Dissertations / Theses on the topic 'Hypertrofia'

Abstract Heart failure (HF) is a complex pathological state, involving simultaneous alterations in several signalling pathways and changes in gene programming. In HF, activation of the neurohumoral factors and renin-angiotensin-aldosterone (RAA) system occurs as a compensatory mechanism to combat the abnormal ventricular function. Developments in cardiac gene delivery methods have exerted a significant impact to treat HF and to discover the novel molecular mechanisms associated with HF and other cardiac diseases. This study demonstrated that adenovirus–mediated gene delivery of B-type natriuretic peptide (BNP) into the anterior wall of the left ventricle decreased myocardial fibrosis and increased capillary density. Post-infarction BNP improved systolic function associated with normalization of cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA) 2 expression and phospholamban phosphorylation at Thr17. On the other hand, (Pro)renin receptor ([P]RR) gene delivery resulted deleterious effects on cardiac function and (P)RR activation induced distinct angiotensin II (Ang II)-independent extracellular matrix remodelling and worsening of cardiac function. (P)RR gene delivery resulted in Ang II-independent activation of extracellular-signal regulated (ERK1/2) phosphorylation and increased myocardial fibrosis. In conclusion, the present study indicates that myocardial BNP gene delivery can achieve pleiotropic, context-dependent, favourable effects on cardiac function and that BNP can act locally as a mechanical load–activated regulator of angiogenesis and fibrosis. These results also implicate that (P)RR blockers may display additional cardiac effects in addition to its ability to evoke effective RAA system blockade. Overall, the findings of this study provide a better understanding of the molecular mechanisms involved in the biological actions of BNP and (P)RR, and identify BNP and (P)RR as potential novel drug targets for the treatment of HF<br>Tiivistelmä Neuroendokriinisellä aktivaatiolla, jonka seurauksena aiheutuu muun muassa verisuonten supistumista ja laajenemista sekä nesteen kertymistä elimistöön, on tärkeä merkitys sydämen vajaatoiminnan kehittymisessä. Neuroendokriininen aktivaatio kompensoi sydämen vajaatoiminnan seurauksena tapahtuvaa kammioiden poikkeavaa toimintaa. Yksi keskeisimmistä verisuonia supistavista tekijöistä on reniini-angiotensiini-aldosteroni (RAA) -järjestelmä, ja verisuonia laajentaviin tekijöihin kuuluvat muun muassa natriureettiset peptidit, kuten B-tyypin natriureettinen peptidi (BNP) ja A-tyypin natriureettinen peptidi. Geeninsiirtomenetelmillä on ollut merkittäviä vaikutuksia uusien hoitomenetelmien kehittämisessä, sydämen vajaatoiminnan syiden selvittämisessä ja uusien kohdegeenien tunnistamisessa sydämen vajaatoiminnan hoitoon. Väitöskirjan tutkimustulokset osoittivat, että suora adenovirusvälitteinen geeninsiirto rotan sydämen vasemman kammion etuseinään on toimiva menetelmä uusien kohdegeenien löytämiseksi sydämen vajaatoiminnan hoitoon. BNP:n geeninsiirto vähensi merkitsevästi fibroosin muodostumista ja lisäsi verisuonten uudismuodostumista sydämessä. Sydäninfarktin jälkeen BNP paransi sydämen systolista toimintaa, johon liittyi aktiivisen kalsiumpumpun, SERCA2:n ja fosfolambaani-proteiinin fosforylaation normalisoituminen. (Pro)reniini reseptorin ([P]RR) geeninsiirto aiheutti angiotensiini II:sta riippumatonta solunulkoisen matriksin uudelleenmuotoutumista ja sydämen toiminnan huonontumista sekä lisääntynyttä sydämen fibroosia. Väitöskirjatutkimus antaa uutta tietoa solunsisäisistä molekulaarisista mekanismeista sydänsoluissa. BNP geeninsiirto aiheutti sydämen tautitilasta riippuvia suotuisia tapahtumia, ja se toimi paikallisesti muun muassa fibroosia ehkäisevänä tekijänä. (P)RR geeninsiirtotulosten perusteella voidaan olettaa, että (P)RR:n salpaus saattaa olla uusi tehokas hoitokeino sydämen vajaatoiminnan hoitoon

Det har forskats mycket på olika signalvägar i det mänskliga genomet, trotts detta finns det många frågetecken som kvarstår. Denna uppsats undersöker några av dem. Syfte: Undersöka förändringar i genuttryck och mRNA-nivåer för hypertrofi- (MRF4) translations- (5.8S &amp; 18S) och proteolysreglerande gener (MuRF1 &amp; GDF-8) efter en 10 veckor lång styrketräningsperiod hos kvinnor och män. Frågeställningar: (1) Finns det en förändring i total mängd RNA före och efter en 10 veckors styrketräningsintervention. (2) Finns det en förändring i uttryck av MRF4, 5.8S, 18S, MuRF1 samt GDF-8 efter en 10 veckors styrketräningsintervention. (3) Finns det en könsskillnad i förändringen av total mängd RNA samt aktivering av MRF4, 5.8S, 18S, MuRF1 och GDF-8 efter en 10 veckors styrketräningsintervention. Metod: Urvalet för analysen bestod av 16 otränade försökspersoner varav 8 var män och 8 var kvinnor. Försökspersonerna utförde unilateral styrketräning av nedre extremiteten under 10 veckor, under 2 av dessa veckor utfördes ocklusionsträning.  Träningsperiodiseringen var vågformig (70-90% av 1RM, 5-12 rep, 3 ggr/vecka). Muskelbiopsier togs i det arbetande benet före träningsperiodens start samt 3-7 dagar efter träningsperiodens avslut. Genuttryck analyserades med qPCR. Resultat: Det fanns ingen signifikant skillnad i förändring mellan män och kvinnors totala RNA eller genuttryck. Total RNA ökade signifikant (p&lt;0,01) med 19,2 %. Kvinnorna hade en signifikant ökning (P&lt;0,05) av RNA på 27,6 % medan männen hade en signifikant ökning (p&lt;0,05) på 14 %. MRF4 hade en signifikant (P&gt;0,05) procentuell ökning i genuttryck med 55,7 % och kvinnor för sig hade en signifikant (P&gt;0,05) ökning på 64 %. GDF-8 ökade signifikant (P&gt;0,05) med 55,5 % medan GAPDH ökade signifikant (P&gt;0,05) för båda könen tillsammans med 70,6 % och för män med 87,8 %. MuRF1 och 5.8S hade inga signifikanta förändringar i genuttryck. Slutsats: Det verkar som att både män och kvinnor får en liknande procentuell förändring av total RNA och mRNA genuttryck 3-7 dagar efter en 10 veckors hypertrofistyrd styrketräningsperiod. För att mäta genuttryck av translationsgenen MRF4 verkar 3-7 dagar efter en 10 veckors styrketräningsperiod vara en tidpunkt då det fortfarande pågår hypertrofi av skelettmuskulaturen.  Av de proteolysreglerande generna GDF-8 och MuRF1 sågs en uppreglering av GDF-8 vilket skulle kunna vara ett tecken på att hypertrofin börjar hämmas. Ett oväntat fynd var att GAPDH visade sig vara olämplig som kontrollgen vid en styrketräningsintervention på 10 veckor och att 18S var väldigt stabil. Detta kan betyda att GAPDH inte skall användas vid längre styrketräningsinterventioner.<br>There have been much research on signaling pathways in the human genome, but there still remain many questions. This paper examines some of them. Aim: Investigate changes in gene expression and mRNA levels of hypertrophy (MRF4), translation (5.8S &amp; 18S) and proteolysis regulating genes (GDF-8) after a 10-week strength training period in men and women. Research questions: (1) Is there a change in the total amount of RNA before and after a 10-week strength training intervention. (2) Is there a change in the expression of MRF4, 5.8S, 18S, Murf1 and GDF-8 after 10 weeks of strength training. (3) Is there a gender difference in the change of total RNA and the expression of MRF4, 5.8S, Murf1 and GDF-8 after a 10-week long strength training intervention. Method: The sample for analysis consisted of 16 untrained subjects, of whom 8 were men and 8 were women. The subjects performed unilateral resistance training of lower extremities for 10 weeks, during two of these weeks blood flow restriction training were performed. The training was undulating (70-90% of 1RM, 5-12 cord, 3 times / week). Muscle biopsies were taken from the working leg before the start and 3-7 days after the training period. Gene expression was analyzed by qPCR. Results: There was no significant gender difference in total RNA or gene expression. Total RNA was significantly increased (p &lt;0.01) with 19.2 %. The women had a significant increase (P &lt;0.05) of RNA at 27.6 %, while the men had a significant increase (p &lt;0.05) at 14 %. MRF4 had a significant (P&gt; 0.05) percentage increase in gene expression by 55.7 %, and women had a significant (P&gt; 0.05) increase of 64 %. GDF-8 increased significantly (P&gt; 0.05) with 55.5 %, while GAPDH increased significantly (P&gt; 0.05) for both sexes with 70.6 % and for men with 87.8 %. Murf1 and 5.8S had no significant changes in gene expression. Conclusions: It seems that both men and women experience a similar percentage difference of total RNA and mRNA gene expression 3-7 days after a 10 weeks long strength training period. To measure the gene expression of MRF4 3-7 days after a 10-week weight-training period seems to be a time when there still is a anabolic responses in the skeletal muscle. Of the proteolysis regulating genes GDF-8 and Murf1 there was an upregulation of GDF-8, which could be a sign that the inhibition of hypertrophy started. An unexpected finding is that GAPDH was found to be unsuitable as a control gene at a strength training intervention at 10 weeks and rRNA 18S was very stable, which could mean that GAPDH should not be used as control gene in longer strength training studies.

Syfte och frågeställningar Syftet med den här studien var att undersöka huruvida högfrekvent (HF) styrketräning motsvarande fem pass/vecka kan generera större muskelhypertrofi och styrka än lågfrekvent (LF) styrketräning motsvarande två pass/vecka. Frågeställning; Kan träningsprogram med högre träningsfrekvens ge större respons på muskelhypertrofi och styrka än normal träningsfrekvens trots samma träningsvolym? Metod Sex försökspersoner (ålder 26 ± 3,3 år, längd 180,4 ± 6 cm, vikt 81,6 ± 6,7 kg) testades för muskeltjocklek (ultraljudsmätning på vastus lateralis och rectus femoris) och muskelstyrka (1RM i unilateral benpress och benspark) på respektive ben. Fp tränade ena benet högfrekvent (fem pass/vecka) och andra benet lågfrekvent (två pass/vecka) under sju veckor. Träningsvolymen kontrollerades så att den var lika mellan benen. Därefter utfördes återtester enligt samma protokoll som före interventionen. Resultat Muskeltjocklek i båda musklerna var oförändrad i LF-benet 2,0 % och ökade i HF-benet 4,7 % (p = 0,04). Vastus lateralis var oförändrad i LF-benet -0,9 % och HF-benet 6,5 %. Rectus femoris ökade i LF-benet 5,1 % (p = 0,04) och var oförändrat i HF-benet 2,5 %. Ingen statistisk differens sågs för muskeltjocklek mellan benen efter interventionen för vastus lateralis och rectus femoris. Muskelstyrka i benpress ökade i LF-benet med 17 % (p = 0,02) och HF-benet med 15,8 % (p = 0,02). Benspark ökade i LF-benet med 15,8 % (p = 0,02) och HF-benet med 17,4 % (p = 0,02). Ingen statistisk differens sågs för muskelstyrka mellan benen efter interventionen för benpress och benspark. Slutsats Slutsatsen av den här studien var att ingen statistisk skillnad uppmättes mellan muskelhypertrofi och styrka för träning enligt det högfrekventa kontra det lågfrekventa träningsprogrammet hos unga aktiva motionärer vana vid styrketräning. Således kan samma träningseffekt i form av muskelhypertrofi och styrka uppnås vid korta pass med låg volym och högre träningsfrekvens som längre pass med högre volym och lägre träningsfrekvens.<br>Aim The purpose of this study was to investigate if high frequency strength training (HF) of five sessions/week can produce larger increases in muscle hypertrophy and strength compared to low frequency strength training (LF) of two sessions/week. Method Six participants (age 26 ± 3,3 years, length 180,4 ± 6 cm, weight 81,6 ± 6,7 kg) were tested for muscle thickness in quadriceps (ultrasound measurements on vastus lateralis and rectus femoris) and strength (1RM in unilateral leg press and leg extension). One leg exercised with a high frequency (five sessions/week) and the other leg with a low frequency (two sessions/week) during seven weeks. The training volume was equated between both legs. Retests were conducted after the intervention. Results Muscle thickness in both muscles together was unchanged in LF 2,0 % and increased in HF 4,7 % (p = 0,04). Vastus lateralis was unchanged in LF -0,9 % and HF 6,5 %. Rectus femoris increased in LF 5,1 % (p = 0,04) and was unchanged in HF 2,5 %. No statistical difference was seen for muscle thickness between legs for vastus lateralis and rectus femoris. Strength increased in leg press for LF with 17 % (p = 0,02) and for HF with 15,8 % (p = 0,02). Leg extension increased for LF with 15,8 % (p = 0,02) and for HF with 17,4 % (p = 0,02). No statistical difference was present for strength between legs for leg press and leg extension. Conclusions The conclusions of this study were that no statistical difference was seen for muscle hypertrophy and strength between high and low frequency training programmes when the volume was equated. This means that comparable training effects can be reached between short duration and low volume strength training workouts at high frequency as to longer duration and higher volume strength training workouts at low frequency.

This thesis is focused on the analysis of experimental ECG records drawn up in isolated rabbit hearts and aims to describe changes in EKG caused by ischemia and left ventricular hypertrophy. It consists of a theoretical analysis of the problems in the evaluation of ECG during ischemia and hypertrophy, and describes an experimental ECG recording. Theoretical part is followed by a practical section which describes the method for calculating morphological parameters, followed by ROC analysis to evaluate their suitability for the classification of hypertrophy and at the end is focused on classification.

Abstract Left ventricular hypertrophy (LVH), a common complication of elevated blood pressure (BP), is a risk factor for cardiovascular (CV) morbidity and mortality. Adiponectin has been shown to have cardioprotective effects and is inversely associated with LVH. BP can be measured at a clinical visit, as a momentary value. Ambulatory blood pressure (APB) measurement (ABPM) is a method of repeated BP measurements through a defined period, targeted to evaluate the circadian BP profile. High BP and ABPM have been shown to be associated with LVH and left ventricular diastolic dysfunction (LVDD). A high sodium intake has been associated with elevated BP and adverse CV outcome. The aim of this study was to investigate the associations between adiponectin and left ventricular mass index (LVMI), a measure of LVH, ABPM and the development of LVDD during long-term follow-up, ABPM and the change in LVMI during long-term follow-up, and the role of dietary sodium intake in the incidence of AF. Adiponectin has been shown to have vasoprotective, anti-inflammatory and cardioprotective effects. Hypoadiponectinemia has been associated with hypertension, coronary artery disease (CAD) and LVH. In this study, adiponectin levels were inversely associated with LVMI, even after adjustment with conventional risk factors of LVH, in a fairly large sample of middle-aged subjects. Elevated BP and pulse pressure (PP) have been associated with echocardiographic measures of LVDD. In this study, the association between APBM and the development of LVDD during a 20-year follow-up was evaluated. Ambulatory PP (APP) was shown to independently associate with the development of LVDD, even after adjustment with conventional risk factors of LVDD. APBM has been associated with LVH in cross-sectional assessments and has also been shown to have predictive value in future LVMI or LVH. In a few studies the predictive value of APP in future LVMI was observed. In the present study, an increase in APP was shown to predict the change in LVMI during long-term follow-up. In this study, the association between dietary sodium intake and the incidence of AF was evaluated. A high sodium intake predicted the occurrence of AF, which is a novel finding. In conclusion, this study offers novel findings about predictive factors in the entity of cardiac remodelling<br>Tiivistelmä Vasemman kammion hypertrofia on yleinen kohonneen verenpaineen seuraus ja sen on todettu olevan sydän- ja verisuonitapahtumien riskitekijä. Adiponektiinin on osoitettu suojaavan vasemman kammion hypertrofialta. Ambulatorinen verenpaineen mittaus on menetelmä, jossa verenpaine mitataan määritellyllä ajanjaksolla toistuvasti, mikä antaa kuvan verenpaineesta vuorokauden eri jaksoissa. Kohonneella ambulatorisella verenpaineella on osoitettu olevan yhteys vasemman kammion hypertrofiaan sekä vasemman kammion diastoliseen vajaatoimintaan. Runsas natriumin saanti on yhteydessä kohonneeseen verenpaineeseen sekä sydän- ja verisuonisairauksiin. Tämän tutkimuksen tarkoituksena on selvittää yhteyksiä adiponektiinin ja vasemman kammion massaindeksin välillä, ambulatorisen verenpaineen ja vasemman kammion diastolisen vajaatoiminnan kehittymisen välillä, ambulatorisen verenpaineen ja vasemman kammion massaindeksin muutoksen välillä sekä natriumin saannin ja eteisvärinän ilmaantuvuuden välillä. Adiponektiinilla on todettu olevan suotuisia vaikutuksia verisuonistoon, tulehdusreaktion hillintään sekä sydänlihakseen. Matalan adiponektiinitason on osoitettu olevan yhteydessä verenpainetautiin, sepelvaltimotautiin sekä vasemman kammion hypertrofiaan. Tässä tutkimuksessa adiponektiinihormonilla osoitettiin olevan käänteinen yhteys vasemman kammion massaindeksiin, vaikka perinteiset riskitekijät otettiin huomioon. Kohonneella verenpaineella sekä pulssipaineella on osoitettu olevan yhteys vasemman kammion diastoliseen vajaatoimintaan. Tässä tutkimuksessa arvioitiin ambulatorisen verenpaineen merkitystä vasemman kammion diastolisen vajaatoiminnan kehittymisessä. Ambulatorinen pulssipaine osoittautui riskitekijäksi, vaikka perinteiset riskitekijät otettiin huomioon. Ambulatorisella verenpaineella ja pulssipaineella on osoitettu olevan yhteys vasemman kammion hypertrofiaan poikkileikkaustutkimuksissa ja seurantatutkimuksissa. Tässä tutkimuksessa ambulatorisen pulssipaineen nousun havaittiin ennustavan vasemman kammion massaindeksin kasvua pitkäaikaisseurannassa. Tässä tutkimuksessa korkean natriumin saannin todettiin olevan yhteydessä lisääntyneeseen eteisvärinän ilmaantuvuuteen. Tätä yhteyttä ei ole aiemmin todettu muissa tutkimuksissa. Tässä tutkimuksessa löydettiin uusia riskitekijöitä sydämen patologisiin ilmentymiin liittyen

Abstract Achilles tendon rupture (ATR) conservative treatment result usually good clinical outcome, but despite the treatment method calf muscle strength deficit persist. Recent evidence suggests that surgery might surpass conservative treatment in restoring strength after ATR, but structural explanations for surgery-related improved strength remain uncertain. The purposes of this thesis were to compare calf muscle isokinetic strength recovery, calf muscle volume, fatty degeneration and AT elongation after conservative treatment or after open surgical repair of ATR. An additional aim was to assess the role of fascial augmentation in terms of calf muscle isokinetic strength recovery, AT elongation, calf muscle volume atrophy and fatty degeneration, and their relationship with calf muscle isokinetic strength in long-term follow-up after ATR surgery. Surgery resulted in 10% to 18% greater plantar flexion strength (P = 0.037) compared to conservative treatment. The mean differences between affected and healthy soleus muscle volumes were -18% after surgery and -25% after conservative treatment (P = 0.042). At 18 months, AT were, on average 19 mm longer in patients treated conservatively compared to surgery (P &#60; 0.001). At 18 months, patients with greater (2–3) fatty degeneration had lower soleus muscle volumes and plantar flexion strength in the healthy leg. In long term, augmentation did not affect any of the strength variables, but the injured side showed 12% to 18% strength deficit compared with the healthy side (P &#60; 0.001). The AT was, on average, 12 mm longer in the affected leg than in the healthy leg (P &#60; 0.001). The mean soleus muscle volume was 13% lower in the affected leg than in the healthy leg (P &#60; 0.001). The mean volumes of the medial- and lateral gastrocnemius muscles were 12% and 11% lower in the affected leg than in the healthy leg, respectively (P &#60; 0.001). AT elongation correlated substantially with plantar strength deficit (ρ = 0.51, P &#60; 0.001) and with both gastrocnemius (ρ = 0.46, P = 0.001) and soleus muscle atrophy (ρ = 0.42, P = 0.002). Calf muscle fatty degeneration was more common in the affected leg compared healthy leg (P &#8804; 0.018). In conclusion, surgery of ATR restored calf muscle isokinetic strength earlier and more completely than conservative treatment. Conservative treatment resulted in greater soleus muscle atrophy and AT elongation compared surgery, which may partly explain the surgery related better strength results. Augmentation provided no long-term benefits compared with simple suturation, and a 12 to 18% plantar flexion strength deficit compared to the healthy side persisted. AT elongation may explain the smaller calf muscle volumes, greater fatty degeneration, and plantar flexion strength deficit observed in long-term follow-up after surgical repair of ATR<br>Tiivistelmä Akillesjännerepeämän (ATR) konservatiivisella ja leikkaushoidolla hoidolla saavutetaan hyvät kliiniset tulokset. Viimeisimmät tutkimukset kuitenkin viittaavat leikkaushoidolla saavutettavan paremmat voimat kuin konservatiivisella hoidolla, mutta rakenteelliset selitykset leikkaushoidon paremmalle pohjelihaksen voimille ovat epäselviä. Työn tarkoituksena oli verrata pohjelihaksen isokineettisten voimien palautumista, pohjelihastilavuuksia, rasvadegeneraatiota ja akillesjänteen (AT) pidentymistä ATR:n konservatiivisen- ja leikkaushoidon jälkeen. Tarkoituksena oli arvioida lihaskalvovahvikkeen merkitystä pohjelihaksen isokineettisten voimien palautumisessa pitkäaikaisseurannassa. Lisäksi tutkimme AT pidentymisen, pohjelihastilavuuksien ja rasvadegeneraation suhdetta pohjelihaksen isokineettisiin voimiin ATR:n leikkaushoidon jälkeen 14 v seurannassa. Leikkaushoidolla saavutettiin 10–18 % paremmat pohjelihaksen voimat verrattuna konservatiiviseen hoitoon. Leikkaushoidon jälkeen soleuslihasten tilavuuksien puoliero terveen jalan hyväksi oli 18 % ja konservatiivisen hoidon jälkeen 25 %. 18 kk kohdalla konservatiivisesti hoidettujen AT oli 19 mm pidempi verrattuna leikkauksella hoidettuihin. 18 kk kohdalla potilaat, joilla vamma jalan soleuslihaksen rasva-degeneraatio oli korkea (2–3), kärsivät suuremmasta soleuslihaksen atrofiasta ja pohjelihaksen voima puolierosta. Voimat eivät muuttuneet 12 kk ja 14 v kontrollien välillä. Lihaskalvovahvikkeella ei ollut merkitystä voimien palautumisessa pelkkään suoraan ompeluun verrattuna, mutta vammapuoli jäi 10–18 % heikommaksi verrattuna terveeseen jalkaan. Vammajalan akillesjänne oli 12 mm pidempi terveeseen jalkaan verrattuna. Vammajalan kolmipäisen pohjelihaksen tilavuus oli 11–13 % pienempi verrattuna terveeseen jalkaan. Akillesjänteen pituus korreloi pohjelihaksen voimapuolieron sekä pohjelihasatrofian kanssa. Akillesjännerepeämän leikkaushoidolla pohjelihaksen isokineettiset voimat palautuvat nopeammin ja täydellisemmin kuin konservatiivisella hoidolla. Leikkaushoitoon verrattuna konservatiivinen hoito johtaa suurempaan soleuslihaksen atrofiaan ja akillesjänteen pidentymään, mikä selittää osittain leikkaushoidon paremmat voimatulokset. 14 v seurannassa lihaskalvovahvikkeesta ei ole etua akillesjännerepeämän leikkaushoidossa. Akillesjännerepeämän leikkaushoidosta huolimatta potilaalle jää terveeseen jalkaan verrattuna 10–18 % pohjelihasten voimapuoliero. Akillesjänteen pidentyminen mahdollisesti selittää pohjelihasten atrofian, rasvadegeneraation ja pysyvän pohjelihasten voimapuolieron akillesjännerepeämän leikkaushoidon jälkeen 14 v seurannassa

Sammanfattning Effekten av styrketräning och energiunderskott på viktminskning hos nybörjarmotionärer. Till dagens datum råder ingen strategi för hur fettförlusten kan maximeras och muskelförlusten minimeras (Katzeff et al, 1995). Lockwood (2008) visar att 50 % av individer som endast använder kostrestriktioner återfår sin ursprungliga vikt igen. Kraemer &amp; Ratamess (2008) visar att regelbunden träning som involverar stora som små muskelgrupper i samma pass frigör mest anabola hormoner. Muskler offras av kroppen eftersom de tar energi och de kan ge energi via glukoneogenes för att ex. jaga byten. I dagens samhälle signalerar stressen ett konstant frigörande av kortisol vilket har en negativ påverkan på bl.a. muskler. Detta hormonpåslag har förstärkts i samband med energiunderskott. Är det möjligt att öka styrka med energiunderskott hos nybörjarmotionärer om protein tillförs för optimal kompenseringseffekt efter träningspass?  4 av 6 överviktiga nybörjarmotionärer genomgick 8 veckor lång träningsperiod med betoning på hypertrofi, energiunderskott och mattiming i denna pilotstudie. 1RM tester har utförts på benpress i maskin, bröstmaskin samt sittande rodd med smalt grepp. Vilopuls har även tagits manuellt på morgonen av varje deltagare vid två tillfällen, före och efter träningsperioden. Testledare har tagit kroppsmått över byst, midja, rumpa samt vardera låren som utvärdering från energiunderskottet. Energiunderskottet har uppskattats till 500 kcal mindre än bibehållandet av ursprunglig vikt. Alla deltagare har ökat sina styrkeresultat och minskat alla kroppsmått. En person har någon extra centimeter kring låren, men kan tyda på hypertrofi. Inga signifikans test har utförts. BMI har minskat på alla deltagare medan kcalvärde har ökat för varje deltagare enligt BIA våg. Ett mål har varit att öka den basala metabolismen i vila via större muskler. Det är främst en ökad fettförbränning som är fördelaktigt för målgruppen, vilket kan uppnås genom en ökad muskelmassa och kolhydratrestriktioner. Trots att pilotstudien har behandlat fysiskt inaktiva nybörjarmotionärer har hypertrofi uppnåtts även efter 4 veckors teknikträning för ökat antal aktiva motorenheter. Inga konkreta slutsatser kan ringas in på en pilotstudie, men positiva resultat har framkommit.

Abstract The β1-adrenergic receptor (β1AR) belongs to the large family of G protein-coupled receptors. It is activated by epinephrine and norepinephrine and thus has a central role in mediating the effects of the sympathetic nervous system. β1AR is the predominant adrenergic receptor in the heart, where it mediates positive inotropy and chronotropy. Thus, it is the most important target receptor for β-adrenergic antagonists, which are widely used in the treatment of cardiovascular diseases. Furthermore, β1AR is also expressed in the brain, where it has a crucial role in regulating memory formation and synaptic plasticity. Human β1AR (hβ1AR) has two polymorphisms, one at each terminus. The carboxyl-terminal (C-terminal) Arg389Gly8.56 polymorphism has previously been shown to have functional significance. Despite the clinical importance of hβ1AR, its biosynthetic profile and post-translational processing have not been well characterized to date. The aims of the present study were to shed light on these events, focusing on the limited proteolysis of hβ1AR and the impact of β-adrenergic ligands on receptor processing. In addition, the C-terminal polymorphism and its associations with certain parameters were investigated in a population consisting of survivors of acute myocardial infarction (AMI). By using a heterologous expression system, hβ1AR biosynthesis was revealed to be efficient and rapid. The N-terminus of the mature receptor was modified with O-glycans and one N-glycan, but despite these modifications it was subject to cleavage at the cell surface that resulted in two C-terminal fragments. The cleavage was mediated by a metalloproteinase, and importantly, it also occurred in vivo. Moreover, receptor activation enhanced the cleavage, which suggests that it represents a novel regulatory mechanism of hβ1AR. Interestingly, those ligands that enhanced the cleavage stabilized intracellular hβ1AR precursors, possibly via a pharmacological chaperone activity. Thus, the present study demonstrates that β-adrenergic ligands can have different regulatory effects on distinct hβ1AR forms. Among the AMI survivors, the Arg3898.56 homozygotes had significantly increased left ventricular mass indexes, when compared to the Gly3898.56 carriers, which suggests an association between Arg3898.56 and left ventricular hypertrophy (LVH). When euglycemic and diabetic patients were analyzed separately, the association existed among the euglycemic patients but was not present in diabetic patients. Diabetes is one of several risk factors that have previously been shown to influence the progression of LVH. Here, diabetes was shown to have a stronger effect on the development of LVH, when compared with the Arg3898.56 variant of hβ1AR<br>Tiivistelmä β1-adrenerginen reseptori (β1AR) kuuluu laajaan G-proteiineihin kytkettyjen reseptorien perheeseen. β1AR on tärkeässä asemassa sympaattisen hermoston toiminnassa. Sydämessä β1AR on vallitseva adrenerginen reseptori, ja sydänlihaksen supistusvireys sekä -taajuus voimistuvat β1AR:n aktivaation kautta. Siten se edustaa sydän- ja verisuonisairauksissa käytettävien β-salpaajien tärkeintä kohdereseptoria. β1AR:n luontaisia agonisteja ovat lisämunuaisytimestä ja hermopäätteistä vapautuvat adrenaliini ja noradrenaliini. Sydänlihaksen lisäksi β1AR:a ilmennetään myös aivoissa, jossa reseptorilla on keskeinen asema muistin ja synaptisen muovautuvuuden kannalta. Ihmisen β1AR (hβ1AR) sisältää kaksi polymorfismia, joista toinen (Arg389Gly8.56) sijaitsee reseptorin karboksyyli- (C-) terminaalissa solulimassa. Tällä polymorfismilla on havaittu olevan toiminnallista merkitystä. Vaikka hβ1AR:n kliininen merkitys on huomattava, sen biosynteesistä ja translaationjälkeisestä muokkauksesta ei ole tähän mennessä ollut juurikaan tutkimustietoa. Tämän väitöskirjatyön tavoite oli kuvata näitä tapahtumia ja erityisesti keskittyä hβ1AR:n solunulkoisen amino- (N-) terminaalin rajoitettuun proteolyysiin. Lisäksi haluttiin tutkia, onko β-adrenergisillä ligandeilla vaikutusta reseptorin prosessointiin. Tutkimuksen kliinisessä osiossa kartoitettiin C-terminaalisen polymorfian yhteyttä valikoituihin muuttujiin aineistossa, joka koostui akuutin sydäninfarktin (AMI) sairastaneista potilaista. hβ1AR:n biosynteesin havaittiin olevan tehokas ja nopea heterologisessa systeemissä. Kypsän reseptorin N-terminaalissa havaittiin useita O-kytkennäisiä ja yksi N-kytkennäinen glykaani. Glykosyloinnista huolimatta N-terminaali pilkkoutui solun pinnalla, mikä tuotti kaksi solukalvolla sijaitsevaa, C-terminaalista reseptoripalasta. Pilkkoutumista, joka havaittiin myös in vivo, katalysoi metalloproteinaasi. Reseptorin aktivaatio kiihdytti pilkkoutumista, joka siten todennäköisesti edustaa uudenlaista hβ1AR:n säätelymekanismia. Ligandit, jotka kiihdyttivät pilkkoutumista, toisaalta stabiloivat solunsisäisiä hβ1AR:n epäkypsiä muotoja toimien luultavasti ns. farmakologisina kaperoneina. Näin ollen väitöskirjatyö osoittaa, että β-adrenergisillä ligandeilla voi olla erilaisia säätelyvaikutuksia eri hβ1AR-muotoihin. Kliinisessä tutkimuksessa Arg3898.56-homotsygooteilla potilailla havaittiin merkittävästi suurentunut vasemman kammion massaindeksi Gly3898.56-kantajiin verrattuina, mikä puoltaa Arg3898.56-polymorfismin ja vasemman kammion hypertrofian (LVH) välistä yhteyttä. Kun euglykeemisiä potilaita ja diabeetikkoja tutkittiin erikseen, yhteys ilmeni vain euglykeemisessä ryhmässä. Diabetes on riskitekijä, joka vaikuttaa LVH:n kehittymiseen. Tässä tutkimuksessa diabeteksellä havaittiin olevan voimakkaampi vaikutus LVH:n kehittymiseen Arg3898.56 -polymorfismiin verrattuna

Hypertrophic cardiomyopathy (HCM), a heart-related abnormality, is the most prevalent cause of sudden death in young athletes at sporting events. A cluster of cardiomyopathy mutations are localized in β-cardiac myosin at the N-terminal region of subfragment-2. Using resonance energy transfer probes, a synthetic peptide model system was developed to study stability of the coiled coil (S2 fragment) structure by determining monomer-dimer equilibrium of the peptide. Fluorescence resonance energy transfer and MacroModel software suite were used to obtain distance measurements along with measurement of coiled coil formation. The model peptide was used to characterize the effects of disease-causing-mutations and examine potential candidate drugs (polyamines) to counteract effects of mutations causing HCM. Distance measurements between donor and acceptor probes obtained by computational simulation and fluorescence resonance energy transfer (FRET) were consistent. Measurements also agreed with simulations of unlabeled wildtype, indicating coiled coil structural stability of the peptide. Interaction of the site-specific antibody with the peptide strongly inhibited dimerization and destabilized coiled coil structure of the peptide. Presence of negatively charged glutamate residues in the region of subfragment-2 strongly suggested a potential interaction site for positively charged polyamines. Binding of certain polyamines, such as poly-L-Lysine 11 residues and poly-D-Lysine 17 residues, demonstrated the ability to enhance dimerization and improve stability of the coiled coil structure, while some other polyamines were shown to have insignificant impact on the structure. In an attempt to characterize the effect of HCM-causing-mutations, peptides containing E924K mutation and lethal mutation E930 deletion were synthesized. Fluorescence resonance probes were conjugated to the mutant peptides to determine coiled coil formation. Results obtained from both dynamic simulations and resonance energy transfer experiments indicated that these mutations strongly inhibit dimerization, and thus, destabilize coiled coil structure of the peptide. Further experiments were conducted using heterodimers containing a chain of wildtype and a chain of mutant peptide. Both E924K & Edel930 mutations destabilized coiled coil formation and prevented dimerization. This peptide model system would provide a promising tool for drug development targeting HCM-causing-mutations along the S2 region of myosin.

Abstract    Aim    The main purpose of this study was to investigate Cross Education (CE), and how gender, detraining and leg dominance affects CE in previously untrained subjects when conducting a unilateral resistance training program. We also investigated if unilateral resistance training can give a hypertrophic response.    Method   Twenty healthy previously untrained individuals, 10 females and 10 males, were recruited as volunteer participants. The participants were randomly assigned to train either left or right leg. The training intervention was 10 weeks (34 sessions) of unilateral resistance training in the leg press and leg extension, sixteen of the participants fulfilled the criteria for inclusion. After two initial familiarization the participants trained conventional resistance training three times a week (week 1-3, 5-7 and 9-10) and Blood Flow Restriction Training (BFRT) five times a week (week 4 and 8). One repetition maximum for both legs in the leg press and leg extension was tested pre-, post and post20 to the training intervention as well as ultrasound measurements of muscle thickness.   Results    The ten-week training period resulted in a significant increase of maximal strength for the untrained leg 18,9 %, (16,6) (p &lt; 0,01) in the leg press and 6,7 %, (3,7) (p &lt; 0,05) in the leg extension. When comparisons between gender were made only men had a significant increase 26,5 %, (16,7) (p &lt; 0,01) in the leg press and 9,9 %, (4,7) (p &lt; 0,05) in the leg extension. Also, we saw a significant difference between women and men on a group level. Comparisons of dominant vs non-dominant leg showed that training the dominant leg resulted in a significant increase of maximal strength in the untrained leg in both the leg press 22 %, (17,9) (p &lt; 0,01) and leg extension 10,1 %, (4,3) (p &lt; 0,05). The maximal strength in the untrained leg was not significantly altered by the detraining period and a significant increase of muscle thickness could be seen in the untrained leg at MP50 4,7 %, (1,3) (p &lt; 0,01).   Conclusion    The conclusions are that a ten week unilateral resistance training intervention results in a CE effect for men but not for women and that this type of training also can result in an increased muscle thickness in the untrained leg. Our findings also supports that training the dominant limb has superior effect on achieving a CE effect. Lastly we conclude that a twenty week detraining period did not affect the CE achieved strength.<br>Abstrakt    Syfte     Studiens huvudsakliga syfte var att undersöka Cross Education (CE) och hur kön, viloperiod och ben-dominans påverkar CE hos otränade individer när man undergår ett unilateralt styrketräningsprogram. Vi undersökte även om ett unilateral styrketräning kunde ge ett hypertrofisvar.    Metod    Tjugo friska otränade och för närvarande inaktiva individer, tio kvinnor och tio män rekryterades som frivilliga deltagare. Deltagarna randomiserades för att träna antingen vänster eller höger ben. Träningsperioden var tio veckor (trettiofyra pass) av unilateral styrketräning i benpress och benspark, sexton deltagare uppfyllde kriterierna för inkludering. Två initiala familjäriseringspass hölls varefter träningen delades in i två typer av träning, dels konventionell styrketräning tre gånger i veckan (vecka 1-3, 5-7 och 9-10) och dels Blood Flow Restriction Training (BFRT) fem gånger i veckan (vecka 4 och 8). Före, efter och efter tjugo veckor testades one repetition maximum för båda benen i benpress och benspark samt att ultraljudsmätningar för muskeltjocklek utfördes.     Resultat    Den tio veckor långa träningsperioden resulterade i en signifikant ökning av den maximala styrkan för det otränade benet 18,9 % (16,6) (p &lt; 0,010) i benpressen och 6,7 % (3,7) (p &lt; 0,050) i bensparken. När jämförelser gjordes mellan könen så hade enbart män en signifikant ökning, 26,5 % (16,7) (p &lt; 0,010) i benpressen och 9,9 % (4,7) (p &lt; 0,050) i bensparken. Vi fann även att det var en signifikant skillnad mellan kvinnor och män på gruppnivå.   Jämförelser mellan dominant och icke-dominant ben visade att träning av det dominanta benet resulterade i en signifikant styrkeökning i både benpress 22 % (17,9) (p &lt; 0,010) och benspark 10,1 % (4,3) (p &lt; 0,050). Den maximala styrkan i det otränade benet påverkades inte signifikant av en viloperiod och en signifikant ökning i muskeltjocklek kunde ses i det otränade benet i MP50 4,7 % (1,3) (p &lt; 0,010)    Konklusion    Slutsatserna är att en tio veckors unilateral styrketräningsintervention resulterar i en CE effekt hos män men inte hos kvinnor, och att denna typ av träning kan resultera i en ökad muskeltjocklek i det otränade benet. Våra fynd styrker att träning av den dominanta lemmen har större effekt på CE. Slutligen drar vi slutsatsen att en tjugo veckors viloperiod inte påverkar CE-styrkan.

Thesis (PhD)--Stellenbosch University, 2013.<br>ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular morbidity and allcause mortality. Significantly, it is considered a modifiable cardiovascular risk factor as its regression increases overall survival and reduces the frequency of adverse cardiac events. A clear understanding of LVH pathogenesis is thus imperative to facilitate improved risk stratification and therapeutic intervention. Hypertrophic cardiomyopathy (HCM), an inherited cardiac disorder, is a model disease for elucidating the molecular mechanisms underlying LVH development. LVH, in the absence of increased external loading conditions, is its quintessential clinical feature, resulting from mutations in genes encoding sarcomeric proteins. The LVH phenotype in HCM exhibits marked variability even amongst family members who carry the same disease-causing mutation. Phenotypic expression is thus determined by the causal mutation and additional determinants including the environment, epigenetics and modifier genes. Thus far, factors investigated as potential hypertrophy modifiers in HCM have been relatively removed from the primary stimulus for LVH; and the few studies that have been replicated yielded inconsistent results. We hypothesized that the factors that closely interact with the primary stimulus of faulty sarcomeric functioning, have a greater capacity to modulate it, and ultimately the LVH phenotype in HCM. Plausible candidate modifiers would include factors relating to the structure or function of the sarcomere, including known HCM-causal genes; and the enzymes that function in sarcomere-based energetics. Indeed, the literature highlights the relevance of sarcomeric proteins, Ca2+-handling and myocardial energetics in the development of LVH in HCM. This study, therefore, set out to evaluate the hypertrophy-modifying capacity of such factors by means of family-based genetic association testing in 27 South African HCM families in which one of three unique HCM-causing founder mutations segregates. Moreover, the single and combined effects of 76 variants within 26 candidate genes encoding sarcomeric or sarcomere-associated proteins were investigated. The study identified a modifying role in the development of hypertrophy in HCM for each of the candidate genes investigated with the exception of the metabolic protein-encoding gene, PRKAG1. More specifically, single variant association analyses identified a modifying role for variants within the genes MYH7, TPM1 and MYL2, which encode proteins of the sarcomere, as well as the genes CPT1B, CKM, ALDOA and PRKAB2, which encode metabolic proteins. Haplotype-based association analyses identified combined modifying effects for variants within the genes ACTC, TPM1, MYL2, MYL3 and MYBPC3, which encode proteins of the sarcomere, as well as the genes CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 and PRKAG3, which encode metabolic proteins. Moreover, a number of variants and haplotypes showed statistically significant differences in effect amongst the three HCM founder mutation groups. The HCM-modifier genes identified were prioritised for future studies according to the number of significant results obtained for the four tests of association performed. The genes TPM1 and MYBPC3, which encode sarcomeric proteins, as well as the genes PFKM and PRKAG2, which encode metabolic proteins, were identified as stronger candidates for future studies as they delivered multiple significant results for various statistical tests. This study makes a novel contribution to the field of hypertrophy research as it tested the hypothesis that structural or energy-related factors located within the sarcomere may act as modifiers of cardiac hypertrophy in HCM, and succeeded in identifying a modifying role for many of the candidate genes selected. The significant results include substantial single and within-genecontext variant effects; and identified sizeable variation in the risk of developing LVH owing to the compound effect of the modifier and the individual founder mutations. Collectively, these findings enhance the current understanding of genotype/phenotype correlations and may, as consequence, improve patient risk stratification and choice of treatment. Moreover, these findings emphasize the potential for modulation of disease by further elucidation of some of the avenues identified.<br>AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) is ‘n onafhanklike voorspeller van kardiovaskulêre morbiditeit en van mortaliteit weens alle oorsake. Van belang is dat dit ‘n wysigbare kardiovaskulêre risiko faktor is, aangesien die afname daarvan algehele oorlewing verhoog en die frekwensie van nadelige kardiale voorvalle verlaag. ‘n Duidelike begrip van LVH patogenese is dus noodsaaklik om verbeterde risiko stratifikasie en terapeutiese intervensie te fasiliteer. Hipertrofiese kardiomiopatie (HKM), ‘n oorerflike hart-siekte, is ‘n model-siekte vir die uitpluis van die molekulêre meganismes onderliggend aan die ontwikkeling van LVH. LVH, in die afwesigheid van verhoogde eksterne lading, is die kern kliniese simptoom van HKM en die gevolg van mutasies in die gene wat kodeer vir sarkomeriese proteïene. Die LVH fenotiepe in HKM toon merkbare veranderlikheid selfs in familie-lede wat dieselfde siekte-veroorsakende mutasie dra. Die fenotiepe word dus bepaal deur die siekte-veroorsakende mutasie asook addisionele determinante insluitend die omgewing, epigenetika en modifiserende gene. Potensiële hipertrofie-modifiseerders wat tot dusver bestudeer is, is betreklik verwyder van die primêre stimulus vir LVH en die paar studies wat gerepliseer is, het teenstrydige resultate gelewer. Ons hipoteseer dat die faktore wat in noue interaksie met die primêre stimulus van foutiewe sarkomeriese funksionering is, ‘n groter kapasitieit het om dit en uiteindelik die LVH fenotiepe in HKM, te moduleer. Aanneemlike kandidaat-modifiseerders sou insluit faktore wat betrekking het tot die struktuur en funksie van die sarkomeer insluitend HKM-oorsaaklike gene en die ensieme wat funksioneer in sarkomeer-gebaseerde energetika. Die literatuur beklemtoon inderdaad die relevansie van sarkomeriese proteïene, Ca2+-hantering en miokardiese energetika in die ontwikkeling van LVM in HKM. Hierdie studie het beoog om die hipertrofie-modifiserende kapasiteit van sulke faktore te evalueer deur middel van familie-gebaseerde genetiese assosiasie toetse in 27 Suid-Afrikaanse HKM families waarin een van drie unieke HKM-stigter mutasies segregeer. Verder was die enkel en gekombineerde effekte van 76 variante binne 26 kandidaat gene wat kodeer vir sarkomeer en sarkomeer-geassosieerde proteïene, ondersoek. Hierdie studie het ‘n modifiserende rol in die ontwikkeling van hipertrofie in HKM geïdentifiseer vir elk van die kandidaat gene wat ondersoek is, met uitsluiting van die PRKAG1, wat kodeer vir ‘n metaboliese proteïen. Meer spesifiek, enkel variant assosiasie analises het ‘n modifiserende rol geïdentifiseer vir variante in die gene MYH7, TPM1 en MYL2, wat kodeer vir sarkomeriese proteïene, asook die gene CPT1B, CKM, ALDOA en PRKAB2, wat kodeer vir metabolise proteïene. Haplotipe-gebaseerde assosiasie-analises het gekombineerde modifiserende effekte geïdentifiseer vir variante in die gene ACTC, TPM1, MYL2, MYL3 en MYBPC3, wat kodeer vir strukturele proteïene van die sarkomeer asook die gene CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 en PRKAG3, wat kodeer vir metabolise proteïene. Verder het ‘n aantal variante en haplotipes statisties betekenisvolle verskille in effek tussen die drie HKM-stigter mutasie groepe getoon. Die HKM-modifiserende gene wat geïdentifiseer is, is verder geprioritiseer vir toekomstige studies volgens die aantal beduidende resultate wat vir die vier assosiasie toetse verkry is. Die gene TPM1 and MYBPC3, wat kodeer vir sarkomeriese proteïene, asook die gene PFKM and PRKAG2, wat kodeer vir metaboliese proteïene, is geïdentifiseer as sterker kandidate vir verdere studies omdat veelvuldige beduidende resultate vir die verskeie statistiese toetse deur hulle gelewer is. Hierdie studie maak ‘n nuwe bydrae tot die veld van hipertrofie navorsing omdat dit die hipotese dat strukturele en energie-verwante faktore, wat binne die sarkomeer geposisioneer is, potensieel as modifiseerders van kardiale hipertropfie in HKM kan optree, ondersoek het. Dit slaag ook daarin om ‘n modifiserende rol vir baie van die geselekteerde kandidaatgene te identifiseer. Die beduidende resultate sluit in aansienlike enkel en binne-geen-konteks variant-effekte en aansienlike variasie in die risiko vir LVH ontwikkeling verskuldig aan die gekombineerde effek van modifiseerder en individuele stigter mutasies. Gesamentlik verbeter hierdie bevindinge die huidige begrip van genotipe/fenotipe korrelasies en dit mag tot gevolg hê verbeterde pasiënt risiko stratifikasie en keuse van behandeling. Verder beklemtoon hierdie bevindinge die potensiaal vir siekte modulering deur verdere uitpluis van sekere van hierdie geïdentifiseerde navorsingsrigtings.<br>National Research Foundation<br>Dr. Paul van Helden<br>Stellenbosch University

Syfte och frågeställning Syftet med denna studie är att identifiera effekten av svänghjulsträning på styrkerelaterade variabler som påverkar idrottslig prestation genom en sammanställning av befintlig vetenskaplig litteratur. Studiens frågeställning var: (1) Vilken effekt har svänghjulsträning på muskeltillväxt (hypertrofi)? (2) Vilken effekt har svänghjulsträning på utvecklingen av maximal styrka? (3) Vilken effekt har svänghjulsträning på utvecklingen av Power (effektutveckling)? (4) Vilken effekt har svänghjulsträning på horisontell förflyttning? (5) Vilken effekt har svänghjulsträning på vertikal förflyttning? Metod En metaanalys för 15 experimentella studier som uppfyllt urvalskriterierna genomfördes. De inkluderade studierna kvalitetsgranskades med Pedros skala. För att möjliggöra en sammanställning av samtliga resultat analyserades resultaten i dataprogrammet Review Manager version 5.3 med Random effekt modell och presenteras med Forest plots. Jämförelserna gjordes över en period på 4-24 veckor. Resultat Svänghjulsträning under en period av 4-24 veckor visar på en statistisk signifikant utveckling  av muskulär hypertrofi (effektstorlek 0,68), maximal styrka (1,40), Power (1,0), horisontell (0,54) och vertikal förflyttning (0,60). Slutsats Det finns stöd i litteraturen för att friska individer presterar bättre på så väl dynamiska styrketest som funktionella test efter svänghjulsträning. Evidensen är särskilt stark för att svänghjulsträning utvecklar maximal styrka och Power för tränade yngre individer samt i kortare mer intensiva block. Denna metaanalys har bara sammanställt skillnader i prestation före och efter svänghjulsträning och kan därför inte säga om effekten av svänghjulsträning är större än effekten av upprepade mätningar eller annan träning.<br>Aim The aim of this study was to identify the effect of the flywheel training on strength-related variables that affect athletic performance by compiling existing scientific literature. Research questions: (1) What effect does flywheel training have on muscle growth (hypertrophy)? (2) What effect does flywheel training have on the development of maximum strength? (3) What effect does flywheel training have on the development of Power (effect development)? (4) What effect does flywheel training have on the development of horizontal movement? (5) What effect does flywheel training have on the development of vertical movement? Method A meta-analysis was conducted from 15 experimental studies that met the selection criteria. The quality of included studies was reviewed by Pedro scale. In order to identify possible bias in the selection process a Funnel plot was carried out. To enable the compilation of all results an analyze with Random effect model was carried out with software Review Manager Version 5.3 and presented with Forest plots. Comparisons were made over a period of 4-24 weeks. Results Flywheel training for a period of 4-24 weeks show a statistically significant increase in effect size for muscular hypertrophy (0,49), maximum strength (1,40), Power (1,00), horizontal-(0,54) and vertical movement (0,60). Conclusions There's support in published studies that healthy individuals perform better on dynamic strength tests as wells as functional test after flywheel training. The evidence is particularly strong that flywheel training develops maximum strength and Power in trained younger individuals and in shorter more intensive blocks. This meta-analysis has just compiled the differences in performance before and after flywheel training and therefore cannot say if the effect of flywheel training is greater than the effect of repeated measurements or other exercise.

STRENGHT TRAINING AND INFLUENCING FACTORS Objectives: The aim of this thesis is to form, apply and find the influence of created workout regarding body composition changes. Methods: In this work we used bioimpedance analysis, antropomotorical measurements of muscle mass and diagnostics of previous physical experience. Results: Considering the following measurement we found out significant changes in fat mass and muscle mass ratio as well as increase of muscle mass in upper extremities. Keyowords: muscle strenght, adaptation, muscle hypertrophy, fat loss, dietary supplements, training programme

Title: Options affect muscle hypertrophy in men age 20 25 years in the fitness centre. Method: Laboratory evaluation of body composition (bioelectric Impedance Analysis) and anthropometric measurement of muscle mass. Results: H1 Volumetric training significantly increased body weight, H2, passing the volume of training significantly increased muscle groups of districts reporting, H3 After completing training, the volume change of FM and FFM in the same order of magnitude ratio - 2:1. H4 After completing the training volume ratio of ECM:BCM linear placements the same as during the initial measurement). The proposed program increased the total weight of 8.9 kg. Similarly, the districts reporting increased body parts. Expected FM:FFM was higher than expected. H1, H2 and H4 is confirmed. Keywords: Volume training, 20 men 25 years, bioimpedences, body composition, fitness centre, hypertrophy Objective: The aim of this work is to create individual training macrocycles. Theme on volume training in the fitness centre. This volume training plan aims to increase the growth of active muscle mass and muscle mass.

Part I. The aldosterone synthase gene (CYP11B2) polymorphism T-344C in blood pressure and left ventricular hypertrophy. BACKGROUND: Aldosterone is a key cardovascular hormone, it significantly influences volume, pressure and electrolyte balance. Aldosterone plays an important role in development of left ventricular (LV) hypertrophy and myocardial fibrosis. The aldosterone synthase gene (CYP11B2) is an important candidate gene region in essential hypertension. DESIGN AND METHODS: We assessed the influence of the T-344C polymorphism of aldosterone synthase - the rate-limiting enzyme in aldosterone biosynthesis - on the structure of the left ventricle in young normotensive men. The population included 113 normotensive mid-European Caucasian men aged 18-40 years (mean 27 +/- 5 years). We also studied the association of -344T/C polymorphism of the CYP11B2 gene with the presence and severity of hypertension in 369 individuals, of whom 213 were hypertensive patients (139 controlled hypertensive, 74 resistant hypertensive) and 156 were healthy normotensive subjects. The genotype was assessed using polymerase chain reaction with subsequent cleavage with restriction enzyme HAEIII (restriction fragment length polymorphism method) and visualization with ethidium bromide. Plasma renin activity (PRA) and plasma...

Hypertrophy of the heart is tightly bound to the metabolic adaptations and a cellular remodeling. An important and dynamic system contributing to the maintenance of energy homeostasis is the creatine kinase system (CK). The microcompartmentalization of CK isoforms maintains the flux of ATP between energy production and consumption sites and ensures the effectiveness of the CK system. Changes in expression and activity of CK isoforms during hypertrophy are already well described - to extend this knowledge, this thesis quantified changes in association of cytosolic CK isoforms and sarcomeres. Another essential system, maintaining homeostasis in overloaded heart is composed of the hexokinase (HK) isoforms, located also in cytosol and in mitochondrial compartment. HK1 is associated with mitochondria under physiological conditions, maintaining mitochondrial membrane potential, while HK2 is located mainly in the cytosol. Under stress conditions translocation of HK2 into mitochondrial membrane occurs, which increases the direct supply of ADP to complex V of the respiratory chain and decreases the probability of apoptosis activation. We analyzed association of individual HK isoforms with mitochondria within the second aim of this thesis. Third aim of the thesis was to characterize changes in the CK and M...

Title: Hormonal changes in strength training Objectives: Perform a systematic review of literature dealing with hormonal changes in strength training. Based on the informations from aforementioned literature, describe wheather acute hormonal response after a bout of strength training significantly influence the proces of hypertrophy or not. Hormone testosterone and changes of its concentrations is for this thesis the most important. Methods: Method of traditional review was used in this thesis. Results: The presence of acute hormonal changes occurred in strength training was confirmed in numerous studies. Role of this hormonal response is because of variability in results not very clear yet. Chronicle changes of resting hormonal levels in strength training are not observed according to results of studies. For better understanding of hormonal strength in strength training, another studies have to be executed. Keywords: endocrinal system, strength training, hormonal response, testosterone, hypertrophy.

It was shown almost 50 years ago that hypothermic incubation of chicken embryos results in a reduction in the size of embryos and an increase in the heart weight, presumably by hypertrophy (increase in cell volume). The chicken embryos were incubated in normothermia (37.5 ř C) and hypothermia (33.5 ř C) from the eleventh embryonic day. On the 17th day, the embryos were weighed and then their hearts were weighed. In agreement with the previous results, hypothermic embryos were 29% smaller and their hearts 18% heavier. The heart-to-body weight ratio was 67% higher in the hypothermic group. The measured cell size was very similar in the target areas and it was also between the two groups. The left ventricle width was twofold that the right one and the difference was not significantly higher in the hypothermia model. Purkinje fibers, the terminal part of the conduction system, were smaller than the working cardiomyocytes. Purkinje fibers were slightly enlarged after hypothermic incubation. The proliferation rate was measured by immunohistochemical labeling of anti-phospho histone H3. The experimental group showed much higher proliferation rate; it reached statistical significance in the right ventricle. Thus, hypothermic incubation resulted in increased growth of embryonic heart based on hyperplasia...

Myocardial damage is one of the most serious consequences of arterial hypertension. Changes in the heart structure and function develop not only due to pressure overload itself, but many other hemodynamic and neurohumoral factors contribute to their formation. Our work has compared echocardiohraphic strucutural anf functional changes of the left ventricle, caused by essential hypertension and hypertension associated with primary aldosteronism (PA) as the most common reason for secondary hypertension. The first part of our work focused on the differences in left ventricle geometry in men with PA and essential hypertension after separating it's low-renin form (where, similarly to PA, the plasma volume expansion was considered to have the dominant effect on left ventricle remodelation). In men with low-renin forms of hypertension including PA, we observed greater both endsystolic and enddiastolic diameter of the left ventricle, lower relative wall thickness and more frequent eccentric type of hypertrophy when compared to essential hypertensives with normal renin levels. Whereas left ventricle cavity diameters were positively correlated to aldosterone levels, wall thicknesses were associated mainly with hypertension severity expressed as an average 24hour blood pressure and number of antihypertensives....

In August 2014 a total die-off of fish stock occurred in Záhumenní velký, a pond with a surface area of 5.85 ha. The investigation of the fish kill revealed that the Jabkenice WWTP located above the pond area had discharged water of inappropriate quality (N-NH4+ -99.3 mg/l-1) into the pond. This event resulted in the monitoring of physical and chemical parameters of water quality, zooplankton sampling and measuring of growth dynamics of fish stock by using control reduction fishing. The survey conducted in 2015 studied three different ponds (Ohrada 0.85 ha, Záhumenní velký 5.85 ha and Vlkava 22.1 ha), located in the fertile lowland areas around Mladá Boleslav where pre-cleaned sewage water from the sewage treatment plants flows. The water samples taken both at the outflow of the waste water treatment plant and in the pond were analysed in an accredited laboratory. The following parameters were examined: BOD5, TN, CODCr, ammoniacal nitrogen, TP, nitrites, nitrates and others.

Short summary: Background: High cardiovascular risk in patients with chronic kidney disease is partly due to mineral dysbalance, microinflammation and oxidative stress. CKD patients accumulate traditional and non-traditional CV risk factors. FGF23, MMPs and PlGF belong among these non-traditional biomarkers of CV risk. FGF23 is a phosphaturic hormone and inhibitor of calcitriol synthesis. It is associated with vascular calcifications. Matrix-metalloproteinases (e.g. MMP-2, MMP-9) are proteolytic, proinflammatory enzymes, contributing to myocardial remodelation. Placental growth factor (PlGF) is a proangiogenic cytokine that is associated with LV hypertrophy in animal model. Plasmatic FGF23, MMPs and PlGF are elevated in CKD. Aim: We aimed to describe dynamic changes between several novel biomarkers of CV risk (FGF23, MMP-2, MMP-9 and PlGF) in CKD stages 1-5, to describe their mutual correlations and possible association with traditional CV risk markers. We studied possible association of laboratory and echocardiographic parameters in patients with CKD stages 2-4. Methods: In a cross-sectional study we evaluated 80 patiens with CKD 1-5 and 44 healthy controls. In a prospective study we evaluated echocardiographic and laboratory parameters in 62 patients with CKD 2-4 for an average study period of 36±10...