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Sports Nutrition – It is essential you include fat in your diet

Dietary FatAn extremely informative article on the vital need for increasing Omega-3 oils in our otherwise highly deficient modern diets, as well as some interesting benefits for endurance athletes when consuming medium-chain fats in sports drinks. Mike.

Fat is necessary to absorb key vitamins and assists carbohydrate in providing you with energy

After all, dietary fat is necessary to absorb key vitamins such as A, D, E, and K. And athletes involved in heavy training often need moderate amounts of fat in their diets just to satisfy their monumental daily caloric needs. Fat also assists carbohydrate in providing the fuel needed for endurance performances

However, not all fats are the same. Athletes can choose from saturated, monounsaturated, and polyunsaturated fats, and there are various kinds of polyunsaturates. There’s also the possibility of choosing between medium-chain fats, such as those found in many dairy products, and long-chain lipids, like those found in meats and plants.

Are certain forms of fat best for maximizing exercise capacity?And which type of fat is superior for your overall health?

Those two key questions have been debated vigorously during the past decade. Lately, the popular press has trumpeted the merits of monounsaturated fat for improved cardiovascular health, and athletic publications have put forth the proposition that medium-chain fats might increase performance under certain circumstances (basically, during ultra-endurance competitions).

Health-conscious athletes have been trying to reduce the amount of saturated fat and cholesterol in their diets, often substituting polyunsaturated fats such as corn oil or mono-unsaturated fats like olive oil for animal fat, and many ultra-athletes have initiated the practice of consuming medium-chain fats during their events

Does low-cholesterol drive you mad?

However, the general move in the athletic world toward lower-cholesterol diets isn’t without potential problems, because some research has linked low-cholesterol diets with increased rates of depression and suicide. Even more surprisingly, carefully documented research has determined that cholesterol levels are often below normal in habitually violent and impulsive homicidal criminals. Among adolescents, individuals who have an ‘aggressive conduct disorder with an attention deficit problem’ frequently have below-normal cholesterol concentrations

Why would cholesterol-poor diets and/or low blood cholesterol levels put people into a funk? The American Meat Council claims that the taste of animal flesh is a basic human need which – if denied – leads to aggressive behavior and poor mental health, but their explanation, while short and sweet, is flavored with a sour hint of conflict of interest. A decent biochemical explanation for the connection between low cholesterol and depression is that cholesterol, in spite of its reputation as the ‘bad boy’ of human nutrition, actually plays some key roles inside the body. One of its important functions is to maintain the integrity of brain-cell membranes

Preserving the integrity of brain cells is a good idea, since keeping the membranes intact keeps the cells working – and the individual possessing those cells alive. Often forgotten, however, is the fact that brain-cell membranes do more than keep the internal contents of brain cells from leaking out; they also contain ‘receptors’ for key chemical messengers in the brain. The receptors are simply attachment points for these messengers, which permit cell-to-cell communication, and cholesterol helps to keep those attachment points functioning properly and the cells communicating normally with each other

One of the key messengers is a chemical called serotonin, which exerts a calming, anti-depressant effect in the human brain. Serotonin levels are low in many individuals suffering from depression, and extremely violent military men and impulsive arsonists have been shown to have impaired serotonin output. Prozac, a widely-prescribed anti-depressant drug, acts to increase brain serotonin concentrations and improve mood and self-confidence. Overall, augmented levels of serotonin seem to be linked with better mental health, while low levels may be correlated with depression, violence, and the impulse to burn down your neighbour’s house

In theory, if your diet were too low in cholesterol, you would have poorly structured brain-cell membranes, reduced numbers of receptors, and therefore brain cells which have a lower capacity to react well with serotonin. In short, you’d get depressed. This link between cholesterol, serotonin, and overall brain function explains why many researchers believe that low-cholesterol diets – such as the ones followed by many athletes – can increase the risk of the blues

But the Finns say no

Sounds good so far, and several studies have linked low cholesterol with depression, but a recent study completed in Finland reached the opposite conclusion. Finnish people who began to consume lower-cholesterol diets actually had reduced rates of depression. In addition, a key problem with the low-cholesterol, high-depression hypothesis is that it means that individuals who are depressed should have lower rates of heart disease (their low cholesterol would downgrade the risk of heart maladies). In reality, depressed people often have higher frequencies of heart troubles

So what’s the real relationship between low-cholesterol diets and depression? Why were Finns with less cholesterol delighted instead of dispirited? The answer might be found by looking at the actions of a fat called DHA (docosahexaenoic acid), which is a polyunsaturated, ‘omega-3’ fat. You may recall that ‘omega-3’ fats shone brilliantly on the nutritional stage several years ago, when research suggested that they might help prevent heart attacks and strokes. Don’t be put off by the term ‘omega-3’. To understand what the term ‘omega-3’ actually means, remember that molecules of fat contain fatty acids, which are long strings of carbon atoms to which hydrogen atoms are attached. Usually, each carbon atom has two hydrogens attached, but sometimes a hydrogen is missing and the carbon is ‘double-bonded’ to an adjacent carbon. The term ‘omega-3’ simply means that the first double bond between carbon atoms is three carbons away from one end of a fatty acid

Certain sources of fat – such as fish oils – are fairly high in omega-3 fats, whereas more commonly used fats like vegetable oils have a preponderance of ‘omega-6’ fats, with the first double bond six carbons away from the end. For now, the only thing you need to remember is that the omega-3 and omega-6 fats are different chemically and play different roles in your body

As mentioned, DHA is an omega-3 fat. It’s critical for our story because – like cholesterol – DHA plays a significant role in the construction of brain-cell membranes. As researchers Joseph R. Hibbeln and Norman Salem of the National Institute of Alcohol Abuse and Alcoholism in Rockville, Maryland, point out, people who attempt to bring down their cholesterol levels often do so by reducing the total amount of fat in their diets. This lowers the amount of DHA they’re taking in – and therefore the amount of DHA which reaches their brains to build brain-cell membranes. In theory, these people are more likely to get depressed, since their brains are low in DHA. This chain of events would make it look as though low cholesterol were causing depression, even though the real culprit was inadequate DHA

Should you fry in fish oil?

In the Finnish study, in which diminished cholesterol intake led to lower – not higher – rates of depression, the study participants added a twist to the usual story: they didn’t lower their cholesterol and saturated-fat intake the usual way – by slipping corn and soybean oil into their pots instead of butter – but primarily by eating increased amounts of fish and less beef. Fish is lower in fat than beef and also turns out to be a rich source of DHA, which may explain why the Finns didn’t get depressed as their cholesterol levels dropped. In contrast, corn oil, which many people turn to as an alternative to saturated fat, is low in DHA. It could be that the corn-oil types are getting depressed in droves because of too-little DHA. Does this mean you should fry in fish oil rather than corn or soybean oil?

Maybe so, because Hibbeln and Salem firmly propose that it’s the reduction in DHA and other omega-3 fats – not the decrease in cholesterol intake – which is the source of the depression problem. They suggest that the direct link between coronary artery disease and depression is simple to explain: the high saturated-fat diets of many people lead to clogged arteries, and the lack of omega-3 unsaturated fat in the saturated-fat regimen raises the risk of depression. Shifting these saturated-fat eaters over to corn, soybean, or safflower oil will keep the arteries cleaner but won’t help the mental side of things, in Hibbeln and Salem’s view, because those vegetable oils are low in omega-3s. Hibbeln and Salem even venture into theories of criminality, proposing that violent, impulsive behavior is associated with low levels of omega-3 fats and high quantities of the more popular omega-6 fats and saturated lipids

While the latter claim may seem extreme, it’s backed up by some pretty decent research. For example, several years ago researchers at the Helsinki University Central Hospital checked out 34 habitually violent, impulsive male criminals. Eleven of these individuals had committed more than two violent crimes and four were impulsive arsonists. When blood samples from the 34 were compared with those from 16 healthy men from the University staff, it was found that the criminals had significantly higher levels of omega-6 fatty acids and appreciably lower quantities of one of the key omega-3 fats, DHA. In addition, men who had attempted suicide had roughly 20 per cent high omega-6 concentrations, compared to men who had never tried to take their own lives. Of course, we can’t say conclusively that low DHA drove the men to crime or suicide: correlations between variables don’t mean that one is the driving force behind the other

Is the future in the past?

However, another interesting observation is that the prevalence of depression in the industrialized world has increased fairly dramatically in the past 100 years or so. In fact, since 1900 each group of people born within a 10-year period has had a higher risk of depression, compared to those born during the previous decade. If you were born between 1950 and 1960, for example, your depression risk is significantly greater, compared to someone born between 1940 and 1950, and appreciably higher than the risk incurred by someone born before 1940. True, the stresses of modern life may contribute to this effect, but it’s also true that this century has seen a fairly dramatic increase in human consumption of omega-6 fatty acids, along with a fall in the intake of omega-3 lipids

There are a couple of reasons for this critical dietary swing. First, the nature of agriculture has shifted, so that just a few plant species (primarily corn and soybeans) are utilized as sources of fatty acids. These plants are relatively poor in omega-3 fats. In contrast, during evolutionary history, humans – especially in hunter-gatherer cultures – tended to eat wide varieties of vegetables and therefore took in products with higher amount of omega-3s. Second, commercial livestock are high in overall fat content but pretty deficient in omega-3 fats. For example, a side of beef coming from the cattle pen to your plate usually has a body-fat content of around 30 per cent, similar to a sedentary human, and virtually no omega-3 fat at all. When you eat the thing, you’re swamping your body with saturated and omega-6 fat and neglecting omega-3 fats totally

In contrast, the free-range and wild animals (including deer, bison, horses, mammoths, and various grazing herbivores) which made up a larger portion of the human diet over the past million years or so were much richer in omega-3s and lower in overall fat. For example, a free-living African herbivore has a body-fat level of just 4 per cent, like the best human endurance athlete, with a good deal of this fat as omega-3

The result of the change in agricultural practices and human eating habits is that the ratio of omega-6 fat to omega-3 fat in the human diet has changed drastically. In fact, the average ratio of omega-6/omega 3 in the modern diet is now estimated to be somewhere between 10/1 and 25/1, a huge change from the ratio which prevailed during two million years of human evolution, which was probably about one to one! The bottom line is that humans are now eating much less omega-3 fat than they did during their long evolutionary history – and perhaps paying the price from a health standpoint

It’s tempting to think that this change in fat intake may be related not only to the modern epidemic of depression but also to the current rampage of coronary artery disease. Critics of the notion that cardiovascular disease is a new thing contend that coronary artery maladies weren’t a big health problem for paleolithic humans because they simply didn’t live long enough to get into trouble, but it’s interesting to note that very young Britons and Americans (age 20 or less) often already show signs of atherosclerosis, whereas currently existing hunter-gatherer tribes in Africa and other parts of the world, with their increased intakes of omega-3 fats, do not. This is in spite of the fact that hunter-gatherers may eat fair amounts of cholesterol, 500-600mg per day by some estimates, about double the amount recommended by the U.S. Senate Select Committee on Nutrition. Individuals from such cultures who reach the age of 60 or more often exhibit little evidence of coronary disease, despite their ample cholesterol intakes

Why Japanese fishermen always smile

Should you consider stepping up your omega-3 intake to improve your mental state? One way to boost omega-3 in your diet would be to eat more fish, and it’s interesting to note that fish-eating people have considerably lower rates of depression, compared to beef- and pork-eating ones. For example, the incidence of depression in North America and Europe is about 10 times greater than the rate in Taiwan, where the people eat large amounts of fish. Studies carried out in the United States reveal that about 4.4 per cent of males and 8.7 per cent of females in New Haven, Connecticut suffer from depression. The rates of depression are 2.3 per cent for males and 4.9 per cent for females in Baltimore, and 2.5 per cent and 8.1 per cent in St. Louis. In contrast, rates of depression in Hong Kong, where people eat huge quantities of fish are about .71 per cent and 1.30 per cent for males and females, respectively. In Japan, where fish consumption is even higher, depression rates are .35 per cent for males and .46 per cent for females, and in some Japanese fishing villages rates of depression have been pegged at zero!

If low omega-3 consumption contributes to both depression and coronary artery disease, then depression and atherosclerosis should be positively correlated, the exact reverse of the hypothesis that depression, as a consequence of low cholesterol, protects against heart disease. In fact, 30 years of research have shown that depression is a good PREDICTOR of heart disease AND poor survival after a heart attack (depression as a REACTION to heart disease was separated from the analysis)

There has not been a lot of experimental work looking at the direct effects of omega-3 fats on depression, but the work that has been done has been favourable. In one study carried out with 494 elderly people, treatment with ‘bovine cortex’, or cow brains, which are a rich source of omega-3s, significantly improved mood and reduced symptoms of withdrawal and apathy, compared to treatment with corn oil (forget about the current scare over BSE)

A digression on breast-feeding

Since omega-3s are so critical for brain function, it’s not surprising that the quantity of omega-3s in infants’ diets can have a significant impact on brain development. In an important study which com-menced in Cambridge, Ipswich, Kings Lynn, Norwich, and Sheffield in 1982 and 1983, investigators kept track of 210 babies who received mother’s milk and 90 babies who were fed only formula. Mother’s milk is an excellent source of omega-3 fat, while formula contains none

At the age of 18 months, developmental scores were obtained for all 300 toddlers, and at the ages of seven to eight, IQ was assessed in the children using the Weschler Intelligence Scale for Children. Developmental scores were higher at 18 months, and IQ was greater at seven to eight years in the children fed breast milk. In fact, IQ scores were eight to 10 points higher in the breast milk-fed kids!

The research team, a group of distinguished British paediatricians, was able to remove most of the problems associated with this kind of research. For example, the breast-fed children received mother’s milk through a tube, eliminating the likelihood that the close bond between mother and child associated with suckling had provided the IQ bonus. And even when the higher social status and educational backgrounds of the mothers who chose to breast feed were adjusted for statistically, the intelligence advantage associated with breast-milk intake remained

Critics have contended that choosing to provide breast milk is an indicator of the tenaciousness of a mother, and that this tenaciousness carries over into the nurturing provided to the child, boosting IQ. However, mothers who chose to furnish breast milk but were then unable to produce milk had kids with IQs similar to those of kids whose mothers chose to dish out formula. There was simply something special in mother’s milk! Overall, getting breast milk raised IQ by about eight points, while higher educational status for the mother nudged IQ up by just two points. Being female rather than male lifted IQ by four points, so mother’s milk was easily the most important IQ-raising factor detected in the study. The researchers also unearthed a ‘dose-response’ relationship between mother’s milk and IQ. Those children who had received more maternal milk were sharper than kids who had imbibed less, particularly with regard to verbal measures of intelligence

What exactly was so good about mother’s milk? The researchers pointed the finger at our old friend DHA, which is not present in infant formula but which occurs in decent concentrations in human breast milk. As the investigators pointed out, DHA is accumulated in large quantities in the developing brain and retina and is crucial for overall mental development

What is the practical meaning of all of this? The addition of fish to your diet several times weekly may decrease your risk of cardiovascular disease and depression. Research suggests that a dietary intake of .5 to 1.0 grams of omega-3 fat per day reduces the risk of cardiovascular death in middle-age men by about 40 per cent, but current actual intake in the United States is only .05 grams daily. If you want to use supplements to obtain more omega-3 fats, experts contend that the supplement should contain high amounts of EPA and DHA but little or no cholesterol or vitamins A and D. Vitamin E should be added to prevent the omega-3s from being oxidized

How omega-3s can affect performance

What about fat type and performance? If you’re already involved in regular training, the effects of omega-3 fats may not be so direct and immediate that ingesting increased quantities of them for six weeks would improve your race times or lift your VO2max.. However, it’s obvious that the less depressed you are, the higher will be your motivation and drive to succeed as an athlete, so inclusion of omega-3 fats in your diet may be favourable to performance from a mental standpoint

It’s also possible that omega-3s might improve performance by upgrading blood flow to the muscles. In one study, blood flow to leg muscles of human subjects was restricted by the application of tourniquets. Some subjects then received a placebo, while others received an infusion of ‘prostaglandin E1′, a chemical which is produced by omega-3 fatty acids. Blood flow was 2.5 times greater in individuals who received E1. Increased blood flow would help endurance athletes by transporting increased oxygen and fuel to muscles and perhaps by improving the buffering of acids produced during intense exercise.

The extra oxygen might raise VO2max, and there’s also some evidence that omega-3 fats could reduce muscle inflammation following overly strenuous workouts

Only one peer-reviewed piece of research has actually looked at whether omega-3 fats can bolster exercise capacity. In that study, carried out at Western Washington University, 32 healthy young males were divided into four groups. One group acted as controls, a second group ingested four grams of omega-3 fat per day, a third group undertook a vigorous aerobic exercise programme, and a fourth group participated in the same exercise programme while taking the omega-3 supplements

After 10 weeks, the non-exercising group which consumed omega-3s was better off than the non-exercised control group without the omegas. Their average VO2max had risen by 11 per cent, against just 4.5 per cent for the controls. In other words, starting to supplement one’s diet with omega-3s is a bit like going on a moderate exercise programme; one’s ability to utilize oxygen seems to increase

However, both exercising groups, the one with omega-3s and the one without, broadened VO2max by about the same amount, 20 per cent, indicating no additional benefit of omega-3 fats when an exercise programme is undertaken. It would be interesting to see this same study carried out for a longer period of time or with a more experienced group of athletes. Perhaps under those conditions, omega-3s could induce some subtle, positive effects

What about medium-chain fats?

Broadening our focus from omega-3 fatty acids to fats in general, there has been some indication that ‘medium-chain’ fats are better for performance than the usual ‘long-chain’ lipids (medium-chain fats have only 10 to 14 carbons in their fatty-acid chains, while long-chain lipids have about 18 to 22).

The advantage of medium-chains may be due to several factors: medium-chain triglycerides (MCTs) are absorbed from the digestive system more quickly than regular lipids, and scientific studies have linked MCTs with an increased metabolism of body fat, preservation of muscle tissue, and significant increases in metabolic rate.

To make themselves look more attractive to finicky humans, MCTs don’t allow themselves to be stored very easily as body fat, and some research has indicated that MCTs are not likely to end up in the fatty deposits which tend to clog the inside walls of your coronary arteries

To make matters even more interesting, exercise scientists have long speculated that MCTs might promote improved endurance performances, primarily because MCTs can slip into the ‘mitochondria’ inside muscle cells much more readily than regular fats. Since muscles create most of the energy they need by breaking down fat and carbohydrate inside their mitochondria, MCTs’ ability to enter the mitochondria quickly should increase energy production and help to conserve muscles’ most precious fuel – glycogen

Until now, however, MCTs’ capacity to enhance exercise was speculative, but a recent study at the University of Cape Town demonstrates that MCTs can indeed improve performances – in certain situations. In the South African study, six experienced cyclists performed the same exercise test on three separate days.

The test consisted of two hours of easy pedalling at just 60% VO2max (about 73 per cent of maximal heart rate), closely followed by a 40-kilometre time trial completed as quickly as possible. During the three tests, the athletes consumed either a 10 per cent carbohydrate solution, a 4.3 per cent MCT beverage, or a drink which contained both 10 per cent carbos AND 4.3 percent MCTs. In all cases, the subjects consumed 400 ml (14 ounces) of drink at the beginning of the test and then 100 ml (3.4 ounces, or three to four normal swallows) every 10 minutes thereafter

The carbohydrate PLUS MCT drink produced the best performances during the 40-K time trial. With carbo plus MCT, cyclists needed just 65 minutes to complete the ride, versus 66:45 with carbohydrate alone and a sluggish 72:08 with only MCTs

Why did adding MCT to the carbohydrate sports drink enhance performance? Basically, MCTs decreased glycogen depletion in the cyclists’ leg muscles during the first two hours of the tests; the MCTs simply replaced glycogen as an energy source during those first two hours. As a result, when the cyclists pedalled along furiously during the 40-K trial, carbo-MCT athletes had more glycogen available to sustain their intense efforts

Why MCTs alone don’t work

It’s important to bear in mind that the MCTs had to be ADDED to carbohydrate in order to shore up performance; the MCT-only drink produced terrible results.

Owen Anderson

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Sports nutrition – A training strategy for protein consumption

A comprehensive and well researched article for those who want to optimise their nutrition to maximise performance which could give them the edge over their competition. Mike.

There is more to protein intake than simply eating the right amount

There’s more to protein nutrition than just eating the optimum amount; the timing of consumption and the type of protein selected can both impact on nitrogen balance; and there are a number of nutritional ‘co-factors’ that are either essential or useful in promoting optimum protein metabolism within the body.

This is especially true where carbohydrate is concerned, because building or even maintaining lean tissue mass is an ‘energy-intensive’ process. Increasing protein intake at the expense of carbohydrate can be a bad strategy for athletes engaged in heavy training, because without sufficient carbohydrate the body simply switches to other fuels for energy, and amino acids from protein (particularly the branched chain amino acids, leucine, isoleucine and valine) provide a ready source of energy!

Muscle tissue is a relatively rich source of branched chain amino acids (BCAAs), and tends to undergo breakdown during periods of highenergy demand, when carbohydrate and/or the amino acid pool becomes depleted. Furthermore, carbohydrates stimulate the release of insulin, a highly anabolic hormone, which helps to drive both glucose and amino acids into muscle cells. Any athlete seeking to optimise his or her protein metabolism should therefore ensure a carbohydrate intake commensurate with training volume.

Protein-carbohydrate mixes

The role of carbohydrate in enhancing endurance during long events and accelerating post- exercise recovery is undisputed, and new research (highlighted in PP 194, March 2004) indicates that carbohydrate feeding before and during high intensity exercise can limit the amount of stress hormone release, thereby reducing the risk of post-exercise immune suppression. However, research suggests that protein has a role to play, too. A study on resistance training examined hormonal responses to water, carbohydrate, protein or a carbohydrate/protein mix, given immediately and then two hours after a training session. As expected, those fed the carbohydrate and carbohydrate-plus-protein mix drinks showed an increased insulin response.

However, those fed the carbohydrate-protein mix also showed a modest but significant increase in growth hormone levels, suggesting that protein combined with carbohydrate following resistance training may create a more favourable hormonal environment for muscle growth.

Post-exercise protein feeding seems to be beneficial for endurance athletes also. In a study on 40 swimmers given either water or water-plusglucose during training sessions and then either water, sucrose or a sucrose-plus-milk protein mix after training, the subjects receiving the posttraining sucrose-protein mix exhibited lower levels of creatine phosphokinase (a marker of muscle damage) than the others. Moreover, creatine phosphokinase levels returned to baseline levels more rapidly in this group, indicating that the ingestion of protein with carbohydrate accelerates recovery.

A study on ultra-endurance athletes, published just a few months ago, showed that a carbohydrate-protein mix maintained a positive nitrogen balance during and after a six-hour training session (five hours of cycling and one hour of running), while a straight carbohydrate drink did not.

The consensus of scientific opinion now is that, following intense exercise, athletes should ingest a carbohydrate and protein mix (around 1 gram per kg of body mass of carbohydrate and 0.5g per kg of protein) within 30 min of completing exercise, as well as consuming a high-carbohydrate meal within two hours. This nutritional strategy has been found to accelerate glycogen resynthesis as well as promoting a more anabolic hormonal profile that may hasten recovery.

Research carried out over a decade ago indicated that ingesting a light carbohydrate/ protein snack 30-60 minutes before exercise is also beneficial. In these studies it was shown that 50g of carbohydrate and 5-10g of protein, taken before a training session, could increase carbohydrate availability towards the end of an intense exercise bout and also enhance the availability of amino acids to muscles, thereby decreasing exercise-induced catabolism (breakdown) of protein.

This research appears to be backed up by a very recent study carried out on 15 trained cyclists, who cycled to exhaustion on two rides 12-15 hours apart, the first at 75% and the second at 85% of VO2max. During the test, riders were split into two groups and given either a 7.3% carbohydrate drink (1.8ml per kg every 15 minutes), or the same drink with protein added at 1.8%. After 7-14 days, the test was repeated and the drink protocol reversed.

The results showed that riders taking the carbohydrate-plus-protein rode for 29% longer than the carbohydrate-only group during the first (75% VO2max) ride and 40% longer during the second (85% VO2max) ride! Furthermore, peak levels of creatine phosphokinase were 83% lower when carbohydrate plus protein was taken. Since the carbohydrate plus protein drink contained 25% more calories overall, further studies are needed to see how much of this effect is due to higher energy intake. However, it seems reasonable to assume that a carbohydrate-protein drink taken during training provides for increased protein concentration outside the cell, which can potentially enhance protein synthesis and repair.

The concept of different glycaemic indexes (the rate at which digested carbohydrate is released into the bloodstream as glucose) for different carbohydrates is now well accepted. However, different proteins display different rates of breakdown into their amino acid building block constituents, and hence uptake into the body.

A study into whey protein and casein (two types of protein supplements that are popular with athletes and bodybuilders) examined the speed at which one of the amino acids (leucine) appeared in the bloodstream after ingestion of a meal of each kind of protein (containing identical amounts of leucine). The researchers found that whey led to a dramatic but short-term increase in plasma amino acids, while casein induced a prolonged plateau of moderately increased levels.

They concluded that the differences were probably explained by the slower gastric emptying of casein. Whey protein is a soluble protein whereas casein clots into the stomach, so delaying its gastric emptying. Likewise, soy protein appears to be digested more rapidly than milk protein, resulting in a higher but more transient peak of plasma amino acids.

The implications are obvious: an athlete seeking to supply a post-training or mid-training boost to the amino acid blood pool would be best advised to consume a fast-release protein, such as whey or soy. However, when a prolonged period of recovery is in store (eg at bedtime) a slowerreleasing casein protein drink, such as milk, would be better. Another implication of this study is that, providing a meal or drink supplies the same quantity of the essential amino acids, one type of protein is not necessarily ‘better’ than another. Of more importance is that its release rate is matched to the timing of ingestion.

The situation also appears to be complicated by age. A recent study, which looked at the effects of protein retention in young men (mean age 25 years) fed protein meals containing either slow-releasing casein proteins or rapid-releasing whey proteins, found a greater retention (ie uptake into muscles) after casein. However, when the same researchers studied protein retention in elderly subjects (mean age 72 years), their findings were reversed, with whey protein producing a significantly higher uptake of amino acids than casein.

The researchers surmised that amino acid availability may limit muscle synthesis in older subjects, and that the higher amino acid peaks produced by whey prevented this from happening. The implication seems to be that ingesting fast-releasing proteins mid- or postexercise may be more important for older athletes than their more youthful counterparts.

‘Free form’ amino acids

The process of digestion releases the amino acid building blocks from ingested protein. However, as we’ve seen, this release rate is variable and the process of digestion itself actually consumes energy. This has prompted some investigators to ask whether the use of ‘free form’ amino acids before, during or after training could be a rapid method of providing athletes with optimum amounts of amino acids exactly when they’re needed.

Particular interest has been shown in the branched chain amino acids (BCAAs), which are readily oxidised for energy and therefore in greater demand when energy output is high. In theory, BCAA supplementation might help to minimise protein degradation, thereby leading to greater gains in fat-free mass, or at least minimise lean tissue loss when training volumes are high.

BCAAs and body composition

There is some evidence to support this hypothesis; for example, a study conducted on trekkers at altitude found that taking 10g of BCAAs per day during a 21-day trek increased fat-free mass by approximately 1.5%, while controls on placebo experienced no such change. Meanwhile, another study found that 30 days of BCAA supplementation (14g per day) promoted a significant increase in muscle mass (+1.3%) and grip strength (+8.1%) in untrained subjects.

These findings suggest that BCAA supplementation may have some impact on body composition. Moreover, some recent evidence suggests that BCAA supplementation can decrease exercise-induced protein degradation and/or muscle enzyme release (an indicator of muscle damage), possibly by promoting an anticatabolic hormonal profile(. However, despite the persuasive rationale, the effects of BCAA supplementation on short- and long-term exercise performance are somewhat mixed, with some studies suggesting an improvement and others showing no effect. More research is needed, therefore, before firm conclusions can be drawn.

Having said that, there is good evidence that BCAAs administered during training can reduce the perception of fatigue, while improving mood and cognitive performance. A study on seven male endurance-trained cyclists with depleted glycogen stores examined the effects of BCAA supplementation (versus placebo) on mental fatigue and perceived exertion. The subjects exercised at a work rate corresponding to approximately 70% VO2max for 60 minutes, followed by another 20 minutes of maximal exercise.

During the 60-minute section, the subjects’ ratings of perceived exertion were 7% lower and mental fatigue 15% lower when they were given BCAAs. In addition, cognitive performance in the ‘Stroops Colour Word Test’ performed after exercise was improved when BCAAs had been ingested during exercise. Interestingly, however, there was no difference in physical performance in the final 20-minute segment of the ride between the placebo and BCAA groups; the amount of work performed during this section was the same regardless of which supplement was taken.

These findings on BCAA supplementation, mental fatigue and perceived exertion were replicated in a study on runners given carbohydrate-plus-BCAA drinks or carbohydrateonly drinks (placebo) during a 30k cross-country run. Subjects on BCAAs improved their postexercise performance in the above-mentioned Stroops test by an average of 3-7% compared with those on placebo. The BCAA group also maintained their performance in two more complex mental tasks (shape rotation and figure identification) after exercise, while the placebo group showed a 25% and 15% reduction respectively in these tasks.

Researchers believe that this cognitive effect may be due to the ability of BCAAs to compete with and therefore reduce the uptake of another amino acid, tryptophan, across the blood-brain barrier and into the brain. Tryptophan is the precursor to a brain neurotransmitter called 5- hydroxytryptamine (5-HT – more commonly known as serotonin), which is involved in fatigue and sleep and is believed to contribute to the development of central/mental fatigue during and after sustained exercise. During exercise, the concentration of tryptophan in the blood relative to other neutral amino acids seems to rise. But supplementing with BCAAs seems to help block this effect, which would, in turn, reduce levels of 5- HT in the brain.

Is leucine a ‘special-case’ BCAA?

Leucine is the most studied of the BCAAs, partly because leucine and its metabolites have been reported to inhibit protein degradation (22). In the body, leucine accounts for about 4.6% of all amino acids and is involved in many important roles in the body, such as regulating protein metabolism by inhibiting degradation and stimulating synthesis .

Of particular interest is the fact that leucine can be oxidised to a compound known as acetylCoA in muscles at a higher rate than the other BCAAs (valine and isoleucine). This is important because acetylCoA is an ‘entry point’ into the citric acid cycle, one of the main energy-producing pathways in the body, and itself the gateway to aerobic metabolism, which explains why the demands for leucine rise substantially during periods of high energy expenditure. Studies have also shown that leucine oxidation is increased under catabolic conditions, such as depleted muscle glycogen.

Some researchers believe that the current leucine requirement, set at 14mg per kg of body weight per day, should be increased to 30mg in people who regularly participate in endurance activities. This argument is supported by research that suggests endurance athletes can actually burn more leucine than they take in through the RDA of protein.

One of the best-known leucine metabolites is a compound called ß-hydroxy ß-methylbutyrate, Is leucine a ‘special-case’ BCAA? more commonly known as HMB, which is popular with bodybuilders and athletes as a muscle/strength building supplement. But what is the evidence that it actually works? Recent research indicates that 1.5-3g per day of HMB supplementation can increase muscle mass and strength, particularly in untrained subjects beginning training and in the elderly. The muscle mass gains in these studies are typically 0.5-1kg greater than for controls during 3-6 weeks of training.

There is also recent evidence that, in athletes, HMB may reduce the catabolic effects of prolonged exercise. In one study, 13 runners were split into two groups, one taking 3g of HMB per day and the other a placebo. Both groups continued with their normal training for six weeks, after which they completed a 20k run. Before and after the run, creatine phosphokinase and lactate dehydrogenase levels (both measures of muscle damage) were measured, with the HMB group showing much smaller increases in both than the placebo group, indicating significantly reduced muscle damage.

However, the long-term effects of HMB supplementation in athletes are less clear. Most studies conducted on trained subjects have reported non-significant gains in muscle mass(34-36), but further research is needed to clarify whether HMB really does enhance training adaptations in athletes.

Essential amino acids

The BCAAs comprise just three of the nine essential amino acids (EAAs), the other six being histidine, lysine, methionine, phenylalanine, threonine and tryptophan. As mentioned, essential amino acids have to be obtained from the diet because they can’t be synthesised in the body from other amino acids. Although the six ‘straight chain’ EAAs are not so readily utilised as fuel, some researchers believe that giving all nine EAAs in a free form (ie as a mix of separate amino acids, not as protein), and in ratios that reflect the amino acid composition of muscle protein, is more beneficial for muscle protein synthesis than giving BCAAs alone.

In recent studies, scientists in Texas have found that ingesting 3-6g of EAAs before and/or after exercise stimulates protein synthesis. Moreover, this stimulation appeared to increase in a dose-dependent manner until plasma EAA concentrations are doubled, and was maximised when EAAs were administered to maintain this doubled concentration over a three-hour period. Adding carbohydrate seemed to enhance this protein synthesis, probably through the anabolic effect of insulin.

Although there has been very little research on EAA ingestion by athletes, studies on resistance training in healthy adults seem to confirm the potential benefits of EAAs; for example, muscle protein synthesis was increased 3.5-fold when 6g of a mixture of EAAs was given along with 35g of carbohydrate after resistance exercise.

In another study, three men and three women resistance trained on three separate occasions and then consumed, in random order, one of the following:

  • a 1 litre solution of mixed amino acids containing both essential and nonessential amino acids (40g);
  • a solution containing only essential amino acids (40g);
  • placebo.

Net muscle protein balance was negative after ingesting placebo but positive to a similar magnitude for both the mixed and essential amino acid drinks. The researchers concluded that: ‘it does not appear necessary to include nonessential amino acids in a formulation designed to elicit an anabolic response from muscle after exercise’.

A comprehensive protein strategy

Given the above findings, what reasonable steps can an athlete take to optimise his or her protein nutrition? Below is a ‘protein checklist’, which crystallises these findings into dietary recommendations:

  • Ensure an adequate intake of dietary protein – ie a minimum of 1.5g of high-quality protein per kg of body weight per day. Power/strength athletes, or those engaged in intense training, should consider increasing this to 2g per kg per day;
  • Ingest protein-carbohydrate drinks after exercise rather than protein alone. Ideally, consume a drink made up of about 1g per kg of carbohydrate and 0.5g per kg of protein within 30 minutes of training, and eat a high-carbohydrate meal within two hours;
  • Consume a light pre-exercise snack: 50g of carbohydrate and 5-10g of protein taken before a training session can increase carbohydrate availability towards the end of an intense exercise bout and also increase the availability of amino acids to muscles. However, make sure your snacks are low in fat to allow for rapid gastric emptying!
  • Use protein/carbohydrate drinks during very long events: a solution containing 73g carbohydrate and 18g protein per litre, consumed at a rate of 1ml per kg of body weight per minute, may delay the onset of fatigue and reduce muscle damage;
  • Consume quick-digesting proteins such as soy and whey immediately after training: this may be especially important for older athletes;
  • At other meals, consume a mix of proteins in order to promote a more sustained release of amino acids into the body;
  • Adding BCAAs to your normal protein intake may be useful for athletes undergoing prolonged or heavy training, and this may be particularly true for events/sports requiring large amounts of mental agility and motor coordination;
  • HMB supplementation, at 3g per day, may be a useful additional strategy for novice athletes, or those returning to training after a layoff;
  • Essential amino acid blends taken 1-3 hours after training may promote additional muscle protein synthesis, although this hypothesis is not proven in athletes;
  • Don’t forget to ensure that your overall diet is of high quality and as whole and unprocessed as possible: this will ensure adequate intakes of other nutrients essential for protein metabolism, such as zinc and the B vitamins.

Andrew Hamilton

References

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Sports Nutrition – Does sodium bicarbonate supplementation improve performance?

Joe Friel in his book “Going Long” talks about the use of potassium bicarbonate to reduce blood acidity as well. His motivation for this revolves around the fact that our blood increases in acidity with age, and the use of this supplement would reduce aging symptoms. From the evidence in this article using sodium bicarbonate to reduce blood acidity for improved sports performance, we have in fact a double benefit. Mike.

New research suggests taking sodium bicarbonate before you train boosts endurance levels

At a glance

It’s been used in baking for years and briefly found favour with athletes, but as Keith Baar and Andy Philp explain, new research suggests that taking sodium bicarbonate before you train really could lead to better endurance performance…

During intense training, our muscles produce a substance called lactate and hydrogen ions (acid) faster than we can use or get rid of them. The result is a build up of these by-products in the exercising muscle. People have long believed that this increase in acid and lactate is a direct cause of fatigue. However, scientists still argue over this point despite over a century of investigation.

Our bodies have a number of protective mechanisms that try to prevent the build up of acid. One of the most important of these is bicarbonate, which is alkaline – ie it helps neutralise acid. Bicarbonate is not only used as a raising agent in baking, but is also made throughout our bodies. One of the biggest bicarbonate producers is the stomach, where bicarbonate is made as a by-product in the process of making our digestive juices. After we eat, the rush to make stomach acid results in an increase in bicarbonate released into the bloodstream. This ‘alkaline tide’ is what makes us feel sleepy after a meal – not what will help us improve performance.

Bicarbonate in the body

During exercise, bicarbonate is initially made as a way to get rid of the carbon dioxide (CO2) produced by our muscles. The increased requirement for ATP to power our muscles results in an increase in CO2 production as a by-product of the breakdown of fats and carbohydrates. In the blood that feeds the muscle, CO2 and water (H2O) are converted to HCO3- (bicarbonate) and H+ (acid) by red blood cells using the enzyme carbonic anhydrase. At the lung, the reaction is reversed and the CO2 and water are released in the breath. This allows us to exhale the waste and maintain the correct acid/alkaline balance in our muscles.

For years, this was believed to be the reason that the lactate threshold and the ventilatory threshold coincided. The idea was that, at our lactate threshold, oxygen delivery to the muscles was insufficient and this resulted in a shift towards energy production without oxygen and the production of lactate and hydrogen ions. Since acid production was turned on, the increase in acid would mean the process above was accelerated, resulting in a sharp rise in ventilation.

While the theory of the relationship between the lactate and ventilatory thresholds makes sense, it doesn’t appear to be right. Newer studies show that oxygen delivery to the muscle is not limited during sub-maximal exercise, so that a lack of oxygen in our muscle cells isn’t what causes lactate production(1). What we really think causes both the lactate and ventilatory thresholds is a rise in the ‘fight or flight’ hormone called adrenaline, and a change in which muscle fibres we use. As the exercise intensity rises, we start to use more type II glycolytic muscle fibres. These fibres produce more lactate than type I or type II oxidative fibres, resulting in increased lactate accumulation in the blood.

At the same time, there is a sharp rise in adrenaline. This is because as the intensity of exercise increases it becomes a greater stress on our body and this activates the flight or flight response: releasing adrenaline. The rise in adrenaline causes our muscles to break down stored carbohydrate (glycogen) faster and decreases blood flow to the liver and kidneys (where lactate is normally removed from the blood), contributing to the accumulation of lactate. Adrenaline also directly increases our respiratory rate, contributing to the ventilatory threshold.

Drinking Sodium Bicarbonate

Bicarbonate and performance

No matter their cause, lactate and ventilatory threshold play a significant role in performance. The higher that we can get our speed/power at lactate threshold, the better our performance will be. Therefore, if we can focus our training on increasing speed/power at lactate threshold, we can maximise our performance adaptation.

One way might be to boost the amount of bicarbonate that we have in our blood on the day of the big event. The extra bicarbonate should buffer the acid our muscles produce and therefore increase the intensity we can maintain before lactate begins to build up in our blood.

People have tested the effects of bicarbonate on performance for over 75 years, on the premise that acid accumulation limits our endurance performance.
In 1931, scientists showed that drinking a solution that contained baking soda (sodium bicarbonate or bicarb) prior to exercise could improve running performance (2). These experiments were confirmed 2 years later, but a huge amount of conflicting research in the following 75 years has made people question whether bicarb can really be used as an ergogenic aid.

Beyond the scientific uncertainty, one of the biggest concerns with using bicarb on the day of performance is that drinking large amounts of baking soda can cause severe intestinal distress (read bloating, nausea and diarrhoea). Since these types of complications are the last thing anyone wants to have to deal with on the day of competition, a lot of athletes have quite understandably shunned the use of bicarb (but see box 1 for tips on decreasing intestinal problems when taking bicarb).

Bicarb training research

While the effects of bicarb on the day of the competition are uncertain and the potential negative effects on the gut might make an athlete unlikely to use bicarb for an important event, there might be good reasons to use bicarb during training. In the last three years, two studies have come out showing that taking bicarbonate during training improves performance.

In the first study, 16 moderately trained women exercised three times a week for eight weeks(3). One group drank a bicarb solution at 90 and 30 minutes prior to performing each high-intensity interval training session (containing 0.2g of bicarb per kilo of bodyweight) while group two drank a similar tasting salt solution.

In weeks one and two, each subject performed six to nine 2-minute intervals on a bike at 140% of their initial power at lactate threshold. The number of intervals and the relative intensity increased every second week until they were performing twelve 2-minute intervals at 160% of the power at lactate threshold in week seven. For week eight, the number of intervals was decreased to six to nine again, but the power was increased to 170%. Before and after training the subjects performed both a graded exercise test for peak VO2 and a time to fatigue test to measure endurance.

In the group that took the bicarb, the alkalinity, the concentration of bicarb, and the amount of lactate in the blood was higher during each training session. This tells us that the drink was absorbed and had the effect of making the blood less acidic. After the 8-week training programme, both groups improved their peak oxygen uptake (VO2) by approximately 18%. However, the group that took bicarb before each training session improved their power at lactate threshold 9.6% more than the group that took the saline solution.

As discussed above, power at lactate threshold is one of the most important parameters for determining endurance performance. Therefore, it was not surprising to see that the bicarb group showed a 41% greater improvement in time to fatigue (see figure 1). While this isn’t a direct measure of performance, the increased endurance and improved power at lactate threshold are strongly associated with better performance.

Increasing Endurance

After discovering that drinking bicarb during training improved performance in humans, some of the same scientists went on to try to determine how bicarb might be exerting its positive effects (4). To do this, they switched from people to rats, allowing a more controlled experiment and detailed analysis of muscle adaptation to training. They split the rats into three groups:

  • A control that didn’t exercise or take bicarb;
  • An exercise group that drank water;
  • An exercise group that drank a bicarb solution 30 minutes before exercise.

Like the human subjects in the first study, the rats increased their training from six to twelve 2-minute intervals, but with a running speed increase of 37 to 52 metres/min over the five weeks of the study.

At the end of training, the bicarb-drinking group had increased the number of mitochondria in one of their running muscles 7.5% more then the water group even though the animals did exactly the same amount of work. The authors of the study also found that the bicarb group increased the production of the transporter protein called MCT4, which helps remove lactate from the muscles (see figure 2). The fact that there was a greater rise in mitochondria tells us that adding baking soda to your training schedule would result in better performance even if you were to do no more work.

Protein and lactate

When we saw this data, we were excited by the fact that simply adding bicarb increased the number of mitochondria in muscle. The fact that they only measured this in a ‘slow’ muscle was interesting because we think that the greatest effect would be in fast twitch muscle where the ability to increase mitochondria is the strongest. Since the number of mitochondria in our fast muscles is one of the best determinants of speed/power at lactate threshold, we wondered whether the improved performance was due to a direct effect of bicarb on our mitochondria.

To study this question, Andy Philp performed a series of experiments on isolated muscle cells. The logic is that if bicarb is exerting its benefits on muscle cells and not the whole body, by just feeding the cells bicarb, we should see the same effects that the researchers above saw in people and rats.
So, Andy set up a (as yet unpublished) cells study in which one cell culture got a salt solution and the other got a solution containing about the same amount of bicarb as would have been circulating in the human study (3). After three days of treating the cells in this way, we saw an increase in the amount of mitochondrial protein in the cells of approximately 50% (see figure 3).

Protein and mitochondria

The reason for this increase in mitochondrial protein appears to be that bicarb is able to directly turn on a regulator of the number of mitochondria in our cells. The amount of this protein, PGC1alpha, is one of the most important factors in making new mitochondria. Simply adding bicarb to the cells resulted in a 5-fold increase in PGC1alpha. This increase in PGC1alpha is almost identical to what is seen after endurance exercise. These data tell us that simply taking bicarb may provide some of the same effects as exercise!

The other interesting findings from this study are that the cells that got the bicarb treatment consumed more energy at rest, they were better able to transport glucose, and they contained more of the glucose and lactate transporters. This tells us that after three days treatment with bicarb, the cells looked more like those in the muscles of an endurance athlete, because endurance athletes have a higher resting metabolism and are better able to take up lactate and sugar from the blood.

The last question that remained was whether the adaptation is a direct effect of the bicarb or whether it is an effect of increasing the alkalinity around the cells. To study this question, Andy employed another popular agent used to control acid/alkaline balance, called sodium citrate. When Andy did the same experiments using citrate, he saw a small increase in PGC1alpha, but not as much as during the bicarb experiments. So, this means that it’s the bicarb that acts directly on our muscle cells to increase mitochondria rather than any change in acid/alkaline balance.

Conclusions

Drinking baking soda solution before exercise means that there is high bicarb concentration in the blood during exercise. Doing high intensity intervals directs that blood to the ‘fast twitch’ muscle fibres (that do a lot of the work at high intensity). The bicarb is taken up in these fast fibres and acts to increase the mitochondrial controller (PGC1alpha). The increase in PGC1alpha signals these fast fibres to make more mitochondria. As discussed above, power at lactate threshold reflects the amount of mitochondria we have in our fast twitch muscle fibres. Therefore, by targeting these fibres with training and nutrition, we can improve their adaptation and, by extension, our performance.
So using sodium bicarbonate during training could be an inexpensive but powerful tool to add to your training regime. It would have a positive effect at any point in training, but the biggest effect on performance will be when you are trying to improve speed/power at lactate threshold using high intensity workouts.

Dietary sodium intake

Keith Baar runs the functional molecular biology laboratory at the University of California.

Andrew Philp is a postdoctoral fellow at the University of California and has performed all of the experiments on the effects of bicarb on muscle mitochondria. Both authors are scientific consultants with the English Institute of Sport and British Cycling

References

1. J. Appl. Physiol. 1998 85: 627-634
2. J Clin Invest. 1931 9: 601-13
3. J Appl Physiol. 2006 101: 918-25
4. Am J Physiol Endocrinol Metab. 2007  293: E916-22

This article was taken from the Peak Performance newsletter, the number one source of sports science, training and research. Click here to access these articles as soon as they are released to maximise your performance