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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ABSTRACT: Astaxanthin (ASTA) is a pinkish-orange carotenoid commonly found in marine organisms, especially salmon. ASTA is a powerful antioxidant and suggested to provide benefits for human health, including the inhibition of LDL oxidation, UV-photoprotection, and prophylaxis of bacterial stomach ulcers. Exercise is associated to overproduction of free radicals in muscles and plasma, with pivotal participation of iron ions and glutathione (GSH). Thus, ASTA was studied here as an auxiliary supplement to improve antioxidant defenses in soleus muscles and plasma against oxidative damage induced by exhaustive exercise. Long-term 1 mg ASTA/kg body weight (BW) supplementation in Wistar rats (for 45 days) significantly delayed time to exhaustion by 29% in a swimming test. ASTA supplementation increased scavenging/iron-chelating capacities (TEAC/FRAP) and limited exercise-induced iron overload and its related pro-oxidant effects in plasma of exercising animals. On the other hand, ASTA induced significant mitochondrial Mn-dependent superoxide dismutase and cytosolic glutathione peroxidase antioxidant responses in soleus muscles that, in turn, increased GSH content during exercise, limited oxidative stress, and delayed exhaustion. We also provided significant discussion about a putative "mitochondrial-targeted" action of ASTA based on previous publications and on the positive results found in the highly mitochondrial populated (oxidative-type) soleus muscles here.Nutrients 01/2014; 6(12):5819-5838. DOI:10.3390/nu6125819 · 3.15 Impact Factor
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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: Astaxanthin, a xanthophyll carotenoid, accelerates lipid utilization during aerobic exercise, although the underlying mechanism is unclear. The present study investigated the effect of astaxanthin intake on lipid metabolism associated with peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in mice. Mice were divided into 4 groups: sedentary, sedentary and astaxanthin-treated, exercised, and exercised and astaxanthin-treated. After 2 weeks of treatment, the exercise groups performed treadmill running at 25 m/min for 30 min. Immediately after running, intermuscular pH was measured in hind limb muscles, and blood was collected for measurements. Proteins were extracted from the muscle samples and PGC-1α and its downstream proteins were measured by western blotting. Levels of plasma fatty acids were significantly decreased after exercise in the astaxanthin-fed mice compared with those fed a normal diet. Intermuscular pH was significantly decreased by exercise, and this decrease was inhibited by intake of astaxanthin. Levels of PGC-1α and its downstream proteins were significantly elevated in astaxanthin-fed mice compared with mice fed a normal diet. Astaxanthin intake resulted in a PGC-1α elevation in skeletal muscle, which can lead to acceleration of lipid utilization through activation of mitochondrial aerobic metabolism.Journal of Clinical Biochemistry and Nutrition 03/2014; 54(2):86-9. DOI:10.3164/jcbn.13-110 · 2.29 Impact Factor