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"No sun, no diabesity protection." The evidence is equivocal and the number of studies low, but there is evidence that this statement could be true.

Ok, its November and not exactly sunny in the Northern hemisphere, but if you look back at the months June-August, how much sun exposure did you actually get, this year? Hardly any? Well, thats bad news, because a recent review of the scant scientific evidence suggests that there is "a role of recreational sun exposure in reducing odds of T2DM incidence" (Shore-Lorenti. 2014).

In view of the fact that the contemporarily available evidence is not exactly comprehensive, you should yet consider the following overview of the potential effects and mechanism as a "work in progress".
As Shore-Lorenti et al. point out, the recent International Diabetes Federation (IDF) Diabetes Atlas (6th edition) describes a snapshot of the global diabetes burden in 2013 and projects this forward to the year 2035.1 Cur rently, an estimated 382 million global citizens have diabetes, costing around $1437 USD in 2013 for each person affected by the condition. Projections based on current trends predict that 592 million people will be living with diabetes by 2035; one in ten people will be affected, with an inordinate amount of fund ing required globally to treat diabetes and manage diabetic com plications ($627 billion USD in 2035).

And while scientists are feverishly searching for a solution for the diabesity epidemic, the ongoing research into the effectiveness of vitamin D supplementation in diabetes have yielded inconsistent results (Mitri. 2011). Against that background it appears almost negligent that only few scientists have yet taken a closer look at the factors that trigger vitamin D sufficiency or rather the global low vitamin D epidemia.

Lack of sun"low vitamin D" - thats not all!

Figure 1: Australians who use sunscreen chronically have 50% reduced vitamin D levels (Matsuoka. 1988)

A lack of sufficient (unprotected) sun exposure - previous studies have shown that chronic sunscreen use decreases circulating concentrations of 25-hydroxyvitamin (Figure 1 | Matsuoka. 1988) - is one of the factors of which researchers speculate that it contributes to the development of vitamin D deficiency even in those of us who live in areas with a high annual sun-exposure.

Now, if restoring the 25-OHD (vitamin D) levels to normal does not work the anti-diabetic magic it is supposed to do and our D-levels are low due to insufficient sun-exposure, it appears only logical to assume that a lack sun-exposure and not a lack of vitamin D is one of the factors that contributes to the ever-increasing rates of diabesity - in conjunction with the usual subjects, obviously: The consumption of a junk-food diet and a lack of exercise, which is without doubt the #1 reason people in the Western Obesity Belt develop obesity, diabetes and the other characteristics of the metabolic syndrome.

Against that background its all the more surprising that evidence for an association between sun exposure and fasting serum glucose level is scarce.

"Typically, the lowest glucose levels occur during summer and levels peak in winter or early spring. One of these analyses [Shore-Lorenti et al. reviewed] went beyond simply observing trends in fasting glucose throughout the year: fasting plasma glucose was positively correlated with a measure of available sun and inversely correlated with temperature." (Shore-Lorenti. 2014)

The study, the researchers from the University of Melbourne have in mind was conducted by Suarez, L. & Barrett-Connor, E. in 1988, already.
If you look at the data Suaraez & Barret-Connor generated, you can see - even without their statistical sophisticated analysis - that there is a significant correlation between possible sun exposure (Figure 1, left) and the fasting plasma glucose levels (Figure 1, right).
Since physical activity may follow a similar circannual rhythm, its yet difficult to exclude that the effects Suarez & Barret-Connor observed were not corroborated (or corrupted?) by an increase in physical activity. However, Shore-Lorenti et al. believe that ...

"[...c]onsidering that the unadjusted analyses and three of four of the studies included in the best evidence synthesis (including the study adjusting for physical activity) are in agreement, it is possible that future research may confirm that sun exposure reduces fasting glucose" (Shore-Lorenti. 2014).

Shore-Lorenti et al. also point out that the highest level of evidence (moderate) for an association between sun exposure and T2DM outcomes in adults originates from the study by Lindqvist et al. (2010). In their paper, the researchers from the Karolinska University Hospital report a reduction in odds of developing T2DM given increased recreational (rather than occupational) sun exposure. 

Figure 2: Leisure time sun exposure is associated with a significantly reduced risk (up to 50%!) of developing T2DM in Swedish adults (Lindqvist. 2010)

In subjects with a low BMI the beneficial effect of using the tanning bed and sunbathing is even more pronounced (-60% risk). In the obese, however, it is significantly reduced (-10%) compared to the average reductions you see in Figure 2.

The fact that only leisure time, but not occupational sun exposure was linked to a significant reduced risk of developing type II diabetes may, as Shore-Lorenti et al. point out be due ...

"[...] to the frequency of sun exposure (perhaps leading to tolerance), duration, intensity and site of exposure (sun protective clothing and behaviour differences between the two settings), or perhaps selection biases for such work (for example, fair-skinned people may avoid occupational sun exposure or a less healthy lifestyle may be associated with manual labour)."

Incidentally, a similar disparity between recreational and occupational sun exposure is well described for risk of developing melanoma (Chang. 2009).

A review by Chen et al. (2008) provides low-level evidence for an association between sun exposure and fasting insulin levels; fasting serum insulin was higher in summer than in winter. Overall, the results are yet inconclusive. A fact, Shore-Lorenti et al. ascribe to "the lack of adjustments made by the included study – particularly for BMI" (Shore-Lorenti. 2014)
Overall, we are thus left with the above overview (Table 1) as a conclusion of which the mere number of "unkown"s and "inconsistent"s tell you that we are not yet at the point to draw a water-proof conclusion.
References:

• Chang, Yu-mei, et al. "Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls." International journal of epidemiology (2009): dyp166. 
• Chen, Shui-Hu, et al. "Community-based study on summer-winter difference in insulin resistance in Kin-Chen, Kinmen, Taiwan." Journal of the Chinese Medical Association 71.12 (2008): 619-627.
• Lindqvist, Pelle G., Håkan Olsson, and Mona Landin-Olsson. "Are active sun exposure habits related to lowering risk of type 2 diabetes mellitus in women, a prospective cohort study?." Diabetes research and clinical practice 90.1 (2010): 109-114.
• Mitri, J., M. D. Muraru, and A. G. Pittas. "Vitamin D and type 2 diabetes: a systematic review." European Journal of Clinical Nutrition 65.9 (2011): 1005-1015.
• Nelemans, P. J., et al. "An addition to the controversy on sunlight exposure and melanoma risk: a meta-analytical approach." Journal of clinical epidemiology 48.11 (1995): 1331-1342.
• Shore?Lorenti, Catherine, et al. "Shining the Light on Sunshine: a systematic review of the influence of sun exposure on type 2 diabetes mellitus?related outcomes." Clinical endocrinology (2014).
• Suarez, L., and E. Barrett-Connor. "Seasonal variation in fasting plasma glucose levels in man." Diabetologia 22.4 (1982): 250-253. 

If you dont have ginger powder, just shred a fresh rhizome. Thats by the way what the researchers did, as well.

Yeah, we all know "Ginger is good for your glucose metabolism". We all know "there are dozens of rodent studies that support its benefits". And we also know that there is evidence from acute interventions that indicate that ginger can ameliorate the glucose response to oral glucose tolerance tests.

But do we know, whether the regular consumption of realistic amounts of pure ginger will have beneficial effects on the glucose levels of those who would benefit the most, i.e. type II aka "lifestyle" diabetics?
The results of the latest study from the Tehran University of Medical Sciences where scientists obviously dont depend on being able to produce patentable agents would suggest: There are benefits!

I have to admit, though, the ginger the 20-60 years old diabetics consumed was not provided in form of whole roots, but rather as a powder made of ginger roots.

"The under study patients were diagnosed with non-insulin dependent diabetes mellitus (NIDDM) by an endocrinologist on the basis of the results of the blood tests and met the criteria of the study. These criteria included: disease duration at least 2 years, HbA1c level of 6-8%, taking no antioxidant supplements such as selenium, zinc and beta-carotene for at least 3 months prior to the study, no smoking and drinking. Exclusion criteria of the study were insulin therapy at baseline or during the study, changes in the type or dose of medication, changes in diet or daily physical activity, any acute illnesses or some chronic diseases including kidney, liver, cardiovascular, and gastrointestinal diseases, smoking pregnancy and lactation, consumption of ginger or other botanical supplements, ginger hypersensitivity, and consumption of less than 80% of supplements during the study period." (Khandouzi. 2015)

Patients were divided randomly into two groups (experiment and control, 25 subjects in each) using computers random numbers to receive either ginger or placebo one capsule twice a day for 12 weeks. All subjects were permitted to consume their usual medications according to their physicians recommendation.

Regular ginger powder, nothing else!

The fresh rhizomes for the ginger powder purchased from local market and were ground as a fine particle after drying. The powder was delivered to a pharmaceutical lab (Tehran university of medical sciences, Iran) to prepare capsules containing 1 gram ginger in each. Lactose was also used to make placebo. Information on when the supplements were ingested is unfortunately, not available, but I assume "twice daily" means with breakfast and dinner or something like that.

Figure 1: Changes in fasting blood sugar, HbA1C, Apo-B/Apo-A1 and MDA levels (Khandouzi. 2015).

What is available, is the most relevant information, i.e. glucose, apolipoproteins and MDA levels we can use to access the effects on glucose and lipid metabolism and the peroxidation of polyunsaturated fatty acids.Parameters of which the data in Figure 1 tells you that they were significantly improved over the course of the 12-week study period. More specifically, this means:

• A 12% and 10% reduction in fasting blood glucose and HbA1c that may reduce many of the nasty chronic side effects of type II diabetes, such as its negative effects on heart health (Patel. 2008)
• A 28% reduction in the Apo B / Apo A-I ratio that signifies a significant reduction in coronary atherosclerosis risk (Van Stiphout. 1986)
• A 23% reduction in malondialdehyde (MDA) levels that signifies a reduction in coronary heart disease risk (Khan. 2000)

Overall, there is thus little question that something as simple as adding 2g of pulverized fresh Zingiber officinale rhizomes will have a significant impact on important health markers in middle-aged type II diabetics.
References:

• Khan, Mudassir Ahmad, and Abdul Baseer. "Increased malondialdehyde levels in coronary heart disease." J Pak Med Assoc 50.8 (2000): 261-264.
• Khandouzi, Nafiseh, et al. "The Effects of Ginger on Fasting Blood Sugar, Hemoglobin A1c, Apolipoprotein B, Apolipoprotein AI and Malondialdehyde in Type 2 Diabetic Patients." Iranian Journal of Pharmaceutical Research: IJPR 14.1 (2015): 131.
• Patel, Anushka, et al. "Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes." (2008).
• Schweizer, A., et al. "Comparison between vildagliptin and metformin to sustain reductions in HbA1c over 1 year in drug?naïve patients with Type 2 diabetes." Diabetic Medicine 24.9 (2007): 955-961.
• Van Stiphout, W. A. H. J., et al. "Is the ratio of apo B/apo AI an early predictor of coronary atherosclerosis?." Atherosclerosis 62.2 (1986): 179-182.

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.

Compared to liquid beverages, gels have the advantage of causing lower GI stress, when significant quantities of CHOs are consumed during exercise. Bars, can be held in the cheek pouch and chewed during critical phases of a race.

The headline gives it away. Todays SuppVersity article is a brief review of the (mostly sponsored) literature on Gatora.... ah, I mean carbohydrate supplementation during exercise. The headline also implies that the usefulness and efficacy of carbohydrate supplements depends on exercise duration and the type of exercise.

As a seasoned student of the SuppVersity you will know that certain paradox involved with regard to the duration / type of exercise. Short exercise durations, for example, shouldnt require large CHO boluses, long duration exercise, on the other hand, is fueled mostly by fat - so why should you supplement with carbohydrates, anyway?
I promise to answer this and other questions in the following paragraphs, but before I do so, I would like to point out that there is as of now no evidence that the much-praised "fat adaptation" increases the exercise performance to an "Olympia" level. Carbohydrate supplements, on the other hand, are still part of the regular supplementation regimen for the 99% of the top athletes.

That being said, the human physiology dictates that the use of carbohydrate supplements during aerobic workouts that last less than 60 minutes is useless, because muscle glycogen is generally not limiting to performance when exercise durations are less than ~60 minutes.

It should not work for short duration exercise, but it still does

Interestingly, 16 out of 23 studies, Trent Stellingwerff and Gregory R. Cox from the Canadian Sport Institute-Pacific and the Australian Institute of Sport reviewed for their recent paper in Applied Physiology have found that carbohydrate supplementation and/or oral (mouth) exposure to carbohydrate can improve performance of tasks less than 1 hour in duration:

You wont fully deplete your muscular glyocogen levels during short duration resistance training (Haff. 2003)

"In 2004 a seminal paper was published showing that a carbohydrate mouth-wash (swirling 25ml of a 6% CHO beverage (only ~1.5g of CHO in 25ml [6.4% maltodextrin solution (CHO)]) around in the mouth for ~10 sec, every 7.5min) significantly improved time trial (TT) performance [in seven male and two female endurance cyclists] by ~3% (Carter et al. 2004a)." (Stellingwerff & Cox. 2014)

This effect of CHO mouth-washing to improve performance in events from 30-60min has now been replicated in several other performance studies (10 of 13 studies) using both cycling and running interventions and with both sweet (sucrose) and non-sweet (maltodextrin) caloric CHO sources,as compared to 5 non-caloric artificial sweetener placebo trials showing no performance enhancing effects.

Figure 1: Hard to believe, but true - In 2010 Pottier et al. observed that CHO mouth-rinsing, but not CHO ingestion increases the 1h high intensity time-trial performance in trained subjects.

 "All these findings have been mechanistically supported with a functional magnetic resonance brain imaging study showing that CHO mouth-washing from both sweet tasting glucose and non-sweet maltodextrin can stimulate the brain areas of the insula/frontal operculum, orbitofrontal cortex and striatum, which are involved with brain centers responsible for reward and motor control (Chambers et al. 2009). Interestingly, if the mouth (oral receptors) and GI tract is by-passed by CHO infusion straight into the blood stream then 1h cycling TT performance was unaltered as compared to no CHO supplementation (Carter et al. 2004b)." (Stellingwerff & Cox. 2014)

Studies evaluating the effects on perceived exertion (Fares et al. 2011) found similar benefits all of which support the idea that the effect does not occur in the musculature, but rather in the head.
It should be obvious that the physiological, or rater intra-muscular benefits of carbohydrate supplements increases with the exercise duration.

CHO supplementation during exercise that lasts 60 minutes or longer

In view of the fact that it is 100% logical and well established by studies by Coyle et al. (Coyle 1992a; Coyle 1992b) that the intake of carbohydrate (glucose alone, and glucose + fructose blends) can significantly improve prolonged endurance capacity and performance (>60min of exercise (Jeukendrup 2010)).

Figure 2: Overview of the performance increases in the 50 studies Stellingwerff & Cox reviewed (2014)

Against that background I will not bother you with another overview of the results, but focus on the efficacy of different carbohydrate supplementation strategies and types of carbohydrate supplements for exercise durations beyond the "magical" hour.

Glucose + fructose - the combination advantage

As a SuppVersity reader youve previously heard about the benefits of combining glucose and fructose in your intra-workout beverage. It is thus only logical that most commercially available formulas are mixtures  glucose + fructose (GLU:FRU) or maltodextrin + fructose - so-called "multi-transportable CHOs". The advantage of using both glucose and fructose is that the carbohydrates will be absorbed via SGLT1 and GLUT5 intestinal transporters.

Specifically during long(er) duration exercise, when the carbohydrate consumption can exceed 60g/h there is a significant performance increase with multi- vs. single source carbohydrate supplements (Stellingwerff & Cox. 2014)

An advantage that has been scientifically established among others by Jeukendrup et al. (2010) who found that this pattern of CHO ingestion results in ~20 to 50% higher CHO oxidation rates compared to the ingestion of a drink that contains nothing but glucose or maltodextrin.


Now an increase in carbohydrate oxidation alone does not sound like something you would aim for as an endurance athlete. In practice, increases in carbohydrate oxidation have yet been shown to increase the performance during prolonged exercise bouts compared to isocaloric glucose-only beverages. (Currell et al. 2008; Triplett et al. 2010; OBrien et al. 2011; OBrien et al. 2013).
Needless to say that there is still research to be done with respect to individual influencing variables of carbohydrate requirements. The currently available evidence, for example, is largely based on results from runners and cyclists. Two other factors / issues that come to mind are...

• the dose-response relationship, which appears to be capped at 75g/h - at least according to a large-scale multi-center study by Smith et al. (Smith. 2013) who found that their subjects, endurance trained cyclists or triathletes experienced significant performance increases, with increasing amounts of carbohydrates (0, 10, 20, 30, 40, 50, 60, 70, 80, 90, 100, 110 and 120g of CHO/h) during a 2h constant load ride.
  
  

  Figure 3: Mean log time to complete time trial (natural) as function of CHO treatment condition with fitted quadratic curve (with 95% CI of mean curves). Differences 100 represent percent change in performance. The quadratic function relating CHO ingestion rate to time complete time trial for 43% (95% CI = 11%–75%,P= 0.059) of the variation in mean performance score (Smith. 2013)

  The CHO given was a 1:1:1 glucose:maltodextrin:fructose blend. Results indicated incremental performance improvements of 1.0%, 2.0%, 3.0%, 4.0%, and 4.7% at 9, 19, 31, 48, and 78g CHO/h, respectively, with diminishing performance enhancement seen at CHO levels >78g/h.
  
  The optimal amount for performance (+4.7%) was 78g/h, with a range of 68 to 88g/h. However, even at 10g/h, a 1.0% increase in performance was observed, showing even a small amount of carbohydrate has the potential to positively impact performance. 
• the optimal mix of glucose, dextrose, fructose, maltodextrin or other "special" carbohydrates  - needless to say that waxy maize, hydroxypropyl distarches (learn more) or the expensive fast absorbing highly insulinogenic patented carbohydrate source Vitargo come to mind, when we are talking about finding the optimal mix of different carbohydrate sources - a mix, by the way, of which you can safely assume that it will differ according to the physiological demands of the workout and the exercise duration.
  
  One thing we shouldnt forget, though, is that next to optimal performance, optimal GI tolerance, i.e. the absence of bloating, diarrhea & co would be an important criteria the "optimal" carbohydrate blend would have to meet.

• Figure 4: CHO suppl. ameliorates  testosterone reductions in 800m runners (de Sousa. 2010)

  the impact of carbohydrate supplementation on hormonal changes during and in response exercise - several human studies suggest that CHO supplementation attenuates the suppression of the hypothalamic-pituitary-gonadal axis and the rise in stress hormones during periods of intense training; a recent rodent study shows that the provision of carbohydrate supple- ments can prevent / reverse exercise-associated menstrual dysfunction (de Sousa. 2010; Zhao. 2014)

I guess, I could come up with additional research gabs, but in the end, a list of "gaps" is not exactly useful for you. Much in contrast to a conclusion, which I am about to formulate in the bottom line, now.
References:

• Carter,  J.,  Jeukendrup,  A.E.,  Mundel,  T.,  and  Jones,  D.A.  (2003).  Carbohydrate  supplementation  improves moderate and high-intensity exercise in the heat. Pflügers Archiv : European journal of physiology446: 211-9.
• Carter, J.M., Jeukendrup, A.E., and Jones, D.A. (2004a). The effect of carbohydrate mouth rinse on 1-h cycle time trial performance. Medicine and science in sports and exercise36: 2107-11.
• Carter, J.M., Jeukendrup, A.E.,  Mann, C.H., and  Jones, D.A. (2004b). The effect of glucose infusion on glucose kinetics during a 1-h time trial. Medicine and science in sports and exercise36: 1543-50. 
• Chambers,  E.S.,  Bridge,  M.W.,  and  Jones,  D.A.  (2009). Carbohydrate  sensing  in  the  human  mouth:  effects  on exercise performance and brain activity. The Journal of physiology587: 1779-94. 
• de Sousa, Maysa Vieira, et al. (2010). Effects of carbohydrate supplementation on competitive runners undergoing overload training followed by a session of intermittent exercise." European journal of applied physiology 109.3: 507-516.
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