No abstract

The fatty acid composition of phospholipids is an important determinant of membrane function. Although the mitochondria play a pivotal role in skeletal muscle function, the fatty acid composition of their individual phospholipids has not been examined. The purpose of this study was to determine the fatty acid profile of each phospholipid in rat skeletal muscle mitochondria and compare it with that of the whole muscle. Lipids were extracted from the gastrocnemius muscles of 10 Wistar rats, and phospholipids were separated by thin-layer chromatography. The fatty acid composition of each phospholipid was then determined by gas chromatography. The same procedure was applied to a mitochondrial preparation from these muscles. We found that the fatty acid composition of the individual mitochondrial phospholipids (phosphatidyl choline, phosphatidyl ethanolamine, cardiolipin, phosphatidyl inositol, phosphatidyl serine, sphingomyelin, and lysophosphatidyl choline) and of the total mitochondrial phospholipids differed markedly (P < 0.05) from the fatty acid composition of the corresponding whole muscle phospholipids. Notably, the mitochondrial phospholipids had higher percentages of MUFA [13.9 (2.1) vs. 10.3 (0.9)] and lower percentages of PUFA [34.8 (4.3) vs. 39.5 (5.2)] and n6 fatty acids [25.0 (2.5) vs. 27.6 (2.5)]. Overall, the mitochondrial phospholipids had a lower unsaturation index than whole muscle phospholipids [135 (20) vs. 161 (26)]. Because PUFA are susceptible to peroxidation, unlike saturated fatty acids and MUFA, we propose that the low polyunsaturation of mitochondrial phospholipids is the result of selective pressure toward membranes that are more resistant to oxidative damage by reactive oxygen species produced in their vicinity. The negative effect of the low polyunsaturation on membrane fluidity may be counterbalanced by the higher percentage of MUFA and the known low cholesterol content of mitochondrial membranes.

Resistance exercise is recommended to individuals following high-protein diets in order to augment changes in body composition. However, alterations in macronutrient composition may compromise physical performance. The present study investigated the effects of an isoenergetic high-protein diet on upper and lower limb strength and fatigue during high-intensity resistance exercise. Ten recreationally active women, aged 25-40 years, followed a control diet (55, 15 and 30 % of energy from carbohydrate, protein and fat, respectively) and a high-protein diet (respective values, 30, 40 and 30) for 7 d each in a random counterbalanced design. Each participant underwent strength testing of upper limb (isometric handgrip strength and endurance) and lower limb (four sets of sixteen maximal knee flexions and extensions on an isokinetic dynamometer) before and after applying each diet. Body weight, body fat and RER were significantly reduced following the high-protein diet (P, 0·05). No differences were found between diets in any of the strength performance parameters (handgrip strength, handgrip endurance, peak torque, total work and fatigue) or the responses of heart rate, systolic and diastolic arterial pressure, blood lactate and blood glucose to exercise. Women on a short-term isoenergetic high-protein, moderate-fat diet maintained muscular strength and endurance of upper and lower limbs during high-intensity resistance exercise without experiencing fatigue earlier compared with a control diet.High-protein diet: Fatigue: Resistance exercise: Handgrip: Women A considerable percentage of the population has reported using a low-carbohydrate, high-protein diet for weight loss and/or maintenance (1) . Although low-carbohydrate ketogenic diets have produced favourable effects on body weight, they have raised concerns on health issues, since these diets are accompanied by increased fat and protein intake. Another criticism of these dietary plans was that they did not recommend physical activity as an integral part of weight loss (1) .Recently proposed high-protein diets advocate the consumption of lean protein sources and allow unrefined carbohydrates from fruits and vegetables. Such high-protein (35 -45 % of energy), low-carbohydrate (20 -35 %) and moderate-fat (, 30 %) diets (high-protein diets) have attracted much attention and are frequently recommended for weight loss and maintenance to individuals with obesity or diabetes (2,3) . There is evidence that high-protein diets induce a number of favourable changes along with weight loss (reduction in body fat, improvement in lipidaemic and glycaemic profiles and resting blood pressure) (2,4) . The addition of exercise (aerobic and/or resistance) to a high-protein diet had additive effects on body composition during weight loss (5) .Despite the popularity of high-protein diets, few studies have investigated their effects on exercise performance (6,7) . These studies reported that a 7 d high-protein diet decreased endurance (aerobic) performance of recreational and trained athle...

We have investigated whether altered hepatic mitochondrial energetics could explain the differential effects of high‐fat diets with low or high ω6 polyunsaturated fatty acid content (lard vs. safflower oil) on the efficiency of body fat recovery (catch‐up fat) during refeeding after caloric restriction. After 2 weeks of caloric restriction, rats were isocalorically refed with a low‐fat diet (LF) or high‐fat diets made from either lard or safflower oil for 1 week, and energy balance and body composition changes were assessed. Hepatic mitochondrial energetics were determined from measurements of liver mitochondrial mass, respiratory capacities, and proton leak. Compared to rats refed the LF, the groups refed high‐fat diets showed lower energy expenditure and increased efficiency of fat gain; these differences were less marked with high‐safflower oil than with high‐lard diet. The increase in efficiency of catch‐up fat by the high‐fat diets could not be attributed to differences in liver mitochondrial activity. By contrast, the lower fat gain with high‐safflower oil than with high‐lard diet is accompanied by higher mitochondrial proton leak and increased proportion of arachidonic acid in mitochondrial membranes. In conclusion, the higher efficiency for catch‐up fat on high‐lard diet than on LF cannot be explained by altered hepatic mitochondrial energetics. By contrast, the ability of the high‐safflower oil diet to produce a less pronounced increase in the efficiency of catch‐up fat may partly reside in increased incorporation of arachidonic acid in hepatic mitochondrial membranes, leading to enhanced proton leak and mitochondrial uncoupling.

The concentration and fatty acid composition of phospholipids in animal cells are important determinants of membrane function. Membrane function may influence apoptosis, a biological process that is crucial for the normal development and function of the body. Few and conflicting data exist regarding the effect of chronic exercise on apoptosis in skeletal muscle, and no data exist regarding the effect of chronic exercise on the fatty acid composition of individual muscle phospholipids. We therefore examined the effects of 8 weeks of voluntary wheel running on DNA fragmentation (an index of apoptosis) and on the concentration and fatty acid composition of individual muscle phospholipids and ceramide (a lipid involved in apoptotic signalling) in rat gastrocnemius muscle by comparing 11 trained and 14 untrained male Wistar rats. The trained animals had significantly (P < 0.05) higher cytochrome c oxidase activity (an index of aerobic adaptation) and lower phosphatidyl inositol concentration compared with their untrained counterparts. Groups did not differ in DNA fragmentation or any other lipid parameter. Our findings suggest that chronic wheel running did not affect apoptosis or the concentration and fatty acid composition of most phospholipids and ceramide in rat gastrocnemius muscle. Given the participation of several phospholipids and ceramide in apoptotic signalling, it appears that the lack of changes in the lipid parameters is in agreement with the lack of change in DNA fragmentation with exercise.