of these hormones. There was no statistically significant difference (p <0.05) between the collections during the training period, but the ES and QC analyzes indicated an upward trend in IGF-I in A3. The biphasic behavior of the GH/IGF-I axis was not observed in this study, possibly due to the planning of the training period, however, IGF-I presented higher concentrations in A3 coinciding with higher jump height results. With these results it was possible to infer that the concentration of IGF-I is positively correlated with the physical performance of volleyball athletes and that the reduction or inability to increase IGF-I may be a warning signal for athletes and coaches. Still, further studies are needed to investigate whether training will have similar effects during long periods of training, more intense training periods, different phases during the preparation or competition period will produce similar hormonal responses.