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Some butter on top of the broccoli would allow for the assimilation of the absorption of the 101.6?g vitamin K 623IU vitamin A (various).

There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the  well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats and oils. The general assumption is thus that the vitamins A, i.e. the retinol and carotenoids, all forms of vitamin D, the tocopherols and -trienols (vitamins E) and the two major forms of vitamin K, i.e. phylloquinone (K1) and menaquinone (K2) will only be absorbed, if you consume them with a sufficient amount of dietary fat. Now, the questions obviously are (a) is this correct and (b) how much is sufficient.
In view of the fact that the answers to (a) and be are not necessarily identical for all four vitamins of interest, it appears sensible to tackle them one after the other.


Starting with vitamin A and the various forms of carotenoids, we can already confirm that (a), i.e. the assumption that we need dietary fats to optimally absorb vitamin A is correct. As Karin van het Hof and her colleagues point out, the "amount of dietary fat required to ensure carotenoid absorption [does yet] seem low (?3–5 g per meal), although it depends on the physicochemical characteristics of the carotenoids ingested." (van het Hof. 2000) In spite of the fact that 5g of fat are not exactly much, the classic uncooked vegetarian orthorexic salad often comes with a total of only 5g of fat of which 95% remain at the bottom of the salad bowl. If that sounds like your favorite dish, you should be aware that you are risking that all the good  beta- and other carotenoids in the salad will pass right through.

Figure 1: Changes in hepatic vitamin A (retinol) and carotenoid stores in gerbils after 14 days on high fat (30%) vs. low fat (10%) diet (Deming. 2000)

In that, the concomitant presence of both dietary fat and carotenoids in a meal is a necessary prerequisite for the absorption of vitamin A, also because the fatty acids will trigger the conversion of of beta-carotene into vitamin A and its subsequent absorption via the lymphatic system (Ribaya?Mercado. 2002). It is thus not surprising that animal studies by Lakshman et al. (1996) and Deming et al. (2000; see Figure 1) suggest that low fat diet can lead to a depletion of the vitamin A tissue stores even if the serum levels remain constant. The amount of fiber in the diet, on the other, has no influence the absorption of vitamin A (Mills. 2009).

Interestingly enough, the provision of the fat blocker Orlistat reduces the absorption of vitamin A only insignificantly, as a 1996 paper by Angela T. Melia, Susan G. Koss?Twardy, and Jianguo Zhi would suggest (Melia. 1996).

Which takes us right to vitamin E, the absoprtion which is - in spite of being "blocked" by the fat blocker orlistat (Melia. 1996) - less susceptible to the absence of dietary fat than you may think. Annet JC Roodenburg, Rianne Leenen, Karin H van het Hof,  Jan A Weststrate, and Lilian BM Tijburg do in fact argue that the optimal intake of vitamin E requires only "a limited amount" of dietary fat (Roodenburg. 2000).

Figure 2: Vitamin E serum levels after 7 days on control (low fat, 3g) or high(er) fat (36g) diet with and without supplemental vitamin E (Roodenburg. 2000)

As you can see in Figure 2. A minimum intake of only 3g per day was sufficient to keep the vitamin E levels stable. The short study period of 7-days (each) and the absence of measures of tissue concentration of vitamin E do yet reduce the practical relevance of the data, Roodenburg et al. present in their Y2k paper in the American Journal of Clinical Nutrition.
If you take a look at the high prevalence of vitamin E dieficiency among the fat (and PUFA) "loving", or at least eating, majority of Americans, it does yet become obvious that a lack of dietary fat is not just theoretically, but also practically not exactly the #1 reason you may become deficient in tocopherols and -trienols. That the latter is an increased demand due to chronic inflammation and the (over-)consumption of exactly those PUFAs that come with a shitload of vitamin E in nature, for a reason would yet be a topic for another SuppVersity article and thus something we will skip to fast forward to ...

...Vitamin K, obviously. Vitamin K is a relative newcomer to the publics understanding of the alphabet soup. Aside from being it a good tool to rip customers vitamin K, or rather K1 (plant sources) and K2 (animal sources) are thus also the only fat soluble vitamins not everyone knows. The fact that the amount of phylloquinone (K1) that makes it into your blood stream is ~70% reduced if you eat your spinach without fat (Gijsbers. 1996).

And if we take the results researchers from the Gifu University School of Medicine present in a 1996 paper in the Journal of Pharmacological Sciences, as a reference, the amount of fat you need to optimally absorb your K2 (menaquinones), is not exactly low.

Figure 3: For optimal absorption of K2, there has got to be a huge amount of fat in the meal - but who wonders. K2 comes with a high amount of fat (Uematsu. 1996)

Uematsu et al. had to supply their subjects, who consumed otherwise identical test meals with 8.8, 20.0 and 34.9g of fat in them with the maximal (i.e. 35g) of fat before the K2 absorption maxed out. In that the total area under the curve did not really differ between those subjects who consumed the K2 before and those who took it immediately after the test meal.

Thats a pity, cause a high intake of vitamin K (menaquinone from animal sources) has been associated with a 27% reduced risk of developing heart disease (Geleijnse. 2004), an ailment of which many still believe that it was brought about by the fat they need to optimally absorb their vitamin K.

For vitamin D, our last "V" on the list, things look differently. For one, everybody knows about this miracle vitamin and for two, it may be "fat soluble", but the amount of fat thats required to optimally absorb it turned out to be much lower than previously thought (see "A Fat D-Ficiency! Do You Really Need More Vitamin D or Simply More Fatty Foods? Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat. " | read more).
In fact, Niramitmahapanya et al. found in 2011 that its not necessarily a high amount, but rather the right type of fat that determines if and how much of the vitamin D you take in capsule form or find in comparably low amounts in your foods that determines how much of the vitamin D actually makes it into your bloodstream:

"The change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was positively associated with MUFA, (? = 0.94; P = 0.016), negatively associated with PUFA, (? = ?0.93; P = 0.038), and positively associated with the MUFA/PUFA ratio (? = 6.46; P = 0.014)."

In plain English this means, that the "good" seed and vegetable oils with their high PUFA content will effectively inhibit the absorption of vitamin D - an observation that adds to the many reasons the modern sedentary, sun-avoiding, sun-screen using, soybean oil (MUFA:PUFA = 0.4) guzzling American is low in or  quasi devoid of vitamin D.

Figure 4: 25(OH)D levels of 30 healthy men and women after ingestion of 50.000IU vitamin D3 supplement in conjunction with a normal or low fat breakfast (Raimundo. 2011)

Against that background its not surprising that you will not find a conclusive answer to the question how much fat you actually need. In a study that used a fatty meal with soybean oil in it, the effect would be totally different from one in which the subjects consumed meals that were made with sunflower oil, an oil with a MUFA:PUFA ratio >1. In view of the results Gnadinger et al present in a recent appear it does still seem appropriate to consume at least some fat alongside your vitamin D supplements. As far as the food-borne vitamin D is concerned, you dont have to worry, anyways. Foods that are high in D3 usually come with all the fat you need to absorb it.

How much fat, exactly you would need to make the most of dietary and supplemental vitamin D, on the other hand, is still not known. The previously mentioned data from the study by Raimondo et al. (see Figure 4, to the right) I wrote about in "A Fat D-Ficiency" is obviously still valid. The extremely high amount of vitamin D (50,000IU!) could yet require a correspondingly high amount of fat to be optimally absorbed and the fact that the fat in the study came from a "vegetable margarine" with an undisclosed ratio of MUFA:PUFA does not make the real-world effects any more predictable.
References:

• Chitchumroonchokchai, Chureeporn, et al. "Dietary fats with increased ratio of unsaturated to saturated fatty acids enhance absorption of carotenoid and vitamin E by increasing both efficiency of micellarization and lipoprotein secretion." FASEB J 24 (2010): 539-3.
• Deming, Denise M., et al. "Amount of dietary fat and type of soluble fiber independently modulate postabsorptive conversion of ?-carotene to vitamin A in Mongolian gerbils." The Journal of nutrition 130.11 (2000): 2789-2796. 
• Geleijnse, Johanna M., et al. "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study." The Journal of nutrition 134.11 (2004): 3100-3105.
• Gijsbers, Birgit LMG, Kon-Siong G. Jie, and Cees Vermeer. "Effect of food composition on vitamin K absorption in human volunteers." British Journal of Nutrition 76.02 (1996): 223-229.
• Goodman, Dew S., et al. "The intestinal absorption and metabolism of vitamin A and beta-carotene in man." Journal of Clinical Investigation 45.10 (1966): 1615.
• Jayarajan, P., Vinodini Reddy, and M. Mohanram. "Effect of dietary fat on absorption of ? carotene from green leafy vegetables in children." Indian journal of medical research 137.5 (2013).
• Kris-Etherton, P. M., et al. "Polyunsaturated fatty acids in the food chain in the United States." The American journal of clinical nutrition 71.1 (2000): 179S-188S.
• Lakshman, M. R., et al. "The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary ??carotene in ferrets." (1996): 49-61.
• Melia, Angela T., Susan G. Koss?Twardy, and Jianguo Zhi. "The effect of orlistat, an inhibitor of dietary fat absorption, on the absorption of vitamins A and E in healthy volunteers." The Journal of Clinical Pharmacology 36.7 (1996): 647-653.
• van het Hof, Karin H., et al. "Dietary factors that affect the bioavailability of carotenoids." The Journal of nutrition 130.3 (2000): 503-506.
• Raimundo, Fabiana Viegas, et al. "Effect of high-versus low-fat meal on serum 25-hydroxyvitamin D levels after a single oral dose of vitamin D: a single-blind, parallel, randomized trial." International journal of endocrinology 2011 (2011).
• Ribaya?Mercado, Judy D. "Influence of Dietary Fat on ??Carotene Absorption and Bioconversion into Vitamin A." Nutrition reviews 60.4 (2002): 104-110.
• Roodenburg, Annet JC, et al. "Amount of fat in the diet affects bioavailability of lutein esters but not of ?-carotene, ?-carotene, and vitamin E in humans." The American journal of clinical nutrition 71.5 (2000): 1187-1193. 
• Uematsu, Toshihiko, et al. "Effect of dietary fat content on oral bioavailability of menatetrenone in humans." Journal of pharmaceutical sciences 85.9 (1996): 1012-1016.

Taking vitamin D pills on their own may be less effective than taking them with a meal containing 30% of the calories from fat - at least for older men & women and high doses of vitamin D3

This is science. Only 6 months ago, I wrote in an article about the effects of fat on the absorption and bioavailability of fat soluble vitamins that vitamin D would be the fat soluble vitamin with the lowest dependence on the co-administration of fat. Rather than the amount, it appeared as if the change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was rather associated with the types of fat, i.e. MUFA = increased absorption vs. PUFA = decreased absorption (Niramitmahapanya. 2011).

Now, half a year later, it appears as if another, previously overlooked variables would force me to reformulate previous recommendations: Age and dosage!
In contrast to previous studies, Bess Dawson- Hughes and colleagues investigated the influence of fat on the absorption of vitamin D3 in older, not young men and women. In that, inclusion criteria for the study were

• no use of not more than 400 IU vitamin D or 1,000 mg calcium per day,
• serum 25(OH)D level in the range 20 to 29.5 ng/mL (49.9 to 73.6 nmol/L),and
• a body mass index in the range 20 to 29.5 (normal weight)

Subjects with kidney problems, hypercalcemia, general issues with malabsorption, Crohn’s disease, disorders of bone metabolism, kidney stones, cancer and those who were using proton pump in hibitors, lipid-lowering medications, fish oil, or flaxseed oil, hormones, osteoporosis medications, or high-dose thiazide diuretic therapy were equally excluded as those subjects who attended tanning salons, regularly.
This was yet not the only difference. Next to the subjects age, the amount of vitamin D3 in the capsules the subjects received differed, as well. While previous studies that reported little to no effect of fat on the absorption of vitamin D3 used small(er) amounts of vitamin D, like 1,000, 2,000 or 5,000 IU per serving, Dawson-Hughes et al. used a single serving of 50,000 IU(!) and thus more than 10x higher dosages than previous studies.

Figure 1: Composition of the test breakfast, lunch, and dinner meals, expressed as % of total energy the 50 healthy older adults consumed in the study at hand (Dawson-Hughes. 2014)

Alongside said vitamin D3 super-dose all 50 subjects ingested one out of three randomly selected meals that were either fat free or contained 30% of the total calories in form of dietary fat - albeit at two different PUFA:MUFA ratios (see Figure 1)

"[The m]eals were provided by the metabolic kitchen and consisted of real food. For example, breakfast consisted of egg whites flavored with small amounts of onion and tomato, fruit, toast, and cranberry juice. The groups were balanced for energy by adjusting the amount of sugar in the cranberry juice (diet or regular juice or a mixture of the two). Protein and fiber were balanced across all groups. MUFA:PUFA was manipulated by adding varying amounts of MUFA (olive oil) and PUFA (corn oil) to achieve a ratio of 1:4 in the low and 4:1 in the high MUFA:PUFA diets. The boxed lunch and the dinner provided to the study subjects on the test day had fat/protein/carbohydrate content similar to that of the test breakfast meals.

Importantly, the subjects were required to (a) eat all of the food provided and (b) refrain from pigging out on anything that was not on the menu for the study day.

Figure 2: Serum vitamin D3 levels in subjects after consuming fat-free or -containing meals (Dawson-Hughes. 2014)

What the scientists found, when they analyzed the vitamin D response of the subjects depending on (a) the fat content and (b) the type of the fat, Dawson-Hughes et al. found:

• In analyses of vitamin D absorption at baseline and the three follow-up time points, there was a significant interaction of fat-free vs fat-containing meal group with time (P < 0.001). As shown in [figure 2], there was no significant difference in plasma vitamin D-3 levels at baseline, but the fat-containing meal group had significantly higher plasma vitamin D-3 concentrations than the fat-free meal group at each time point thereafter.
  
  At 12 hours, the fat-containing vs fat-free meal mean difference in plasma D-3 concentration was 26.9 ng/mL (95% CI 9.6 to 44.1 ng/mL) (69.9 nmol/L). Differences at the other time points were for 10 hours, 30.5 ng/mL (95% CI 14.4 to 46.7 ng/mL) (79.3 nmol/L) and for 14 hours, 21.3 ng/mL (95% CI 4.6 to 37.9 ng/mL) (55.4 nmol/L).

• Vitamin D-3 levels at 12 hours after the dose were 116.0 3 ng/mL (301.5 nmol/L) in the low MUFA:PUFA group and 104.2 ng/mL (270.8 nmol/L) in the high MUFA: PUFA group.
  
  Potential covariates, body mass index, total body fat mass, and screening plasma 25(OH)D level were not associated with vitamin D absorption and neither modified the effect of fat on vitamin D absorption.

As the researchers point out, "[t]here were no serious adverse events during the study" and "[c]ompliance with the vitamin D supplement was 100%" (Dawson-Hughes. 2014). So, non of these obvious, but undesirable confounding factors could explain the observed differences between (a) the non-fat vs. fat-meals and (b) the influence of the PUFA:MUFA ratio.
References:

• Dawson-Hughes, Bess, et al. "Dietary Fat Increases Vitamin D-3 Absorption." Journal of the Academy of Nutrition and Dietetics (2014).
• Niramitmahapanya, Sathit, Susan S. Harris, and Bess Dawson-Hughes. "Type of dietary fat is associated with the 25-hydroxyvitamin D3 increment in response to vitamin D supplementation." The Journal of Clinical Endocrinology & Metabolism 96.10 (2011): 3170-3174. 
• Wortsman, Jacobo, et al. "Decreased bioavailability of vitamin D in obesity." The American journal of clinical nutrition 72.3 (2000): 690-693.

Marathon de Sable ? Tomato juice

Its about time for another quickie, a news quickie about exercise & supplementation, about vitamin D and tomato juice... actually its rather about tomato juice, a special carbohydrate + protein bar and the notorious "Gatorate(R)-ish" carbohydrate supplement every endurance athlete believes he must be taking. But lets be honest, who cares about tomato juice, carbohydrate, protein bars, pseudo Gatorade and their individual and joint effects on the health and performance of constantly (over-)taxed ultra-marathoners, if the other new item in todays article deals with the potential beneficial effect of vitamin D on IGF-1 and its anabolic consequences?
You care? Ok, in that case, you may be inclined to hear that the bar contained 30.20 g (19.7 g sugars) carbohydrates, 5.2g fiber, a surprisingly high amount of fat (15.6g) and. of course, protein 30.8g to be precise (14.3 g whey protein). If we add the energy content of carbs, fats and protein up, we get an energy content of ~400kcal for the bar and thus approx 24x more than in 100ml of the tomato juice, which is - as you can see in Table 1 more or less devoid of "nutrients", but packed with antioxidants.

Table 1: Average nutritional value per 100 g of tomato juice and protein bar used in the present study (canned, salt added) and the carbohydrate supplementation beverage, as provided by the manufacturer (Samaras. 2014)

As you can see in Figure 1, enough antioxidants to elicit significant increases in flow-mediated dilatation, which was used as an estimate of endothelial function, by the researchers from the  General Hospital of Giannitsa in Greece.

Figure 1: Changes (% pre) in response to tomato juice & protein bar supplementation (Samaras. 2014)

Interestingly, the thiobarbituric-acid reactive substances, and protein carbonyls were significantly decreased in both supplementation groups - a good indicator that these changes were not mediated by the red night-shade elixir, but rather by the protein + carbohydrate bar, which lead to a "whey-typical" increase in reduced glutathione.

Is the vitamin D you produce at the beach youre visiting only rarely the secret to perfect glucose control? Learn more in the "Beyond Carbohydrate Series"

If the marathoners had now had low vitamin D levels, they may even had gained some muscle, if they had followed a similar protocol as the subjects in another recently published study from the St. John Fisher College Rochester NY.

And the results of this study dont even seem completely nonsensical. As a SuppVersity reader you do after all know about the existing evidence of the negative effects low vitamin D levels will have on the function and strength of skeletal muscle ("low" in this context means less than 30ng 25-OHD on the lab report). Against that background, it does after all appear to be logical that refilling the levels would in one way or another help maintain or even build skeletal muscle.

The actual news here is yet not that vitamin D could potentially prevent muscle atrophy and increase hypertrophy. Its rather that these effects could be brought about by the significant increases in total IGF-1, as well as the IGF-1 binding proteins 1 + 3 researchers from the College of Rochester observed, when they added 4,000 IU of vitamin D to the diets of 6 vitamin D insufficient and deficient men (39.0±8.6yo with 25OH D 20.0±7.7ng/mL) who participated in a one-hour exercise program consisting of stretching (ST), aerobic (AB), and resistive (RT) exercises (Darr. 2014)

Suggested Read: "Underestimated Vitamin D Sources: Especially Eggs, But Also Chicken, Pork, Fish & Dairy Contain an Overlooked, Physiologically Relevant Amount of Ready-Made 25OHD" | more

The aerobic training was a intensity treadmill walk, which was rotated with a moderate strength (50% 1-RM, 15, 10 repetitions) full body workout consisting of squats, bench presses, leg presses, and lat pull downs. As previously said, the scientists found that the vitamin D binding protein 3 levels (BP3) were increased after the resistance training in the vitamin D (n=6) vs. placebo (n=7) group (30%). And while the total IGF-1 levels decrease in the placebeo group, the increase in various binding proteins buffered this effect in the vitamin D group. Similar, yet less pronounced effects were observed in response to the aerobic training.

Whether the scientists assumption that the increases in BP3 and BP1 levels and the maintenance of the total IGF-1 levels "potentially alter [...] the IGF system for enhanced muscle health" is accurate, let alone practically relevant is something this study cannot actually confirm.

And lets be honest, is it even likely? For someone without a pre-existing vitamin D deficiency? No. For someone with similarly low vitamin D levels as the deficient and insufficient subjects in a 2011 study by Stockton et al. (2011)? Probably, yes - but are you actually D-ficient?
References:

• Ceglia, Lisa, et al. "Effects of alkali supplementation and vitamin D insufficiency on rat skeletal muscle." Endocrine 44.2 (2013): 454-464.
• Darr, Rachel, et al. "Vitamin D supplementation effects on the IGF system in men after acute exercise (828.15)." The FASEB Journal 28.1 Supplement (2014): 828-15.
• Samaras, Antonios, et al. "Effect of a special carbohydrate-protein bar and tomato juice supplementation on oxidative stress markers and vascular endothelial dynamics in ultra-marathon runners." Food and Chemical Toxicology (2014).
• Stockton, K. A., et al. "Effect of vitamin D supplementation on muscle strength: a systematic review and meta-analysis." Osteoporosis international 22.3 (2011): 859-871.

The study at hand used plain ascorbic acid, no quack supplements with "advanced vitamin C".

While people tend to believe that vitamin C is good for anything, the evidence that it actually does anything good is relatively scarce. Against that background I am happy to tell you that a group of Greek researchers from the School of Physical Education and Sport Science, the European University Cyprus and theAristotle University of Thessaloniki have now finally confirmed what many of you probably thought was a long-established fact: "[L]ow vitamin C concentration is linked with decreased physical performance and increased oxidative stress and that vitamin C supplementation decreases oxidative stress and might increase exercise performance only in those with low initial concentration of vitamin C." (Paschalis. 2014)
When they came up with the study design, Paschalis et al. simply assumed that the mythical ergogenic effect of vitamin C actually existed. To test this hypothesis, they screened 100 males for vitamin C baseline values in blood, picked the 10 individuals with the lowest and the 10 with the highest vitamin C values from their baseline sample and assigned them to two groups.

Figure 1: Overview of the study design (Paschalis. 2014)

Using a placebo-controlled crossover design, the 20 selected subjects performed aerobic exercise to exhaustion (oxidant stimulus) before and after vitamin C supplementation for 30 days.

An overview of the study design is shown in Fig. 1. All measurements were performed between 08:00 and 11:00 h after overnight fasting. Initially, to examine whether rest ing blood vitamin C concentration affects aerobic perfor mance, VO2max was assessed (using incremental cycling test to volitional exhaustion) and was compared in both the low and the high vitamin C groups (Monark, Vansbro, Swe den). More specifially, the protocol started with a 50 W load at 50 rpm and increased by 10 W every 2 min until volitional fatigue. The test was terminated when three of the following four criteria VO2max were met: (1) volitional fatigue, (2) a lower than 2 mL/kg/min increase in VO2 despite an increase in workload, (3) a respiratory exchange ratio greater than or equal to 1.10, and (4) heart rate within 10 bpm of the predicted maximal heart rate (220–age). Res piratory gas variables were measured using a metabolic cart (Quark b2, Cosmed, Italy), which was calibrated before each test using standard gases of known concentration. The VO 2max assessment was used as a reference value to cal culate the workload at the relative intensity of each subject and ensured that all subjects would cycle at similar relative intensity during the following aerobic exercise sessions.

After the baseline testing had been done, the subjects within both the low and the high vitamin C groups received either placebo (3x333mg of lactose) or vitamin C supplementation (3x333mg of vitamin C), in a double-blind randomized crossover fashion (see Figure 1).

Figure 2: Changes in VO2max (left) and redox status (right) in subjects according to initial vitamin C status before and after vitamin C supplementation for 30 days (Paschalis. 2014).

As you can see in Figure 2 there were measurable differences in the response to the acute exhaustive exercise protocol (an oxidant stimulus), the subjects in both groups performed before and after vitamin C or placebo supplementation for 30 days. The data in Figure 2 does yet also show that the subjects who had been randomly assigned to the vitamin C supplement group had lower baseline VO2max levels. A fact that raises the question whether this is the result of a lower vitamin C intake or whether the vitamin C intake correlates with an unhealthier lifestyle that left the subjects unfit and with low vitamin C levels.
Unfortunately, this question is hard to answer based on the available research on vitamin C. While we have conflicting results with respect to its ability to impair the adaptational response to exercise (Close. 2014), there is very little evidence that it will actually have beneficial effects on any meaningful performance parameters. In fact, a study by Huck et al. that was published in the scientific journal Nutrition in 2013 is probably what comes closest to the results of the study at hand.

Figure 3: Effects of 500mg vitamin C per day on selected parameters in a 4 week chronic exercise + diet supplementation in obese men and women (Huck. 2013)

In said study Huck et al. observed that the provision of 500mg of vitamin C as an adjunct to exercise and diet in obese individuals lead to significant reductions in heart rate and the ratings of perceived exertion during exercise. The data in in Figure 3 does yet also tell you that there were no beneficial effects on VO2max, which best reflects the adaptational response to exercise.

This results of stands in contrast to the study at hand, but in line with previous results of studies in athletes, where only more or less irrelevant reductions of the acute inflammatory response to exercise were observed (Nieman. 2000; Peters. 2001; Tauler. 2002). A response of which you as a SuppVersity reader know that it is an essential part of the signalling cascade that triggers the adaptational response to. If we eventually get back to the Paschalis study, it would thus appear that athletes who are usually consuming more than enough vitamin C in their diets and are not at particular risk of developing low serum vitamin C levels would see similar results as the "high vitamin C" subjects in the Paschalis study, i.e. none - even worse, in view of the potential negative effects on the training induced adaptations that could not become visible in the study at hand, because there was no exercise protocol involved, it could even harm their progress.
References:

• Close, G. L., and M. J. Jackson. "Antioxidants and exercise: a tale of the complexities of relating signalling processes to physiological function?." The Journal of physiology 592.8 (2014): 1721-1722.
• Huck, Corey J., et al. "Vitamin C status and perception of effort during exercise in obese adults adhering to a calorie-reduced diet." Nutrition 29.1 (2013): 42-45.
• Nieman, David C., et al. "Influence of vitamin C supplementation on cytokine changes following an ultramarathon." Journal of Interferon & Cytokine Research 20.11 (2000): 1029-1035.
• Paschilis, V. et al. "Low vitamin C values are linked with decreased physical performance and increased oxidative stress: reversal by vitamin C supplementation." Eur J Nutr (2014). Ahead of print.
• Paulsen, Gøran, et al. "Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double?blind, randomised, controlled trial." The Journal of physiology 592.8 (2014): 1887-1901.
• Peters, E. M., et al. "Vitamin C supplementation attenuates the increases in circulating cortisol, adrenaline and anti-inflammatory polypeptides following ultramarathon running." International journal of sports medicine 22.7 (2001): 537-543.
• Picklo, Matthew. "Supplementation with vitamin E and vitamin C inversely alters mitochondrial copy number and mitochondrial protein in obese, exercising rats (1030.5)." The FASEB Journal 28.1 Supplement (2014): 1030-5. 
• Powers, Scott K., et al. "Dietary antioxidants and exercise." Journal of sports sciences 22.1 (2004): 81-94.
• Powers, Scott K., And Kurt J. Sollanek. "Endurance Exercise And Antioxidant Supplementation: Sense Or Nonsense?-Part." Sports Science 27.137 (2014): 1-4.
• Tauler, P., et al. "Diet supplementation with vitamin E, vitamin C and ?-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes." Pflügers Archiv 443.5-6 (2002): 791-797.