Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren,David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fishoil and vitamin E supplementation in oxidative stress at rest and afterphysical exercise. J. Appl. Physiol.83(1): 189-195, 1997.Fish oil supplementation and physicalexercise may induce oxidative stress. We tested the effects of 8 wk of-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats(n = 80) were divided into groupssupplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO andvitamin E (SOVE), and for FOVE and SOVE they were dividedinto corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipidperoxidation [thiobarbituric acid-reacting substances(TBARS)] was 33% higher in FO compared with SO in the liver, butoxidative protein damage (carbonyl levels) remained similar in bothliver and red gastrocnemius muscle (RG). Vitamin E supplementation,compared with FO and SO, markedly decreased liver and RG TBARS, butliver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E alsomarkedly decreased liver and RG protein carbonyl levels, althoughlevels in FOVE and SOVE were similar. Exercise increased liver and RGTBARS and RG protein carbonyl levels markedly, with similar levels inFOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not proteinoxidation in a tissue-specific manner. Vitamin E markedly decreasedlipid peroxidation and protein oxidation in both FOVE and SOVE,although liver lipid peroxidation remained higher in FOVE. Despitehigher levels of hepatic lipid peroxidation at rest in FOVE comparedwith SOVE, liver appeared to be relatively less susceptible toexercise-induced oxidative stress in FOVE.

     

Oxidation of low-density lipoproteins: effect of antioxidant content,fatty acid composition and intrinsic phospholipase activity on susceptibility to metal ion-induced oxidation

The oxidative modification of low-density lipoprotein (LDL) may play an important role in atherogenesis. Our understanding of the mechanism of LDL oxidation and the factors that determine its susceptibility to oxidation is still incomplete. We have isolated LDL from 45 healthy individuals and studied the relationship between LDL fatty acid, vitamin E and β-carotene composition, intrinsic phospholipase A₂-like activity and parameters of LDL oxidation. LDL was exposed to a copper ion-dependent oxidising system and the kinetics of oxidation studied by monitoring formation of fatty acid conjugated dienes. The length of the lag phase of inhibited lipid peroxidation was measured as well as the rate of lipid peroxidation during the propagation phase. There was no significant correlation between LDL antioxidant vitamin or fatty acid composition and lag time to LDL oxidation. Oleic acid was negatively correlated with the rate of LDL oxidation (r = −0.41, P < 0.01) whilst linoleic acid was significantly correlated with the extent of LDL oxidation measured by the production of total dienes (r = 0.34, P < 0.05). Interestingly, LDL vitamin E content was positively correlated with both the rate (r = 0.28, P < 0.05) and extent of LDL oxidation (r = 0.43, P < 0.01). LDL isolated from this group of subjects showed significant intrinsic phospholipase-like activity. The phospholipase activity, whilst not correlated with lag time, was significantly correlated with both rate (r = 0.43, P < 0.01) and total diene production (r = 0.44, P < 0.01) of LDL oxidation. We conclude that antioxidant content, fatty acid composition and intrinsic phospholipase activity have little influence on the lag time of Cu-induced LDL oxidation. These components do however, significantly influence both the rate and extent of LDL oxidation, with increased vitamin E, linoleic acid content and phospholipase activity associated with faster and more extensive oxidation. The possible pro-oxidant effect of vitamin E has interesting implications for the postulated ‘protective’ effects of vitamin E on atherogenesis.     

Supercritical fluid-aerosolized vitamin E pretreatment decreases leak in isolated oxidant-perfused rat lungs

Hybertson, Brooks M., Roger P. Kitlowski, Eric K. Jepson,and John E. Repine. Supercritical fluid-aerosolized vitamin Epretreatment decreases leak in isolated oxidant-perfused rat lungs.J. Appl. Physiol. 84(1): 263-268, 1998.We hypothesized that direct pulmonary administration ofsupercritical fluid-aerosolized (SFA) vitamin E would decrease acuteoxidative lung injury. We previously reported that rapid expansion ofsupercritical CO₂ formedrespirable particles of vitamin E and that administering SFA vitamin Eto rats increased lung vitamin E levels and decreased neutrophil-mediated lung leak. In the present investigation, we foundthat pretreatment with SFA vitamin E protected isolated rat lungsagainst the oxidant-induced lung leak caused by perfusion with xanthineoxidase (XO) and purine, an enzyme system that generates superoxideanion () and hydrogenperoxide. SFA vitamin E droplets were 0.7-3 µm in diameter, andinhalation of the airborne droplets for 30 min deposited ~55 µg ofvitamin E in rat lungs. Isolated rat lungs perfused with XO (0.02 U/ml) and purine (10 mM) gained more weight (1.75 ± 0.12 g,n = 8), retained more Ficoll(11.5 ± 1.2 mg/left lung,n = 7), and accumulated more Ficoll intheir lung lavages (700 ± 146 µg/ml,n = 8) than control lungs [0.25 ± 0.06 g (n = 10), 6.2 ± 1.2 mg/left lung (n = 9), and 141 ± 31 µg/ml (n = 8), respectively,P < 0.05]. In contrast,isolated lungs from rats that were pretreated with SFA vitamin E haddecreased (P < 0.05) weight gains(0.32 ± 0.06 g, n = 7), Ficollretentions (3.3 ± 1.1 mg/left lung,n = 7), and lung lavage Ficollconcentrations (91 ± 26 µg/ml,n = 6) after perfusion with XO andpurine compared with isolated lungs from control rats perfused with XOand purine. This protective effect was not observed in rat lungs givensham treatments (CO₂ alone orvitamin E acetate aerosolized with supercriticalCO₂). Our results suggest thatdirect pulmonary supplementation of vitamin E decreases susceptibilityto vascular leakage caused by XO-derived oxidants.

     

Oral supplements of vitamin E improve measures of oxidative stress in plasma and reduce oxidative damage to LDL and erythrocytes in β-thalassemia intermedia patients

Fifteen β-thalassemia intermedia patients, not requiring chronic transfusional therapy, were monitored in order to check their antioxidant status, and the lipid oxidation products in plasma, LDL, and erythrocytes before and during a 9-month oral treatment with 600 mg/day vitamin E. The low level of vitamin E, and high level of malondialdehyde in plasma clearly tended to normalize after three months (P<.001), and were quite similar to control after six months. The abnormally low level of vitamin E in LDL and the four times higher than control basal level of conjugated dienes (LDL-CD), were not modified after three months of treatment. Significant changes of LDL-VE (P<.05) and of the basal LDL-CD (P<.001) were evident after six months. LDL-VE was within the normal range after nine months, whereas LDL-CD still appeared twice as higher than control.

Plasma vitamin A, ascorbate, β-carotene, and lycopene increased markedly at the end of the trial (P<.005).

The level of vitamin E in red blood cells was normalized after six months of supplementation. A decrease of the baseline value of conjugated dienes was observed after nine months, although it remained 1.4-fold higher than control. The RBC count and hematocrit appeared higher at the end of the trial (P<.05 and P<.001, respectively). The hemoglobin value did not show variations. A shift to normal of the resistance of erythrocytes to osmotic lysis was observed.

Our findings provide evidence that an oral treatment with vitamin E improves the antioxidant/oxidant balance in plasma, LDL particles, and red blood cells, and counteracts lipid peroxidation processes in β-thalassemia intermedia patients.     

Oral supplements of vitamin E improve measures of oxidative stress in plasma and reduce oxidative damage to LDL and erythrocytes in beta-thalassemia intermedia patients

Fifteen beta-thalassemia intermedia patients, not requiring chronic transfusional therapy, were monitored in order to check their antioxidant status, and the lipid oxidation products in plasma, LDL, and erythrocytes before and during a 9-month oral treatment with 600 mg/day vitamin E. The low level of vitamin E, and high level of malondialdehyde in plasma clearly tended to normalize after three months (P < .001), and were quite similar to control after six months. The abnormally low level of vitamin E in LDL and the four times higher than control basal level of conjugated dienes (LDL-CD), were not modified after three months of treatment. Significant changes of LDL-VE (P < .05) and of the basal LDL-CD (P < .001) were evident after six months. LDL-VE was within the normal range after nine months, whereas LDL-CD still appeared twice as higher than control. Plasma vitamin A, ascorbate, beta-carotene, and lycopene increased markedly at the end of the trial (P < .005). The level of vitamin E in red blood cells was normalized after six months of supplementation. A decrease of the baseline value of conjugated dienes was observed after nine months, although it remained 1.4-fold higher than control. The RBC count and hematocrit appeared higher at the end of the trial (P < .05 and P < .001, respectively). The hemoglobin value did not show variations. A shift to normal of the resistance of erythrocytes to osmotic lysis was observed. Our findings provide evidence that an oral treatment with vitamin E improves the antioxidant/oxidant balance in plasma, LDL particles, and red blood cells, and counteracts lipid peroxidation processes in beta-thalassemia intermedia patients.     

Oxidative stress and antioxidant status in mouse kidney: effects of dietary lipid and vitamin E plus iron

The purpose of this study was to determine the effects of dietary fat, vitamin E, and iron on oxidative damage and antioxidant status in kidneys of mice. Sixty 1-month-old male Swiss-Webster mice were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g all-rac-alpha-tocopherol acetate or 0.74 g ferric citrate per kilogram of diet for 4 weeks. Significantly (P < 0.05) higher levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), and conjugated dienes were found in the kidneys of mice fed with fish oil compared with mice fed lard irrespective of vitamin E status. Mice maintained on a vitamin E-deficient diet had significantly higher renal levels of TBAR, but not conjugated dienes, than the supplemented group. Fish oil fed mice receiving vitamin E supplementation had lower levels of alpha-tocopherol than did mice in the lard fed group. Significantly higher levels of ascorbic acid were also found in the kidneys of mice fed with fish oil than were found in mice fed lard. The levels of protein carbonyls and glutathione (GSH), and activities of catalase, superoxide dismutase, selenium (Se)-GSH peroxidase, and non-Se-GSH peroxidase were not significantly altered by dietary fat or vitamin E. Dietary iron had no significant effect on any of the oxidative stress and antioxidant indices measured. The results obtained provide experimental evidence for the pro-oxidant effect of high fish oil intake in mouse kidney and suggest that dietary lipids play a key role in determining cellular susceptibility to oxidative stress.     

Effect of caffeinated drinks on substrate metabolism, caffeine excretion, and performance

The effect ofaddition of different dosages of caffeine (Caf) to acarbohydrate-electrolyte solution (CES) on metabolism, Caf excretion,and performance was examined. Subjects(n = 15) ingested 8 ml/kg of waterplacebo (Pla-W), 7% CES (Pla-CES), or 7% CES with 150, 225, and 320 mg/l Caf (CES-150, CES-225, and CES-320, respectively) during a warm-upprotocol (20 min) and 3 ml/kg at one-third and two-thirds of a 1-h timetrial. Performance was improved with Caf supplementation: 62.5 ± 1.3, 61.5 ± 1.1, 60.4 ± 1.0, 58.9 ± 1.0, and 58.9 ± 1.2 min for Pla-W, Pla-CES, CES-150, CES-225, and CES-320, respectively.The postexercise urinary Caf concentration (range 1.3-2.5 µg/ml)was dose dependent and always far below the doping level of theInternational Olympic Committee (12 µg/ml) in all subjects. Sweat Cafexcretion during exercise exceeded postexercise early-void urinary Cafexcretion. Caffeinated CES did not enhance free fatty acidavailability, ruling out the fact that performance improvement resultedfrom enhanced fat oxidation. It is concluded that addition ofrelatively low amounts of Caf to CES improves performance and thatpostexercise urinary Caf concentration remained low.

     

Effect of dietary lipid and vitamin E on mitochondrial lipid peroxidation and hepatic injury in the bile duct-ligated rat.

To assess whether lipid peroxidation of hepatic mitochondria is associated with cholestatic hepatic injury we examined the effect of bile duct ligation (BDL) versus sham surgery on mitochondrial lipids of rats maintained on one of seven diets. Diets included vitamin E-deficient (E-) and vitamin E-sufficient (E+) combined with normal lipid (11.9% calories as stripped corn oil), high lipid (35% calories as stripped corn oil), or n-3 fatty acid (fish oil) supplementation. Rats were killed 17 days after surgery, mitochondria were isolated by differential centrifugation, and lipid-conjugated dienes and thiobarbituric acid-reacting substances (TBARS) were measured in mitochondrial lipids as indices of lipid peroxidation. BDL resulted in significant increases in lipid peroxidation in all dietary groups. The E- high lipid diets (with either corn oil or fish oil) were associated with higher lipid peroxide and serum bilirubin values in BDL rats compared to the normal lipid diets. Fish oil supplementation did not ameliorate cholestatic or oxidative injury. Serum alanine aminotransferase, bilirubin, alkaline phosphatase, and cholylglycine levels correlated significantly with levels of mitochondrial conjugated dienes and TBARS. These data suggest that free radical stress occurs during BDL in the rat and may result in mitochondrial lipid peroxidation, and that diets high in lipid may increase free radical damage to hepatic mitochondria. The role of free radicals in cholestatic hepatic injury requires further investigation.     

Zinc status affects p53, gadd45, and c-fos expression and caspase-3 activity in human bronchial epithelial cells

This study was designed to examine theinfluence of zinc depletion and supplementation on the expression ofp53 gene, target genes of p53, andcaspase-3 activity in normal human bronchial epithelial (NHBE) cells. Aserum-free, low-zinc medium containing 0.4 µmol/l of zinc [zincdeficient (ZD)] was used to deplete cellular zinc over one passage. Inaddition, cells were cultured for one passage in media containing 4.0 µmol/l of zinc [zinc normal (ZN)], which represents normal cultureconcentrations (Clonetics); 16 µmol/l of zinc [zinc adequate (ZA)],which represents normal human plasma zinc levels; or 32 µmol/l ofzinc [zinc supplemented (ZS)], which represents the high end ofplasma zinc levels attainable by oral supplementation in humans.Compared with ZN cells, cellular zinc levels were 76% lower in ZDcells but 3.5-fold and 6-fold higher in ZA and ZS cells, respectively.Abundances of p53 mRNA and nuclear p53 protein were elevatedin treatment groups compared with controls (ZN). For p53mRNA abundance, the highest increase (3-fold) was observed in ZD cells.In contrast, the highest increase (17-fold) in p53 nuclearprotein levels was detected in ZS cells. Moreover, gadd45mRNA abundance was moderately elevated in ZD and ZA cells and was notaltered in ZS cells compared with ZN cells. Furthermore, the onlyalteration in c-fos mRNA and caspase-3 activity was thetwofold increase and the 25% reduction, respectively, detected in ZScompared with ZN cells. Thus p53, gadd45, andc-fos and caspase-3 activity appeared to be modulated bycellular zinc status in NHBE cells.

     

Effect of antioxidant protection by p-coumaric acid on low-density lipoprotein cholesterol oxidation

Mechanisms inwhich p-coumaric acid (CA) acts as an antioxidant are notwell understood. This study investigated whether CA can act as a directscavenger of reactive oxygen species (ROS) and whether it minimizes theoxidation of low-density lipoprotein (LDL). Rats were administered CAin drinking water at low or high doses for 10, 21, and 30 days (uptakeswere 29 and 317 mg/day, respectively). Blood levels of8-epiprostaglandin F₂ were monitored as a marker of LDLoxidation. Oral administration of CA (317 mg/day) for 30 dayssignificantly inhibited LDL oxidation. CA also reduced LDL cholesterollevels in serum but had no effect on levels of high-density lipoproteincholesterol. In vitro studies that used electron spin resonance incombination with spin trapping techniques were used to determine theability of CA to scavenge ROS and alter LDL oxidation. CA effectivelyscavenged ·OH in a dose-dependent manner. IC₅₀ andmaximum velocity for CA scavenging of ·OH were 4.72 µM and 1.2 µM/s, respectively, with a rate constant of 1.8 × 10¹¹ M¹ · s¹. Ourstudies suggest that the antioxidant properties of CA may involve thedirect scavenging of ROS such as ·OH.

     

Effects of glucose, glucose plus branched-chain amino acids, or placebo on bike performance over 100km

Madsen, Klavs, Dave A. MacLean, Bente Kiens, and DirkChristensen. Effects of glucose, glucose plus branched-chain aminoacids, or placebo on bike performance over 100 km. J. Appl. Physiol. 81(6): 2644-2650, 1996.This studywas undertaken to determine the effects of ingesting either glucose(trial G) or glucose plusbranched-chain amino acids (BCAA; trialB), compared with placebo (trialP), during prolonged exercise. Nine well-trained cyclists with a maximal oxygen uptake of 63.1 ± 1.5 mlO₂ ^· min^{1 ·} kg¹performed three laboratory trials consisting of 100 km of cycling separated by 7 days between each trial. During these trials, the subjects were encouraged to complete the 100 km as fast as possible ontheir own bicycles connected to a magnetic brake. No differences inperformance times were observed between the three trials (160.1 ± 4.1, 157.2 ± 4.5, and 159.8 ± 3.7 min, respectively). Intrial B, plasma BCAA levels increased from339 ± 28 µM at rest to 1,026 ± 62 µM after exercise(P < 0.01). Plasma ammoniaconcentrations increased during the entire exercise period for allthree trials and were significantly higher intrial B compared withtrials G andP (P < 0.05). The respiratory exchange ratio was similar in the threetrials during the first 90 min of exercise; thereafter, it tended todrop more in trial P than intrials G andB. These data suggest that neitherglucose nor glucose plus BCAA ingestion during 100 km of cyclingenhance performance in well-trained cyclists.

     

The influence of dietary vitamin E, fat, and methionine on blood cholesterol profile, homocysteine levels, and oxidizability of low density lipoprotein in the gerbil

A 90-day feeding study with gerbils was conducted to evaluate the influence of dietary vitamin E levels (25 mg/kg diet, 75 mg/kg, 300 mg/kg, and 900 mg/kg), two levels of dietary methionione (casein or casein+L-methionine (1% w/w)) and two sources of lipid (soybean oil [20%] or soybean oil [4%]+coconut oil [16%, 1:4 w/w]) upon serum lipids (total cholesterol, HDL-cholesterol, LDL-cholesterol). In addition, this study examined the effects of diet-induced hyperhomocysteinemia and supplemental dietary vitamin E on the oxidation of low density lipoproteins. Tissue vitamin E (heart, liver, and plasma) demonstrated a dose response (P≤0.001) following the supplementation with increasing dietary vitamin E (25, 75, 300, and 900 mg/kg). In addition, tissue vitamin E levels were found to be higher (P≤0.001) in those animals receiving a combination of coconut oil+soybean oil as compared to the group receiving soybean oil solely. Blood cholesterol profiles indicated an increase (P≤0.001) in total cholesterol and LDL cholesterol by the influence of saturated fat and supplemental methionine. Low-density lipoprotein cholesterol profile demonstrated a reduction (P≤0.001) at the higher dietary vitamin E levels (300 and 900 mg/kg) as compared to the 25 mg/kg and 75 mg/kg dietary vitamin E. Plasma protein carbonyls were not influenced by dietary vitamin E nor by supplemental methionine intake. In vitro oxidation of LDL showed that vitamin E delayed the lag time of the oxidation phase (P≤0.001) and reduced total diene production (P≤0.001). On the contrary, supplemental methionine decreased (P≤0.001) the delay time of the lag phase, whereas total diene production was increased (P≤0.001). Plasma lipid hydroperoxides were significantly reduced (P≤0.05) with supplemental dietary vitamin E, whereas supplemental L-methionine (1%) resulted in a significant (P≤0.05) increase in lipid plasma hydroperoxide formation. Plasma homocysteine was elevated (P≤0.001) with supplemental dietary L-methionine (1%) as well as the inclusion of dietary saturated fat. The present data showed that 1) a combination of dietary lipids (saturated and unsaturated fatty acids) as well as vitamin E and methionine supplementation altered blood cholesterol lipoprotein profiles; 2) in vitro oxidation parameters including LDL (lag time and diene production) and plasma hydroperoxide formations were affected by vitamin E and methionine supplementation; and 3) plasma homocysteine concentrations were influenced by supplemental methionine and the inclusion of dietary saturated fat.     

Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability

Jeukendrup, Asker E., Lars B. Borghouts, Wim H. M. Saris,and Anton J. M. Wagenmakers. Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability. J. Appl. Physiol. 81(5):1952-1957, 1996.This study investigated the effect of endogenouscarbohydrate (CHO) availability on oxidation rates of ingested glucoseduring moderate-intensity exercise. Seven well-trained cyclistsperformed two trials of 120 min of cycling exercise in random order at57% maximal O₂ consumption. Preexercise glycogen concentrations were manipulated byglycogen-lowering exercise in combination with CHO restriction[low-glycogen (LG) trial] or CHO loading[moderate-to-high-glycogen (HG) trial]. In the LG and HGtrials, subjects ingested 4 ml/kg body wt of an 8% corn-derivedglucose solution of high natural¹³C abundance at the start,followed by boluses of 2 ml/kg every 15 min. The third trial, in whichpotato-derived glucose was ingested, served as a control test forbackground correction. Exogenous glucose oxidation rates werecalculated from the ¹³C enrichmentof the ingested glucose and of the breathCO₂. Total CHO oxidation was lowerin the LG trial than in the HG trial during 60-120 min of exercise[84 ± 7 (SE) vs. 116 ± 8 g;P < 0.05]. Exogenous CHOoxidation in this period was 28% lower in the LG trial compared withthe HG trial. Maximal exogenous oxidation rates were also lower(P < 0.05) in the LG trial (0.64 ± 0.05 g/min) than in the HG trial (0.88 ± 0.04 g/min). Thisdecreased utilization of exogenous glucose was accompanied by increased plasma free fatty acid levels (2-3 times higher) and lower insulin concentrations. It is concluded that glycogen-lowering exercise, performed the evening before an exercise bout, in combination with CHOrestriction leads to a reduction of the oxidation rate of ingestedglucose during moderate-intensity exercise.

     

Fuel metabolism in men and women during and after long-duration exercise

This study aimed to determine gender-baseddifferences in fuel metabolism in response to long-duration exercise.Fuel oxidation and the metabolic response to exercise were compared inmen (n = 14) and women(n = 13) during 2 h (40% of maximalO₂ uptake) of cycling and 2 h ofpostexercise recovery. In addition, subjects completed a separatecontrol day on which no exercise was performed. Fuel oxidation wasmeasured using indirect calorimetry, and blood samples were drawn forthe determination of circulating substrate and hormone levels. Duringexercise, women derived proportionally more of the total energyexpended from fat oxidation (50.9 ± 1.8 and 43.7 ± 2.1% forwomen and men, respectively, P < 0.02), whereas men derived proportionally more energy from carbohydrateoxidation (53.1 ± 2.1 and 45.7 ± 1.8% for men and women,respectively, P < 0.01). Thesegender-based differences were not observed before exercise, afterexercise, or on the control day. Epinephrine(P < 0.007) and norepinephrine(P < 0.0009) levels weresignificantly greater during exercise in men than in women (peakepinephrine concentrations: 208 ± 36 and 121 ± 15 pg/ml in menand women, respectively; peak norepinephrine concentrations: 924 ± 125 and 659 ± 68 pg/ml in men and women, respectively). Ascirculating glycerol levels were not different between the two groups,this suggests that women may be more sensitive to the lipolytic action of the catecholamines. In conclusion, these data support the view thatdifferent priorities are placed on lipid and carbohydrate oxidationduring exercise in men and women and that these gender-based differences extend to the catecholamine response to exercise.

     

Modulation of whole body protein metabolism, during and after exercise, by variation of dietary protein

The aim of this study was to investigate dietaryprotein-induced changes in whole body leucine turnover and oxidationand in skeletal muscle branched chain 2-oxo acid dehydrogenase (BCOADH) activity, at rest and during exercise. Postabsorptive subjects receiveda primed constant infusion ofL-[1-¹³C,¹⁵N]leucinefor 6 h, after previous consumption of a high- (HP; 1.8 g · kg¹ · day¹,n = 8) or a low-protein diet (LP; 0.7 g · kg¹ · day¹,n = 8) for 7 days. The subjects werestudied at rest for 2 h, during 2-h exercise at 60% maximum oxygenconsumption, then again for 2 h at rest. Exercise induced a doubling ofboth leucine oxidation from 20 µmol · kg¹ · h¹and BCOADH percent activation from 7% in all subjects. Leucine oxidation was greater before (+46%) and during (+40%,P < 0.05) the first hour of exercisein subjects consuming the HP rather than the LP diet, but there was noadditional change in muscle BCOADH activity. The results suggest thatleucine oxidation was increased by previous ingestion of an HP diet,attributable to an increase in leucine availability rather than to astimulation of the skeletal muscle BCOADH activity.

     

Composition of α-tocopherol and fatty acids in porcine tissues after dietary supplementation with vitamin E and different fat sources

The present study evaluated the effect of increasing supplementation of all-rac-α-tocopheryl acetate and dietary fatty acid composition during a four week period after weaning on porcine tissue composition of α-tocopherol stereoisomers and fatty acids, and on hepatic expression of genes involved in transfer of α-tocopherol, and oxidation and metabolism of fatty acids. From day 28 to 56 of age, pigs were provided 5% of tallow, fish oil or sunflower oil and 85, 150, or 300 mg/kg of all-rac-α-tocopheryl acetate. Samples of liver, heart, and adipose tissue were obtained from littermates at day 56. Tissue fatty acid composition was highly influenced by dietary fat sources. Dietary fatty acid composition (P<0.001) and vitamin E supplementation (P<0.001) influenced the α-tocopherol stereoisomer composition in liver, i.e. less proportion of the RRR-α-tocopherol was observed in pigs provided fish oil and the highest dose of vitamin E in comparison with other dietary treatments. In addition, the stereoisomer composition of α-tocopherol in heart, and adipose tissue was influenced by dietary treatments. Expression of genes in liver involved in the regulation of FA conversion, SCD (P=0.002) and D6D (P=0.04) were lower in pigs fed fish oil compared to other treatments, whereas the fatty acid oxidation, as indicated by the expression of PPAR-α, was higher when sunflower and fish oil was provided (P=0.03). Expression of α-TTP in liver was higher in pigs fed fish oil (P=0.01). Vitamin E supplementation did not influence significantly the hepatic gene expression.     

Increased GLUT-4 translocation mediates enhanced insulin sensitivity of muscle glucose transport after exercise

The purpose of this study was to determinewhether the increase in insulin sensitivity of skeletal muscle glucosetransport induced by a single bout of exercise is mediated by enhancedtranslocation of the GLUT-4 glucose transporter to the cell surface.The rate of3-O-[³H]methyl-D-glucosetransport stimulated by a submaximally effective concentration ofinsulin (30 µU/ml) was approximately twofold greater in the musclesstudied 3.5 h after exercise than in those of the sedentary controls(0.89 ± 0.10 vs. 0.43 ± 0.05 µmol · ml¹ · 10 min¹; means ± SE forn = 6/group). GLUT-4 translocation wasassessed by using theATB-[2-³H]BMPAexofacial photolabeling technique. Prior exercise resulted in greatercell surface GLUT-4 labeling in response to submaximal insulintreatment (5.36 ± 0.45 dpm × 10³/g in exercised vs. 3.00 ± 0.38 dpm × 10³/g insedentary group; n = 10/group) thatclosely mirrored the increase in glucose transport activity. The signalgenerated by the insulin receptor, as reflected in the extent ofinsulin receptor substrate-1 tyrosine phosphorylation, was unchangedafter the exercise. We conclude that the increase in muscle insulinsensitivity of glucose transport after exercise is due to translocationof more GLUT-4 to the cell surface and that this effect is not due topotentiation of insulin-stimulated tyrosine phosphorylation.

     

Coenzyme Q10: Absorption,Antioxidative Properties,Determinants, and Plasma Levels

The purpose of this article is to summarise our studies, in which the main determinants and absorption of plasma coenzyme Q10 (Q10, ubiquinone) have been assessed, and the effects of moderate dose oral Q10 supplementation on plasma antioxidative capacity, lipoprotein oxidation resistance and on plasma lipid peroxidation investigated. All the supplementation trials carried out have been blinded and placebo-controlled clinical studies. Of the determinants of Q10, serum cholesterol, serum triglycerides, male gender, alcohol consumption and age were found to be associated positively with plasma Q10 concentration. A single dose of 30 mg of Q10, which is the maximum daily dose recommended by Q10 producers, had only a marginal elevating effect on plasma Q10 levels in non-Q10-deficient subjects. Following supplementation, a dose-dependent increase in plasma Q10 levels was observed up to a daily dose of 200 mg, which resulted in a 6.1-fold increase in plasma Q10 levels. However, simultaneous supplementation with vitamin E resulted in lower plasma Q10 levels. Of the lipid peroxidation measurements, Q10 supplementation did not increase LDL TRAP, plasma TRAP, VLDL+LDL oxidation resistance nor did it decrease LDL oxidation susceptibility ex vivo. Q10 with minor vitamin E dose neither decreased exercise-induced lipid peroxidation ex vivo nor muscular damage. Q10 supplementation might, however, decrease plasma lipid peroxidation in vivo, as assessed by the increased proportion of plasma ubiquinol (reduced form, Q10H 2 ) of total Q10. High dose vitamin E supplementation decreased this proportion, which suggests in vivo regeneration of tocopheryl radicals by ubiquinol.     

Coenzyme Q10: absorption, antioxidative properties, determinants, and plasma levels

The purpose of this article is to summarise our studies, in which the main determinants and absorption of plasma coenzyme Q10 (Q10, ubiquinone) have been assessed, and the effects of moderate dose oral Q10 supplementation on plasma antioxidative capacity, lipoprotein oxidation resistance and on plasma lipid peroxidation investigated. All the supplementation trials carried out have been blinded and placebo-controlled clinical studies. Of the determinants of Q10, serum cholesterol, serum triglycerides, male gender, alcohol consumption and age were found to be associated positively with plasma Q10 concentration. A single dose of 30 mg of Q10, which is the maximum daily dose recommended by Q10 producers, had only a marginal elevating effect on plasma Q10 levels in non-Q10-deficient subjects. Following supplementation, a dose-dependent increase in plasma Q10 levels was observed up to a daily dose of 200 mg, which resulted in a 6.1-fold increase in plasma Q10 levels. However, simultaneous supplementation with vitamin E resulted in lower plasma Q10 levels. Of the lipid peroxidation measurements, Q10 supplementation did not increase LDL TRAP, plasma TRAP, VLDL+LDL oxidation resistance nor did it decrease LDL oxidation susceptibility ex vivo. Q10 with minor vitamin E dose neither decreased exercise-induced lipid peroxidation ex vivo nor muscular damage. Q10 supplementation might, however, decrease plasma lipid peroxidation in vivo , as assessed by the increased proportion of plasma ubiquinol (reduced form, Q10H 2 ) of total Q10. High dose vitamin E supplementation decreased this proportion, which suggests in vivo regeneration of tocopheryl radicals by ubiquinol.     

Effect of vitamin E deprivation and exercise training on induction of HSP70

Kelly, D. A., P. M. Tiidus, M. E. Houston, and E. G. Noble.Effect of vitamin E deprivation and exercise training on inductionof HSP70. J. Appl. Physiol. 81(6):2379-2385, 1996.To investigate the effects of dietary vitamin Edeprivation and chronic exercise on the relative content of selectedisoforms of the heat-shock protein 70 (HSP70) family in rat hindlimbmuscle, vitamin E was withheld for 16 wk from female rats thatunderwent treadmill run training during the final 8 wk. As indicated byincreased (P < 0.05) content of thestress-inducible isoform (HSP72), training did stress the exercisingmuscles. However, vitamin E deficiency did not alter HSP72 content innontrained rats and was associated with a lesser induction(P < 0.01) in some muscles oftrained animals. The constitutive isoform, which exhibited similarlevels in muscles of varying fiber types, was demonstrated to belargely refractory to exercise, with an equivocal response to vitamin Edeprivation. HSP72 content was correlated to type I myosin heavy chain(MHC-I) content but only in muscles of sedentary normal-diet rats.After training, HSP72 content in a muscle essentially devoid of MHC-I(superficial vastus lateralis) reached levels comparable to those in amuscle high in MHC-I (soleus).