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.

Carbohydrate-Dependent, Exercise-Induced Gastrointestinal Distress

Gastrointestinal (GI) problems are a common concern of athletes during intense exercise. Ultimately, these symptoms can impair performance and possibly prevent athletes from winning or even finishing a race. The main causes of GI problems during exercise are mechanical, ischemic and nutritional factors. Among the nutritional factors, a high intake of carbohydrate and hyperosmolar solutions increases GI problems. A number of nutritional manipulations have been proposed to minimize gastrointestinal symptoms, including the use of multiple transportable carbohydrates. This type of CHO intake increases the oxidation rates and can prevent the accumulation of carbohydrate in the intestine. Glucose (6%) or glucose plus fructose (8%-10%) beverages are recommended in order to increase CHO intake while avoiding the gastric emptying delay. Training the gut with high intake of CHO may increase absorption capacity and probably prevent GI distress. CHO mouth rinse may be a good strategy to enhance performance without using GI tract in exercises lasting less than an hour. Future strategies should be investigated comparing different CHO types, doses, and concentration in exercises with the same characteristics.

Mechanical strain induces the production of spheroid mineralized microparticles in the aortic valve through a RhoA/ROCK-dependent mechanism

Calcific aortic valve disease (CAVD) is a chronic disorder characterized by an abnormal mineralization of the leaflets, which is accelerated in bicuspid aortic valve (BAV). It is suspected that mechanical strain may promote/enhance mineralization of the aortic valve. However, the effect of mechanical strain and the involved pathways during mineralization of the aortic valve remains largely unknown. Valve interstitial cells (VICs) were isolated and studied under strain conditions. Human bicuspid aortic valves were examined as a model relevant to increase mechanical strain. Cyclic strain increased mineralization of VICs by several-fold. Scanning electron microscope (SEM) and energy dispersive X-ray (EDX) analyses revealed that mechanical strain promoted the formation of mineralized spheroid microparticles, which coalesced into larger structure at the surface of apoptotic VICs. Apoptosis and mineralization were closely associated with expression of ENPP1. Inhibition of ENPP1 greatly reduced mineralization of VIC cultures. Through several lines of evidence we showed that mechanical strain promoted the export of ENPP1-containing vesicles to the plasma membrane through a RhoA/ROCK pathway. Studies conducted in human BAV revealed the presence of spheroid mineralized structures along with the expression of ENPP1 in areas of high mechanical strain. Mechanical strain promotes the production and accumulation of spheroid mineralized microparticles by VICs, which may represent one important underlying mechanism involved in aortic valve mineralization. RhoA/ROCK-mediated export of ENPP1 to the plasma membrane promotes strain-induced mineralization of VICs.