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.

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.


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.

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? 

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.


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.

A little something to learn from McArdle’s disease

Muscle glycogen phosphorylase deficiency (glycogenosis type V or McArdle’s disease) is a disorder characterized by marked exercise intolerance—that is, premature fatigue and cramps during exertion, with frequent episodes of rhabdomyolysis.

Unfortunately, sedentary behavior may worsen exercise intolerance by further reducing the limited oxidative capacity caused by blocked glycogenolysis.” [7]

Glycogen matters. Having chronic full glycogen stores, while continuing to consume ample amounts of carbohydrates, is a bad idea, especially if your fat tissue does not easily expand.

Glycogen is a treat the body gives us when we need extra and fast energy. Even on a low carb diet we never fully deplete our glycogen stores (skeletal muscle and liver) and high intensity exercise on a low carb diet still makes you dig into your glycogen stores. But what if you were all out of glycogen and tried to exercise? There are in fact people who are unable to use glycogen during exercise. Some of these people lack myophosphorylase, an enzyme that breaks glycogen down to glucose-1-phosphate. These people have what is known as glycogen storage disease type V, commonly called McArdle’s disease. The disease was recognized by Dr. Brian McArdle who first noticed it when he came across a patient who experienced pain and weakness after exercise. McArdle did an exercise test on the patient and noticed that he failed to increase lactate levels. This prompted him to believe that the patient had a glycogen breakdown problem.

If you are one of the 1:100 000 who has McArdle’s, proper warm up is very important. Gradual warm up causes a gradual increase in fat metabolism which reduces the need for glycogen. This is also a tip to everyone on ketogenic diets who like to engage in vigorous exercise. Proper and gradually increasing warm up exercises makes sure as much fat as possible is ready for use. Patients with McArdle’s are known to experience a “second wind” which happens when alternative sources of energy are increasing in availability.

Keeping muscle glycogen stores from being full is perhaps one of the most important strategies when it comes to treating insulin resistance. Once glycogen stores are full, the muscles become insulin resistant, to keep from getting “sugar poisoned.” When glycogen stores are low, muscles increase the uptake of glucose from the blood by increasing the glucose transporter GLUT4 in the cellular membrane. This protects us from high blood sugar. In patients with McArdle’s, due to their inability to convert glycogen to glucose-1-phosphate, the muscles increase GLUT4 in order to get enough fuel [1]. But in McArdle’s the glycogen stores are full, and so they have impaired glucose tolerance and are in fact insulin resistant, despite increased GLUT4[2] .

One of the problems with not being able to break down glycogen is that the body must burn alternative fuels. These fuels are proteins or fats. For those of you reasonably versed in physiology you probably see how this can be problematic. On a high carbohydrate diet and little or no ability to break down glycogen, protein breakdown will be high. As the body breaks down proteins to glucose, the McArdle’s patients experience muscle wasting and renal failure due to myoglobinuria (muscle form of hemoglobin in the urine).

There is more to learn from these strange myopathies. For one, it is postulated that the exercise induced growth hormone (GH) response is stimulated by lactate. Lactate is produced when the muscles break down glycogen. Thus, exercising patients with McArdle’s disease should provide a clue. This was the reasoning of a research group from the UK [3]. They exercised 11 patients with McArdle’s and found that lactate remained at a resting level throughout the exercise and 9 of the 11 patients failed to show a significant exercise induced increase in growth hormone. Thus, it seems likely that lactate really is an important growth hormone stimulus.

If you are interested in a large GH response, high intensity does it. Although circulating levels of GH rise in response to low intensity exercise, a sevenfold and sustained rise (60–90 min post-exercise) in GH is observed with exercise above the lactate threshold.

You would think that if you can’t rely on glycogen for fuel, it would be wise to optimize fat burning, for example going on a ketogenic diet. And a few observations suggest that you would think right. A ketogenic diet seems to help [4,5], as does a high fat diet [6]. Also, if you have trouble using glycogen, insulin should be reduced to a minimum, as insulin inhibits glycogen breakdown. German researchers report of a

 “…55 year-old man with McArdle disease. By increasing the fat content of his diet to 80% with 14% protein (1 g/kg/d) to totally 1.760 kcal, ketosis of 2-6 mmol/l 3-OH-butyrate was established. The principal effects comprise absence of carbohydrate-based stimulation of insulin secretion leading to activation of glycogen synthesis, and repletion of the tricarboxylic cycle with acetyl-CoA from ketone bodies. With a continuous one-year diet his exercise tolerance was 3- to 10-fold increased dependent of the endurance level.”[4]

McArdle’s patients easily become sedentary. This just serves to exacerbate muscle breakdown and worsen muscular quality. But you don’t need glycogen to exercise or build muscles. Simple running has proven very effective in one case report [7]. Running also involves eccentric exercise which has a low energy cost for a given level of muscle force.

From Perez et al 2007
Although a ketogenic diet seems the natural choice for patients with McArdle’s, there are no real good studies of the strategy. A few small studies have examined high protein feeding with some very modest results [8], but high protein seems a bit of, as fat and ketones can replace glycogen more easily than proteins. Other strategies such as supplementing with creatine or vitamin B6 or ingesting glucose prior to exercise has been tested, but with varying results.


1. Robertshaw HA, Raha S, Kaczor JJ, Tarnopolsky MA: Increased PFK activity and GLUT4 protein content in McArdle’s disease. Muscle Nerve 2008, 37: 431-437.

2. Nielsen JN, Vissing J, Wojtaszewski JF, Haller RG, Begum N, Richter EA: Decreased insulin action in skeletal muscle from patients with McArdle’s disease. Am J Physiol Endocrinol Metab 2002, 282: E1267-E1275.

3. Godfrey RJ, Whyte GP, Buckley J, Quinlivan R: The role of lactate in the exercise-induced human growth hormone response: evidence from McArdle disease. Br J Sports Med 2009, 43: 521-525.

4. Vorgerd M, Zange J: Treatment of glycogenosys type V (McArdle disease) with creatine and ketogenic diet with clinical scores and with 31P-MRS on working leg muscle. Acta Myol 2007, 26: 61-63.

5. Busch V, Gempel K, Hack A, Muller K, Vorgerd M, Lochmuller H, Baumeister FA: Treatment of glycogenosis type V with ketogenic diet. Ann Neurol 2005, 58: 341.

6. Viskoper RJ, Wolf E, Chaco J, Katz R, Chowers I: McArdle’s syndrome: the reaction to a fat-rich diet. Am J Med Sci 1975, 269: 217-221.

7. Perez M, Moran M, Cardona C, Mate-Munoz JL, Rubio JC, Andreu AL, Martin MA, Arenas J, Lucia A: Can patients with McArdle’s disease run? Br J Sports Med 2007, 41: 53-54.

8. Quinlivan R, Beynon RJ: Pharmacological and nutritional treatment for McArdle’s disease (Glycogen Storage Disease type V). Cochrane Database Syst Rev 2004, CD003458. 

Do you exercise like a predator or prey?

I have little time for writing these days. I mostly hover quietly in the background of the blogosphere and the twittering realm, plotting for the lifestyle revolution to come.

But a thought hit me in the shower one day.

Exercise is stress. It is a voluntarily induced stressing of our physiology which triggers certain responses. It is usually the response were after, though the exercise in itself can be very rewarding. What we want is for our body to grow stronger and fitter, which it does in response to exercise. It is the rest following exercise that makes us stronger, not the exercise in itself. That is all well and good, but I’ve been wondering how much our mental state while exercising affects the exercise and thus the response. I have often said that if exercise is nothing but a stressful element in your life, something you dread and that gives you no pleasure at all, then don’t exercise. Life’s too short and mental stress is so harmful I am unsure if there’s a point in exercising if you hate it.

This got me thinking of people I know who do not exercise, but still lead relatively active lives. These are people who walk and half run through the day, rarely having time even to eat sitting down. Although they are fairly non sedentary and probably have an energy expenditure easily exceeding that of many healthy hunter gatherers, they are not very fit. Then I realized that much of the “exercise” they do, happens while being in a state of mental stress – hastening from meeting to meeting or from any other A to B. Some of these people almost never have time to walk calmly, do some thinking or enjoy the scenery. In these peoples’ lives there is also a relationship between the intensity of an activity and the amount of mental stress – the highest intensities are reached when things are crazy stressful.

These people remind me of prey animals. This form of physical activity is like that of a nervous prey animal running for its life several times a day. And this is why I am wondering if there is anything to gain, even in pure physiological factors. Does exercise while being stressed negate the normal positive effects of exercise?

Although I don’t know the answer to the above question, the way I would like people to exercise is like a predator. Do some workouts on an empty stomach like you would if you needed to hunt for food. Exercise with high intensities and reward yourself with a big slice of meat and total relaxation after. And don’t exercise like this every day. Like a predator we may move around a lot when we don’t hunt, but we don’t hunt every day.



…then rest.

The fittest person in the morgue

I have to admit that the title is stolen from an article by Mary Sheppard. The article is about the strange phenomenon of athletes keeling over and dying during strenuous exercise. The irony is that a marathoner will probably be the most worn out specimen at the morgue despite having a high VO2max before death.

The Hormesis

If we accept the validity of the general concept of physiological hormesis as being the phenomenon of achieving health beneficial effects by exposure to mild stress, then hormesis is being applied already and successfully to humans. The evidence for this is the well-demonstrated health benefits of regular and moderate exercise.”[1]

Running is good for us. It has to be, we’ve been told so for years and years. There’s just no doubt about it. There usually isn’t much need for running in a modern society, except for perhaps trying to catch a bus or escaping the occasional bully or mugger. But despite the lack of need to run, many of us still prefer to run, and some run a lot. We even learn to enjoy the burning lungs, the taste of blood and a heart rate that would otherwise have us seriously worried. We are mimicking the thrill of the hunt. Humans are truly made to run. But, contrary to our hunting forefathers there is no reward following the hunt. No big mammoth to cut up and bring home. No great mammal that feeds your family for a week and that makes running unnecessary until the meat is gone.

Modern humans do things differently. Instead of following the natural evolutionary approach and wait with exerting ourselves until more food is needed, we run again the very next day, and the day after that, and the day after that. The total amount of physical activity is staggering. There is nothing natural about it. Recreational joggers and marathon runners burn through an extreme amount of energy, usually supported by a high carbohydrate diet. Many also claim they do it for their health. But is it really that healthy?

Exercise is the perfect example of the principle of hormesis. The term is usually used to describe favorable effects of small amounts of something that is unfavorable in larger amounts, like a toxin or a stressor. Exercise is a stressor. If you want to test it, you can start exercising and don’t stop. You will get weaker and weaker until you fall and your body will be in a far worse shape than when you started. Exercise is really and truly bad for us, but only acutely and only if we forget to rest after.

…the occurrence of SCD [Sudden Cardiac Death] associated to training and competitions for athletes is increased by 2.8 times compared to the average relative risk of non-competitive practitioners, hence giving rise to the following question: Does sports activity causes sudden death in young people?”[2]

It is important to remember that it is the physiological response to exercise, the repairing of damaged tissues, and increasing of tolerability that causes exercise to make us stronger. It is the rest, the restitution that increases our potential, our endurance and our strength. Exercise makes us weak, rest makes us stronger.

Energy and glucose restriction has been shown to increase the lifespan of several species. It also increases formation of reactive oxygen species (ROS) in the mitochondria. The organism however, seem to adapt and acquire an increased resistance to oxidative stress. Antioxidants, which decrease ROS levels, limit the life extending effects of glucose restriction and exercise [3]. It has also been suggested that high antioxidant intakes lessens the adaptive response to exercise. But not all data show this [4].

The bottom line is that if you want exercise to be healthy, you better learn to rest.

The Metabolism
Everybody is free to do what they want and to exercise as they please. But the marathon runner lies, consciously or not, if he says he runs for his physical health. Although top athletes are marvelous examples of how far we can push the boundaries of the human body, they are not in it for the health. Injuries, wear and tear, infections and long term side effects are all part of the deal. This deal also needs to be remembered by recreational runners.

If you run for hours a day, you do it for the joy of exercising. You do it for the brake it gives you from the everyday hassle. You do it for shear competitiveness. But you do not do it for your physical health. That is bollocks.

From a metabolic standpoint is makes little sense to participate in long duration exercise of an intensity that is way over in the carbohydrate burning zone. Our carbohydrate fuel stores are quickly depleted. From en evolutionary standpoint these stores are there for short and intense bouts of exercise. As a hunter or gatherer we would spend most of our time in a fat burning low intensity zone and only occasionally do shorter high intensity work. Imagine foraging or tracking prey or working around the camp – all low intensity physical activities. Or you can watch Robb Wolf and his “caveman” friends hunting big game with atlatls. There is little sprinting involved.

Many runners (or other endurance athletes) however, spend much of their time in a carbohydrate burning zone. I was taught in school that intensities around the anaerobic threshold, where much of the energy (ATP) is produced outside of the mitochondria, are ideal for improving endurance performance. But the long time spent exercising at these intensities, may cause serious problems.

One obvious aspect is that the high intensity exercise many do requires them to stuff themselves with carbohydrates. Stuffing yourself with carbs is probably more of a problem if you don’t exercise much, but it might still be problematic. High carbohydrate for an endurance performer is usually synonymous with high sugar high starch which will in itself have a negative impact on the body. What’s worse is that high starch usually means high grain low fat. The stage is set for gut problems, infections, allergies and asthmas, muscle cramping and soreness, slow wound healing and general poor health. Remember, the apparent absence of disease does not equal good health. Poor diet might be the reason why the 50 year old marathon runner often does not look anything like a healthy human specimen.

The Body
But there are other problems, directly related to the exercising itself. One obvious aspect is the amount of wear and tear. The higher intensity exercise you perform the longer restitution needed to fully repair the body. Injuries and frailty is part of the deal. Endurance athletes are more osteoporotic than the rest of us [5-8].

Too little rest and too much exercise results in increased cortisol and other stress parameters. Marathon running is a huge stress to the body. One group of researchers from Canada used data from magnetic resonance imaging (MRI) to find out how marathon running affects the heart over time. Headed by Dr. Eric Larose, the group found that the magnitude of abnormal heart segments was more widespread and significant in a group of less fit runners. Runners with lower VO2max showed more signs of heart injury than more fit runners.

Wu et al [9] found that a 24hour ultra marathon damaged about every part of the body measured, including the liver and gallbladder. They also found that HDL decreased, LDL increased, red and white blood cell count decreased as well as testosterone. Their conclusion: “Ultra-marathon running is associated with a wide range of significant changes in hematological parameters, several of which are injury related.

Lippi et al noticed that enzyme biomarkers indicating liver damage are increased after a half marathon run to such a degree that there is no point testing for liver damage close to a race [10].

Skenderi et al [11] examined thirty-nine runners competing in the Spartathlon race (a 246km continuous race from Athens to Sparta) who managed to complete the race within a 36h time limit. They found that “Muscle and liver damage indicators were elevated at the highest level ever reported as a result of prolonged exercise…

There is more data showing muscle damage from this kind of exercising. Warhol et al [12] found that the muscles of veteran runners had intercellular collagen deposition suggesting repeated injury. Tissue from non runner controls did not show this.

Since oxidative modifications of DNA can lead to mutations and exceptionally high volumes of exercise are also associated with a substantial oxidative stress, concerns have arisen about the health effects of competing in endurance and ultraendurance exercise events, particularly when participants are not optimally trained.”[13]

As if damaging your muscles and organs weren’t enough, both ultra endurance exercise and half marathon results in DNA damage [13,14]. There is however need for follow up studies of DNA damage and instability. So far the effects are only proven acutely. Rae et al fount that telomere length in the vastus lateralis muscle in experienced endurance runners was inversely related to years spent running and hours spent training [15]. Shortening of telomere length is a sure sign of aging. Collins et al [16] found that Athletes with exercise-associated fatigue (fatigued athlete myopathic syndrome) had significantly shorter telomere length in their vastus lateralis compared to matched controls. Results from Ludlow et al suggest that hormesis is in fact a factor and that when it comes to telomere length moderate physical activity is better than both low and high levels [17].

As heart-healthy as running is supposed to be the heart is still one of the body parts placed under the most pressure and cardiac damage is easily measured [18,19]. I was taught in school that endurance exercise increases left ventricular volume and thus produces a greater cardiac output. Strength exercise on the other hand was supposed to increase heart wall thickness because of the high blood pressure, and thus increase the risk of cardiac arrhythmias. I think this is what is called the “Morganroth hypothesis.” Trouble is that much data refute the hypothesis. The most recent comes from Australia, showing increased left ventricular wall thickness after endurance exercise, but not after strength exercise.

Cardiac troponin (part of contraction process in skeletal and cardiac muscle) increases greatly after a half marathon in young runners, and “…reach levels typically diagnostic for acute myocardial infarction…”[20]. The level is higher in less trained athletes [21]. Whether cardiac injury markers are indicative of real damage is uncertain. Jassal et al puts it this way “Elevations of cardiac injury markers in non-elite athletes are extremely common following the completion of endurance events and correlate with the increased endurance time. Whether the increase in the levels of these enzymes represents true myocardial injury or a result of the release of cTnT from the myocytes requires further investigation.”[21].

The clinical significance of chronic exposure to endurance exercise is unknown. The development of myocardial fibrosis has been suggested as a long-term outcome to chronic exposure to repetitive bouts of endurance exercise and has been linked to an exercise-induced inflammatory process observed in an animal model. This hypothesis is supported by a limited number of studies reporting postmortem studies in athletes and an increased prevalence of complex arrhythmia in veteran athletes.”[22]

There are other parts of the cardiovascular system negatively affected by extreme exercise. A 96 fold increased serum level of calprotectin after both half and full marathon is indicative of damage to the vascular endothelium and microthrombi [23].

Marathon running has also been shown to induce kidney damage/renal abnormalities [24], and especially if you get dehydrated.

It has been suggested that marathon running also induce brain damage, as measured by increase levels of S100beta, a common marker of brain damage. A study from 2004 however, indicates that the increased S100beta levels come from extracranial sources [25]. But it’s still tissue damage. By the way, S100beta is also a marker of cancer.

The Conclusion
Exercise breaks us down. Rest is what makes us stronger. There is little indication that marathon running is worth participating in for health reasons. Running is in itself fine, but too much and too high intensity combined with an unnatural diet makes it very unhealthy. If I was to give an advice based on the best of my knowledge for optimal health I would recommend short high intensity exercise such as interval or strength training. Do this 2-4 times a week and keep any other exercise you partake in in a fat burning, moderate intensity zone. This is also an exercise advice that can be easily coupled with low carbohydrate dieting.


1. Rattan SI, Demirovic D: Hormesis can and does work in humans. Dose Response 2009, 8: 58-63.

2. Ferreira M, Santos-Silva PR, de Abreu LC, Valenti VE, Crispim V, Imaizumi C, Filho CF, Murad N, Meneghini A, Riera AR, de Carvalho TD, Vanderlei LC, Valenti EE, Cisternas JR, Moura Filho OF, Ferreira C: Sudden cardiac death athletes: a systematic review. Sports Med Arthrosc Rehabil Ther Technol 2010, 2: 19.

3. Ristow M, Zarse K: How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). Exp Gerontol 2010, 45: 410-418.

4. Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH: Normal Adaptations to Exercise Despite Protection Against Oxidative Stress. Am J Physiol Endocrinol Metab 2011.

5. Campion F, Nevill AM, Karlsson MK, Lounana J, Shabani M, Fardellone P, Medelli J: Bone status in professional cyclists. Int J Sports Med 2010, 31: 511-515.

6. Smathers AM, Bemben MG, Bemben DA: Bone density comparisons in male competitive road cyclists and untrained controls. Med Sci Sports Exerc 2009, 41: 290-296.

7. Burrows M, Nevill AM, Bird S, Simpson D: Physiological factors associated with low bone mineral density in female endurance runners. Br J Sports Med 2003, 37: 67-71.

8. Schmitt H, Friebe C, Schneider S, Sabo D: Bone mineral density and degenerative changes of the lumbar spine in former elite athletes. Int J Sports Med 2005, 26: 457-463.

9. Wu HJ, Chen KT, Shee BW, Chang HC, Huang YJ, Yang RS: Effects of 24 h ultra-marathon on biochemical and hematological parameters. World J Gastroenterol 2004, 10: 2711-2714.

10. Lippi G, Schena F, Montagnana M, Salvagno GL, Banfi G, Guidi GC: Significant variation of traditional markers of liver injury after a half-marathon run. Eur J Intern Med 2011, 22: e36-e38.

11. Skenderi KP, Kavouras SA, Anastasiou CA, Yiannakouris N, Matalas AL: Exertional Rhabdomyolysis during a 246-km continuous running race. Med Sci Sports Exerc 2006, 38: 1054-1057.

12. Warhol MJ, Siegel AJ, Evans WJ, Silverman LM: Skeletal muscle injury and repair in marathon runners after competition. Am J Pathol 1985, 118: 331-339.

13. Wagner KH, Reichhold S, Neubauer O: Impact of endurance and ultraendurance exercise on DNA damage. Ann N Y Acad Sci 2011, 1229: 115-123.

14. Niess AM, Baumann M, Roecker K, Horstmann T, Mayer F, Dickhuth HH: Effects of intensive endurance exercise on DNA damage in leucocytes. J Sports Med Phys Fitness 1998, 38: 111-115.

15. Rae DE, Vignaud A, Butler-Browne GS, Thornell LE, Sinclair-Smith C, Derman EW, Lambert MI, Collins M: Skeletal muscle telomere length in healthy, experienced, endurance runners. Eur J Appl Physiol 2010, 109: 323-330.

16. Collins M, Renault V, Grobler LA, St Clair GA, Lambert MI, Wayne DE, Butler-Browne GS, Noakes TD, Mouly V: Athletes with exercise-associated fatigue have abnormally short muscle DNA telomeres. Med Sci Sports Exerc 2003, 35: 1524-1528.

17. Ludlow AT, Zimmerman JB, Witkowski S, Hearn JW, Hatfield BD, Roth SM: Relationship between physical activity level, telomere length, and telomerase activity. Med Sci Sports Exerc 2008, 40: 1764-1771.

18. Whyte GP, George K, Sharma S, Lumley S, Gates P, Prasad K, McKenna WJ: Cardiac fatigue following prolonged endurance exercise of differing distances. Med Sci Sports Exerc 2000, 32: 1067-1072.

19. Dawson EA, Whyte GP, Black MA, Jones H, Hopkins N, Oxborough D, Gaze D, Shave RE, Wilson M, George KP, Green DJ: Changes in vascular and cardiac function after prolonged strenuous exercise in humans. J Appl Physiol 2008, 105: 1562-1568.

20. Nie J, George KP, Tong TK, Gaze D, Tian Y, Lin H, Shi Q: The influence of a half-marathon race upon cardiac troponin T release in adolescent runners. Curr Med Chem 2011, 18: 3452-3456.

21. Jassal DS, Moffat D, Krahn J, Ahmadie R, Fang T, Eschun G, Sharma S: Cardiac injury markers in non-elite marathon runners. Int J Sports Med 2009, 30: 75-79.

22. Whyte GP: Clinical significance of cardiac damage and changes in function after exercise. Med Sci Sports Exerc 2008, 40: 1416-1423.

23. Fagerhol MK, Nielsen HG, Vetlesen A, Sandvik K, Lyberg T: Increase in plasma calprotectin during long-distance running. Scand J Clin Lab Invest 2005, 65: 211-220.

24. Neviackas JA, Bauer JH: Renal function abnormalities induced by marathon running. South Med J 1981, 74: 1457-1460.

25. Hasselblatt M, Mooren FC, von Ahsen N, Keyvani K, Fromme A, Schwarze-Eicker K, Senner V, Paulus W: Serum S100beta increases in marathon runners reflect extracranial release rather than glial damage. Neurology 2004, 62: 1634-1636.