Effects of prolonged running performed at the intensity corresponding to the onset of blood lactate accumulation, on maximum isokinetic strength in active non-athletic individuals

OBJETIVO: O objetivo deste estudo foi analisar os efeitos da corrida contínua prolongada realizada na intensidade correspondente ao início do acúmulo do lactato no sangue (OBLA) sobre o torque máximo dos extensores do joelho analisado em diferentes tipos de contração e velocidade de movimento em indivíduos ativos. MÉTODO: Oito indivíduos do gênero masculino (23,4 ± 2,1 anos; 75,8 ± 8,7 kg; 171,1 ± 4,5 cm) participaram deste estudo. Primeiramente, os sujeitos realizaram um teste incremental até a exaustão voluntária para determinar a velocidade correspondente ao OBLA. Posteriormente, os sujeitos retornaram ao laboratório em duas ocasiões, separadas por pelo menos sete dias, para realizar 5 contrações isocinéticas máximas para os extensores do joelho em duas velocidades angulares (60 e 180º.s-1) sob as condições excêntrica (PTE) e concêntrica (PTC). Uma sessão foi realizada após um período de aquecimento padronizado (5 min a 50%VO2max). A outra sessão foi realizada após uma corrida contínua no OBLA até a exaustão voluntária. Essas sessões foram executadas em ordem randômica. RESULTADOS: Houve redução significante do PTC somente a 60º.s-1 (259,0 ± 46,4 e 244,0 ± 41,4 N.m). Entretanto, a redução do PTE foi significante a 60º.s-1 (337,3 ± 43,2 e 321,7 ± 60,0 N.m) e 180º.s-1 (346,1 ± 38,0 e 319,7 ± 43,6 N.m). As reduções relativas da força após o exercício de corrida foram significantemente diferentes entre os tipos de contração somente a 180º.s-1. CONCLUSÃO: Podemos concluir que, em indivíduos ativos, a redução no torque máximo após uma corrida contínua prolongada no OBLA pode ser dependente do tipo de contração e da velocidade angular.

Synthesis, characterization and molecular structures of the pyridinium trans-bis(pyridine)tetrachlororuthenate(III) and pyridinium trans-(carbonyl)(pyridine)tetrachlororuthenate(III)

The pyH[trans-RuCl4(py)2](1) and pyH[trans-RuCl4(CO)(py)](2) complexes were synthesized and found to crystallize in space group P21/n, Z = 4 with a = 8.080(7), b = 22.503(7), c = 10.125(6) Å, β = 93.19(6)° for (1) and a = 7.821(1), b = 10.337(3), c = 19.763(3) Å, β = 93.07(1)° for (2). The structures were solved by Patterson and difference Fourier techniques and refined to R = 0.062 for (1) and R = 0.038 for (2). In both cases the Ru(III) ion is octahedrally coordinated to four co-planar chlorine atoms, the nitrogen of the pyridine rings or carbon from the carbon monoxide. Another protonated pyridine group, which forms the counter-cation completes the crystal structures. The UV-Vis absorption spectra show three bands: (1) 360 (ε = 1180 M-1 cm-1), 441 (ε = 3200 M-1 cm-1) and 532 nm (ε = 400 M-1 cm-1); (2) 315(ε = 1150 M-1 cm-1), 442 (ε = 3170 M-1 cm-1) and 530 nm (ε = 390 M-1 cm-1). The two higher energy bands were associated with ligand-to-metal charge transfer transitions and a third band at lower energy was assigned to a d-d transition. Low temperature EPR data confirmed the presence of the paramagnetically active Ru(III) and it is consistent with axial symmetry of the complexes. The position of the stretching CO band in complex (2) is discussed in terms of metal-CO backbonding.

Histological study of hamster buccal mucosa following topical application of DMBA and exposition to low power 337 nm laser light

The aim of the present work is to analyze the histological changes on hamster buccal mucosa caused by the topical use of 7,12-dimethylbenzanthracene (DMBA) and exposition to a 220 μJ/pulse nitrogen laser light (@ 337 nm) at an average power of 2,3 mW. Twenty-one hamsters divided into two experimental groups were treated six times with DMBA. One hamster was kept as control. Group I was composed by ten hamsters and was submitted only to DMBA. Group II, also with ten hamsters, received the same treatment as group I and was exposed to the laser radiation. The time duration of each irradiation section was 10 seconds. All the treatment happened in alternated days. The histological analysis took place twice, after the end of the treatment and after sixty days. Both experimental groups presented dilatation of vessels, thickening of the epithelial tissue and the presence of inflammatory infiltrates. The preliminary results indicates that in group II the number of dilated vessels and its new area are much more significant than in group I.

Mirabegron relaxes urethral smooth muscle by a dual mechanism involving β3-adrenoceptor activation and α1-adrenoceptor blockade

Mirabegron is the first β3-adrenoceptor (AR) agonist approved for treatment of overactive bladder syndrome (OAB). This study aimed to investigate the effects of β3-adrenoceptor (AR) agonist mirabegron in mouse urethra. The possibility that mirabegron exerts α1-AR antagonism was also tested in rat smooth muscle preparations presenting α1A- (vas deferens and prostate), α1D- (aorta) and α1B-AR (spleen). Functional assays were carried out in mouse and rat isolated tissues. Competition assays for the specific binding of [(3) H]Prazosin to membrane preparations of HEK 293 cells expressing each of the human α1-ARs, as well as β-AR mRNA expression and cyclic AMP measurements in mouse urethra were performed. Mirabegron produced concentration-dependent urethral relaxations that were right shifted by the selective β3-AR antagonist L 748,337, but unaffected by β1- and β2-AR antagonists (atenolol and ICI 118,551, respectively). Mirabegron-induced relaxations were enhanced by the phosphodiesterase-4 inhibitor rolipram, and this agonist stimulated cAMP synthesis. Mirabegron also produced rightward shifts in urethral contractions induced by the α1-AR agonist phenylephrine. Schild regression analysis revealed that mirabegron behaves as a competitive antagonist of α1-AR in urethra, vas deferens and prostate (α1A-AR, pA2  ≅ 5.6) and aorta (α1D-AR, pA2  ≅ 5.4), but not in spleen (α1B-AR). The affinities estimated for mirabegron in functional assays were consistent with those estimated in radioligand binding with human recombinant α1A- and α1D-ARs (pKi ≅ 6.0). The effects of mirabegron in urethral smooth muscle are the result of β3-AR agonism together with α1A / α1D-AR antagonism.