Dietary Intake of Soccer Players before, during and after an Official Game: Influence of Competition Level and Playing Position.

Physical demands in soccer differ according to league level and playing position and may influence nutritional requirements. This study examined the effect of competition level and playing position on dietary intake in male soccer players (SP). Diet was weighed and recorded by 123 SP for 3 days; before, on the day, and the day after an official match. SP in the Super League (SL, n = 33) division reported higher (p < 0.05) average three-day energy (195 ± 36 kJ/kg), carbohydrate (6.0 ± 1.1 g/kg), and protein (2.2 ± 0.5 g/kg) intakes compared to the intakes reported by SP in the 2nd (n = 30) (energy: 159 ± 31 kJ/kg; carbohydrate: 4.6 ± 1.2 g/kg; protein: 1.9 ± 0.4 g/kg), 3rd (n = 30) (energy: 153 ± 34 kJ/kg; carbohydrate: 4.5 ± 1.2 g/kg; protein: 1.7 ± 0.4 g/kg), and 4th (n = 30) (energy: 152 ± 36 kJ/kg; carbohydrate: 4.2 ± 1.2 g/kg; protein: 1.7 ± 0.5 g/kg) national leagues (mean ± SD). Furthermore, when data were analyzed by playing position (pooled data), wide midfielders reported higher (p < 0.05) energy (183 ± 33 kJ/kg), carbohydrate (5.4 ± 1.2 g/kg), and fat (1.5 ± 0.4 g/kg) intakes compared to central defenders (energy: 147 ± 37 kJ/kg; carbohydrate: 4.1 ± 1.1 g/kg; fat: 1.2 ± 0.4 g/kg). The dietary intake of SP may differ according to the playing position and competition level, possibly due to different metabolic demands in training and competition.

Effect of chronic exercise on DNA fragmentation and on lipid profiles in rat skeletal muscle.

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.

An isoenergetic high-protein, moderate-fat diet does not compromise strength and fatigue during resistance exercise in women.

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.

Long-term exercise increases the DNA binding activity of peroxisome proliferator-activated receptor gamma in rat adipose tissue.

The aim of the present study was to examine the effect of 8 weeks of voluntary wheel running on the gene expression, at the protein level, of 2 enzymes involved in lipogenesis (fatty acid synthase [FAS] and diacylglycerol acyl transferase 1), 2 proteins involved in lipolysis (hormone-sensitive lipase [HSL] and perilipin), and 3 transcription factors mediating the induction of genes involved in lipid metabolism (the alpha, gamma, and delta members of the peroxisome proliferator-activated receptor, or PPAR, family) in rat liver, gastrocnemius muscle, epididymal fat, and subcutaneous fat. Proteins were measured through Western blot analysis in the tissues of 11 trained and 14 untrained rats. The trained rats had lower FAS in the liver; higher FAS, HSL, and perilipin in epididymal fat; and higher HSL in subcutaneous fat. In addition, the trained rats had higher total protein concentrations in both fat depots. No significant differences in the liver, muscle, or adipose tissue PPAR contents were found between groups. However, the DNA binding activity of PPARgamma, measured through an enzyme immunoassay-based method, was higher in both fat depots of the trained rats. Our findings suggest that long-term wheel running had significant effects on the concentrations of proteins playing key roles in lipogenesis and lipolysis in rat liver and adipose tissue. These effects may be due to PPAR activation rather than induction, rendering the transcriptional regulation of target genes more economical and flexible. The activation of PPARgamma with exercise may mediate its beneficial effect on insulin sensitivity.

Hepatic mitochondrial energetics during catch-up fat with high-fat diets rich in lard or safflower oil.

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.