The effects of exercise on skeletal and heart muscle citrate synthase and carnitine palmitoyltransferase mRNA expressions in high-calorie fed rats.

In this study, the effect of high-calorie feeding and aerobic exercise on skeletal and cardiac muscle citrate synthase (CS), carnitine palmitoyltransferase-I (CPT-I), and -II (CPT-II) mRNA expressions were evaluated. Genetically non-obese rats were grouped as normal-high calorie and sedentary-exercising. Gastrocnemius-soleus and heart muscles' CS, CPT-I, and CPT-II expressions and skeletal muscles' histopathological characteristics were evaluated. High-fat diet had increased body weight by 10% and aerobic exercise did not make any difference. Skeletal muscle CS expression was increased significantly in normal-calorie exercising group. Exercise and high-fat diet did not change CPT-I and CPT-II expressions in both heart and skeletal muscle. Histopathological evaluations demonstrated increased cytoplasmic lipid droplets in high-calorie fed sedentary rats, and exercise had reduced lipid droplets in skeletal muscle. Also, both mitochondria and nuclei distribution were impaired in high-calorie groups. In conclusion, aerobic exercise without food restriction was not enough to make significant changes in fat transportation mechanism into skeletal and heart muscle.

A Comparison of the Maximal Fat Oxidation Rates of Three Different Time Periods in The Fatmax Stage.

This study aimed to compare the maximal fat oxidation (MFO) rates obtained from the stage average, last 2 min average, and highest value in the Fatmax stage determined with a 6 min step protocol. A total of 35 overweight, sedentary healthy men (age: 25.4 ± 0.7 years, body mass index: 26.0 ± 0.6 kg/m2) participated in the study. Substrate oxidation was calculated using breath-by-breath gas exchange data for each stage. When the change in the fat oxidation rate for every min throughout the Fatmax stage was evaluated, the average value of the 4th min was significantly lower than that of the 2nd and 3rd min (p < 0.01). In addition, the 5th and 6th min fat oxidation rates were significantly lower than the rates of the 1st, 2nd, 3rd, and 4th min (0.30 ± 0.01 and 0.29 ± 0.01 g/min for the 5th and 6th min, respectively, vs. 0.35 ± 0.02, 0.34 ± 0.02, 0.33 ± 0.02, and 0.31 ± 0.01 g/min for the 1st, 2nd, 3rd, and 4th min, respectively; p < 0.01). Most of the participants had MFO rates in the 1st min of the stage (16/35 participants), and the MFO rates of the remaining participants were observed in the 2nd, 3rd, and 4th min (7/35, 4/35, and 8/35 participants, respectively). None of the participants had MFO rates in the 5th or 6th min. The individual MFO rate (highest fat oxidation rate during Fatmax) was significantly higher than the fat oxidation rate calculated with the last 2 min average values (0.36 ± 0.02 and 0.30 ± 0.01 g/min, respectively; p < 0.05). In conclusion, the calculation of the fat oxidation rate by averaging the last portion of the Fatmax stage data may cause the underestimation of the MFO rate, which probably occurs earlier in the Fatmax stage.

Pathogenesis of high-altitude pulmonary edema / Patogénesis de la edeme pulmonar en la altura

Ratas Sprague-Dawley de la especie Madison fueron expuestas a baja presión barométrica de 294 y 236 torr, o 8.5 por ciento de oxígeno a presió normal por 8-10 horas. Esto resultó en un aumento de la presión de la arteria pulmonar y de la presión sistólica ventricular derecha de 30.5 a 49 torr. Los estudios ultraestructurales del pulmón mostraron evidencia de una insuficiencia por stress de los capilares pulmonares que incluyen una interrupción de la capa endotelial capilar, la capa epitelial alveolar, o todas las capas de la pared, eritrocitos y edema en el intersticio de la pared alveolar, fluido proteinaceo y eritrocitos en los espacios alveolares, y protusiones llenas del líquido del endotelio en la luza de los capilares. Estas características son consistentes con los cambios estructurales previamente hemos descrito en pulmones de conejos cuando los capilares son expuestos a altas presiones transmurales, lo que fuertemente sugiere que la patogénesis de HAPE es una insuficiencia por stress de los capilares pulmonares.