there is not a whole lot of good news for vitamin C supplementation here. it may reduce soreness, but at a cost. just suck it up. maybe drink some http://www.bodyrecomposition.com/muscle-gain/an-objective-comparison-of-chocolate-milk-and-surge-recovery.html" .
Antioxidants Do Not Prevent Postexercise Peroxidation and May Delay Muscle Recovery.
Teixeira VH, Valente HF, Casal SI, Marques AF, Moreira PA.
Med Sci Sports Exerc. 2009 Aug 5. [Epub ahead of print]
PMID: 19657294
PURPOSE:: This study aimed to determine the effects of 4 wk of antioxidants (AOX) supplementation on exercise-induced lipid peroxidation, muscle damage, and inflammation in kayakers. METHODS:: Subjects (n = 20) were randomly assigned to receive a placebo (PLA) or an AOX capsule (AOX; 272 mg of alpha-tocopherol, 400 mg of vitamin C, 30 mg of beta-carotene, 2 mg of lutein, 400 mug of selenium, 30 mg of zinc, and 600 mg of magnesium). Blood samples were collected at rest and 15 min after a 1000-m kayak race, both before and after the supplementation period, for analysis of alpha-tocopherol, alpha-carotene, beta-carotene, lycopene, lutein plus zeaxanthin, vitamin C, uric acid, total AOX status (TAS), thiobarbituric reactive acid substances (TBARS) and interleukin-6 (IL-6) levels, and creatine kinase (CK), superoxide dismutase (SOD), glutathione reductase (Gr), and glutathione peroxidase (GPx) activities. RESULTS:: With supplementation, plasma alpha-tocopherol (P = 0.003) and beta-carotene (P = 0.007) augmented significantly in the AOX group. IL-6 (exercise, P = 0.039), TBARS (exercise, P < 0.001), and uric acid (exercise, P = 0.032) increased significantly in response to the exercise regardless of treatment group. Cortisol level raised more from pre- to postsupplementation period in the PLA group (time x supplementation, P = 0.002). Although TAS declined after exercise before intervention, it increased above preexercise values after the 4-wk period in the AOX group (supplementation x time x exercise, P = 0.034). CK increased after exercise in both groups (exercise effect, P < 0.001) and decreased from week 0 to week 4 more markedly in the PLA group (supplementation x time, P = 0.049). CONCLUSIONS:: AOX supplementation does not offer protection against exercise-induced lipid peroxidation and inflammation and may hinder the recovery of muscle damage.
Antioxidants prevent health-promoting effects of physical exercise in humans.
Ristow M, Zarse K, Oberbach A, Klöting N, Birringer M, Kiehntopf M, Stumvoll M, Kahn CR, Blüher M.
Proc Natl Acad Sci U S A. 2009 May 11. [Epub ahead of print]
PMID: 19433800 [PubMed - as supplied by publisher]
Exercise promotes longevity and ameliorates type 2 diabetes mellitus and insulin resistance. However, exercise also increases
mitochondrial formation of presumably harmful reactive oxygen species (ROS). Antioxidants are widely used as supplements but whether they affect the health-promoting effects of exercise is unknown. We evaluated the effects of a combination of vitamin C (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as measured by glucose infusion rates (GIR) during a hyperinsulinemic, euglycemic clamp in previously untrained (n = 19) and pretrained (n = 20) healthy young men. Before and after a 4 week intervention of physical exercise, GIR was determined, and muscle biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential influences of vitamins on exercise effects. Exercise increased parameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals. This was paralleled by increased expression of ROS-sensitive transcriptional regulators of insulin sensitivity and ROS defense capacity, peroxisome-proliferator-activated receptor gamma (PPARgamma), and PPARgamma coactivators PGC1alpha and PGC1beta only in the absence of antioxidants (P < 0.001 for all). Molecular mediators of endogenous ROS defense (superoxide dismutases 1 and 2; glutathione peroxidase) were also induced by exercise, and this effect too was blocked by antioxidant supplementation. Consistent with the concept of mitohormesis, exercise-induced oxidative stress ameliorates insulin resistance and causes an adaptive response promoting endogenous antioxidant defense capacity. Supplementation with antioxidants may preclude these health-promoting effects of exercise in humans.
American Journal of Clinical Nutrition, Vol. 87, No. 1, 142-149, January 2008
Oral administration of vitamin C decreases muscle
mitochondrial biogenesis and hampers training-induced adaptations in endurance performance1,2,3
Mari-Carmen Gomez-Cabrera, Elena Domenech, Marco Romagnoli, Alessandro Arduini, Consuelo Borras, Federico V Pallardo, Juan Sastre and Jose Viña
1 From the Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain (M-CG-C, ED, AA, FVP, JS, and JV); the Catholic University of Valencia, Valencia, Spain (CB); and the Polytechnic University of Valencia, Valencia, Spain (MR)
Background: Exercise practitioners often take vitamin C supplements because intense muscular contractile activity can result in oxidative stress, as indicated by altered muscle and blood glutathione concentrations and increases in protein, DNA, and lipid peroxidation. There is, however, considerable debate regarding the beneficial health effects of vitamin C supplementation.
Objective: This study was designed to study the effect of vitamin C on training efficiency in rats and in humans.
Design: The human study was double-blind and randomized. Fourteen men (27–36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 male Wistar rats were exercised under 2 different protocols for 3 and 6 wk. Twelve of the rats were treated with a daily dose of vitamin C (0.24 mg/cm2 body surface area).
Results: The administration of vitamin C significantly (P = 0.014) hampered endurance capacity. The adverse effects of vitamin C may result from its capacity to reduce the exercise-induced expression of key transcription factors involved in
mitochondrial biogenesis. These factors are peroxisome proliferator–activated receptor co-activator 1, nuclear respiratory factor 1, and
mitochondrial transcription factor A. Vitamin C also prevented the exercise-induced expression of cytochrome C (a marker of
mitochondrial content) and of the antioxidant enzymes superoxide dismutase and glutathione peroxidase.
Conclusion: Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.
J Sports Med Phys Fitness. 2006 Sep;46(3):462-7. Links
The effects of vitamin C supplementation on symptoms of delayed onset muscle soreness.
* Connolly DA,
* Lauzon C,
* Agnew J,
* Dunn M,
* Reed B.
Human Performance Laboratory, University of Vermont, Burlington, VT, USA.
AIM: The aim of this study was to compare the effects of 8 days of vitamin C (VC) supplementation on elbow flexor delayed onset muscle soreness (DOMS) to 8 days of placebo ingestion. METHODS: For 3 days prior to an exercise bout (2x20 eccentric elbow extensions), and for 5 days after, a treatment group ingested 3x1 000 mg/day of VC versus 3x50 mg/day of glucose ingestion for the placebo group over the same time period. All subjects were prescreened via dietary recall to exclude any subjects with habitual VC consumption greater than 400 mg/day. Subject comprised 24 subjects (male and female) randomly divided into 2 groups of 12 subjects. Treatment group comprised 5 females and placebo group comprised 8 females. RESULTS: Data from a repeated measures ANOVA indicate that DOMS was successfully induced in both groups via significant time effects for strength loss (P=0.0001), point tenderness (P=0.0001), elbow flexor decreased range of motion (P=0.013), and subjective pain (P=0.0001). However, there were no significant between group differences in response to any of the aforementioned variables: strength loss (P=0.202), point tenderness (P=0.824), elbow flexor range of motion (P=0.208), subjective pain (P=0.342). CONCLUSIONS: The results of this study suggest that a VC supplementation protocol of 3x1 000 mg/day for 8 days is ineffective in protecting against selected markers of DOMS.
Int J Sport Nutr Exerc Metab. 2006 Jun;16(3):270-80. Links
Effect of high dose vitamin C supplementation on muscle soreness, damage, function, and oxidative stress to eccentric exercise.
* Bryer SC,
* Goldfarb AH.
Exercise and Sport Science Dept, University of North Carolina Greensboro, 27402-6170, USA.
This study investigated if vitamin C supplementation before and after eccentric exercise could reduce muscle soreness (MS), oxidative stress, and muscle function. Eighteen healthy men randomly assigned to either a placebo (P) or vitamin C (VC) (3 g/d) treatment group took pills for 2 wk prior and 4 d after performing 70 eccentric elbow extensions with their non-dominant arm. MS increased in both groups with significantly reduced MS for the first 24 h with VC. Range of motion was reduced equally in both groups after the exercise (P > or = 0.05). Muscle force declined equally and was unaffected by treatment. VC attenuated the creatine kinase (CK) increase at 48 h after exercise with similar CK after this time. Glutathione ratio (oxidized glutathione/total glutathione) was significantly increased at 4 and 24 h with P but VC prevented this change. These data suggest that vitamin C pretreatment can reduce MS, delay CK increase, and prevent blood glutathione oxidation with little influence on muscle function loss.