Effect of Astaxanthin on Cycling Time Trial Performance
ABSTRACT We examined the effect of Astaxanthin (AST) on substrate metabolism and cycling time trial (TT) performance by randomly assigning 21 competitive cyclists to 28 d of encapsulated AST (4 mg/d) or placebo (PLA) supplementation. Testing included a VO2max test and on a separate day a 2 h constant intensity pre-exhaustion ride, after a 10 h fast, at 5% below VO2max stimulated onset of 4 mmol/L lactic acid followed 5 min later by a 20 km TT. Analysis included ANOVA and post-hoc testing. Data are Mean (SD) and (95% CI) when expressed as change (pre vs. post). Fourteen participants successfully completed the trial. Overall, we observed significant improvements in 20 km TT performance in the AST group (n=7; -121 s; 95% CI, -185, -53), but not the PLA (n=7; -19 s; 95% CI, -84, 45). The AST group was significantly different vs. PLA (P<0.05). The AST group significantly increased power output (20 W; 95% CI, 1, 38), while the PLA group did not (1.6 W; 95% CI, -17, 20). The mechanism of action for these improvements remains unclear, as we observed no treatment effects for carbohydrate and fat oxidation, or blood indices indicative of fuel mobilization. While AST significantly improved TT performance the mechanism of action explaining this effect remains obscure.
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- "Astaxanthin exerts an antioxidant effect (Ambati et al. 2014) that is many times stronger than that of Vitamin E, and it has a documented anti-inflammatory activity (Fassett et al. 2008). It reduces phospholipid hydroxides and may support brain function (Nakagawa et al. 2011), reduces stress-induced modifications that impair lipid utilization in the mitochondria (Aoi et al. 2014), and improves muscular performance (Earnest et al. 2011) as well as recovery of muscle damage after exercise (Djordjevic et al. 2012). The anti-oxidant Ubiquinone Q10 (25 mg/day) improves mitochondrial function (Rosenfeldt et al. 2005) and energy production (Cordero et al. 2012), reducing lipid peroxidation (Liao et al. 2007). "
ABSTRACT: Many patients with myalgic encephalopathy (fibromyalgia/chronic fatigue syndrome) localise the beginning of their disease at a time period of emotional, or professional, or social stress, or an infectious or traumatic/surgical incident. It is suggested that these may have temporarily suppressed their immunological system, after which a "rebound" of hyper-immunity has occurred. Hyper-immunity against external aggressors is commonly characterized by an extremely high titre of Immunolobulin G against the Epstein-Barr virus (Herpes 4), or elevated Anti-Streptolysin-O titre (ASLO). In a proportion of patients, hyper-immunity proceeds to auto-immunity with IgG antibodies against the thyroid gland (Hashimoto's disease), Antinuclear antibodies (ANF or ANA), and sometimes positive rheumatism-tests. The IgG covalently binds to Complement C3, which complex is cytotoxic by damaging the cell membrane, and induces inflammation. Simultaneously large quantities of reactive oxygen species (ROS) are produced. This causes muscular pain, poor energy production by the mitochondria, and increased permeability of the capillary vessels, also in the brain. The latter disturbs the thalamo-hypothalamo-pituitary regulation, impairs cognitive function, mood and the working memory. It disturbs the nycthemeral rhythm and the sleep pattern, and may cause neuro-vegetative dysfunction. Antibodies against the myelin sheet as well as impaired neurotransmission may be involved in polyneuropathy. Conventional treatment must correct possible endocrine deficiencies and can help alleviating particular symptoms. Causal treatment addresses the immune dysfunction using corticosteroids, gamma globulin infusions, or immune-suppressors. Immune modulators can selectively be attempted. However, treatment should also address the pathogenic mechanisms by prescribing an appropriate diet, and particular food supplements (Complementary and Alternative Medicine, CAM). We have developed a * Frank@comhaire.com; Brakelmeersstraat, 18; B 9830 Sint Martens-Latem; Belgium. Frank H. Comhaire 2 specific nutraceutical containing several anti-oxidants (Astaxanthin, Oxido-reductase ubiquinone Q10), a strong natural anti-inflammatory substance (pine bark extract, Pycnogenol®), the fyto-adaptogen Lepidium meyenii (MACA), acetyl-carnitine, zinc, and vitamins B6, B9 and B12. To this supplement long-chain poly-unsaturated omega-3 fatty acids are added (docosahexaenoic acid, DHA, and eicosapentaenoic acid, EPA). The CAM approach induces and maintains improvement in 85% of patients, but it seldom results in the complete disappearance of signs and symptoms.
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ABSTRACT: Osteoarthritis (OA) is the most common cause of musculoskeletal disability in elderly individuals, and it places an enormous economic burden on society. Management of OA is primarily focused on palliative relief by using agents such as nonsteroidal anti-inflammatory drugs and analgesics. However, such an approach is limited by a narrow therapeutic focus that fails to address the progressive and multimodal nature of OA. Given the favorable safety profile of most nutritional interventions, identifying disease-modifying nutritional agents capable of improving symptoms and also preventing, slowing, or even reversing the degenerative process in OA should remain an important paradigm in translational and clinical research. Applying advances in nutritional science to musculoskeletal medicine remains challenging, given the fluid and dynamic nature of the field, along with a rapidly developing regulatory climate over manufacturing and commerce requirements. The aim of this article is to review the available literature on effectiveness and potential mechanism of macronutrients for OA, with a focus on the following: long-chain ω-3 essential fatty acids eicosapentaenoic acid and docosahexaenoic acid, functional ω-6 fatty acid γ-linolenic acid, and macronutrient composition of background diet. There also is a discussion about the concept of rational polysupplementation via the strategic integration of multiple nutraceuticals with potential complementary mechanisms for improving outcomes in OA. As applied nutritional science evolves, it will be important to stay on the forefront of proteomics, metabolomics, epigenetics, and nutrigenomics, because they hold enormous potential for developing novel therapeutic and prognostic breakthroughs in many areas of medicine, including OA.PM&R 05/2012; 4(5 Suppl):S145-54. DOI:10.1016/j.pmrj.2012.02.022 · 1.66 Impact Factor
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ABSTRACT: Oxidative stress and inflammation are established processes contributing to cardiovascular disease caused by atherosclerosis. However, antioxidant therapies tested in cardiovascular disease such as vitamin E, C and β-carotene have proved unsuccessful at reducing cardiovascular events and mortality. Although these outcomes may reflect limitations in trial design, new, more potent antioxidant therapies are being pursued. Astaxanthin, a carotenoid found in microalgae, fungi, complex plants, seafood, flamingos and quail is one such agent. It has antioxidant and anti-inflammatory effects. Limited, short duration and small sample size studies have assessed the effects of astaxanthin on oxidative stress and inflammation biomarkers and have investigated bioavailability and safety. So far no significant adverse events have been observed and biomarkers of oxidative stress and inflammation are attenuated with astaxanthin supplementation. Experimental investigations in a range of species using a cardiac ischaemia-reperfusion model demonstrated cardiac muscle preservation when astaxanthin is administered either orally or intravenously prior to the induction of ischaemia. Human clinical cardiovascular studies using astaxanthin therapy have not yet been reported. On the basis of the promising results of experimental cardiovascular studies and the physicochemical and antioxidant properties and safety profile of astaxanthin, clinical trials should be undertaken.Molecules 12/2012; 17(2):2030-48. DOI:10.3390/molecules17022030 · 2.42 Impact Factor