Abstract Background: Resistance training promotes cardiovascular health benefits that may affected by sleep deprivation. Objective: To evaluate the effect of high-intensity resistance training on ...myocardial contractility in rats subsequently subjected to paradoxical sleep deprivation. Methods: Forty male Wistar rats were distributed into control group (CTRL), resistance training (REST), 96-hour paradoxical sleep deprivation (PSD96) and resistance training followed by 96-hour paradoxical sleep deprivation (REST/PSD96). The animals underwent high-intensity resistance training for 8 weeks, 5x/week. Twenty-four hours after the last training session, the PSD96 and REST/PSD96 groups were submitted to paradoxical sleep deprivation, which was followed by the in vitro study of isolated papillary muscle contractile mechanics. Results: In comparison with the CTRL group, a lower papillary muscle length and increased cross sectional area were found in PSD96 and RETS/PSD96, which were associated with decreased temporal parameters of contraction force and relaxation. Decreased resting tension and slowing of relaxation time were found in the PSD96 group only. This effect was attenuated by previous resistance training. Conclusion: Resistance training partially prevented contractile changes induced by PSD, minimizing the slowing in relaxation time. Thus, high-intensity exercise seems to not fully protect the cardiac tissue from PSD-induced effects.
Abstract only
We tested the efficacy of modified cardiac fibroblasts (CF) expressing VEGF (
vascular endothelial growth factor
) and/or IGF‐1
(insulin‐like growth factor)
associated to fibrin polymer ...to induce angiogenesis, vasculogenesis and improve cardiac function post myocardium infarction. The groups: VEHICLE= control, POLYMER= fibrin polymer, CELL= 10
6
CF, NULL, VEGF, IGF‐1 and IGF+VEGF= 10
6
modified CF by AdNULL, AdIGF‐1EGFP or AdVEGFEGFP, were directly injected in the left ventricle muscle of rats 24 h following ligation of the descending coronary artery. After 4 weeks, VEGF and IGF‐1 protein increased in IGF‐1, VEGF and IGF‐1+VEGF groups, p<0.0001. Interestingly, only groups receiving VEGF alone or combined with IGF‐1 increased capillary and vascular densities and reduced total myocardial collagen area (35,12 ± 7,05 vs. 31,28 ± 5,03 vs. 30,07 ± 6,21 vs. 25,89 ± 2,92 vs. 15,43 ± 2,02* vs. 16,07 ± 1,83%*, *p<0,05, respectively). Basal morphometric and functional cardiac indices remained unchanged in all groups; however, under pharmacologic stress, the VEGF groups displayed a significant improvement in cardiac work with maintenance of stroke volume and end‐diastolic pressure. Altogether, CF expressing VEGF alone or in combination with IGF‐1 can induce angiogenesis and vasculogenesis in ischemic myocardium decreasing collagen content and improving cardiac performance 4 weeks after coronary ligation.
FUNDAMENTO: Poucos estudos analisaram os efeitos cardíacos do exercício físico prévio à oclusão coronariana. OBJETIVO: Avaliar, em ratas submetidas a exercício físico, as repercussões do infarto do ...miocárdio. MÉTODOS: Ratas foram submetidas à natação ou permaneceram sedentárias por oito semanas e foram randomizadas para oclusão coronariana ou cirurgia simulada, compondo quatro grupos: Sedentário (S), Exercício (E), Sedentário infarto (SIM) e Exercício infarto (EIM). Após seis semanas, foram analisados biometria, ecodopplercardiograma, hemodinâmica e mecânica miocárdica. RESULTADOS: Não foram observados cardioproteção nos animais EIM e diferença no tamanho do infarto (%VE) entre EIM (38,50 ± 4,60%) e SIM (36,58 ± 4,11%). Os teores de água pulmonar (%) de SIM (80 ± 0,59) e EIM (80 ± 0,57) foram maiores do que em S (78 ± 0,15) e E (78 ± 0,57). A pressão sistólica (mmHg) do ventrículo esquerdo (S: 130 ± 5; E: 118 ± 8; SIM: 91 ± 3; EIM: 98 ± 3) e a primeira derivada temporal (mmHg/s) positiva da pressão (S: 8.216 ± 385; E: 8.437 ± 572; SIM: 4.674 ± 455; EIM: 5.080 ± 412) de S e E foram maiores do que em SIM e EIM. As frações de encurtamento da área transversa (%) de SIM (27 ± 2) e EIM (25 ± 2) foram similares e menores do que E (65 ± 2) e S (69 ± 2). A relação E/A foi maior em SIM (5,14 ± 0,61) e EIM (4,73 ± 0,57) em relação a S (2,96 ± 0,24) e E (2,83 ± 0,21). Em estudos de músculos papilares isolados foi verificada depressão da capacidade contrátil semelhante em SIM e EIM, e não houve alteração da rigidez miocárdica. CONCLUSÃO: O treinamento prévio por natação não atenuou as repercussões cardíacas em virtude do infarto do miocárdio.BACKGROUND: Few studies have analyzed the cardiac effects of exercise prior to coronary occlusion. OBJECTIVE: To evaluate the effects of myocardial infarction in rats undergoing physical exercise. METHODS: Female rats underwent swimming exercise or were kept sedentary for eight weeks and were randomized to coronary occlusion or sham surgery, in one of the following four groups: Sedentary (S), exercise (E), Sedentary myocardial infarction (SMI) and Exercise myocardial infarction (EMI). After six weeks, their biometrics, Doppler echocardiography, hemodynamics and myocardial mechanics were analyzed. RESULTS: No cardioprotection was observed in EMI animals and there was no difference in infarct size (%LV) between EMI (38.50 ± 4.60%) and SMI (36.58 ± 4.11%). Water content of the lung (%) of SMI (80 ± 0.59) and EMI (80 ± 0.57) was higher than that of S (78 ± 0.15) and E (78 ± 0.57) groups. Left ventricular systolic pressure (mmHg) (S: 130 ± 5, E: 118 ± 8; SMI: 91 ± 3; EMI: 98 ± 3) and the first positive time derivative (mmHg) positive pressure (S: 8216 ± 385; E: 8437 ± 572; SMI: 4674 ± 455; EMI: 5080 ± 412) of S and E were higher than those of SMI and EMI. The transverse fractional shortening (%) of SMI (27 ± 2) and EMI (25 ± 2) were similar and lower than that of E (65 ± 2) and S (69 ± 2). The E/A ratio was higher in SMI (5.14 ± 0.61) and EMI (4.73 ± 0.57) compared to S (2.96 ± 0.24) and E (2.83 ± 0 21). In studies of isolated papillary muscle, depression of the contractile capacity observed was similar to that of SMI and EMI, and there was no change in myocardial stiffness. CONCLUSION: Previous training by swimming did not attenuate cardiac implications due to myocardial infarction.
FUNDAMENTO: A Contração Pós-Repouso (CPR) do músculo cardíaco fornece informações indiretas sobre a manipulação de cálcio intracelular. OBJETIVO: Nosso objetivo foi estudar o comportamento da CPR e ...seus mecanismos subjacentes em camundongos com infarto do miocárdio. MÉTODOS: Seis semanas após a oclusão coronariana, a contratilidade dos Músculos Papilares (MP) obtidos a partir de camundongos submetidos à cirurgia sham (C, n = 17), com infarto moderado (MMI, n = 10) e grande infarto (LMI, n = 14), foi avaliada após intervalos de repouso de 10 a 60 segundos antes e depois da incubação com cloreto de lítio (Li+) em substituição ao cloreto de sódio ou rianodina (Ry). A expressão proteica de SR Ca(2+)-ATPase (SERCA2), trocador Na+/Ca2+ (NCX), fosfolambam (PLB) e fosfo-Ser (16)-PLB foi analisada por Western blotting. RESULTADOS: Os camundongos MMI apresentaram potenciação de CPR reduzida em comparação aos camundongos C. Em oposição à potenciação normal para camundongos C, foram observadas degradações de força pós-repouso nos músculos de camundongos LMI. Além disso, a Ry bloqueou a degradação ou potenciação de PRC observada em camundongos LMI e C; o Li+ inibiu o NCX e converteu a degradação em potenciação de CPR em camundongos LMI. Embora os camundongos MMI e LMI tenham apresentado diminuição no SERCA2 (72 ± 7% e 47 ± 9% de camundongos controle, respectivamente) e expressão protéica de fosfo-Ser16-PLB (75 ± 5% e 46 ± 11%, respectivamente), a superexpressão do NCX (175 ± 20%) só foi observada nos músculos de camundongos LMI. CONCLUSÃO: Nossos resultados mostraram, pela primeira vez, que a remodelação miocárdica pós-IAM em camundongos pode mudar a potenciação regular para degradação pós-repouso, afetando as proteínas de manipulação de Ca(2+) em miócitos.FUNDAMENTO: La Contracción pos pausa (CPP) del músculo cardíaco provee informaciones indirectas sobre la manejo del calcio intracelular. OBJETIVO: Nuestro objetivo fue estudiar el comportamiento de la CPP y sus mecanismos subyacentes en Ratas con infarto de miocardio. MÉTODOS: Seis semanas después de la oclusión coronaria, la contractilidad de los Músculos Papilares (MP) obtenidos a partir de Ratas sometidos a falsa cirurgia (C, n = 17), con infarto moderado (MMI, n = 10) y gran infarto (LMI, n = 14), fue evaluada después de pausas de estímulos de 10 a 60 segundos antes y después de la incubación con cloruro de litio (Li+) en substitución del cloruro de sodio o rianodina (Ry). La expresión proteica de SR Ca(2+)-ATPasa (SERCA2), intercambiador Na+/Ca2+ (NCX), fosfolamban (PLB) y fosfo-Ser (16)-PLB fue analizada por Western blotting. RESULTADOS: Los Ratas MMI presentaron potenciación de CPP reducida en comparación a los Ratas C. En oposición a la potenciación normal para Ratas C, fueron observadas decaimientos de fuerza post-reposo en los músculos de Ratas LMI. Además de eso, la Ry bloqueó la decaimiento o potenciación de PRC observada en Ratas LMI y C; el Li+ inhibió el NCX y convirtió la decaimiento en potenciación de CPP en Ratas LMI. Aunque los Ratas MMI y LMI hayan presentado disminución en el SERCA2 (72 ± 7% y 47 ± 9% de Ratas control, respectivamente) y expresión proteica de fosfo-Ser16-PLB (75 ± 5% y 46 ± 11%, respectivamente), la superexpresión del NCX (175 ± 20%) sólo fue observada en los músculos de Ratas LMI. CONCLUSIÓN: Nuestros resultados mostraron, por primera vez, que el remodelado miocárdico post-IAM en Ratas puede cambiar la potenciación regular para decaimiento post-reposo, afectando las proteínas de manejo del Ca(2+) en miocitos.BACKGROUND: Post-rest contraction (PRC) of cardiac muscle provides indirect information about the intracellular calcium handling. OBJECTIVE: Our aim was to study the behavior of PRC, and its underlying mechanisms, in rats with myocardial infarction. METHODS: Six weeks after coronary occlusion, the contractility of papillary muscles (PM) obtained from sham-operated (C, n=17), moderate infarcted (MMI, n=10) and large infarcted (LMI, n=14) rats was evaluated, following rest intervals of 10 to 60 seconds before and after incubation with lithium chloride (Li+) substituting sodium chloride or ryanodine (Ry). Protein expression of SR Ca(2+)-ATPase (SERCA2), Na+/Ca2+ exchanger (NCX), phospholamban (PLB) and phospho-Ser(16)-PLB were analyzed by Western blotting. RESULTS: MMI exhibited reduced PRC potentiation when compared to C. Opposing the normal potentiation for C, post-rest decays of force were observed in LMI muscles. In addition, Ry blocked PRC decay or potentiation observed in LMI and C; Li+ inhibited NCX and converted PRC decay to potentiation in LMI. Although MMI and LMI presented decreased SERCA2 (72±7% and 47±9% of Control, respectively) and phospho-Ser16-PLB (75±5% and 46±11%, respectively) protein expression, overexpression of NCX (175±20%) was only observed in LMI muscles. CONCLUSION: Our results showed, for the first time ever, that myocardial remodeling after MI in rats may change the regular potentiation to post-rest decay by affecting myocyte Ca(2+) handling proteins.
FUNDAMENTO: Poucos estudos analisaram os efeitos cardíacos do exercício físico prévio à oclusão coronariana. OBJETIVO: Avaliar, em ratas submetidas a exercício físico, as repercussões do infarto do ...miocárdio. MÉTODOS: Ratas foram submetidas à natação ou permaneceram sedentárias por oito semanas e foram randomizadas para oclusão coronariana ou cirurgia simulada, compondo quatro grupos: Sedentário (S), Exercício (E), Sedentário infarto (SIM) e Exercício infarto (EIM). Após seis semanas, foram analisados biometria, ecodopplercardiograma, hemodinâmica e mecânica miocárdica. RESULTADOS: Não foram observados cardioproteção nos animais EIM e diferença no tamanho do infarto (%VE) entre EIM (38,50 ± 4,60%) e SIM (36,58 ± 4,11%). Os teores de água pulmonar (%) de SIM (80 ± 0,59) e EIM (80 ± 0,57) foram maiores do que em S (78 ± 0,15) e E (78 ± 0,57). A pressão sistólica (mmHg) do ventrículo esquerdo (S: 130 ± 5; E: 118 ± 8; SIM: 91 ± 3; EIM: 98 ± 3) e a primeira derivada temporal (mmHg/s) positiva da pressão (S: 8.216 ± 385; E: 8.437 ± 572; SIM: 4.674 ± 455; EIM: 5.080 ± 412) de S e E foram maiores do que em SIM e EIM. As frações de encurtamento da área transversa (%) de SIM (27 ± 2) e EIM (25 ± 2) foram similares e menores do que E (65 ± 2) e S (69 ± 2). A relação E/A foi maior em SIM (5,14 ± 0,61) e EIM (4,73 ± 0,57) em relação a S (2,96 ± 0,24) e E (2,83 ± 0,21). Em estudos de músculos papilares isolados foi verificada depressão da capacidade contrátil semelhante em SIM e EIM, e não houve alteração da rigidez miocárdica. CONCLUSÃO: O treinamento prévio por natação não atenuou as repercussões cardíacas em virtude do infarto do miocárdio.BACKGROUND: Few studies have analyzed the cardiac effects of exercise prior to coronary occlusion. OBJECTIVE: To evaluate the effects of myocardial infarction in rats undergoing physical exercise. METHODS: Female rats underwent swimming exercise or were kept sedentary for eight weeks and were randomized to coronary occlusion or sham surgery, in one of the following four groups: Sedentary (S), exercise (E), Sedentary myocardial infarction (SMI) and Exercise myocardial infarction (EMI). After six weeks, their biometrics, Doppler echocardiography, hemodynamics and myocardial mechanics were analyzed. RESULTS: No cardioprotection was observed in EMI animals and there was no difference in infarct size (%LV) between EMI (38.50 ± 4.60%) and SMI (36.58 ± 4.11%). Water content of the lung (%) of SMI (80 ± 0.59) and EMI (80 ± 0.57) was higher than that of S (78 ± 0.15) and E (78 ± 0.57) groups. Left ventricular systolic pressure (mmHg) (S: 130 ± 5, E: 118 ± 8; SMI: 91 ± 3; EMI: 98 ± 3) and the first positive time derivative (mmHg) positive pressure (S: 8216 ± 385; E: 8437 ± 572; SMI: 4674 ± 455; EMI: 5080 ± 412) of S and E were higher than those of SMI and EMI. The transverse fractional shortening (%) of SMI (27 ± 2) and EMI (25 ± 2) were similar and lower than that of E (65 ± 2) and S (69 ± 2). The E/A ratio was higher in SMI (5.14 ± 0.61) and EMI (4.73 ± 0.57) compared to S (2.96 ± 0.24) and E (2.83 ± 0 21). In studies of isolated papillary muscle, depression of the contractile capacity observed was similar to that of SMI and EMI, and there was no change in myocardial stiffness. CONCLUSION: Previous training by swimming did not attenuate cardiac implications due to myocardial infarction.
Male Wistar rats (150–200 g) were divided in six groups: 1) sedentary rats (S, n=7), 2) SLD, sedentary‐treated with anabolic steroid (stanozolol, 5 mg/Kg/week, n=6), 3) SHD (stanozolol, 5 mg/Kg/day ...for 5days on week, n=6), 4) trained (T) rats (treadmill‐16 m/min, n=5), 5) TLD, trained‐treated with anabolic steroid (stanozolol, 5 mg/Kg/week, n=6) and 6) THD, trained‐treated with anabolic steroid (stanozolol, 5 mg/Kg/day for 5 days on week, n=6). The whole treatment and exercise protocol were carried out during 8 weeks. After this period, the animals were anesthetized with urethane (1.4 g/kg, IP) and the papillary muscle was quickly removed from the left ventricle and attached to a force transducer and perfused with 1.5 mM Ca2+ containing Krebs‐Ringer's solution enriched with O2 and maintained at 29°C. Muscles were stimulated at 5‐ms pulses, 0.2 Hz for 60 min in Lmax and the data were on‐line recorded (Biopac System). Following that, ryanodine (1μM) was added in the preparation to induce tetanus (10 Hz). The steroid treatment did not cause any change in maximal muscle twitch (S 5.3±0.5, SLD 4.7±0.4, SHD 4.6±0.5 g/mm2). However, the exercise and the association of exercise and the low dose of stanozolol significantly increased the papillary performance (T 6.5±0.3#, TLD 6±0.5#, THD 5.6±0.4 g/mm2# P<0.05 Trained vs. respective sedentary group). The difference disappeared after ryanodine treatment (S 4.5±0.4, SLD 5.2±0.4, SHD 5.3±0.3, T 5±0.3, TLD 5.5±0.2, THD 5.6±0.7 g/mm2). Taken together, the results suggest that the association between exercise and stanozolol was able to improve the papillary performance. The best responses were probably mediated by Ca2+ of SERCA due to ryanodine blocked calcium release.
Supported by FAPESP, CNPq (PRONEX).
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