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The role of vitamin C in athletic performance
Abstract
There is widespread belief among athletes that special nutritional practices--in particular high-protein diets--will enhance their achievements in competition. Supplementation with vitamins, especially vitamin C, is equally popular. But because genetic predisposition, hard physical training and psychological factors play a most important role in determining performance, and because any potential difference in achievement will be small, it is almost impossible to obtain scientific evidence of a beneficial effect of a particular nutrient. There have been many investigations during the past four decades of the potential effect of high-dose vitamin C supplementation on physical performance. The variables used have included maximum oxygen uptake, blood lactic acid levels, and heart rate after exercise, and in some cases performance was assessed in competitive events. The results have been equivocal: Most studies could not demonstrate an effect. On the other hand, a suboptimal vitamin C status results in an impaired working capacity which can be normalized by restoring vitamin C body pools. Athletes, who follow irrational, unhealthy eating patterns often not including vitamin-C-containing fruit and vegetables, are in need of nutrition education.
... Vitamin D has genomic and non-genomic actions on musculoskeletal tissues [266,267]. The genomic pathway involves activation of the 1,25(OH) 2 D nuclear receptors, resulting in expression of several messenger RNAs and synthesis of key proteins [265,268]. ...
... The genomic pathway involves activation of the 1,25(OH) 2 D nuclear receptors, resulting in expression of several messenger RNAs and synthesis of key proteins [265,268]. The non-genomic pathway acts directly through secondary messenger systems in the cell and/or by activating protein kinase C [267,269,270]. ...
... References Musculoskeletal 20 to 32 ng/mL Sarcopenia and muscle weakness [266,267,275,277,278] General fractures 32 ng/mL [79,349,350] Hip fractures [79,87,[351][352][353][354][355] Rickets and osteomalacia 20 ng/mL [271,272,[352][353][354]356] Fall prevention [62,87,171,276,357] Frailty [87,103,338,339] Dysphagia in the elderly [280][281][282][283] Urgency and overactive bladder [284,285] Cardiovascular (CVD): 30 to 40 ng/mL Blood pressure [87,176,187,193,195,[235][236][237]241,242,358,359] Regulate renin-angiotensin system [234,238] Protective effects on CVD [178,179,360,361] Vascular tone [180,181,238,239] Vascular calcification [41,177,182,183] Smooth muscle cell and endothelial functions [184][185][186] Decreasing CVD risks; stroke, myocardial infarction, heart failure [51,176,177,187,193,195] Mechanisms of CVD risk-reduction [192,238] Cardiovascular mortality [172][173][174][175][176][177] Lipids/apo-proteins (Apo A1 and B) [191,362] Cancer: 40 ng/mL Cancer [46,94,[108][109][110][111][112]120,[130][131][132][133]143,[149][150][151][363][364][365] Breast cancer and survival [108][109][110][111][112][127][128][129]162,[366][367][368] Colorectal cancers [76,[108][109][110][111][112]124,126,[152][153][154]162,342] Lymphoma [156][157][158][159][160][161] VDR polymorphisms [116][117][118][119][120][121] Relationship to living in higher latitudes [108,109,[113][114][115]124,[144][145][146][147][148] Relationship to serum 25(OH)D levels [46,94,124,[127][128][129][130][131][132][133]135,154,[164][165][166][167] Mechanisms of cancer reduction [125,134,135,163] UVB/sun exposure and cancer reduction [44,[46][47][48][49][50][51][52][53][54][108][109][110][111][112][113][114][115][123][124][125]135] Cancer metastasis [137][138][139][140] Respiratory system: 30 to 40 ng/mL Respiratory infections [228,369] Asthma and chronic obstructive airway diseases [286][287][288]364,370,371] Cystic fibrosis [361,364,372,373] Forced expiratory volume and vital capacity [286][287][288] Metabolic disorders: 30 to 40 ng/mL Type 1 diabetes mellitus [249][250][251] Type 2 diabetes mellitus [44,54,97,177,200,201,235,243,244,248,374,375] Insulin resistance [44,50,[52][53][54]97,201,246,247,253,254,[376][377][378][379] Metabolic syndrome [246,247,380] stabilize Parkinson's disease for a short period without triggering hypercalcemia [322]. A prospective 30-year follow-up study reported that low 25 (OH)D levels were associated with a 20% increased risk of Alzheimer's disease and vascular dementia [323]. ...
... Markers of exercise performance have been lower in individuals with suboptimal vitamin C intakes; such individuals have also encountered higher concentrations of oxidative-stress biomarkers [189][190][191][192]. This is the only definitive situation for which supplementation of vitamin C has been suggested [193,194]. ...
Saliva is easily obtainable for medical research and requires little effort or training for collection. Because saliva contains a variety of biological compounds, including vitamin C, malondialdehyde, amylase, and proteomes, it has been successfully used as a biospecimen for the reflection of health status. A popular topic of discussion in medical research is the potential association between oxidative stress and negative outcomes. Systemic biomarkers that represent oxidative stress can be found in saliva. It is unclear, however, if saliva is an accurate biospecimen as is blood and/or plasma. Exercise can induce oxidative stress, resulting in a trend of antioxidant supplementation to combat its assumed detriments. Vitamin C is a popular antioxidant supplement in the realm of sports and exercise. One potential avenue for evaluating exercise induced oxidative stress is through assessment of biomarkers like vitamin C and malondialdehyde in saliva. At present, limited research has been done in this area. The current state of research involving exercise-induced oxidative stress, salivary biomarkers, and vitamin C supplementation is reviewed in this article.
... The roles of vitamin D in the regulation of bone-mineral metabolism [19][20][21][22][23][24], the musculoskeletal system [25][26][27], and fracture prevention [28][29][30][31][32] have been well established. Recent data suggest associations between hypovitaminosis D and metabolic syndrome, diabetes, hypertension, and immune diseases [33][34][35][36]. ...
Vitamin D regulates blood pressure, cardiac functions, and endothelial and smooth muscle cell functions, thus playing an important role in cardiovascular health. Observational studies report associations between vitamin D deficiency and hypertension and cardiovascular-related deaths. Peer-reviewed papers in several research databases were examined, per the guidelines of the Preferred Reporting Items for Systematic Reviews, using key words that address the relationship between vitamin D and cardiovascular disease. Correlations and interpretations were made considering the risks-benefits, broader evidence, and implications. This review analyzed current knowledge regarding the effects of vitamin D on the cardiovascular system. 1,25(OH)2D and related epigenetic modifications subdue cellular inflammation, improve overall endothelial functions, reduce age-related systolic hypertension and vascular rigidity, and attenuate the actions of the renin-angiotensin-aldosterone system. Most observational and ecological studies support 25(OH) vitamin D having protective effects on the cardiovascular system. However, the association of vitamin D deficiency with cardiovascular diseases is based primarily on observational and ecological studies and thus is a matter of controversy. Adequately powered, randomized controlled clinical trial data are not available to confirm the association. Thus, to test the hypothesis that correction of vitamin D deficiency protects the cardiovascular system, well-designed, statistically powered, longer-term clinical trials are needed in persons with vitamin D deficiency. Nevertheless, the available data support that adequate vitamin D supplementation and sensible sunlight exposure to achieve optimal vitamin D status are important in the prevention of cardiovascular disease and other chronic diseases.
Aims
Aldehyde reductase (AKR1A) is involved in the synthesis of ascorbic acid (AsA) as well as the detoxification of aldehydes. AKR1A−/− (KO) mice produce about 10% of the normal amounts of AsA compared to AKR1A+/+ (WT) mice. We investigated physiologic roles of AKR1A in running using the KO mice.
Main methods
The KO mice were subjected to a treadmill test under either restricted AsA production or a sufficiency by supplementation and compared the results with those of WT mice. Contents of glucose, aspartate aminotransferase, AsA and free fatty acids in blood were measured. Glycogen contents were measured in the liver and skeletal muscle, and hepatic proteins were examined by immunoblot analyses.
Key findings
Running performance was higher in the KO mice than the WT mice irrespective of the AsA status. After the exercise period, blood glucose levels were decreased in the WT mice but were preserved in the KO mice. Liver glycogen levels were also consistently preserved in the KO mice after exercise. Free fatty acid levels tended to be originally high in blood plasma compared to those of the WT mice and were increased to similar extent in them. A key regulator of energy metabolism, PGC-1α, and the products of downstream target genes that encode for glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphatase, were constitutively at high levels in the KO mice.
Significance
The genetic ablation of AKR1A activates the PGC-1α pathway and spare glucose, which would consequently confer exercise endurance.
The ultimate symptom of vitamin C deficiency is scurvy, which is lethal if not adequately and promptly treated. Man is one of the few animal species which is unable to synthesize its own ascorbic acid, the antiscorbutic agent. Among mammals, only the guinea-pig, flying mammals and primates lack this ability. The metabolic deficiency is the same: lack l-gulono-gamma-lactone oxidase, the last enzymatic step in the biosynthesis of ascorbate from glucose. Interestingly, ascorbic acid is synthesized in the liver by mammals whereas the kidney is the site of biosynthesis in other vertebrates. It is likely that species which now do not have the ability to produce ascorbate lost this ability during evolution.
Over the last decade, research involving nutritional supplementation and sport performance has increased substantially. Strength and power athletes have specific needs to optimize their performance. Nutritional supplementation cannot be viewed as a replacement for a balanced diet, but an important addition to it. However, diet and supplementation are neither mutually exclusive nor does one depend on the other. Strength and power athletes have four general areas of supplementation needs. First strength athletes need supplements that have a direct effect on performance. The second areas of supplements are those that promote recovery. The third group is the supplements that enhance immune function. The last group of supplements is those that provide energy or have a direct effect on the workout. This chapter will review the key supplements needed to optimize performance and training of the strength athlete.
The primary factors that affect exercise performance capacity include an individual’s genetic endowment, the quality of training, and the effectiveness of coaching (see Fig. 1). Beyond these factors, nutrition plays a critical role in optimizing performance capacity. In order for an athlete to perform well, their training and diet must be optimal. If an athlete does not train enough or has an inadequate diet, their performance may be decreased (1). On the other hand, if an athlete trains too much without a sufficient diet, they maybe susceptible to become overtrained (see Fig. 2).
It has been postulated that supplemental doses of ascorbic acid (vitamin C) may improve endurance performance and perhaps reduce the severity and morbidity of athletic injuries.1-4 The present study was designed to answer these questions and to determine the long-term effects of a large supplemental dose of ascorbic acid in contrast to those of a placebo.
Materials and Methods
Two hundred and eighty-six male officers (average age, 28.0 years) participated in this study while attending the 12-week Squadron Officers School, Maxwell Air Force Base, Ala. Each officer ran the 12-minute field test5 at the beginning of training and then was given a bottle containing either 500-mg tablets of ascorbic acid or a placebo. The bottles were numbered at random with a code that was kept in strict secrecy until completion of the study. The subjects were instructed to take two pills each day throughout the training period. Also
