Monday, 30 September 2013

Have some ATP

If, a little while back, someone had told me I should ingest more ATP to improve my performance I certainly would have reacted with disbelief. It sounds like eating chlorophyll in order to give my cells more oxygen (it is not how it works). After some smaller studies and some theorizing in media and science journals, a member over at Paleohacks asked the following question in 2012:

PEAK ATP...? Total Marketing Hype or the Next Big Performance Supplement?
Well, to answer the above question, it seems like it might just be the next big thing. Just recently a wonderfully interesting study was published in Nutrition and Metabolism where the effect of ATP supplementation was examined.

The company, TSI has marketed a supplement with ATP for a while. ATP, as most of you know, is an energy substrate, or the energy substrate which drives all energy demanding processes in our body. In addition to driving processes within the cell, ATP also has important extracellular functions. Most importantly via purinergic (P2Y and P2X) membrane receptors. ATP plays many important roles such as relaxing smooth gut muscles, affecting neurotransmission and also modifying muscle excitability by modifying ion gradient across muscle cell membranes. 

Once ATP enters the body it is readily used. If injected into the blood it is undetectable in a matter of seconds. Once in our blood, ATP is taken up by our red blood cells. This in turn enables them to more efficiently transport oxygen to the parts of the body in need of oxygen.

When oxygen demands of muscle cells increase, this is sensed by red blood cells, which in turn deforms and releases ATP. The result is dilated blood vessels that can supply more blood with more nutrients and oxygen to the working musculature.

So in this study 21 healthy, trained young men were either given daily doses of ATP (the supplement was TSI’s PEAK-ATP (ATP-disodium) TSI partially sponsored the study) or a placebo (maltodextrine). What makes this study particularly interesting is its rigid design which makes the results obtained less likely to be affected by errors. Both participants and researchers were blinded to what supplement was used, until all results were in.

The study was also divided into three phases: Phase one consisted of a three times per week non-linear periodized resistance training for 8 weeks. Phase two consisted of a two-week overreaching cycle. Phase three consisted of participants tapering for weeks 11 and 12.

Researchers measured a whole lot of factors ranging from muscle strength (back squat, bench press, and deadlift), vertical jump power, Wingate peak power (anaerobic test on ergometer cycle), creatine kinase, C-reactive protein, free and total testosterone, perceived recovery, protein breakdown (urinary 3-methylhistidine) and body composition determined by dual-energy x-ray absorptiometry.

What perhaps most are interested in is what happened to strength and muscle mass. Well, both groups increased strength but the ATP-group experienced a significantly greater increase. ATP caused a 12,9% and 16,4% strength increase in deadlift and back squat respectively. In the placebo group the corresponding results were 4,4% and 8,5%. Total strength increase with ATP was 12,6% and 5,9% in the control group.

During the overreaching cycle the placebo group experienced a 22,6kg average decrease in strength while the number in the ATP-group was only 12kg. The vertical jump power test showed that the ATP-group had a significantly higher power output compared to controls (15,7% vs. 11,6%). During the overreaching cycle ATP subjects reduced power output by 2,2% while controls reduced it by 5%.

In addition the ATP-group increased lean body mass by 4kg versus only 2,1kg in control group.

In sum this study shows that ATP supplementation can be considered an ergogenic aid with quite considerable effects on muscle strength, volume, power production and recovery. ATP also seemed to cause higher training volume tolerability and reduced muscle breakdown. These results should be of interest for both competition athletes as well as recreational athletes with a considerable time spent exercising.

It should be considered though that this is just the first study to show these effects and it needs to be replicated. No test has yet been done on females or older participants. But considering the above results, more studies of ATP supplementation should pop up soon.

Monday, 29 April 2013

Don't blame lactate

I've been thinking about lactate and low carb lately, and haunted by guilt for not writing anything here in some while, I thought I'd share my thoughts.

If you're even just remotely interested in exercise, chances are that you still know buildup of lactate should be avoided. Those with more exercise experience will have heard of the benefits of exercising at the lactate threshold, the exercise level where lactate production will exceed the rate of  removal, and lactate accumulates. Those with expert knowledge will perhaps pray for more lactate while exercising. It's a funny thing really.

Lactate is produced when glucose is broken down. Glucose is first broken down to pyruvate, and lactate is then made from pyruvate via the enzyme lactate dehydrogenase (LDH). Lactate can be burned as energy and can also be turned back into glucose in the process called gluconeogenesis. The thing with lactate production is that we produce more at higher intensities of exercise. It is with dread that i remember the 800 meter competitions I competed in when I was younger. The last 100 m of those races was an exercise in willing my legs to move even though they felt like they would burst from pressure of lactate build up. Lactate has a poor reputation, but as it seems, it is quite undeserved.

Because lactate is produced from glucose, an athlete primarily fueling his body on carbohydrates will produce more lactate than one primarily fueled on fat.

In fact, lactate levels are notoriously lower after low carb, high fat diets and this is in one of the hallmarks of fat adaptation. Even 4 days of high fat dieting followed by a carb loading day will make you produce less lactate during exercise (and also burn proportionately more fat) (1).

In "The art and science of low carbohydrate performance", Volek and Phinney has this to say on the matter:

"An increased reliance on fat and a corresponding decrease in glycolysis during exercise is associated with less accumulation of lactate (a surrogate for hydrogen ion accumulation). As cellular lactate and hydrogen ion levels increase at higher intensities of exercise, there are several events that cause force production and work capacity to decrease. A key contributor in this process is the acidity (i.e., decreasing pH) associated with hydrogen ion buildup. Along with maximal oxygen consumption, lactate threshold (the exercise intensity where blood lactate begins to accumulate) is a major determinant of endurance performance. With the enhanced ability to oxidize lipid associated with keto-adaptation, there is less lactate production at any one workload, and thus an elevation in the threshold exercise intensity associated with increased acidity."

As you see, reduced lactate production is used as an argument in favor of low carbohydrate dieting. But, this reasoning might be based on a shaky foundation. It rest on the assumption that more lactate is bad and that less is good. Also, acidity doesn't seem to be the problem (2).

When we exercise, potassium ions (K+) leak out of the muscle cells and into the extracellular compartment causing the muscles be depolarized and losing their excitability. Muscles are sort of like batteries. There has to be a difference in electrical charge between the inside and the outside of the cell to make them contract. Loss of contractile force has often been blamed on lactic acid build up and the reduced pH that follows. 

Quite recently, a group of Danish researchers showed that rat muscles produced less force if potassium ion level in the incubation medium was high, but if lactic acid was added to the incubation, the muscles regained their force producing ability (3). Lactic acid acts on chloride channels in the muscles and prevents the muscles from becoming more depolarized (2). There is also an added effect on excitability by adding both lactic acid and adrenaline (4).

So it seems that lactate is in fact what keeps muscles from fatiguing when extracellular potassium is high and removing lactic acid would only cause us to fatigue earlier. We can no longer blame lactate.

But if this is true, as it seems to be, what then of the claims that low carb is beneficial because less lactate is produced?

Studies of low carbohydrate diets and endurance exercise performance indicate that lower carb may reduce the ability for high intensity sprints during endurance races (5). I wonder if this may in fact partly be explained by the reduced lactate output (of course it could simply be because fatty acids takes too darn long to oxidize). I asked Kristian Overgaard, one of the Danish researchers, and he answered:

"I would say that if a dietary intervention influences the glycolytic flux and production of lactic acid, this may affect muscle function through a number of different mechanisms – one of them being a reduction in excitability-protective effect of acidification, which our group has demonstrated in skeletal muscle. Whether this particular mechanism is important in explaining the reduced performance is speculative. But it is a possibility."

Now, it was first believed that the effect of lactic acid on depolarization was due to the fact that it was an acid. For example, the Danish researchers exposed rat muscles, that were incubated in a high potassium ion solution, to CO2 and this caused an increased excitability. Because of this, my thinking was that increased levels of the ketone bodies beta-hydroxybutyrate and acetoacetate, might fulfill the same function as lactic acid, because they also are acids. But results from the Danish group suggested that the effect of lactic acid was on chloride channels and not a result of reduced pH. This does not however mean that ketone bodies may not exert some other positive influence, minimizing the proposed negative consequence of the reduced lactate output. 

Anyway, these were my thoughts. Now they are yours. Have a nice day.


References

(1) Burke LM, Hawley JA, Angus DJ, Cox GR, Clark SA, Cummings NK et al. Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability. Med Sci Sports Exerc 2002; 34(1):83-91.

(2) de Paoli FV, Ortenblad N, Pedersen TH, Jorgensen R, Nielsen OB. Lactate per se improves the excitability of depolarized rat skeletal muscle by reducing the Cl- conductance. J Physiol 2010; 588(Pt 23):4785-4794.

(3) Overgaard K, Hojfeldt GW, Nielsen OB. Effects of acidification and increased extracellular potassium on dynamic muscle contractions in isolated rat muscles. J Physiol 2010; 588(Pt 24):5065-5076.

(4) de Paoli FV, Overgaard K, Pedersen TH, Nielsen OB. Additive protective effects of the addition of lactic acid and adrenaline on excitability and force in isolated rat skeletal muscle depressed by elevated extracellular K+. J Physiol 2007; 581(Pt 2):829-839.

(5) Havemann L, West SJ, Goedecke JH, Macdonald IA, St Clair GA, Noakes TD et al. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. J Appl Physiol 2006; 100(1):194-202.



Wednesday, 26 December 2012

Diet, weight loss and body composition changes

This is an unfortunately long post, and I apologize for it, but the reason is that I find all this so darn interesting.  Hope you do to.

A little while back I looked closer at some of the science behind diet, weight loss and body re-composition. I have heard people say on several occasions that a low carbohydrate diet will prevent loss of muscle mass and that all weight lost is fat. So I wanted to find out once and for all what really happens with our body when we lose weight. I'll show you some of the data, and although these studies are not the only ones, I am confident that the studies presented here give a satisfactory accurateness

So there is much debate about what happens to our body composition when we lose weight and perhaps especially when we do it using a low carbohydrate diet. This quote is from Sachiko T. et al 2001. Dietary Protein and Weight Reduction: A Statement for Healthcare Professionals From the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association:
Some popular high-protein/low-carbohydrate diets limit carbohydrates to 10 to 20 g/d, which is one fifth of the minimum 100 g/d that is necessary to prevent loss of lean muscle tissue.
Clearly the AHA suggests that we will lose muscle tissue by going low carb. In my school we used the exercise physiology textbook from McArdle, Katch and Katch (2007) which said this:
…low carbohydrate diet sets the stage for a significant loss of lean tissue as the body recruits amino acids from muscle to maintain blood glucose via gluconeogenesis.
Once again, low carbohydrate dieting does not seem a good idea if we want to preserve muscle mass while we lose fat mass.

But the questions remains unanswered; how much muscle mass do we lose if we go low carb and can we do anything to prevent a potential loss of muscle tissue?

Let us look at some studies and see what they tell us.

Studies
This study from Bonnie Brehm and coworkers compared a low carbohydrate diet to a low fat diet:


All participants in the above study were women and they were obese. Dietary energy content was reduced in both diets and body composition was measured using Dual Energy X-ray Absorptiometry (DEXA). As you can see, weight loss was greater with low carb, but so was loss of lean body mass (LBM) and the percentage loss of LBM was not much different between diets. 

Here's another study:


This was a crossover study where all the participants tried two different diets in random order. The results are given under:


As is usually the case in weight loss trials, the men lost more weight than the women. And once again low carb caused a greater weight loss, but also quite the loss of lean body mass. The women eating low fat seemed to lose the greatest percentage LBM, which is also a recurrent theme in weight loss trials. 

Next, here's Kelly Meckling and coworkers:


One of the goals in this study was for the low fat group to reduce their calorie intake to the naturally reduced level of the low carbers. Weight loss did not differ between groups, but loss of LBM was significantly larger in the low carb group and over 25% of the LC weight loss was lean body mass. Body composition was measured using bioelectrical impedance analysis (BIA).

Next, as study from William Yancy and coworkers from 2004:

  
Weight loss with low carb was double that of low fat and this time loss of fat free mass (FFM) was actually quite larger in the low fat group. LBM is what is left if we remove fat mass and skeletal mass. Fat free mass is, not surprisingly, total mass minus fat mass. LBM and FFM are used interchangeably. 

It seems that loss of non-fat mass is common, regardless of diet, but we need to look at some more studies to get a clearer picture.

Here's one from down under, from Manny Noakes:


This is a short study, but with 83 participants. The results are pretty similar, both when it comes to weight and LBM loss, but in both diets around 30% of the lost weight was LBM and that is rather much.

Another one from Australia. Here's Jennifer Keogh and coworkers:


Both diets were 30% energy restricted and designed to be isocaloric. Once again there was a significant loss of fat free mass with both diet strategies.

Jeff Volek brought us this study in 2008:


An Atkins type diet was compared to a regular calorie restricted low fat diet in 40 men and women. Weight loss was greater with low carb, but so was loss of LBM. So far, there seems to be little truth to any claim that low carb preserves LBM.

This next one is another crossover study:


Alexandra Johnstone and coworkers showed us yet again that weight loss is greater with low carb, but that so is loss of FFM. Notice that this is a study of men only and so the percentage loss of FFM is much smaller than in studies of women.

One last study. Third one from Australia, this time by Grant D. Brinkworth:


118 people participated in this eight week study and were scanned with DEXA. Weight loss was greater with low carb and both groups lost about 20% FFM.

To summarize, loss of fat mass is greater with LC than LF diets. Loss of LBM is common on both LF and LC diets, but as we will see, not obligate. But there are some considerations to make first.

Considerations
First of all, any loss of water will usually be considered LBM and so if there is a difference in water loss between diets, this will affect loss of LBM/FFM. Carbohydrate restriction usually does cause a greater loss of body water, at least in the initial phase of the diet. Loss of glycogen with low carb will cause a parallel loss of water and so there is reason to expect a larger loss of LBM with low carb, and we need to remember that LBM is not a measure of muscle proteins.  

Contradictory findings
Although loss of LBM is clearly common on low carb diets, there are studies suggesting that such a loss can be avoided.

In a very small crossover study by Benoit et al from 1965 we can see the obvious advantage of low carb dieting compared to fasting:


Notice the difference in LBM loss. One likely advantage of carbohydrate restriction is that the combination of adequate protein intake and high ketone body production spares muscle proteins from being used to produce glucose. The Benoit study is small, but it suggests that loss of LBM is not a necessary consequence of low carb dieting.

And look at this one:


In this study of twelve men, LBM increased during the diet period, even though there was no change in the exercise pattern of the subjects. It is results like these, which sometimes appear, that suggests that it is possible to lose weight in a way that spares muscle tissue. In another very small study of very obese adolescents, similar results were found:



After eight weeks of a very low calorie ketogenic diet, lean body mass increased by almost 1,5kg while 15kg of fat was lost.

So I think it's time to ask what the difference between these few studies where LBM increases (in spite of water loss) and the RCT's where a low carbohydrate diet always leads to some LBM loss. But remember also that not all LBM is functional LBM. That is, we expect some loss of LBM and some LBM can be lost without negative consequences. We must remember to keep our feet on the ground, there is no problem with some loss of LBM with large losses of fat mass.

To make a long story short, there are some important factors we can manipulate in order to reduce loss of LBM. Being a man is perhaps the most effective. Men lose more fat and less LBM when they lose weight. It's just the way it is. But both men and women can increase their protein intake. In many of the RCT's in this post, average protein intake was low, often around 1g/kg body weight/day. The optimal intake is probably closer to 1.8g/kg/day (severely overweight people should use ideal body weight instead of actual body weight).

Several studies have found a correlation between protein intake and LBM loss. James Krieger wrote this in 2006:

  
And he concluded thusly:


In a very recent review article, Stuart Philips and Luc van Loon has this to say:


The thing with carbohydrate restriction is that is causes a greater fat loss and greater LBM loss than low fat strategies, but the end result is that low carb thus causes a greater reduction in body fat percentage and so the greater change in body composition. To optimize the results, protein intake should most likely be kept at >1,5g/kg/day. Here's another quote from Phillips and van Loon:


There is also the matter of sodium and potassium that might play a part in the results. Potassium is an important intracellular ion in our muscles and adequate potassium is important for creating an anabolic environment. The trouble with ketosis or severe carbohydrate restriction is that it causes our kidneys to excrete sodium and unless that sodium is properly replaced the kidneys compensate by excreting potassium. In short, when optimal body composition changes is the goal, or optimal performance, salt intake is important and should be a good deal higher than the daily recommended intake.

In addition to minding our protein and salt intake, we can of course also do resistance exercise in order to increase lean mass retention or even increase lean mass while reducing fat mass. It is, not surprisingly, well documented that resistance exercise, as a part of weight loss, is very effective at reducing lean mass loss, regardless of diet. But in order for resistance exercise to yield optimal results, protein and salt intake must be optimized.  

Richard Wood and coworkers just published results from a study where overweight older men were put on two different diets with or without resistance exercise. Here are the results:


Even though the results favor both low carbohydrate dieting and resistance exercise, I must say that I was surprised at the amount of FFM loss in the low carbohydrate and resistance exercise group, even when considering that some is water loss. After 12 weeks I would have suspected FFM to have increased. But there are once again some factors to consider. First of all, the mean age of the participants were 60 years. This may have caused the results to be smaller than if younger men participated. Also the resistance exercise was not very heavy, it could have been a good deal heavier and it is likely that muscle hypertrophy would then have been greater.

Donald K. Layman and coworkers compared the effects of two different diets varying in protein and carbohydrate content, with or without resistance exercise. The graphs on the left are women and the ones on the right are men:



Clearly, both increasing protein/decreasing carbohydrate and resistance exercise improve body composition changes. The low carbohydrate diet in this study was not very low. Average carb intake during the intervention was 141g in LC and 126g in LC+RE. Protein intake was 110g and 102g respectively.

I'd like to compare the results of a study I conducted in 2010 with that of a study from Donnely from 1991:


These are two very different strategies. In our study the participant were told to be in dietary ketosis, but could eat as much as they liked. In Donnely's study calories was severely restricted. Also in our study the participants exercised twice a week, whereas in Donnely's they exercised four times per week (resistance exercise). They are both effective strategies both for losing weight and changing body composition, so it is up to us what we prefer. I for one would like to eat as much as I please and not have to exercise that much to get the results I want.

The conclusion
Loss of LBM with weight loss is common but not obligate. A low carbohydrate diet is no grantee for all weigh loss being fat. In order to achieve optimal body re-composition one should reduce carbohydrates, make sure to eat enough protein and salt, and do regular heavy resistance exercise. The results one can achieve are quite astonishing.

Tuesday, 4 September 2012

Jump!



With ageing, skeletal muscle atrophy in humans appears to be inevitable. A gradual loss of muscle fibres begins at approximately 50 years of age and continues such that by 80 years of age, approximately 50% of the fibres are lost from the limb muscles that have been studied.
[1]

The loss of muscle mass with age (sarcopenia) is associated with a decline in muscle strength, muscle power, muscle quality, and physical function and increases in fat infiltration and mortality.[2]

Robert Oppenheimer did it.

I love jumping. Been doing it as long as I can remember. Jumped long jump, high jump and triple jump when I was young. Played basketball, and preferred jumping for rebounds. Did martial arts and preferred jump kicks. Now I've quit all organized exercise and generally just jump around. Oh, and landing is also great.

But jumping is more than childish fun for me. When I worked as an exercise instructor for older people, most all of them told me that the ability that was most quickly reduced with aging, and one of the things they missed the most, was the explosiveness – the spring in their feet. But they also told me that they just stopped moving in this way as they got older. Not because jumping became more difficult in any way, but because they just did. Truth be told, you rarely see older people jumping. They usually prefer less explosive ways of moving, and I really think that is sad.




An important part of our health as we age is the ability to be self-sufficient and good physical function is paramount to our quality of life. Both strength training and power training are effective at increasing physical performance in older adults [5], although power training may yield similar results with less total work performed per training session [6]. Power training has also been found to be superior to regular strength training in older adults [7]. Even moderate plyometric training improves chair-rise performance in older adults [8] and all in all it seems that we should keep jumping as we age. It really matters.

A decline in muscle mass and strength with aging can be found in every living creature endowed with muscle tissue. Worms, flies, fish, frogs, mice, rats, dogs, and primates are among the many species that have been studied that show atrophic and structural degeneration in aging muscles often with the accumulation of abnormal degenerative proteins. [3]  

As we age our muscles atrophy. We lose muscle cells and the reason seems to be that we lose motor neurons: the neurons that signal the muscles to move. Our body has no interest in having a lot of energy demanding muscle tissue hanging around if it's not being used. Less signal to move means less muscle tissue. This first graph from Faulkner et al [1] show the relationship between the total number of fibres in the vastus lateralis muscles and the age of men between 18 to 82 years of age. The second graph shows the relationship between the number of motor units in the extensor digitorum brevis muscles (muscle in the foot that extends a couple of toes) and the age of men between 5 and 88 years of age.





Why we lose these motor neurons is not well understood. Some people will say that aging in itself is the cause, but the reason for believing this seem simply to be that older people have less motor neurons, as does other animals as they age. Exercise will slow this process, but by how much we cannot say. We really do not know how much off the neuron loss is caused by aging and how much is caused by inactivity or lack of challenge to skeletal muscles. Still, exercise helps, and particularly explosive exercise.

For most elderly people, the decrease in muscle mass is accompanied by at least an equal, but usually even greater, decrease in strength and power, as well as an increase in muscle weakness (the strength per unit of cross-sectional area of muscle) and fatigability. The sum total of these effects is that age-related changes in the musculoskeletal system have a significant impact on the everyday activities of the elderly.[1] 

It is also usually said that aging causes a preferential degradation of fast muscle fibers and this is has always made sense, given how old people actually move less explosively. New research however, indicate that there might also be quite a large loss of slow muscle fibers [9].

An important difference between regular resistance exercise and plyometric (high velocity strength) exercise is that while resistance exercise promotes more muscle hypertrophy, plyometric will more so improve neuron-muscle cooperation, increase strength per unit of cross-sectional area and also a preferential stimulation of fast twitch type II fibers. Plyometrics will improve the ability to generate a lot of power in a short time.

Consider the high jumper. The force generated to fling a 2 meter high man over a 2.4 meter obstacle is massive, and yet the high jumpers are not known for their large leg muscles. An incredible amount of force can be generated even by normal sized muscles. This video shows Swedish high jumper and Olympic gold medalist, Stefan Holm jumping over some hurdles (He is 1.81m tall and his personal best indoor is 2.40m.) I wonder how he will move when he is 60.



An important benefit of resistance exercise is prevention of osteoporosis, and all sorts of high power exercises are particularly effective at building bone mass. But we should remember that the main problem with osteoporosis is falling. If we don't fall or injure ourselves, it does not matter much if our bones are a bit brittle. So we also need to focus on preventing falling and this is where speed may be important and where plyometrics could be more important than resistance exercise.

Now, I wasn’t joking about also liking landing. Landing is in itself a perfectly fine exercise. Remember that landing is great eccentric exercise. For obvious reasons we are stronger landing than we are jumping. This is good; as it will prevent us from jumping so high that the body cannot take the force of the landing. Further, it means that if you want to exercise using landing, you need to either go higher than you can jump, find some extra weights or land on one foot.



I use landing as an exercise form and often do several jumps per session down from hights that will really challenge my leg muscles.

Sarcopenia is a multifactorial consequence of aging that will affect many adults. Resistance training is the most effective and safe intervention to attenuate or recover some of the loss of muscle mass and strength that accompanies aging. [4]  

I think the take home message here is this: we don't have to become week; we don't have to lose the spring in our steps. We don’t have to stop jumping if we don’t want to. What we need to do in order to live long independent lives is simply to keep moving and keep jumping.




References

1. Faulkner JA, Larkin LM, Claflin DR, Brooks SV: Age-related changes in the structure and function of skeletal muscles. Clin Exp Pharmacol Physiol 2007, 34: 1091-1096.

2. Hanson ED, Srivatsan SR, Agrawal S, Menon KS, Delmonico MJ, Wang MQ et al.: Effects of strength training on physical function: influence of power, strength, and body composition. J Strength Cond Res 2009, 23: 2627-2637.

3. Ferrucci L, de Cabo R, Knuth ND, Studenski S: Of Greek heroes, wiggling worms, mighty mice, and old body builders. J Gerontol A Biol Sci Med Sci 2012, 67: 13-16.

4. Jones TE, Stephenson KW, King JG, Knight KR, Marshall TL, Scott WB: Sarcopenia--mechanisms and treatments. J Geriatr Phys Ther 2009, 32: 83-89.

5. Drey M, Zech A, Freiberger E, Bertsch T, Uter W, Sieber CC et al.: Effects of Strength Training versus Power Training on Physical Performance in Prefrail Community-Dwelling Older Adults. Gerontology 2011.

6. Henwood TR, Riek S, Taaffe DR: Strength versus muscle power-specific resistance training in community-dwelling older adults. J Gerontol A Biol Sci Med Sci 2008, 63: 83-91.

7. Miszko TA, Cress ME, Slade JM, Covey CJ, Agrawal SK, Doerr CE: Effect of strength and power training on physical function in community-dwelling older adults. J Gerontol A Biol Sci Med Sci 2003, 58: 171-175.

8. Saez SD, V, Requena B, Arampatzi F, Salonikidis K: Effect of plyometric training on chair-rise, jumping and sprinting performance in three age groups of women. J Sports Med Phys Fitness 2010, 50: 166-173.

9. Purves-Smith FM, Solbak NM, Rowan SL, Hepple RT: Severe atrophy of slow myofibers in aging muscle is concealed by myosin heavy chain co-expression. Exp Gerontol 2012.

Monday, 13 August 2012

How competitive sports might take the fun out of exercising



Exercise is done against one's wishes and maintained only because the alternative is worse.
George A. Sheehan


AP Photo/Anja Niedringhaus
The Olympics is over (Paralympics has yet to start) and the super humans has left the TV screen. It was all great fun (except of course for the things that weren't fun, such as doping, poor sportsmanship and the occasional dislocated elbow) and for many, very inspiring. I certainly feel more inspired and eager to exercise than in quite a long while.

But as I am reading through scientific articles, all about the relationship between exercise and various health parameters, I am suddenly struck by the meaninglessness of it all. Exercise is healthy in so many ways, but it really should not be something we partake in to improve our cholesterol levels. It is not something we should do to prevent osteoporosis or fatty liver and it is not something to do to hopefully feel or look good in 10 years' time. Exercise should be about having a good time here and now, and any extra beneficial effects should be considered bonuses.

Of course, many do consider exercise to be nothing more than fun and a break from every day hassle, but many do not and that is a shame. Exercise is one of those things we humans so easily overthink and make so much more than is really is. Movement is the most natural thing in the world. We are truly made to move and undoubtedly sicken if we don’t.

One of the reasons that so many of us struggle to just have fun moving and not being caught by the big monster that is stress, pressure and expectations, might be the influence from competitive sports. There is a big difference between exercising for the joy of exercise and exercising to become the best. Undoubtedly, competitive athletes also have fun exercising, but the presence of competition is what makes all the difference and we should not strive to become like competitive athletes. Once we set our goals high we start to specialize and we exclude so many ways of moving that would have been rewarding in so many ways.

I'm am not trying be some exercise hippie here, setting high goals and going for them is all good, but I feel that it should be easier for people to just play and have fun with exercise without all the fuss about high quality equipment or the neurotic focusing on numbers.

I know many of you are like me in that we feel we have too little time to exercise and so when we do get some time we try to make our exercise sessions count and try to make them as effective as possible, often heavy high intensity exercise that really wears you out. But think about it, what kind of inane way to exercise is that? 


I guess what I'm trying to say is something like this. If exercising in a physiologically less effective, but more enjoyable way makes you happier, then do it. Finding the joy in exercise is about not asking too many questions. Generally speaking we are so concerned with effects and numbers and comparing one form of exercise with another, that we reduce the chance of just having fun with being active. Being happy is what makes you look good, not high intensity. It is about setting your goals straight. Remember, you only live once and there is so much fun to be had.

So if you ask me, the best exercise is the exercise that makes you happy. How about we just have some fun, eh? 



Tuesday, 12 June 2012

The folly of the mean - Why do they differ so?

A few years ago I did a small study where we combined a ketogenic diet with resistance exercise [1]. After 10 weeks the 8 women in the diet group experienced a mean weight loss of 5,6kg. DEXA-scanning (Dual Energy X-ray Absorptiometry) showed that the mean fat mass loss was 5,6kg and that the fat free mass was unchanged. But, it would be wrong of me to say that this strategy conserves lean body mass, because the truth of the matter is that it all depends. Because 4 of the women in the diet group increased lean body mass, while 4 lost some despite the 10 weeks of resistance exercise. The individual results from the study are illustrated below.



As you can see, there are large individual variations. But individual variations are often not presented in scientific articles. Instead we are given results as means, and the means do not tell us what happens at the individual level. Of course, results also commonly include a measure of variation such as standard deviation (SD) or confidence interval (CI), but that still does not tell us what the true variation was and exactly how the different individuals responded. And this is the trouble with presenting study results as means; there are always individual variations and the funny thing is that it is usually these very variations we really want to understand.

Exercise studies are good examples of how misleading averages and means can be. Generally speaking we have to say that exercise at best is a very poor weight loss strategy. The reason is that exercise studies rarely yield weight loss of any significance. Even if we didn't have exercise studies we would still know that exercise does not make us lean, because we all know that our body weight does not change with changes in exercise volume. My body weight is practically constant, no matter how much or how little I exercise, and most people seem to be like me. Of course, if we do resistance or strength training we will build muscles, and often gain weight, but there is just no obvious link between energy expended during exercise and concomitant weight loss.

However, if we look closer at exercise studies it may seem that it is possible to lose weight from exercising, but that it doesn't happen to all of us. Take for example a study lead by Neil A. King at Queensland University of Technology [2]. Fifty-eight overweight and obese men and women completed 12 weeks of supervised exercise in a laboratory. The exercise sessions were designed to expend 2500 kcal/week and involved exercising at 70% of each individual’s maximum heart rate for 5 days a week. The aim of the study was to assess the effects of 12 weeks of mandatory exercise on appetite control.

After the 12 weeks of exercise the mean weight loss was 3,6kg. Now, we cannot conclude that this loss was caused by the exercise itself. Usually when people are recruited to studies such as these, they tend to change their behavior towards a more healthy lifestyle. Unless we can control for eating behavior, stress, alcohol intake or any other factor known to influence weight loss we cannot say that exercise is a causal factor. Anyway these are the individual results from the study:




About 22 of the participants, or roughly half, lost more weight than the mean. And 10 participants gained weight. So the really interesting question is; what is the cause of the difference in the individual responses? Although the mean weight loss was small and likely affected by non-exercise factors the above results do not exclude the possibility that some of these people lost weight simply by exercising and without significant changes in other lifestyle factors. In fact the very statement that I usually make, that exercise does not cause significant weight loss, is based on results given as means. But what if there's always responders and non-responders equaling each other out?

Still, we need to remember that if exercise by itself caused some of the people in the King study to lose weight, it is more likely because of factors such as reduced insulin resistance, reduced glycogen stores or improved fat metabolism, than because of increased energy expenditure.

Diet studies are also hard to interpret based on results presented as means. The Look AHEAD (Action for Health in Diabetes) [3,4] documented the effect of a traditional lifestyle intervention on overweight and type 2 diabetics. More than 5000 overweight men and women were randomized into an intensive lifestyle intervention group (ILI) or a control group that only received information and support. The study lasted 4 years (this is a gigantic study and one of very few randomized controlled trials of this size) and the goal of the ILI group was to achieve a 7% weight loss and to maintain the loss throughout the 4 years. The participants in the ILI group were asked to eat 1200-1800 kcal per day of which less than 30% was to come from fat. In addition the goal was to exercise 175 minutes per week, and they participated in regular group and individual counseling. All in all, the researchers did all they could to make sure the participants lost weight.

After 4 years of dieting the mean weight loss in the ILI group was 4,9kg or 4,7% of baseline body weight. The below graph illustrates that many achieved a great weight loss after 1 year, but as the study progressed, the participants gradually regained their lost weight, and if the study had lasted any longer the mean weight loss would probably have been even smaller.



But once again the mean results don't really tell us much. Wadden and coworkers reveals that only 74% of the participants lost weight and that the remaining 26% gained weight. Only 46% lost more than 5% of initial body weight (which was 95kg in women and 109 in men, so roughly 5kg), and only 35% lost more than 7% of initial weight. With so much effort in so heavy people these results are a strong indication that traditional dieting simply does not work. But once again we need to ask what the difference between the participants who lost a lot of weight and those who lost little was. This is the really important question, and a question that is asked to rarely. Those who continue to cling to the old dogma might say that those who lost the most weight probably were those who followed the given advice the most and that those who lost little did not do as told.

And they might be right. But we need to know. We can be pretty sure that many of the participants did not do as told and that many did more. That's just how people are and had this been a smaller and more tightly controlled study, anyone who did more or less than asked would have been excluded from the analysis. But there might also be large individual variations in response to the same intervention, and once again it is these variations – the reason we respond differently to the same stimuli – we truly want to understand.

One way we sometimes try to shed light on some of the individual variations is to do correlation analyses. For example, if in the above study, there was a strong correlation between protein intake and weight loss, then differences in protein intake was probably an important reason for the individual variations. But the ting is that we rarely find such strong correlations in weight loss studies and so we are left in the dark when it comes to understanding what biological mechanisms are hidden in the mean.

Even though studies fail to elucidate the reason for individual variations, I would still like the individual results to be presented more often, because this acts as a strong reminder that we cannot truly understand the world if we cannot understand why we differ so.



References

1. Jabekk PT, Moe IA, Meen HD, Tomten SE, Hostmark AT: Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat. Nutr Metab (Lond) 2010, 7: 17.

2. King NA, Caudwell PP, Hopkins M, Stubbs JR, Naslund E, Blundell JE: Dual-process action of exercise on appetite control: increase in orexigenic drive but improvement in meal-induced satiety. Am J Clin Nutr 2009, 90: 921-927.

3. Wing RR: Long-term effects of a lifestyle intervention on weight and cardiovascular risk factors in individuals with type 2 diabetes mellitus: four-year results of the Look AHEAD trial. Arch Intern Med 2010, 170: 1566-1575.

4. Wadden TA, Neiberg RH, Wing RR, Clark JM, Delahanty LM, Hill JO, Krakoff J, Otto A, Ryan DH, Vitolins MZ: Four-year weight losses in the Look AHEAD study: factors associated with long-term success. Obesity (Silver Spring) 2011, 19: 1987-1998.

Monday, 28 May 2012

Homo cerebrum portans, can you trust your body?


"How little do we know that which we are! How less what we may be!"
Lord Byron, Don Juan 



I've been thinking about the way we advise when it comes to health. I wanted to write some of it down and also write something about the carrying of brains, but I realize this all turned out a bit incoherent. Still, I'll put this out there as some loose thoughts as I do not feel that the title of this blog in any way promises coherency.

Hundreds of thousands of years of evolution has made us smarter than any other animal ever to exist. But might we have become too smart for our own good? As modern science has advanced and we've gradually become more urban, we have removed ourselves from what's natural and embraced the unnatural. Not because the unnatural has given us better health, but because leading theories say is gives us better health. We have embraced the theoretical knowledge of nutrition and health, yet we seem to have forgotten simple facts such as what type of foods humans actually eat. We no longer trust our bodies to tell us if what we do is right, instead we are willing to eat foods our body tells us make us sick, but that our head is telling us are healthy. And most often, we trust our head. Truth and reality has long since parted ways and the human body has been reduced to an instrument for carrying our brain from A to B. When the body resists, we force it to submission with medication. 


iStockphoto

When we start our search for health we soon realize the importance of listening to our body, and as soon as we feel we've learnt how to do this we are quick to pass the insight on to others. "You need to listen to your body!" It is easy to say, but I fear the advice is oft based as much on self-illusion as on self-insight. Telling an average modern human to listen to his body is much like telling an average modern human to listen for the mating calls of the common black bird – we have no idea what to listen for.

We might feel healthy, and arguably feeling healthy is in many ways the same as being healthy, but how healthy we feel is a matter of perspective. Compared to the other animals, the human animal is unarguably in a terrible state. Our ancestors are accused of hunting down huge and dangerous mammals, such as mammoths, with simple handheld weapons and so contributing to their extinction. The Inuit hunt whales in kayaks and hunters living in the central Kalahari still do persistence hunting.  A few thousand years ago we must have been a fierce and impressive animal, but if modern humans were to return to nature, pale, fat, unfit and allergic to trees, I fear the other animals would laugh their heads of if they could.

We might feel healthy, but how well we feel depends on how well we've been. If the norm is a condition characterized by illness and un-health, we will not know what it feels like to be really healthy. In fact, we might feel super healthy and still be far from how healthy we could be. Generally speaking, it seems that we no longer know what good health feels like. I am not even sure I do. I know it should be possible to feel strong and fit every day. I know we should all be able to climb a tree if we wanted to, or run a few miles if we feel like it. I know that it is possible to view physical challenges in everyday life as welcome challenges rather than as frustrating obstacles. But in order to achieve good health we do in fact need to listen to our body. 





Trusting in one's body must have been far easier for earlier humans. When there was little theoretical and written knowledge, our bodies was basically the thing we relied on. But a hunter gatherer will learn to listen to his body and to interpret its answers from birth. We however, have learned to trust theory and have little or no body-listening skills. So if you start listening to your body at 30, you cannot actually trust it. You just do not have the listening skills. That is why we still need to rely on skepticism and theoretical knowledge. For example, if you start working out at 30 and feel that the way you are working out is amazingly effective and so effective that you feel the need to share it with everybody, you should probably calm down and reflect a little. Most likely you would have gotten amazing results with other exercise forms and maybe even better results. It is important to remember that no matter how good we feel, we often do not know how good we could have felt. The same can be said about foods which by some are added to the diet and seemingly changes life and health for the better. Your body might feel better, but there is a good chance that it isn’t better and your seemingly improved health might very well be an illusion. (God I'm tired of wheat grass drinking health evangelists convinced that their green goo is the reason for their newfound vigour.)

No, it's not telling you to drink this!
 
A mother recently said to me "I am overweight and know I should eat fewer carbohydrates, but what about my son who is lean? Should he too reduce his intake of carbs to prevent becoming overweight or sick?"

It is a very good question, but the premise is sort of wrong. Overweight does not equal poor health. In fact, a person who easily gains weight might be protected against the ill effects of high blood sugar that cause harm in a lean person who does not convert glucose to fat so easily. Anyway, her son definitely cannot leave these decisions his body, although the body should be listened to. His body might tell him he should lay off grains, because it makes his stomach upset and painful, it's an easy enough signal to understand. But when it comes to preventing illness, out body tells us very little. Often enough we feel great and then we die. So we need theory and science.

Our best bet for optimal nutrition is, as far as I can tell, a paleo(-ish) diet with fewer carbohydrates than what is recommended by the government, but exactly how many carbohydrates, I don't know.

In the paleosphere the Kitavans are often used to show that humans can live on a diet based on carbohydrates without ill health. From this observation many conclude that we too can live on just as much carbohydrate with just as little ill health as the Kitavans. But this conclusion excludes all other lifestyle factors that differ between us and the Kitavans. Some of these factors really matters a lot. Perhaps the most important of these is stress.

Stress makes us insulin resistant and ill in so many ways. For example, a single night of poor sleep is enough to make us a good deal more insulin resistant. This makes us poorer at burning fat and may lead to blood sugar fluctuations and sugar cravings and this is unhealthy for all of us, regardless of weight. The question we should ask is not if humans can live on a diet with 50-60% carbohydrates and be healthy, but if we, here and now, with our current lifestyle and currents stress levels, can live on such a diet. Even if those 50-60% are from healthy paleo foods, I am not so sure.

In the end, knowing our body is an important step towards good health, and getting to know our body is a constant process of trial and error. It takes time to get good at it. But listening to physiologic feedback is not enough to prevent illness. We need theory as well and together they will take us most of the way.