Supplementation with α-lipoic acid, CoQ10, and vitamin E augments running performance and mitochondrial function in female mice.
ABSTRACT: Antioxidant supplements are widely consumed by the general public; however, their effects of on exercise performance are controversial. The aim of this study was to examine the effects of an antioxidant cocktail (α-lipoic acid, vitamin E and coenzyme Q10) on exercise performance, muscle function and training adaptations in mice. C57Bl/J6 mice were placed on antioxidant supplement or placebo-control diets (n = 36/group) and divided into trained (8 wks treadmill running) (n = 12/group) and untrained groups (n = 24/group). Antioxidant supplementation had no effect on the running performance of trained mice nor did it affect training adaptations; however, untrained female mice that received antioxidants performed significantly better than placebo-control mice (p ≤ 0.05). Furthermore, antioxidant-supplemented females (untrained) showed elevated respiratory capacity in freshly excised muscle fibers (quadriceps femoris) (p ≤ 0.05), reduced oxidative damage to muscle proteins (p ≤ 0.05), and increased expression of mitochondrial proteins (p ≤ 0.05) compared to placebo-controls. These changes were attributed to increased expression of proliferator-activated receptor gamma coactivator 1α (PGC-1α) (p ≤ 0.05) via activation of AMP-activated protein kinase (AMPK) (p ≤ 0.05) by antioxidant supplementation. Overall, these results indicate that this antioxidant supplement exerts gender specific effects; augmenting performance and mitochondrial function in untrained females, but does not attenuate training adaptations.
Project description:Diets containing fats of different proportions and types have been demonstrated to influence metabolism. These fats differ in long chain fatty acids (LCFAs) or medium chain fatty acids (MCFAs) content. In our laboratory using swimming as the training modality, MCFAs increased endurance attributed to increased activities of oxidative enzymes. How it affects whole-body metabolism remains unexplored. The present study investigated the metabolic, biochemical and genetic adaptations with treadmill running as the training modality.C57BL/6N mice were divided into untrained and trained groups and provided with low-fat (10% kcal from soybean oil), coconut oil (10% kcal from soybean oil, 20% kcal from coconut oil) or soybean oil (30% kcal from soybean oil) diet. Training was performed on a treadmill for 30 days. After recovery, whole-body metabolism at rest and during exercise, endurance, substrate metabolism, mitochondrial enzyme activities, and gene expression of training-adaptive genes in the muscle and liver were measured.At rest, medium-fat diets decreased respiratory exchange ratio (RER) (p?< 0.05). Training increased RER in all diet groups without affecting oxygen consumption (p?< 0.05). During exercise, diets had no overt effects on metabolism while training decreased oxygen consumption indicating decreased energy expenditure (p?< 0.05). Coconut oil without training improved endurance based on work (p?< 0.05). Training improved all endurance parameters without overt effects of diet (p?< 0.05). Moreover, training increased the activities of mitochondrial enzymes likely related to the increased expression of estrogen related receptor (ERR) ? and ERR? (p?< 0.05). Coconut oil inhibited peroxisome proliferator-activated receptor (PPAR) ?/? activation and glycogen accumulation in the muscle but activated PPAR? in the liver in the trained state (p?< 0.05). Substrate utilization data suggested that coconut oil and/or resulting ketone bodies spared glycogen utilization in the trained muscle during exercise thereby preserving endurance.Our data demonstrated the various roles of diet and fat types in training adaptation. Diets exerted different roles in PPAR activation and substrate handling in the context of endurance exercise training. However, the role of fat types in training adaptations is limited as training overwhelms and normalizes the effects of diet in the untrained state particularly on endurance performance, mitochondrial biogenesis, and ERR expression.
Project description:Milk and/or whey protein plus resistance exercise (RT) increase strength and muscle size, and optimize body composition in adult males and females. Greek yogurt (GY) contains similar muscle-supporting nutrients as milk yet it is different in several ways including being a semi-solid food, containing bacterial cultures and having a higher protein content (mostly casein) per serving. GY has yet to be investigated in the context of a RT program. The purpose of this study was to assess the effects of GY consumption plus RT on strength, muscle thickness and body composition in lean, untrained, university-aged males. Thirty untrained, university-aged (20.6 ± 2.2 years) males were randomized to 2 groups (n = 15/group): fat-free, plain GY or a Placebo Pudding (PP; isoenergetic carbohydrate-based pudding) and underwent a combined RT/plyometric training program 3 days/week for 12 weeks. They consumed either GY (20 g protein/dose) or PP (0 g protein/dose) daily, 3 times on training days and 2 times on non-training days. After 12 weeks, both groups significantly increased strength, muscle thickness and fat-free mass (FFM) (p < 0.05). The GY group gained more total strength (GY; 98 ± 37 kg, PP; 57 ± 15 kg), more biceps brachii muscular thickness (GY; 0.46 ± 0.3 cm, PP; 0.12 ± 0.2 cm), more FFM (GY; 2.4 ± 1.5 kg, PP; 1.3 ± 1.3 kg), and reduced % body fat (GY; -1.1 ± 2.2%, PP; 0.1 ± 2.6%) than PP group (p < 0.05 expressed as absolute change). Thus, consumption of GY during a training program resulted in improved strength, muscle thickness and body composition over a carbohydrate-based placebo. Given the results of our study, the general benefits of consuming GY and its distinctiveness from milk, GY can be a plausible, post-exercise, nutrient-rich alternative for positive strength, muscle, and body composition adaptations.
Project description:<h4>Background</h4>Acute capsaicinoid and capsinoid supplementation has endurance and resistance exercise benefits; however, if these short-term performance benefits translate into chronic benefits when combined with resistance training is currently unknown. This study investigated changes of chronic Capsiate supplementation on muscular adaptations, inflammatory response and performance in untrained men.<h4>Methods</h4>Twenty untrained men were randomized to ingest 12 mg Capsiate (CAP) or placebo in a parallel, double-blind design. Body composition and performance were measured at pre-training and after 6 weeks of resistance training. An acute resistance exercise session test was performed pre and post-intervention. Blood samples were collected at rest and post-resistance exercise to analyze Tumor necrosis factor- (TNF-), Soluble TNF- receptor (sTNF-r), Interleukin-6 (IL-6) and Interleukin-10 (IL-10).<h4>Results</h4>Exercise and CAP supplementation increased fat-free mass in comparison to baseline by 1.5 kg (P < 0.001), however, the majority of the increase (1.0 kg) resulted from an increase in total body water. The CAP change scores for fat-free mass were significantly greater in comparison to the placebo (CAP ∆%= 2.1 ± 1.8 %, PLA ∆%= 0.7 ± 1.3 %, P = 0.043) and there was a significant difference between groups in the bench press exercise (P = 0.034) with greater upper body strength change score for CAP (∆%= 13.4 ± 9.1 %) compared to placebo (∆%= 5.8 ± 5.2 %), P = 0.041. CAP had no effect on lower body strength and no supplementation interactions were observed for all cytokines in response to acute resistance exercise (P > 0.05).<h4>Conclusion</h4>Chronic Capsiate supplementation combined with resistance training during short period (6 weeks) increased fat-free mass and upper body strength but not inflammatory response and performance in young untrained men.
Project description:The kynurenine pathway (KP) is gaining attention in several clinical fields. Recent studies show that physical exercise offers a therapeutic way to improve ratios of neurotoxic to neuroprotective KP metabolites. Antioxidant supplementation can blunt beneficial responses to physical exercise. We here studied the effects of endurance training in the form of sprint interval training (SIT; three sessions of 4-6 × 30 s cycling sprints per week for three weeks) in elderly (~65 years) men exposed to either placebo (<i>n</i> = 9) or the antioxidants vitamin C (1 g/day) and E (235 mg/day) (<i>n</i> = 11). Blood samples and muscle biopsies were taken under resting conditions in association with the first (untrained state) and last (trained state) SIT sessions. In the placebo group, the blood plasma level of the neurotoxic quinolinic acid was lower (~30%) and the neuroprotective kynurenic acid to quinolinic acid ratio was higher (~50%) in the trained than in the untrained state. Moreover, muscle biopsies showed a training-induced increase in kynurenine aminotransferase (KAT) III in the placebo group. All these training effects were absent in the vitamin-treated group. In conclusion, KP metabolism was shifted towards neuroprotection after three weeks of SIT in elderly men and this shift was blocked by antioxidant treatment.
Project description:Exercise training influences phospholipid fatty acid composition in skeletal muscle and these changes are associated with physiological phenotypes; however, the molecular mechanism of this influence on compositional changes is poorly understood. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a nuclear receptor coactivator, promotes mitochondrial biogenesis, the fiber-type switch to oxidative fibers, and angiogenesis in skeletal muscle. Because exercise training induces these adaptations, together with increased PGC-1α, PGC-1α may contribute to the exercise-mediated change in phospholipid fatty acid composition. To determine the role of PGC-1α, we performed lipidomic analyses of skeletal muscle from genetically modified mice that overexpress PGC-1α in skeletal muscle or that carry KO alleles of PGC-1α. We found that PGC-1α affected lipid profiles in skeletal muscle and increased several phospholipid species in glycolytic muscle, namely phosphatidylcholine (PC) (18:0/22:6) and phosphatidylethanolamine (PE) (18:0/22:6). We also found that exercise training increased PC (18:0/22:6) and PE (18:0/22:6) in glycolytic muscle and that PGC-1α was required for these alterations. Because phospholipid fatty acid composition influences cell permeability and receptor stability at the cell membrane, these phospholipids may contribute to exercise training-mediated functional changes in the skeletal muscle.
Project description:Factors underpinning the time-course of resistance-type exercise training (RET) adaptations are not fully understood. This study hypothesized that consuming a twice-daily protein-polyphenol beverage (PPB; <i>n</i> = 15; age, 24 ± 1 yr; BMI, 22.3 ± 0.7 kg·m<sup>-2</sup>) previously shown to accelerate recovery from muscle damage and increase daily myofibrillar protein synthesis (MyoPS) rates would accelerate early (10 sessions) improvements in muscle function and potentiate quadriceps volume and muscle fiber cross-sectional area (fCSA) following 30 unilateral RET sessions in healthy, recreationally active, adults. Versus isocaloric placebo (PLA; <i>n</i> = 14; age, 25 ± 2 yr; BMI, 23.9 ± 1.0 kg·m<sup>-2</sup>), PPB increased 48 h MyoPS rates after the first RET session measured using deuterated water (2.01 ± 0.15 vs. 1.51 ± 0.16%·day<sup>-1</sup>, respectively; <i>P</i> < 0.05). In addition, PPB increased isokinetic muscle function over 10 sessions of training relative to the untrained control leg (%U) from 99.9 ± 1.8 pretraining to 107.2 ± 2.4%U at <i>session 10</i> (vs. 102.6 ± 3.9 to 100.8 ± 2.4%U at <i>session 10</i> in PLA; interaction <i>P</i> < 0.05). Pre to posttraining, PPB increased type II fCSA (PLA: 120.8 ± 8.2 to 109.5 ± 8.6%U; PPB: 92.8 ± 6.2 to 108.4 ± 9.7%U; interaction <i>P</i> < 0.05), but the gain in quadriceps muscle volume was similar between groups. Similarly, PPB did not further increase peak isometric torque, muscle function, or MyoPS measured posttraining. This suggests that although PPB increases MyoPS and early adaptation, it may not influence longer term adaptations to unilateral RET.<b>NEW & NOTEWORTHY</b> Using a unilateral model of resistance training, we show for the first time that a protein-polyphenol beverage increases initial rates of myofibrillar protein synthesis and promotes early functional improvements. Following a prolonged period of training, this strategy also increases type II fiber hypertrophy and causes large individual variation in gains in quadricep muscle cross-sectional area.
Project description:Background:Supplementation with large doses of antioxidants, such as vitamin C and E, has been shown to blunt some adaptations to endurance training. The effects of antioxidant supplementation on adaptations to strength training is sparsely studied. Herein we investigated the effects of vitamin C and E supplementation on acute stress responses to exercise and adaptation to traditional heavy load strength training. Methods:In a double blind placebo-controlled design, twenty-eight, young, trained males and females were randomly assigned to receive either vitamin C and E (C: 1000 mg, E: 235 mg, per day) or placebo supplements, and underwent strength training for 10 weeks. After five weeks, a subgroup conducted a strength training session to investigate acute stress responses. Muscle samples were obtained to investigate changes in stress responses and in proteins and mRNA related to the heat shock proteins (HSPs) or antioxidant enzymes. Results:The acute responses to the exercise session revealed activation of the NF?B pathway indicated by degradation of I?B? in both groups. Vitamin C and E supplementation had, however, no effects on the acute stress responses. Furthermore, ten weeks of strength training did not change muscle ?B-crystallin, HSP27, HSP70, GPx1 or mnSOD levels, with no influence of supplementation. Conclusions:Our results showed that although vitamin C and E supplementation has been shown to interfere with training adaptations, it did not affect acute stress responses or long-term training adaptations in the HSPs or antioxidant enzymes in this study.
Project description:We examined if resistance training affected muscle NAD+ and NADH concentrations as well as nicotinamide phosphoribosyltransferase (NAMPT) protein levels and sirtuin (SIRT) activity markers in middle-aged, untrained (MA) individuals. MA participants (59±4 years old; n=16) completed 10 weeks of full-body resistance training (2 d/wk). Body composition, knee extensor strength, and vastus lateralis muscle biopsies were obtained prior to training (Pre) and 72 hours following the last training bout (Post). Data from trained college-aged men (22±3 years old, training age: 6±2 years old; n=15) were also obtained for comparative purposes. Muscle NAD+ (+127%, p<0.001), NADH (+99%, p=0.002), global SIRT activity (+13%, p=0.036), and NAMPT protein (+15%, p=0.014) increased from Pre to Post in MA participants. Additionally, Pre muscle NAD+ and NADH in MA participants were lower than college-aged participants (p<0.05), whereas Post values were similar between cohorts (p>0.10). Interestingly, muscle citrate synthase activity levels (i.e., mitochondrial density) increased in MA participants from Pre to Post (+183%, p<0.001), and this increase was significantly associated with increases in muscle NAD+ (r2=0.592, p=0.001). In summary, muscle NAD+, NADH, and global SIRT activity are positively affected by resistance training in middle-aged, untrained individuals. Whether these adaptations facilitated mitochondrial biogenesis remains to be determined.
Project description:The effects of antioxidant supplements on exercise-induced oxidative stress have not been investigated in untrained leisure horses. We investigated the effects of 14-day supplementation with vitamin E (1.8 IU/kg/day), coenzyme Q<sub>10</sub> (CoQ<sub>10</sub>; ubiquinone; 800 mg/day), and a combination of both (the same doses as in mono-supplementation) on the blood levels of CoQ<sub>10</sub>, vitamin E, and oxidative stress parameters in untrained leisure horses subjected to acute moderate exercise. Correlations between lipid peroxidation and muscle enzyme leakage were also determined. Forty client-owned horses were included in the study, with 10 horses in each of the antioxidant and placebo (paraffin oil) groups. Blood parameters were measured before supplementation, before and immediately after exercise, and after 24 h of rest. The differences in individual parameters between blood collection times and groups were analysed with linear mixed models (<i>p</i> ˂ 0.05). None of the supplemented antioxidants affected vitamin E and CoQ<sub>10</sub> concentrations, oxidative stress parameters, or serum muscle enzymes. Lipid peroxidation occurred in horses supplemented with placebo and CoQ<sub>10</sub> but not in horses supplemented with vitamin E or the combination of both antioxidants. These results suggest that vitamin E alone or in combination with CoQ<sub>10</sub> prevented lipid peroxidation in untrained leisure horses subjected to acute moderate exercise.
Project description:<h4>Background</h4>In the context of mass regulation, 'muscle memory' can be defined as long-lasting cellular adaptations to hypertrophic exercise training that persist during detraining-induced atrophy and may facilitate future adaptation. The cellular basis of muscle memory is not clearly defined but may be related to myonuclear number and/or epigenetic changes within muscle fibres.<h4>Methods</h4>Utilizing progressive weighted wheel running (PoWeR), a novel murine exercise training model, we explored myonuclear dynamics and skeletal muscle miRNA levels with training and detraining utilizing immunohistochemistry, single fibre myonuclear analysis, and quantitative analysis of miRNAs. We also used a genetically inducible mouse model of fluorescent myonuclear labelling to study myonuclear adaptations early during exercise.<h4>Results</h4>In the soleus, oxidative type 2a fibres were larger after 2 months of PoWeR (P = 0.02), but muscle fibre size and myonuclear number did not return to untrained levels after 6 months of detraining. Soleus type 1 fibres were not larger after PoWeR but had significantly more myonuclei, as well as central nuclei (P < 0.0001), the latter from satellite cell-derived or resident myonuclei, appearing early during training and remaining with detraining. In the gastrocnemius muscle, oxidative type 2a fibres of the deep region were larger and contained more myonuclei after PoWeR (P < 0.003), both of which returned to untrained levels after detraining. In the gastrocnemius and plantaris, two muscles where myonuclear number was comparable with untrained levels after 6 months of detraining, myonuclei were significantly elongated with detraining (P < 0.0001). In the gastrocnemius, miR-1 was lower with training and remained lower after detraining (P < 0.002).<h4>Conclusions</h4>This study found that (i) myonuclei gained during hypertrophy are lost with detraining across muscles, even in oxidative fibres; (ii) complete reversal of muscle adaptations, including myonuclear number, to untrained levels occurs within 6 months in the plantaris and gastrocnemius; (iii) the murine soleus is resistant to detraining; (iv) myonuclear accretion occurs early with wheel running and can be uncoupled from muscle fibre hypertrophy; (v) resident (non-satellite cell-derived) myonuclei can adopt a central location; (vi) myonuclei change shape with training and detraining; and (vii) miR-1 levels may reflect a memory of previous adaptation that facilitates future growth.