Differential IL 10 serum production between an arm-based and a leg-based maximal resistance test.

Bench press (i.e. arm-based) and half-squat (i.e. leg-based) are exercises commonly used to increase and evaluate muscular strength. In addition to differences in the location of the muscles that participate in each exercise, the total muscle mass required for the latter is larger than that involved in the former. The aim of this study is to analyze the effects of a maximal incremental strength test when performed by bench press and by half-squat on myocellular damage, oxidative damage and the inflammatory cytokine response. Ten male athletes were subjected to half-squat and bench press incremental strength tests. Blood samples were collected at rest, 15-minutes and 24 h post-test. Hydroperoxide and malondialdehyde concentrations were determined as lipid peroxidation markers. Lactate dehydrogenase (LDH) and creatine kinase isoenzyme MB (CK-MB) activities were determined as markers of muscle damage. α-Actin concentration was determined as a marker of sarcomeric damage. Serum interleukin (IL) 6, IL10, and tumor necrosis factor alpha (TNFα) were determined to assess the inflammatory response. LDH and CK-MB values were greater at 15 min and 24 h post bench press exercise (p < 0.05). No differences were found in lipid peroxidation or α-actin. Interestingly, IL10 values were greater in response to the press bench at 24 h post-test (p < 0.05). Our results suggest that, at equivalent workloads, an arm-based exercise induced higher anti-inflammatory effects and more severe muscle damage compared with a leg-based exercise.

Comparison of the inflammatory and stress response between sprint interval swimming and running.

The aim of the study was to compare myocellular damage, metabolic stress, and inflammatory responses as well as circulating sodium (Na+ ) and potassium (K+ ) between a single sprint swimming and running training. Eighteen subjects regularly involved in swimming and running training for at least 2 years were recruited. The subjects performed 8 × 30 seconds "all out" exercise on different days either by running or by swimming in a random order. Blood was collected before each training session, after the cessation of exercise (post) and after 2 hours of rest (2 hours). We then analyzed tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10), interleukin 6 (IL-6), cortisol, creatine kinase MB isoform (CK-MB), lactate dehydrogenase (LDH), K+ , and Na+ . Neither TNF-α nor IL-10 differed between swimming and running. Most of the subjects showed a non-statistically significant increase of LDH and CK-MB after swimming. On the other hand, IL-6 (P < .05) and cortisol (P < .05) were significantly lower after 2 hours of swimming than after running. In addition, post-exercise K+ was significantly lower (P < .001) for swimming than for running. Our results provide evidence of similar inflammatory responses between exercise modes but lower metabolic stress in response to swimming than in response to running.

Antioxidant effect of exercise: Exploring the role of the mitochondrial complex I superassembly.

Mitochondrial respiratory complexes become assembled into supercomplexes (SC) under physiological conditions. One of the functional roles of these entities is the limitation of reactive oxygen species (ROS) produced by complex I (CI) of the respiratory chain. We sought to determine whether the systemic antioxidant effect of exercise is mediated by the assembly of mitochondrial CIs into SCs in rats. Male Wistar rats were exercise trained or remained sedentary for ten weeks; then, blood samples were collected, and the gastrocnemius muscle was isolated. The assembly of mitochondrial SCs and the lipid peroxidation of the mitochondrial and plasmatic fractions were assessed. Our results demonstrate that exercise induced the assembly of CI into SCs in the gastrocnemius and induced a systemic decrease in lipid peroxidation. We also found an inverse association between the superassembly of CIs and mitochondrial lipid peroxidation (p < 0.01) and protein carbonyls (p < 0.05). We conclude that exercise induces the chronic assembly of CIs into SCs, which provide mitochondrial protection against oxidative damage, at least in the studied muscle. Given the relevant role that mitochondria play in health and disease, these findings should help to elucidate the role of exercise as a therapeutic approach for metabolic diseases.

Coenzyme Q differentially modulates phospholipid hydroperoxide glutathione peroxidase gene expression and free radicals production in malignant and non-malignant prostate cells.

The aim of this study was to investigate the role of coenzyme Q on the mRNA abundance of PHGPx and the reactive oxygen species (ROS) production in two different cell lines from human prostate, a line of non cancer cells (PNT2) and a line of cancer cells (PC3). Results showed that malignant cells markedly differ in their response to coenzyme Q compared to non-malignant cells, with no changes in PHGPx expression and greater ROS production. Furthermore coenzyme Q supplementation significantly lowered cell growth of the PC3 cancer line without affecting the PNT2. If these results are confirmed with additional experiments, it could represent a novel and interesting approach on the biomedical use of coenzyme Q10 in cancer therapy.

Dietary oils high in oleic acid, but with different non-glyceride contents, have different effects on lipid profiles and peroxidation in rabbit hepatic mitochondria.

The influence on the lipid profile and lipid peroxidation in rabbit-liver mitochondria exerted by different edible oils high in oleic acid but different non-glyceride phenolic fractions was studied. High-phenolic virgin olive oil from the variety "Picual", the same oil submitted to an exhaustive process of washing to eliminate the phenolic fraction without altering the lipid profile and high-oleic sunflower oil (poor in phenolic compounds) were added to rabbit diets. The results reveal the importance of the different oleic: linoleic ratio of the lipid sources on the lipid profile of mitochondrial membranes. This is highlighted by the greater proportion of saturated fatty acids and the lower content in oleic acid (p < 0.05) shown by the rabbits fed on high-oleic sunflower oil. The group fed on the fat rich in phenolics exhibited the highest level of antioxidants (alpha-tocopherol, ubiquinone 10) and the highest activity of glutathione peroxidase as well as the lowest content in hydroperoxides and TBARS. The study provides evidences in vivo about the considerable antioxidant capacity of the phenolic fraction of virgin olive oil in rabbit-liver mitochondria and the important role that this non-glyceride fraction can play in the overall antioxidant benefits attributed to this oil.

Dietary fat type and regular exercise affect mitochondrial composition and function depending on specific tissue in the rat.

Physical exercise and fatty acids have been studied in relation to mitochondrial composition and function in rat liver, heart, and skeletal muscle. Male rats were divided into two groups according to dietary fat type (virgin olive and sunflower oils). One-half of the animals from each group were subjected to a submaximal exercise for 8 weeks; the other half acted as sedentary controls. Coenzyme Q, cytochromes b, c + c1, a + a3 concentrations, and the activity of cytochrome c oxidase were determined. Regular exercise increased (P < 0.05) the concentration of the above-mentioned elements and the activity of the cytochrome c oxidase by roughly 50% in liver and skeletal muscle. In contrast, physical exercise decreased (P < 0.05) cytochrome c oxidase activity in the heart (in micromol/min/g, from 8.4+/-0.1 to 4.9+/-0.1 in virgin olive oil group and from 9.7+/-0.1 to 6.7+/-0.2 in sunflower oil animals). Dietary fat type raised the levels of coenzyme Q, cytochromes, and cytochrome c oxidase activity in skeletal muscle (P < 0.05) among the rats fed sunflower oil. In conclusion, dietary fat type, regular exercise, and the specific tissue modulate composition and function of rat mitochondria.

Cerebral cortex synaptic heavy mitochondria may represent the oldest synaptic mitochondrial population: biochemical heterogeneity and effects of L-acetylcarnitine.

The microheterogeneous nature of intrasynaptic mitochondria has been demonstrated and is widely accepted. However, evidence is still lacking about the role played by the different intrasynaptic mitochondrial subpopulations. The data obtained support the hypothesis that "heavy" mitochondria could represent old mitochondrial populations: in fact, in addition to the well known impairment of typical mitochondrial functions, they possess the highest levels of hydroperoxides and their fatty acids pattern is completely modified. The qualitative and quantitative fatty acid modifications suffered by these organelles deeply altered their protein/lipid ratio, thus modifying their mode of action. The present work also collects a large body of evidence that a subchronic L-acetylcarnitine treatment in 28 days does not structurally affect both nonsynaptic and intrasynaptic mitochondria of normal rat in a "steady-state" metabolic condition.

Oxidative stress induced by exercise and dietary fat modulates the coenzyme Q and vitamin A balance between plasma and mitochondria.

Physical exercise induces oxidative stress. Dietary fat modulates lipid composition of plasma and fatty acid profile of mitochondrial membranes. Over 8 wk, two groups of rats were fed virgin olive oil or sunflower oil as the only fat sources. Both groups were divided into 4 subgroups according to exercise: one of sedentary rats and the other three of rats subjected to different exercises on a treadmill. There was a lower concentration of vitamin A and coenzyme Q in the plasma of animals subjected to exercise compared to the sedentary animals. The concentrations of these molecules in liver and skeletal muscle mitochondria of animals exercised until exhaustion were higher than in sedentary animals. This can suggest the existence of a balance between plasma and mitochondrial membrane for these antioxidants as a response to an oxidative attack.

Olive oil supplemented with vitamin E affects mitochondrial coenzyme Q levels in liver of rats after an oxidative stress induced by adriamycin.

In this study we have evaluated the supplementation of olive oil with vitamin E on coenzyme Q concentration and lipid peroxidation in rat liver mitochondrial membranes. Four groups of rats were fed on virgin olive, olive plus 200 mg/kg of vitamin E or sunflower oils as lipid dietary source. To provoke an oxidative stress rats were administered intraperitoneally 10 mg/kg/day of adriamycin the last two days of the experiment. Animals fed on olive oil plus vitamin E had significantly higher coenzyme Q and vitamin E levels but a lower mitochondrial hydroperoxide concentration than rats fed on olive oil. Retinol levels were not affected, by either different diets or adriamycin treatment. In conclusion, an increase in coenzyme Q and alpha-tocopherol in these membranes can be a basis for protection against oxidation and improvement in antioxidant capacity.

Virgin olive oil and coenzyme Q10 protect heart mitochondria from peroxidative damage during aging.

The mitochondrial theory of aging suggests that this phenomenon is the consequence of random somatic mutations in mitochondrial DNA, induced by long-term exposure to free radical attack. There are two potential dietary means of delaying the effects of free radicals on cellular aging, i.e., enrichment of mitochondrial membranes with monounsaturated fatty acids and supplementation with antioxidants. We have performed a preliminary study on male rats, 6 or 12 month old, fed with diets differing in the nature of the fat (virgin olive oil or sunflower oil) and/or with antioxidant supplementation (coenzyme Q10), analysing hydroperoxide and coenzyme Q9 and Q10 in heart mitochondria. Preliminary results allow us to conclude that the CoQ10 dietetic supplementation as well as the enrichment of the cellular membranes with monounsaturated fatty acids, successfully protect mitochondrial membranes from aged rats against the free radical insult.

Physical exercise affects the lipid profile of mitochondrial membranes in rats fed with virgin olive oil or sunflower oil.

The effects of physical exercise on the lipid profile in mitochondrial membranes of liver and skeletal muscle were examined in rats fed with virgin olive oil or sunflower oil. Thirty male Wistar rats, 21 d old, were randomly assigned to four groups according to fat ingestion and physical activity over an 8-week period. For each type of oil, one group acted as a control group while rats from the other were trained to run for 40 min daily on a horizontal treadmill, at a speed of 35 m/min. The results show that diet affected the fatty acid profile of the mitochondrial membranes from skeletal muscle and liver. Physical exercise also modified the fatty acid profile of the mitochondrial membranes. Total monounsaturated fatty acids decreased (P < 0.001) in liver mitochondria of exercised animals. Total polyunsaturated fatty acids in mitochondrial membranes of liver increased (P < 0.005) after exercise but those in mitochondrial membranes of skeletal muscle decreased (P < 0.05). These changes due to the exercise may arise via several mechanisms, e.g. fluidity regulation; changes in the eicosanoid metabolism; differences in the availability or oxidation rate of the different fatty acids.

Relative importance of the saponified and unsaponified fractions of dietary olive oil on mitochondrial lipid peroxidation in rabbit heart.

The effects of four edible oils on lipid peroxidation have been investigated in rabbit heart mitochondrial membranes. The experimental oils (olive oil from the variety "picual", washed olive oil from the variety "picual", olive oil from the variety "arbequina" and high-oleic sunflower oil) had a similar fatty-acid composition, but differed in their unsaponified fraction (polyphenols, tocopherols, and others). The lowest hydroperoxide levels were found with picual and washed picual. No differences in mitochondrial membrane thiobarbituric acid reactive substance (TBARS), alpha-tocopherol concentrations and cytosolic antioxidant enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase) were found, whereas the CoQ10 content correlated inversely with hydroperoxide levels in all groups. These results suggest that mitochondrial membranes with high levels of monounsaturated fatty acids generate low levels of lipid peroxidation. Moreover, the saponified fraction of the experimental diets proved more important in preventing lipid peroxidation than the unsaponified fraction. Lastly, coenzyme Q may help to prevent peroxidative stress damage in rabbit heart mitochondria.

Vitamin E supplementation increases the stability and the in vivo antioxidant capacity of refined olive oil.

Two experiments were carried out to investigate if the supplementation with vitamin E affects refined olive oil response to oxidation regarding the stability of the oil and the protection in vivo against lipid peroxidation in rats after its intake in comparison with other edible oils. In experiment 1, samples of virgin olive oil, refined olive oil, refined olive oil supplemented by us with 200 mg/kg vitamin E, and sunflower oil were collected before and after a 60 min frying process. After frying, refined olive oil supplemented with vitamin E compared with the non-supplemented refined olive oil had a higher concentration of alpha-tocopherol (240.34+/-6.07 mg/kg vs. 131.94+/-8.14 mg/kg), more resistance against oxidation (19.01+/-1.88% vs. 10.6+/-2.08%) and less polar components (4.2+/-0.06% vs. 5.45+/-0.22%). In experiment 2, 24 male Wistar rats, divided into 4 groups, were fed on diets based on the same unfried oils (8% w/w) as in experiment 1, for 4 weeks. Two days prior to the end of the experiment, the rats were intraperitoneally administered with adriamycin (10 mg/kg/ day) to provoke an oxidative stress. The rats fed on refined olive oil plus vitamin E compared to the rats fed on non-supplemented refined olive oil had lower hydroperoxides concentrations (26.8+/-2.6 nmol/mg vs. 35.6+/-2.49 nmol/mg) higher coenzyme Q levels (128.1+/-11.97 pmol/mg vs. 81.25+/-9.25 pmol/mg) and higher alpha-tocopherol values (1.23+/-0.04 mmol/mg vs. 0.93+/-0.06 mmol/mg) in microsomes of liver. In conclusion, the supplementation of refined olive oil with 200 mg/kg of vitamin E increases the stability of this oil under pro-oxidant conditions, and its intake decreases the oxidative damage generated by adriamycin in rats.

Plasma antioxidants are strongly affected by iron-induced lipid peroxidation in rats subjected to physical exercise and different dietary fats.

Plasma is an important vehicle through which antioxidant molecules are conveyed and in which they may show different behaviors, either acting as a protective factor for oxidative damage to different blood elements or using it as a vehicle through which dietary antioxidant factors would be distributed to the body. The aim of the study was to determine the plasma level of vitamin E, coenzyme Q, uric acid and vitamin A and their relation with the cellular oxidative damage mediated by physical training and the ingestion of different fat (virgin olive and sunflower oils). Male Wistar rats were divided into 8 subgroups based on the dietary fat intake and their physical activity. Results show that both dietary fat and physical training affect susceptibility to iron-induced lipid peroxidation in plasma and the tissues that were studied. The increase of this lipid peroxidation parallels a decrease of the level of all the plasma antioxidants that were studied.

Lipid peroxidation and antioxidants in erythrocyte membranes of full-term and preterm newborns.

The most probable factor connecting premature infant problems such as retinopathy, intraventricular hemorrhage and chronic lung disease appears to be the excessive production of oxygen free radicals which can occur as a consequence of oxygen therapy. The aim of our investigation was to elucidate the possible correlations between lipid peroxidation, in this study measured as hydroperoxides production, and antioxidant concentrations in erythrocyte membranes of both full term and preterm infants. Hydroperoxide concentrations were found to be high, especially in premature infants, in erythrocyte membranes at birth and in the initial days of life. The erythrocyte membranes were also found to contain low levels and/or low activities of antioxidant defense mechanisms which was more evident in premature newborns where alpha-tochopherol levels were significantly lower in comparison to full term infant levels. Furthermore, when premature infants undergo oxygen therapy these effects were exacerbated. These results demonstrate that at birth, particularly in the premature newborn, the degree of oxidative stress outweighs the antioxidant defense mechanisms.

Tissue specific interactions of exercise, dietary fatty acids, and vitamin E in lipid peroxidation.

Both physical exercise and ingestion of polyunsaturated fatty acids that play an essential role in free radical-mediated damages cause lipid peroxidation. The intake of specific fatty acids can modulate the membrane susceptibility to lipid peroxidation. Data confirmed that liver, skeletal muscle, and heart have different capabilities to adapt their membrane composition to dietary fatty acids, the heart being the most resistant to changes. Such specificity affects membrane hydroperoxide levels that depend on the type of dietary fats and the rate of fatty acid incorporation into the membrane. Sedentary rats fed a monounsaturated fatty acid-rich diet (virgin olive oil) showed a higher protection of their mitochondrial membranes against peroxidation than sedentary rats fed a polyunsaturated fatty acid-rich diet (sunflower oil). Rats subjected to training showed higher hydroperoxide contents than sedentary animals, and exhaustive effort enhanced the aforementioned results as well as in vitro peroxidation with a free radical inducer. This study suggests that peroxide levels first depend on tissue, then on diet and lastly on exercise, both in liver and muscle but not in heart. Finally, it appears that alpha-tocopherol is a less relevant protective agent against lipid peroxidation than monounsaturated fatty acids.

Effects of the amount and type of dietary fat on exocrine pancreatic secretion in dogs after different periods of adaptation.

Mongrel dogs were fed, from weaning to 6 months of age, on one of two 9% lipid diets that differed only in the type of fat content (sunflower oil or virgin olive oil) to study their effects on exocrine pancreatic secretion, in the basal period and in response to food. In addition, the results were compared with those obtained in a previous work performed by us on dogs adapted for 8 months to diets containing a higher (15%) amount of the same dietary fats to further evaluate the influence of the amount of dietary fat and the length of the adaptation period. The results from the present study show that both the volume and bicarbonate secreted in the absence of stimuli are unaffected by the quality of dietary fat. In contrast, in response to food, the pancreatic juice flow and the bicarbonate output were significantly higher in the group of animals given the sunflower oil diet. The differences seem to be related with the oleic acid content in the diets and the effectiveness of this fatty acid in triggering the release of inhibitory peptides such as pancreatic polypeptide and peptide YY. The comparison between the results from our present and previous studies supports the afore-mentioned hypothesis and confirms the existence of a clear influence of the amount and type of dietary fat, especially the oleic acid content, upon the pancreatic response to food, without ruling out a role for the duration of the adaptation period.

Coenzyme Q content depends upon oxidative stress and dietary fat unsaturation.

The presence of Coenzyme Q (CoQ) in food, its role in cellular bioenergetics and antioxidant protection and the key role played by dietary fatty acids on membrane structure support the interest for a wide research concerning the relationship between dietary fats, CoQ content and biochemical behaviour. Several models of peroxidative stress 'in vivo' have been extensively investigated in our laboratory, with particular regards to the influence of dietary fat upon mitochondrial CoQ levels. First studies showed that the unsaturation degree of dietary fat leads to different CoQ9 and CoQ10 mitochondrial contents. The highest levels were found using polyunsaturated fat. A significant CoQ9 decrease after adriamycin peroxidative induction was found when dietary fat was polyunsaturated; on the contrary, a light increase was found in the case of monounsaturated fat. Another example of oxidative stress is that produced by food frying. The results obtained were in some cases similar to those of the previous experimental design: in fact monounsaturated dietary fats increased CoQ mitochondrial contents, whereas the polyunsaturated ones decreased CoQ levels. Finally, the combined effect of physical exercise and dietary fats on tissue and plasma CoQ levels has been studied. CoQ levels did not change during aerobic performances when dietary fat was monounsaturated whereas light increases were detected in the case of polyunsaturated fats. On the contrary, in anaerobic conditions, CoQ levels clearly increased with monounsaturated fats and no alterations were found in the case of polyunsaturated ones.

Lipid peroxidation and antioxidants in newborns.

The aim of this investigation was to elucidate a possible correlation between lipid peroxidation, antioxidant concentrations and erythrocyte membrane fluidity in plasma from newborns. Ten healthy newborns were recruited. Venous blood samples were collected at birth, and thereafter at 3 and 72 h postnatal age. The following parameters were assessed: hydroperoxides, Coenzyme Q10 and alpha-tocopherol both in plasma and in erythrocyte membranes, and fluorescence polarization (as a tool for assessing membrane fluidity). Hydroperoxides were shown to be high in erythrocyte membranes at birth and significantly decreased at 3 and 72 h after birth. In the erythrocyte membranes, coenzyme Q10 content showed an opposite behaviour with respect to the plasma compartment. Membrane fluidity appeared unchanged even in the presence of the above mentioned modifications.

Absence of rapid adaptation of the exocrine pancreas of conscious dogs to diets enriched in fat or carbohydrates.

Adult mongrel dogs were fed during 8 days on one of two diets, one rich in fat (FR) and the other rich in carbohydrates (CR), in order to compare the exocrine pancreatic secretion in the basal period and in response to food. Under resting conditions, mean pancreatic juice flow and mean values of protein content, amylase and lipase activity and production were similar in both experimental groups, suggesting that the period of adaptation used did not produce any influence on the measured parameters. No significant difference between the two dietary groups was found in postprandial volume of pancreatic juice. The peak of pancreatic juice flow in FR-group was smaller but remained elevated until the end of the 5th h, possibly due to the fact of delayed gastric emptying when animals are fed with a high fat diet. No significant differences were found between the groups in neither postprandial amylase activity and secretion nor lipase activity. On the other hand, lipase output was significantly higher in FR-group but only during the 5 postprandial h. This fact may be related to some intestinal factor stimulated by the hydrolysis products of fat. Finally, our findings show that no rapid adaptation of exocrine pancreatic secretion exist to the diet, at least in our experimental conditions. Of course, this does not exclude that the phenomenon of adaptation may appear in the dog under long-term adaptation to the diet.