Acute effects of free fatty acids (FFA) were investigated on: (1) glucose oxidation, and UCP-2 and -3 mRNA and protein levels in 1 h incubated rat soleus and extensor digitorium longus (EDL) muscles, (2) mitochondrial membrane potential in cultured skeletal muscle cells, (3) respiratory activity and transmembrane electrical potential in mitochondria isolated from rat skeletal muscle, and (4) oxygen consumption by anesthetized rats. Long-chain FFA increased both basal and insulin-stimulated glucose oxidation in incubated rat soleus and EDL muscles and reduced mitochondrial membrane potential in C2C12 myotubes and rat skeletal muscle cells. Caprylic, palmitic, oleic, and linoleic acid increased O(2) consumption and decreased electrical membrane potential in isolated mitochondria from rat skeletal muscles. FFA did not alter UCP-2 and -3 mRNA and protein levels in rat soleus and EDL muscles. Palmitic acid increased oxygen consumption by anesthetized rats. These results suggest that long-chain FFA acutely lead to mitochondrial uncoupling in skeletal muscle.
RESUMOO exercício físico prolongado reduz os estoques de glicogênio muscular. Nessas condições, os processos de fadiga muscular são estimulados coincidindo com um aumento na produção de espécies reativas de oxigênio. A suplementação de carboidratos ou de antioxidantes isoladamente contribui para a melhora da performance muscular, sugerindo um efeito importante da depleção de substrato (glicose) e do aumento da produção de EROs no desenvolvimento da fadiga muscular durante a atividade física. Embora o mecanismo seja desconhecido, estamos propondo neste estudo que uma maior disponibilidade de glicogênio poderia favorecer uma maior atividade da via das pentoses fosfato, aumentando a disponibilidade de NADPH e GSH no tecido muscular esquelético. Uma maior capacidade antioxidante aumentaria a capacidade do tecido muscular em atividade, mantendo o equilíbrio redox durante atividade física prolongada e melhorando o desempenho. Neste processo, o ciclo glicose-ácido graxo pode ser importante aumentando a oxidação de lipídio e reduzindo o consumo de glicogênio durante a atividade prolongada. Além disso, um aumento na produção de EROs pode reduzir a atividade de enzimas importantes do metabolismo celular incluindo a aconitase e a a-cetoglutarato desidrogenase, comprometendo a produção de energia oxidativa, via predominante na produção de ATP durante a atividade muscular prolongada. Palavras-chave: fadiga, antioxidantes, metabolismo, músculo esquelético, exercício prolongado. ABSTRACTFatigue is closely related to the depletion of glycogen in the skeletal muscle during prolonged exercise. Under this condition, the production of oxygen reactive species (ROS) is substantially increased. It has been shown that dietary supplementation of carbohydrate or antioxidant attenuates muscle fatigue during contraction. This suggests that glycogen availability and/or elevated ROS production plays an important role on muscle fatigue development during prolonged muscle activity. Although the mechanism is still unknown, we propose that elevated muscle glycogen availability may lead to a high activity of hexose monophosphate pathway, increasing the NADPH and glutathione concentration in the skeletal muscle tissue. Elevated antioxidant capacity would increase the muscle redox balance during muscle contraction, improving performance. In this process, the glucose-fatty acid cycle may be important to increase lipid oxidation and consequently decrease glycogen utilization during prolonged activity. In addition, an elevated ROS production could reduce the activity of key metabolic enzymes including aconitase and a-ketoglutarate dehydrogenase, decreasing the oxidative energy production in the skeletal muscle during prolonged activity. Keywords: fatigue, antioxidants, metabolism, skeletal muscle, prolonged exercise. INTRODUÇÃOO papel protetor da glutationa como antioxidante durante a atividade física tem sido extensivamente investigado. Há muitas evidências de que a glutationa é um dos principais antioxidantes do tecido muscular esquelético exercend...
In recent decades, the high incidence of infectious and parasitic diseases has been replaced by a high prevalence of chronic and degenerative diseases. Concomitantly, there have been profound changes in the behavior and eating habits of families around the world, characterizing a “nutritional transition” phenomenon, which refers to a shift in diet in response to modernization, urbanization, or economic development from undernutrition to the excessive consumption of hypercaloric and ultra-processed foods. Protein malnutrition that was a health problem in the first half of the 20th century has now been replaced by high-fat diets, especially diets high in saturated fat, predisposing consumers to overweight and obesity. This panorama points us to the alarming coexistence of both malnutrition and obesity in the same population. In this way, individuals whose mothers were undernourished early in pregnancy and then exposed to postnatal hyperlipidic nutrition have increased risk factors for developing metabolic dysfunction and cardiovascular diseases in adulthood. Thus, our major aim was to review the cardiometabolic effects resulting from postnatal hyperlipidic diets in protein-restricted subjects, as well as to examine the epigenetic repercussions occasioned by the nutritional transition.
We evaluated the effects of perinatal protein undernutrition on the respiratory pattern and responses to hypercapnia and hypoxia. Pregnant Wistar rats received normoproteic (NP, 17% of protein) or hypoproteic diet (HP, 8% of protein) during gestation and lactation. Male offspring (NP: n=10; HP: n=10) at the 30‐day‐old were evaluated for respiratory frequency (Rf), tidal volume (VT) and ventilation (VE), and ventilatory responses to hypercapnia (10% CO2) and hypoxia (7% O2). At rest, HP rats showed increased Rf (NP: 105.3±3.1 vs. HP: 135.1±2.2 cycles.min−1, P<0.0001) and Ve (NP: 987.4±36.1 vs. HP: 1384.9±57.1 mL.kg− 1.min−1, P<0.0001), but no change in VT. After exposure to hypercapnia, HP showed higher ventilatory responses than NP rats in Rf (NP: 170.5±2.8 vs. E: 181±3.5 cycles.min−1, P=0.02) and Ve (C: 2349.1±111.1 vs. E:2769.8±151.8 mL.kg−1.min−1, P=0.03). Likewise, hypoxia‐induced ventilatory responses were increased in HP rats in Rf (NP: 116.9 ±4.1 n= 5 vs. HP: 146.1±4.4 resp.min−1, p=0.0010), VT (NP: 12.0±0.7 vs HP: 16.5 ±1.2 mL.kg−1, p=0.0135) and Ve (NP: 1449.5 ±114.9 vs. HP: 2454.3 ± 175.0 mL.kg−1.min−1, p=0.0013). Our data suggest that juvenile rats submitted to perinatal protein undernutrition had increase in ventilation at rest and in ventilatory responses to hypercania and hypoxia, which could be a potential hidden basis for the development of arterial hypertension in adulthood.Support: FACEPE and CNPq.
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