The idea that dietary supplements can improve athletic performance is popular among athletes. The use of antioxidant supplements is widespread among endurance athletes because of evidence that free radicals contribute to muscle fatigue during prolonged exercise. Furthermore, interest in vitamin D supplementation is increasing in response to studies indicating that vitamin D deficiency exists in athletic populations. This review explores the rationale for supplementation with both antioxidants and vitamin D and discusses the evidence to support and deny the benefits of these dietary supplements. The issue of whether athletes should use antioxidant supplements remains highly controversial. Nonetheless, at present there is limited scientific evidence to recommend antioxidant supplements to athletes or other physically active individuals. Therefore, athletes should consult with their health care professional and/or nutritionist when considering antioxidant supplementation. The issue of whether athletes should supplement with vitamin D is also controversial. While arguments for and against vitamin D supplementation exist, additional research is required to determine whether vitamin D supplementation is beneficial to athletes. Nevertheless, based upon the growing evidence that many athletic populations are vitamin D deficient or insufficient, it is recommended that athletes monitor their serum vitamin D concentration and consult with their health care professional and/or nutritionist to determine if they would derive health benefits from vitamin D supplementation.

Background

Supplements for athletic performance have been a part of the landscape for decades and athletes are always looking for an edge in terms of either promoting adaptations to training, recovery, or outright performance.    And while many in the field tend to think of me as anti-supplement, this really sort of misses my issue with supplements.  Because I’m not anti-supplement; rather I’m simply anti-bs. 

I’m also anti-anything that takes focus away from the factors that actually do matter, namely things like training, diet, lifestyle, etc.  And the sad fact is that all too many athletes try to use supplements in place of proper training, attention to their diet, etc.  It goes to something I discussed ad nauseum in the thankfully finished Why the US Sucks at Olympic Lifting series, quick fixes are more appealing than things that take work.  And popping a pill is easier than working your nuts off in the gym or watching your diet.

And the reality is that most claims made for most supplements are about 99% bs and 1% “Well, maybe”.   Of course, that never stops athletes, who fall prey to the logic of “IF this is the next big thing, I don’t want to miss out on it.”  Of course, supplement industries pander to that very thought process; that’s how they make shocking amounts of money off of desperate athletes.

I’ve been in this field for over 2 decades and in that time I’ve seen thousands of products come and go, always with the same hype and exciting ad copy claiming that they are the solution for the woes of athletes, only to disappear months later to be replaced by the newest crop of crap.  Because over that 20 years, I can count the number of products that even came close to living up on maybe two hands.  That gives supplements about a 99.9% failure rate; in my mind it’s absurd to hold any opinion about anything new except to assume it’s crap until proven otherwise.  But I’m sort of getting off track here and really only want to focus on two specific supplements since they relate to today’s paper. 

Because for about three decades, one ‘class’ of supplements that has been popular (and very often recommended) is that of anti-oxidants.  In short, these are compounds that help to scavenge or ‘deal with’ what are called reactive oxygen species (ROS) in the body. These are produced under various conditions (including exercise) and one early theory of aging and bodily damage was that the production of ROS was part of the overall breaking down of the body.  With the logical solution being to simply take these nutrients in doses ranging from reasonable to ‘Oh my god, you want me to take how much?’ levels.  I can fondly remember Colgan and his laundry list of high-dose anti-oxidants in Optimum Sports Nutrition (an excellent book so long as you ignore every word about supplements) for example.

More recently, there has been great interest in Vitamin D status, both from a general health standpoint (Vitamin D deficiency is literally being considered a current vitamin deficiency epidemic and there is actually a staggering amount of data that this is the case) and from an athletic standpoint (and data going back to the 1920′s actually suggested this very early on).  Vitamin D does about a million and one things in the body but one thing it is strongly related to is muscular function and performance; I even mentioned explicitly in the Why the US Sucks at Olympic Lifting that one advantage that Kenyan runners may have is the ability to train outdoors year round (the same holds for Jamaican sprinters) and this may maintain better Vitamin D status compared to athletes who live in harsher environments.

Which is all just a lead up to today’s paper, a relatively short review on both anti-oxidant and Vitamin D (and calcium) supplementation for athletes, looking at the role that they play in the body and arguments both for and against the use of either by athletes.

The Paper

The paper starts by looking at the role of antioxidants in the body.  As I mentioned above, ROS are produced in the body under a variety of conditions including exercise and there is at least some evidence that ROS may cause fatigue during exercise when they are produced in large quantities; this is along with potentially causing overall bodily damage through oxidative stress (also caused by things like pollution and smoking for example) and muscle damage.

And this provided the idea that providing supplemental anti-oxidants (which include but are not limited to compounds such as Vitamin A, Vitamin C, Vitamin E, beta-carotone and a host of others; the list of potential anti-oxidant compound seems to grow daily).  However, with the exception of N-Acetyl Cysteine, which appears to reduce fatigue during some types of submaximal exercise (and it’s thought that this occurs by reducing ROS fatigue in breathing muscles, believe it or not), most studies supplementing anti-oxidants have not found any impact on performance.

Even the studies on anti-oxidant supplementation on muscle damage and oxidative damage are pretty mixed, probably reflecting differences in the type, amount and intensity of exercise along with the specific anti-oxidants and doses that were supplemented.  Basically, outside of NAC and submaximal endurance performance, the data is far from conclusive.

Moving to arguments for anti-oxidant supplementation, the paper examines three potential reasons that athletes might consider anti-oxidant supplementation.  First is the known increase in ROS production during activity, coupled with the general principle that the compounds are pretty much non-toxic even at relatively high levels. This is sort of a ‘It probably won’t hurt and might help’ kind of argument.  Kind of weak.

A second argument has to do with the role of excessive ROS on muscle fatigue but, as I noted above, with the exception of NAC, most supplementation studies have shown no performance benefit of anti-oxidants so this argument pretty much fails.  The final argument that they address is the idea that many athletes have poor or insufficient diets (note that most anti-oxidants in the diet come from fruits and vegetables) and that an athlete who’s diet is poor may need supplementation.  Which is equally weak for a number of reasons I won’t go into just yet.

In terms of arguments against anti-oxidants, the paper examines a number of arguments against supplementation. First they point out that while exercise certainly does increase ROS production it’s very transient (and this does distinguish it from the pollution or smoking examples which may be generating more chronic levels).  As well, the body already has an in-built system to deal with ROS production; quite in fact it increases it’s activity with training. 

That is, by exposing the body to ROS in moderate amounts, it adapts by being better able to handle further ROS production (some have even theorized that high-dose antioxidant supplementation might be harmful down the road by limiting the body’s upregulation of it’s inbuilt system).

In a related vein, there is considerable evidence and this has been accumulating for a while that the production of ROS is part of the overall adaptation to training (and the data here is more geared towards endurance athletes than strength/power athletes).  That is, the production of ROS, like inflammation and a whole host of other things that occur with training appear to be part of the overall training stimulus; blocking this with high-dose supplementation could conceivably limit the adaptations to training.

Finally is the simple fact that studies are routinely showing that individual anti-0xidant supplementation (as opposed to diets high in natural anti-oxidants; that is diets including lots of fruits and vegetables) either have no real benefit to health or may actually be harmful and increase mortality in the long-term.    The authors conclude that outside of ensuring a mixed, energy sufficient diet (which should provide adequate ‘natural’ anti-oxidants) that there is no reason for athletes to supplement with individual high-dose anti-oxidants.  I’ll come back to this when I wrap-up below.

Moving on the authors next address Vitamin D along with calcium (since it’s a bit tough to separate the two).  Vitamin D is a bit odd among the vitamins for a number of reasons, not the least of which that it can actually be produced by the body specifically in response to sun exposure.  The authors overview the metabolism of Vitamin D but I won’t repeat that here, go Wikipedia it if you must know.

Vitamin D is critical in the body for a number of reasons, not the least of which is bone health; in this vein, adequate Vitamin D status is required for optimal calcium absorption in the body.  As well, Vitamin D regulates genes all over the body, controls inflammation and immune system function; a great deal of research has focused on low Vitamin D status and colon cancer.   Of more relevance to athletes is that Vitamin D status is tied to muscular function and Vitamin D is involved in the expression of a number of genes involved in muscular function and performance; all issues relevant to athletes.

There’s actual a considerable history of evidence on the issue of Vitamin D and performance although it’s only recently that researchers have realized that Vitamin D might be playing a role.  Let me explain: back in the early part of the 20th century, it was observed that athletes often made less progress during the winter months in terms of strength or performance and that exposure to ultraviolet light improved trainability and strength gains.  We now clearly know that UVB exposure would have had one effect of increasing Vitamin D synthesis in the body and as discussed in Athletic Performance and Vitamin D, this may have been the mechanism at work.

Of more relevance, recent research is finding that almost everyone is Vitamin D deficient, all over the world. This is due to a number of factors including things like overuse of sunscreen, working indoors, poor diet, etc.  Both calcium and Vitamin D come from the diet (and many foods are fortified with both) but, as I mentioned, Vitamin D is an oddity among the vitamins in that it can be produced by the body, specifically in response to direct sun exposure.

Moving to Vitamin D status, the authors point out that determination of optimal level of Vitamin D in the body is still a bit of a controversial area.  It’s generally considered that Vitamin D levels below 50 nmol/L (or 20 ng/mL) is a sign of deficiency while levels below 80 nmol/L (32 ng/mL) is insufficient.  What level is optimal is harder to determine but a concentration of 100-250 nmol/l (or 40-100 ng/ML) is thought to be ideal.

It’s worth mentioning that while there is less work on the Vitamin D status of athletes, what work exists suggests that many athletes show Vitamin D insufficiency or outright deficiency levels; depending on the study and the definition used this may be as high as 90% of the athletes tested.  This is especially true for athletes involved in indoor sports, or who train in areas with a harsh winter that limits sun exposure (while Vitamin D levels go up during summer training, they are only maintained for perhaps a month or so without supplementation or sun exposure.  Interestingly, even athletes in sunny areas, such as Qatar may be at risk for deficiency, probably due to athletes preferring to train after sundown since it’s about a billion degrees during the day.  It’s only athletes who live in temperate year round sunny climates that are likely to not be at risk for Vitamin D deficiency.

And from that standpoint alone, supplementation is probably warranted for athletes who train indoors or who live in cold weather areas where sun exposure for a great part of the year simply isn’t available (note that the use of a tanning bed would be another option so long as the duration are moderate).

Mind you, the direct data on Vitamin D and athletic performance isn’t major except for what I talked about above, a handful of studies have examined it and there does appear to be a positive correlation between Vitamin D status and things like strength and muscle force, along with decreased risk of stress fracture (important for athletes in high-impact activities).  Mind you, claims such as “The higher the Vitamin D status the better your performance” are absolutely not supported by current research; it’s likely that it’s more an issue of correcting a highly likely deficiency or insufficiency.

In terms of arguments against supplementation, the main one is the overall lack of data indicating a performance boost; mind you that keeping an athlete healthy in general terms (and Vitamin D contributes to immune system function and bone health) is just as critical here.  An injured or sick athlete isn’t training nor performing and the realities of Vitamin D deficiency should be addressed regardless of whether or not it improves performance.

The other argument against has to do with toxicity, as a fat soluble vitamin, it is possible to take too much Vitamin D.  It does take pretty stupid levels but athletes often fall into a ‘more is better’ trap.  But this is more to do with ensuring that athletes don’t do stupid things and take 5X the recommended dose than the supplement itself.  I’d note that roughly 30 minutes of direct sun exposure pretty much maxes out Vitamin D synthesis (at roughly 10,000 IU’s) in the body and this might be taken as a rough realistic maximum daily intake level.  Others have set more conservative maximum intake levels of 4000 IU’s/day; at the current time it’s not really known what level of supplementation is toxic or problematic.

Finally the authors note that there is individual difference in the absorption and utilization of Vitamin D and this could conceivably impact on how a given athlete responds to supplementation (a great deal of research suggested a problem with Vitamin D levels in obesity but that’s a different research review).  The authors recommend that, while there is little evidence that Vitamin D supplementation will improve performance (outside of correcting a deficiency), athletes should monitor their Vitamin D levels and supplement as needed.  Again I’ll give my recommendations below.

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My Comments

For the most part what I wrote above doesn’t really differ to any signicant degree from what I wrote in the articles Supplements Part 1 and Supplements Part 2.  In terms of anti-oxidant supplementation, I’m really not a fan under most circumstances.  Not only do they not appear to have much if any benefit, especially taken in isolated form in high-doses, they may actually be detrimental to training adaptations.  Using them during a primary training phase could slow adaptations.  In contrast, athletes in heavy competition might consider supplementation; some studies do show decreased muscle soreness and damage and taking them during a heavy competition schedule might be worthwhile simply to keep the athlete in one piece.  That’s in addition to NAC having a potential ergogenic benefit before certain types of endurance performance.

In terms of Vitamin D, outside of those athletes who can train consistently in the sun, I think supplementation is probably mandatory.  Few athletes live in climates where outdoor sun exposure is available year round and the simple fact is that even if optimal levels occur during summer training, they only maintain about a month or so after the stimulus of regular sun exposure is removed. 

Athletes who’s sports keep them indoors, or who live in areas with actual winter (where training is done indoors by choice or there is simply limited sun exposure) will find Vitamin D levels falling rapidly, potentially compromising immune system function, bone health and even trainability.  Supplementation (or going to the tanning bed a few times per week for reasonable amounts of time, perhaps 30 minutes 2-3X/week) will serve to maintain optimal Vitamin D status during those time periods.

And while it would be ideal for athletes to get regular blood work to determine levels along with their response to supplementation it’s not cheap work to do and has to be done at least twice.  For athletes that can get it done, I’d mention that it takes, on average, 100 IU of Vitamin D to raise levels by 1 ng/mL.  So an athlete with a Vitamin D level of 30 ng/mL who wants to get to 50 ng/mL would need 2000 IU’s per day.

As I noted above, 30 minutes of direct sun exposure generates 10,000 IU’s of Vitamin D and that appears to be the maximum the body will synthesize.  A daily intake of half that should be more than safe and is in keeping with other maximum daily recommendations of 4000 IU/day.  And outside of extreme deficiencies, that level should cover most folks (that is if we assume levels drop to an insufficient 20-30 ng/mL during the winter, 5000 IU/day would be expected to raise that to 70-80 ng/mL right in the middle of the optimal range).

I’d note in closing that, as a fat soluble vitamin, Vitamin D should be taken with a fat containing meal for optimal absorption, Vitamin D is also a supplement that can be taken only weekly (i.e. 35,000 IU’s all at once or what they’d get from 5000 IU’s per day for a week) for athletes who are bad about taking pills.

With the sheer volume of research appearing on a weekly basis, this will at least help me to look at data in a more timely fashion.  I’d mention that, for anyone who wants an even better look at a lot of studies, you’d be well served to consider Alan Aragon’s monthly Research Review which I reviewed in the confusingly titled Alan Aragon Research Review – Product Review.

In any case, today I want to look at two recent studies which are:

1. Deglaire et al. Hydrolyzed dietary casein as compared with the intact protein reduces postprandial peripheral, but not whole-body, uptake of nitrogen in humans. Am J Clin Nutr. (2009) 90(4):1011-22.
2. West et. al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J Appl Physiol. 2009 Nov 12.

For each study I’ll give a brief background to the topic, look at what was done and then jump straight to the conclusions with some final summing up.  As noted above, some of the detail will be left out but I figure that anyone who is that interested in the details of methodology and such will simply get ahold of the full paper and read it themselves.

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Deglaire et al.  Hydrolyzed dietary casein as compared with the intact protein reduces postprandial peripheral, but not whole-body, uptake of nitrogen in humans. Am J Clin Nutr. (2009) 90(4):1011-22.

BACKGROUND: Compared with slow proteins, fast proteins are more completely extracted in the splanchnic bed but contribute less to peripheral protein accretion; however, the independent influence of absorption kinetics and the amino acid (AA) pattern of dietary protein on AA anabolism in individual tissues remains unknown. OBJECTIVE: We aimed to compare the postprandial regional utilization of proteins with similar AA profiles but different absorption kinetics by coupling clinical experiments with compartmental modeling. DESIGN: Experimental data pertaining to the intestine, blood, and urine for dietary nitrogen kinetics after a 15N-labeled intact (IC) or hydrolyzed (HC) casein meal were obtained in parallel groups of healthy adults (n = 21) and were analyzed by using a 13-compartment model to predict the cascade of dietary nitrogen absorption and regional metabolism. RESULTS: IC and HC elicited a similar whole-body postprandial retention of dietary nitrogen, but HC was associated with a faster rate of absorption than was IC, resulting in earlier and stronger hyperaminoacidemia and hyperinsulinemia. An enhancement of both catabolic (26%) and anabolic (37%) utilization of dietary nitrogen occurred in the splanchnic bed at the expense of its further peripheral availability, which reached 18% and 11% of ingested nitrogen 8 h after the IC and HC meals, respectively. CONCLUSIONS: The form of delivery of dietary AAs constituted an independent factor of modulation of their postprandial regional metabolism, with a fast supply favoring the splanchnic dietary nitrogen uptake over its peripheral anabolic use. These results question a possible effect of ingestion of protein hydrolysates on tissue nitrogen metabolism and accretion.

My Comments: Ever since the pioneering work in the 90′s on fast and slow proteins, there has been continued interest in the digestion speed of proteins and how that impacts on metabolism, performance and, of course, muscle growth. In recent years, there have been many claims made for the superiority of faster proteins to slower in terms of ‘speeding amino acids to muscle’ in terms of promoting growth.

As well, as many may note, a recent commercial product (T-nations Anaconda), who’s anabolic claims were analyzed in perhaps the most commented article on the site in Alan’s Aragon’s guest article Supplement Marketing on Steroids, has recently been released to the market.

For background, hydrolysates are simply whole proteins that have been pre-digested (through the addition of enzymes during production) to some degree.  The theory being that, due to this pre-digestion, the hydrolysate will be digested in the stomach faster, getting aminos into the bloodstream faster and, presumably, having a better effect on skeletal muscle than slower proteins.

But is it true?  Guess.

The above study examined this issue by feeding 21 subjects 2 test meals containing ~26.5 grams of either intact casein or it’s hydrolysate; the protein had been marked with radioactive nitrogen so that it’s fate after ingestion could be tracked over the next 8 hours.  The test meals also contained 96 grams of carbohydrate and 23 grams of fat; this is worth noting as adding other nutrients to fast proteins often makes them behave more like slow proteins.  I’ll spare you the methodology, sufficed to say that tracking protein after it enters the body is brutally complicated and involves a lot of modelling and various measurements of blood amino acid levels and such.

Here’s what the study found.  Over the time course studied (8 hours after ingestion), the hydrolyzed casein product showed greater losses from digestion (that is, less was absorbed).  As well, a greater amount of the hydrolysate was oxidized for energy through deamination (a process by which the amino group is stripped off the carbon backbone).  Finally, a larger amount of the casein hydrolysate was used by the splanchnic bed (gut and intestines) with significantly less of the total protein reaching the bloodstream or peripheral tissues (muscles).

To quote the researchers:

Despite similar overall net postprandial protein utilization, our results indicate important differences in metabolic partitioning and kinetics between protein sources characterized by a preferential utilization of dietary nitrogen by for splanchnic protein syntheses after HC [hydrolyzed casein] ingestion at the expense of the incorporation into peripheral tissues.

Translating that into English: hydrolyzed casein is digested more poorly, gets burned for energy to a greater degree and gets used more by the gut than intact casein; the end result of this is that hydrolyzed casein provides LESS amino acids to skeletal muscle after ingestion than intact casein protein.

So not only is the claim that hydrolysates are better at providing aminos faster to skeletal muscle wrong, the reality is actually exactly reversed: intact casein is better for providing aminos to the muscle.  I’d note that other studies have found this as well: in one, intact protein provided MORE branched-chain amino acids into the bloodstream than a hydrolyzed form.

I’d add to this that, as I discussed in The Protein Book, other data supports the idea that slower proteins may actually be superior to faster proteins for muscle growth; in one set of studies, for example, milk protein (a mix of slow and fast proteins) resulted in greater hypertophy than soy (a fast protein) over 8 weeks of training and supplementation.  As well hydrolyzed proteins tend to taste like bleach; it’s no coincidence that Anaconda has to come with a separate flavoring intensifier: hydrolysates are gag-inducing.  They can’t be consumed straight.

Summing up: Hydrolysates are not only not superior to intact protein in terms of providing amino acids to skeletal muscle, they are distinctly inferior.  Their fast digestion speed leads to greater digestive losses, more oxidation via deamination and provides less amino acids to skeletal muscle.  That’s on top of tasting like vomit.  Or at least making you want to.

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West et. al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J Appl Physiol. 2009 Nov 12.

The aim of our study was to determine whether resistance exercise-induced elevations in endogenous hormones enhance muscle strength and hypertrophy with training. Twelve healthy young men (21.8 +/- 1.2 y, BMI = 23.1 +/- 0.6 kg(.)m(-2)) independently trained their elbow flexors for 15 weeks on separate days and under different hormonal milieu. In one training condition, participants performed isolated arm curl exercise designed to maintain basal hormone concentrations (low hormone, LH); in the other training condition, participants performed identical arm exercise to the LH condition followed immediately by a high volume of leg resistance exercise to elicit a large increase in endogenous hormones (High Hormone, HH). There was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1) or testosterone after the LH protocol, but significant (P < 0.001) elevations in these hormones immediately and 15 and 30 min after the HH protocol. The hormone responses elicited by each respective exercise protocol late in the training period were similar to the response elicited early in the training period indicating that a divergent post-exercise hormone response was maintained over the training period. Muscle cross-sectional area increased by 12% in LH and 10% in HH (P < 0.001) with no difference between conditions (condition x training interaction, P = 0.25). Similarly, type I (P < 0.01) and type II (P < 0.001) muscle fiber CSA increased with training with no effect of hormone elevation in the HH condition. Strength increased in both arms but the increase was not different between the LH and HH conditions. We conclude that exposure of loaded muscle to acute exercise-induced elevations in endogenous anabolic hormones enhances neither muscle hypertrophy nor strength with resistance training in young men. Key words: testosterone, growth hormone, IGF-1, anabolism.

My Comments: For several decades now, there has been intense focus on the acute hormonal response to training.  This started back in the 80′s where researchers, interested in growth did a rather cursory examination of elite powerlifters and bodybuilders, made some assumptions about muscle size, made some even bigger assumptions about how they trained, and then proceeded to reach some staggeringly poor conclusions.

Basically, what they observed was that bodybuilders were bigger than powerlifters, which is debatable in the first place.  They also observed that powerlifters typically used low reps and long rest periods and bodybuilders (remember: this was the Arnold era) trained with high reps and short rest periods.  Thus they concluded that high reps and short rest stimulated muscle growth and went looking for reasons why this was the case.  I’d note that this is not really how you’re supposed to do science: you don’t reach your conclusion and go find reasons why it’s right.  You test hypotheses and draw your conclusions from that.  But I digress.

And the main focus for a while was potential differences in hormonal response to training, primarily focusing on testosterone and growth hormone (GH).  The basic study design that was followed was to compare the acute hormonal response to either 3 sets of 5 repetitions with a long rest interval (3 minutes) to sets of 10 with a 1 minute rest interval.  Repeatedly, studies showed that the first type of training boosted testosterone and the second GH.  Entire training schemes have grown out of this but there was a problem: nobody ever bothered to see if these acute (usually less than 10-15 minute) bumps in hormones actually did anything.

Nevermind that this makes little sense anyhow for a variety of reasons.  Not the least of which is that women have higher GH levels than men and get a bigger GH response to training, yet they don’t grow better.  If anything, with the known impact of testosterone on muscle growth, if there was to be any benefit to this, you’d expect the lower rep/heavy work to be superior.  Yet the researchers were arguing that it wasn’t.   There was a logic missing in the argument (not the least of which being the assumption that powerlifters had smaller muscles than bodybuilders) that seemed to get skipped over.

In addition to the science, there is a long held belief, echoed in various places (including the comments section of another contentious article I wrote titled Squats vs. Leg Press for Big Legs) that certain movements, notably squats and deadlifts, will have full-body growth stimulating properties, generally mediated through the hormonal response.

It’s not uncommon to see people recommending things like “If you want big arms, squat/train legs.” for example.  Essentially, heavy leg work is touted as being the key to overall growth.  Nevermind that the same people who make this argument will often complain about “All those guys in the gym with huge upper bodies and no legs” without realizing that the two ideas contradict one another (that is, if leg training is required for growth, how can guys get huge upper bodies without training legs).  But I digress again.

In any case, this study examined the issue directly with a somewhat confusing study design: twelve healthy young men trained their biceps on different days of the week under different training conditions.  In what they called the low-hormone condition, the biceps were trained all by themselves; no other exercise was done.  In the other called the high-hormone condition, the biceps were trained and then a large-volume of leg training was done to elevate the supposedly anabolic hormones.

Does that make sense, all subjects trained both arms, but on different days and under different conditions.  And the training was far enough apart that the hormonal response from the leg training wouldn’t have impacted the low-hormone training session.  This training was followed for 15 weeks and subjects consumed protein both before and after the training (so there was nutritional support).

Hormone levels were measured and while there was no significant change in hormones in the low-hormone situation, in the high-hormone situation, there were increases in lactate, growth hormone, free and total testosterone and IGF-1 with the peak occurring approximately 15 minutes after the leg work.

And, if the hormonal response to heavy leg training actually has any impact, what you’d expect to see is that one arm, the one trained along with the leg training, would grow better.

Did it happen? Guess.

Both maximal strength and muscle cross sectional area increased identically in both arms to the tune of a 20% vs. 19% increase in strength for low- vs. high-hormones and an increase in skeletal muscle cross sectional area of 12% vs. 10% in low- vs. high-hormones.  These differences were not statistically significant. Quoting the researchers:

Despite vast differences in hormone availability in the immediate post- exercise period, we found no differences in the increases in strength or hypertrophy in muscle exercised under low or high hormone conditions after 15 weeks of resistance training. These findings are in agreement with our hypothesis and previous work showing that exercise-induced hormone elevations do not stimulate myofibrillar protein synthesis (36) and are not necessary for hypertrophy (37). Thus, our data ((36) and present observations), when viewed collectively, lead us to conclude that local mechanisms are of far greater relevance in regulating muscle protein accretion occurring with resistance training, and that acute changes in hormones, such as GH, IGF-1, and testosterone, do not predict or in any way reflect a capacity for hypertrophy.

I don’t think it gets any clearer than that and I’d note that another recent study titled “Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men.” by the same group found the exact same thing.

Summing Up: Leg training has no magic impact on overall growth, most of which is determined locally (through mechanisms of tension and fatigue mediated by changes in local muscular metabolism).  If you want big arms, train arms.  If you want big legs, train legs.

And if folks are wondering why empirically ‘folks who train legs hard’ seem to get big compared to those who don’t, I’d offer the following explanation: folks willing to toil on heavy leg work work hard.  Folks too lazy to train legs hard often don’t.  And it’s the overall intensity of the training that is causing the difference, not the presence or absence of squats per se. Which is why guys who only hammer pecs and guns get big pecs and guns even if they couldn’t find the squat rack in the gym: the small acute hormonal responses to training are simply irrelevant to overall growth.

Greenberg JA et. al. Coffee, diabetes, and weight control. Am J Clin Nutr. (2006) 84(4):682-93.

Several prospective epidemiologic studies over the past 4 y concluded that ingestion of caffeinated and decaffeinated coffee can reduce the risk of diabetes. This finding is at odds with the results of trials in humans showing that glucose tolerance is reduced shortly after ingestion of caffeine or caffeinated coffee and suggesting that coffee consumption could increase the risk of diabetes. This review discusses epidemiologic and laboratory studies of the effects of coffee and its constituents, with a focus on diabetes risk. Weight loss may be an explanatory factor, because one prospective epidemiologic study found that consumption of coffee was followed by lower diabetes risk but only in participants who had lost weight. A second such study found that both caffeine and coffee intakes were modestly and inversely associated with weight gain. It is possible that caffeine and other constituents of coffee, such as chlorogenic acid and quinides, are involved in causing weight loss. Caffeine and caffeinated coffee have been shown to acutely increase blood pressure and thereby to pose a health threat to persons with cardiovascular disease risk. One short-term study found that ground decaffeinated coffee did not increase blood pressure. Decaffeinated coffee, therefore, may be the type of coffee that can safely help persons decrease diabetes risk. However, the ability of decaffeinated coffee to achieve these effects is based on a limited number of studies, and the underlying biological mechanisms have yet to be elucidated.

My Comments

Caffeine is another one of those compounds about which there is endless argument and debate.  Some feel that it is evil, too much causes all manners of problems, and should be eliminated completely. Others like me feel that the only problem with caffeine is when there isn’t enough of it.

Specific to this research review, it’s often been claimed that caffeine raises insulin, causes insulin resistance and deteriorates blood glucose control.  Thus individuals suffering from the Metabolic Syndrome/Insulin Resistance/Pre-Type II diabetes (all being the same name for essentially the same thing) should avoid it.

But what does the research actually say in this regards?

First and foremost, there is actual some truth to the idea that caffeine can cause problems with blood glucose control and insulin levels,  at least if you’re looking at high doses of caffeine right before a meal tested under acute (single meal) conditions.

Typically doses of 5 mg/kg are given which is 500 mg of caffeine for a 100kg (220 lb) person.  Under those conditions, at least in short-term studies, problems are often seen.  This is an enormous amount of caffeine.

Putting this in a real world perspective, a typical soda or cup of coffee might contain 60-100 mg of caffeine, or approximately 1/5th to 1/8th the amount used in most studies.  Of course, we all know people who’s idea of caffeine intake means drinking the entire pot and, in that situation, the above might actually apply.  But the person drinking a soda with a meal or a cup of coffee won’t even be close.

At the same time, epidemiological studies (which are not the strongest data set in my opinion) suggest that regular caffeine/coffee intake may actually be beneficial in terms of limiting the incidence of diabetes and may play a role in weight loss.

So clearly it’s a bit more complicated than it looks (or is claimed) and this paper set out to uncomplicate things.

The first data set the review looked at was epidemiological data. Now, I’m no fan of epidemiology in general, there can be a lot of confounding factors when you’re trying to determine what causes what. At best, that kind of data gives a starting point and some possible correlational data to do direct work; at worst it’s useless.

That said, looking at 20 studies on the topic, the researchers found that 17 of the 20 showed a beneficial effect of habitual coffee/caffeine intake on diabetes and glucose metabolism, 3 found no effect and none showed a negative effect.

Getting a bit more detailed, four of the studies suggested that non-caffeine components of coffee were involved (that is, pure caffeine and coffee per se may have different effects, a topic I’ll come back to below) and four studies found an effect of decaf coffee (suggesting that non-caffeine components are playing a role here). One study suggested that the impact of coffee was due to an effect on body weight (weight loss) which was the next topic of the paper and what I’ll discuss next.

Looking first at rat data, the paper examines data showing that caffeine can reduce bodyweight, fat pad weight and even fat cell number. However, humans aren’t rats and human data on this topic is mixed at best. One human study found no impact of caffeine on weight loss but as mentioned above it may be that coffee and other non-caffeine components explains the epidemiological data.

Next up, the paper looked at the impact of caffeine on thermogenesis (calorie burning) and lipolysis (fat mobilization). It comments that a habitual caffeine of 600 mg/day (~6 strong cups of coffee) could lead to an extra caloric expenditure of 100 cal/day (equivalent to walking about 1 mile for a 150 lb person). This effect also occurs with ground and instant coffee, but not decaf so the effect is probably mediated via the caffeine itself. Do note that the body can develop tolerance to these effects so any effect might not be very long lasting.

Related to this, caffeine has also been shown to increase lipolysis (fat mobilization) and fat oxidation and both caffeine and coffee have this effect; decaf does not so it’s clearly an effect of the caffeine per se. Interestingly, both the impact on lipolysis and fat oxidation is more pronounced in non-obese than obese individuals; leaner individuals, probably due to a greater sensitivity to lipolytic stimuli, get a larger effect.

In any case, I want to expand on that a bit, even if caffeine is having a negative impact on insulin sensitivity or insulin levels, the simple fact is that it increases fat mobilization.  Combined with a caloric deficit or exercise, this means that those fatty acids can be burned off the body.  The idea that caffeine is somehow bad on a diet because of an impact on insulin sensitivity is missing the forest for the trees; caffeine increases fat mobilization and burning and that’s what matters in the long run for losing body fat.

The paper also mentions that caffeine may increase energy expenditure. Doses of 3-30 mg/kg in rats increase spontaneous activity and this type of activity (called NEAT or non-exercise activity thermogenesis in humans) can amount to a fairly considerable energy expenditure. Basically, caffeine may help with weight loss by making you move around more.   Again, decaf does not have this effect.

Additionally, a very well known effect of caffeine is improved exercise performance. Caffeine pre workout decreases fatigue, causes more fat to be used (sparing glycogen) and has a host of other effects. By allowing exercisers to work harder, caloric expenditure can be increased.  Which can only facilitate fat loss.

The next topic discussed has to do with the direct impact of caffeine/coffee on insulin and blood glucose tolerance with a majority of short-term studies showing a negative impact of coffee/caffeine on glucose tolerance when given right before a carbohydrate containing meal.

Note that caffeine was not found to raise insulin or blood glucose when not given with a carbohydrate meal; the fear of caffeine on low-carb diets (it’s often claimed that caffeine will raise insulin and should be avoided on such diets) appears to be unfounded. However, this data is at odds with the epidemiological data suggesting that chronic caffeine/coffee intake decreases diabetes risk.

Data comparing the effects of decaf to caffeinated coffee suggests a possible explanation; decaf coffee tends to lower blood glucose, suggesting the presence of non-caffeine compounds in coffee that may beneficially impact on blood glucose levels.

Note also that animal research suggests a tolerance to any impact of caffeine on blood glucose levels although this has not been studied in humans. However, humans are known to develop a tolerance to the stimulant, thermogenic and other effects of caffeine, it may be that chronic intake of caffeine has a very different effect on blood glucose levels that studies looking at single dose intakes.

Mechanistically, caffeine probably impacts on blood glucose tolerance by raising blood fatty acids and catecholamine levels, both of which impair skeletal muscle insulin sensitivity.  That is, the way that caffeine might have an impact on insulin resistance (and thus indirectly insulin levels when carbohydrates are consumed) is by its effects on lipolysis.

Additionally, the potential impact of coffee/caffeine on fullness was noted but this has not been well researched in humans, some studies indicate higher satiety in folks using coffee/caffeine habitually.

Next the paper delved into other potential health effects. Acutely, caffeine/coffee can raise blood pressure a bit but the body develops partial tolerance rapidly. High caffeine intakes have been found, in animal studies, to cause problems with pregnancy; as well, it may potentiate the negative effects of alcohol and tobacco in this regards. Intakes of >3 cups/day of coffee can decrease fetal birth weight.

Additionally, caffeine withdrawal can cause headaches, irritability, anxiety, depression, drowsiness and fatigue. Folks wanting to reduce their caffeine/coffee intake (for whatever reason) should do so gradually to avoid problems.

High doses of caffeine can also contribute to the risk of kidney stones in elderly individuals and could cause problems with osteoporosis; this is mainly seen with daily calcium intake is low to begin with.
Early research suggested a link between coffee and an elevation of blood lipids but this turns out to only hold for boiled coffee, not brewed.

Finally, the paper discussed the issue of non-caffeine compounds in coffee that might have additional effects on the body. One (I’ll spare you the name) has been shown to decrease glucose uptake from the intestine, this might offset negative potential effects of caffeine on blood glucose levels (caffeine alone accelerates glucose uptake from the gut).

Another compound (called a quinide) was shown to enhance glucose uptake and insulin sensitivity in rats, and both the high antioxidant content of coffee along with the magnesium intake may improve insulin sensitivity in the long-term; this might explain the discrepancy in the short-term and epidemiological data.
More research into the non-caffeine components of coffee still needs to be done.

Application

So what’s the take home in this? Caffeine/coffee intake appears to have different effects when looked at in the short and long term; looking only at acute dosing studies (esp with extremely high doses of caffeine) aren’t that relevant to how people actually consume caffeine (over the long term).

In the short-term, caffeine can impact positively on a number of factors (such as delaying fatigue during exercise, increasing lipolysis, and increasing fat oxidation and caloric expenditure) but negatively on others (decreased glucose tolerance/increased insulin response, slight increase in blood pressure).

However, longer term studies suggest that habitual caffeine/coffee intake is, overall, beneficial: it decreases the risk of diabetes and may contribute to preventing weight gain Tangentially, of course, any benefit of coffee/caffeine itself is going to be more than outweighed if you fill it up with sugar, cream and other high calorie goodies.

My take on the topic: used in reasonable amounts, caffeine pretty much does nothing but help fat loss.  The impact on insulin sensitivity is overstated (in my opinion) only applying to acute studies with massive doses.  The known impact of caffeine on lipolysis and improving exercise performance is so well-established as to be beyond debate.

So use caffeine, just don’t go nuts with it.

(-)-Hydroxycitrate (HCA) might promote weight maintenance by limiting the capacity for de novo lipogenesis (DNL). It was investigated whether HCA may reduce DNL in humans during a persistent excess of energy intake as carbohydrate. In a double-blind, placebo-controlled, randomized and cross-over design, 10 sedentary lean male subjects (mean+/-S.D., age: 24+/-5 years, BMI: 21.8+/-2.1 kg/m(2)) performed a glycogen depletion exercise test followed by a 3-day high-fat diet (F/CHO/P, 60/25/15% energy; 100% of energy expenditure (EE)) and a 7-day high-CHO diet (F/CHO/P, <5/>85/10% energy; 130-175% of EE; overfeeding). During overfeeding, they ingested 3×500 mg/day HCA or placebo (PLA). Each intervention ended with a 60-h stay in the respiration chamber (days 9 and 10). Body weight increased during overfeeding (mean+/-S.E., HCA: 2.9+/-0.2 kg, PLA: 2.8+/-0.2 kg). Respiratory quotient (RQ) was >1.00 in all subjects indicating that DNL was present. On day 9, 24-h EE was lower with HCA compared to PLA (P<0.05). On day 10, resting metabolic rate and RQ during night were lower (P<0.01 and P<0.05, respectively). Non-protein RQ, fat balance and net fat synthesis as DNL tended to be lower (P<0.1) with HCA compared to PLA indicating lower DNL; activity-induced EE was higher with HCA (P<0.05) indicating the urge to eliminate the excess of energy ingested. We conclude that an experimental condition resulting in DNL in humans was created and that treatment with HCA during overfeeding with carbohydrates may reduce DNL.

My comments: I choose this week’s study for two reasons as it addresses two separate issues, that of de novo lipogenesis (DNL, the synthesis of fat from carbohydrates) as well as the supplement hydroxycitric acid (HCA) which has been touted as a ‘fat-burner’ (for use on a fat loss diet) for quite some time.

DNL has been the subject of much debate for years and many readers have probably seen it claimed that ‘carbs in excess of needs simply get converted to fat and stored’. This is true if you’re looking at rats, mice and hamsters. One study (Acheson et. al., 1982) in humans gave the subjects 500 grams of carbohydrates (2000 calories) all at once; conversion of carbs to fat was insignificant. The majority of research in humans has not found DNL to contribute significantly to fat gain except under a few very extreme conditions. They are

1. An artificially low-fat diet: less than 10% of total calories which well-meaning but otherwise misguided athletes and bodybuilders sometimes try to achieve.
2. Chronic massive carbohydrate overfeeding: one study (Acheson et. al., 1988) gave 700-900 grams of carbohydrates for 3 straight days following glycogen depletion. In the first 24 hours, as glycogen was refilled, there was no net DNL. Over the next 2 days, as carb intake remained massive and sustained, DNL increased and a significant amount of fat was synthesized. This is part of why diets like Bodyopus and my Ultimate Diet 2.0 taper carbohydrates down as the carb-load continues.

This study created a situation similar to both, for the first 3 days, the subjects followed a low-carbohydrate diet with glycogen depletion (sound familiar). Then they were overfed for the next 7 days on 85% carbohydrates(5% fat and 10% protein) with caloric intake at 130-170% over maintenance. Massive carbohydrate overfeeding accompanied by a very low fat intake, and DNL increased significantly as indicated by a respiratory quotient (RQ) greater than 1.0.

Along with this, the researchers gave the subjects HCA to see if it blunted DNL during the overfeeding, which it did. Back in my first book The Ketogenic Diet, I mentioned that HCA might have some use during CKD style carb-loads for this very reason: empirically, some people found that HCA would limit bloating and puffiness during their carb-load.

But what relevance does this study have to normal conditions? Essentially none. Unless you’re deliberately overfeeding carbs for many days in a row (along with an extremely low-fat intake), DNL generally contributes minimally, if at all to fat gain (for review, see Hellerstein, 1999). As well, HCA only has an impact in humans during massive carbohydrate overfeeding, although one study (Westerterp-Plantenga, 2002) suggested it might help reduce food intake. Its use as a fat-burner on a diet (by definiton you can’t be overfeeding carbs, except during refeeds or CKD style carb-loads) was misguided anyhow, since that’s not how it works.

Summing up: except under the most extreme of dietary conditions, DNL contributes almost insignificantly to fat gain in humans. Which isn’t to say that carbs don’t contribute to fat gain, it’s simply generally not through direct conversion to fat. And while HCA might have some use during those types of extreme dietary conditions, in general it’s fairly useless as a supplement; especially as any kind of fat burner on a diet.