Why dieting is bad for you

By Simon Cork, Neurophysiologist, Imperial College London, @SimonCorkPhD

According to a 2016 survey of 2000 people in the UK, almost two thirds of us are on a diet at any one time. For most people, the typical diet consists of eating a salad for lunch, and cutting out desserts and snacks. NHS guidelines for weight loss recommend reducing calorie intake by around 600 calories each day. But is this advice right?

There is a theory among many scientists in the obesity field that body weight is fixed around a “set point”. That means that for the majority of people, body weight is typically static (unless drastic changes are made to exercise or diet). Any fluctuations in our body weight are compensated for by either increasing or decreasing energy input or output. You might feel this if you’re on a low calorie diet by feeling constantly tired and feeling like you just want to sit down. That’s your body’s way of trying to conserve energy.

One method our body uses to keep its weight constant is a hormone called leptin, released by fat cells into our bloodstream. The more fat we have, the more leptin we have flowing through our blood. Normally, leptin acts in the brain to restrict appetite, effectively acting as the brake to restrict major changes in body weight. Minor increases in fat lead to increases in leptin, which reduces appetite. Loss of body fat causes decreases in leptin and thus increases in appetite to compensate. Leptin is therefore the body’s messenger to the brain, informing it of our weight.

The problem occurs when we override the effects of leptin, typically with respect to its appetite-restricting effects. More fat means more leptin, which should reduce our appetite, and thus reduce our body weight back to what our brains perceive as “normal”. However, if we override these effects (e.g. by ordering dessert after starters and a main, or eating large portions, thus eating past the point of feeling full), our brains eventually become resistant to leptin.

simon cork dieting

Leptin levels are directly correlated with body weight. Bronsky et al, 2007.

This leptin resistance effectively means that our brains are tricked into underestimating what our body weight truly is. Although a 150 kg person has more circulating leptin than a 70 kg person, the extra leptin doesn’t decrease appetite as it should because the brain has become resistant to leptin: it needs more leptin to have the same effect. The brain is therefore “tricked” into thinking the body has less fat than it really does.

This has significant consequences when people who want to lose weight go on low calorie diets. As we restrict food intake, we lose body fat. For reasons not fully understood, the levels of leptin fall at a greater rate than body fat. Our brains react by activating mechanisms to restrict any further loss of body fat and promote energy storage. One such reaction is lowering the resting metabolic rate – effectively the minimum amount of energy required to keep us alive.

You may remember a US TV series called “The Biggest Loser”. This show took overweight or obese people and subjected them to a gruelling exercise and diet regime. The contestant who lost the most weight by the end of the show won a significant cash prize. In 2016, the results of a study were released which followed the contestants after they finished the show. They found that almost all contestants regained their weight and found that some regained more weight than before they started.

And this is the crux of the matter. It has been found that people who go on crash diets significantly reduce their resting metabolic rate – effectively, they are using less energy just by being alive than before the diet. And this metabolic rate may never recover – even after stopping the diet.

This may explain why a number of contestants regained more weight after the show than they started with. Their bodies are constantly fighting against a famine. It may also be why most people who go on a diet fail to maintain their low body weight long term. This is the key issue that many people developing weight loss therapeutics are facing.

simon cork dieting 2

Calorie restriction (CR – blue line) results in significant decreases in resting metabolic rate (RMR) Davoodi et al, 2014

For many people, losing weight is relatively easy. Simply restricting calories and/or increasing the amount of energy we use, usually by exercising, will result in weight loss. Maintaining that weight loss is the key issue. Exercise is often the key to maintaining weight loss, but is difficult to maintain the necessary levels of exercise required to compensate for the decreases in energy use that occurs following dieting.

Scientists are currently investigating how to manipulate the body weight set point, by both re-sensitising the body to leptin (i.e. countering the leptin resistance), and/or by increasing the levels of naturally occurring hunger-suppressing hormones that our bodies release after eating.

If decades of dieting advice has told us anything, it’s that dieting doesn’t work to bring about long-term weight loss. But importantly, by permanently reducing the resting metabolic rate, dieting may actually be preventing our bodies ability to lose weight in the future.

Microbiome – fad or future?

By Simon Cork, Neurophysiologist, Imperial College London, @SimonCorkPhD

You may have heard many scientists and media types getting excited over the term “microbiome” recently. There was a series on BBC Radio 4 termed “The Second Genome” recently dedicated to it, and a succession of articles on the BBC News website 1 2. But what exactly is it, what does it do, and should we all be excited?

The microbiome is the term scientists give the community of bacteria that live in your guts (micro meaning small, and biome meaning biological community). People have been studying the microbiome for many years, and there is a remarkable amount of literature around the microbiome of insects. But recently, the microbiome of humans, and specifically the effects our microbiomes have on our overall health, has entered the spotlight.

In insects and other animals, the bacteria that live in and around them have remarkable effects not only on their heath but on their development. For many insects and animals, interactions with bacteria are a requirement for their survival. One particularly powerful example of the influence of bacteria on a host’s behaviour is in the fruit fly.

Feeding fruit flies different diets (and thus altering their gut microbiome composition) causes them to preferentially mate with flies fed on the same diet. When given antibiotics, which wipe out their bacteria, this preference disappears.

In humans, we are only just beginning to understand (or perhaps recognise) the importance that the microbiome has on our health. We are also beginning to understand how changes in our microbiome predispose, or even cause, certain diseases.


Less bacteria, more weight?

Take obesity for example. Worldwide, over 2.1 billion people are overweight or obese. The causes of obesity vary from person to person, but one common factor found in obese individuals is the lack of diversity of their gut bacteria. In a lean individual, the gut bacteria will contain a variety of different strains and species of bacteria. However, in individuals with obesity, this diversity is significantly reduced (with an increase in the ratio of the Firmicutes and a decrease in the Bacteoridates species).

We also know that babies who are born via caesarean section are at a higher risk of developing a number of health conditions in later life, one of which is obesity. The reasons why are not completely understood, but we know that C-section babies do not get the full complement of bacteria that babies born naturally get.

Essentially, in the first few months of life, a baby born via C-section has a gut bacterial population that more closely resembles that found on the skin, as this is often the first bacteria that they come into contact with.

Quite astonishingly, it may be possible that gut bacterial populations that predispose to disease act as a form of non-genetic inheritance of disease. For example, an obese mother, who likely has a bacterial population with a low diversity, may pass this low diversity to her child during delivery, thus predisposing them to obesity in later life.

So what does this mean? Well, the honest answer is we don’t quite know. At the moment, these observations are simply that, observations. We can predict whether or not a person will be obese or lean with 90% accuracy simply by studying the diversity of their microbiome, but what we don’t fully understand is how the bacteria are contributing to weight gain.


What’s in it for them: bacteria causing obesity? And other diseases?

One theory is that certain bacteria have the ability to harvest energy from our diets more effectively than others. Couple this with a sedentary lifestyle and you have the recipe for weight gain.

Another theory is that the bacteria are interfering with our brain chemistry. We know that many species of bacteria can secrete molecules that are either the same or have very similar chemistry to many of the molecules found in our brain, and we know that bacteria are able to secrete these chemicals in response to certain foods.

Could it be then, that our bacteria are driving our food choices? Imagine a population of gut bacteria that have a penchant for sugar; they use this as their main source of energy and want to make sure that it keeps coming. Is it possible that in response to their host eating a sugary meal, the bacteria release chemicals that tells their brain to eat more? This may sound far-fetched, but there’s increasing evidence that this may actually be happening.

There’s also increasing evidence that our gut bacteria may be driving a number of other conditions, including asthma, depression and anxiety, possibly through chemicals they release which interfere with our normal brain chemistry.

To each their own: individual differences and possible ways to shift them

So what can we do about this? Well, the bad news is this area of research is still very much in its infancy.

There are a few things we do know.

Our gut bacterial populations vary considerably from person to person, which makes a one-size fits all approach to fixing a dysfunctional microbiome tricky (although the microbiomes of people living in the same house are more similar than they are to the rest of the population).

The difficulty now is figuring out how we can shift this composition in later life. Unfortunately, downing a yoghurty probiotic drink containing a single strain of bacteria doesn’t really have much of an effect on the overall composition of the community in our guts. Many of the bacteria found in these drinks are not normally found in the guts of anyone – in fact they’re chosen largely because they can survive both the hostile journey from mouth to gut, and through the factory.

Our diets play a large role in the composition of our microbiome. And our microbiome populations become fixed during our early life. Differences in how we were delivered, whether we are breast fed or bottle fed, which country we grow up in and whether we share our house with pets, all affect the composition of our microbiome.

Perhaps the easiest way of shifting our microbiome is related to how much fibre we eat. Our bodies can’t digest dietary fibre on its own, and most of the fibre we eat makes its way to the end of our digestive tracts. This is where it feeds the bacteria in our guts, who in response not only increase their diversity (fibre feeds a lot of different kinds of bacterial species, who can all grow in its presence), but also release chemicals which are beneficial to our bodies’ health.


Poop pills: what do we know about this surprising possible obesity treatment?

However, there is another way we can shift our microbial population – faecal transplants. If we take an obese mouse, and feed its droppings to a lean mouse (thus transplanting its bacteria), that lean mouse will become obese – regardless of what it eats. The same is true if you take the gut bacteria from an obese human and transplant it into the gut of a lean mouse. That in itself is amazing.

But is the same true for humans? Well, faecal transplant (or FT) has been used clinically to treat C. difficile (or C-diff as it’s commonly known) infection. This nasty hospital-acquired infection is difficult to treat with standard antibiotics and, left unchecked, can be fatal. However, FT is an effective treatment for C-diff and is a cure for many people.

On the other hand, the literature surrounding its effectiveness for treating obesity in humans is controversial, and also risky. A lack of proper clinical trials means we don’t fully know whether it works or to what extent. Furthermore, FT has the potential to transmit a number of diseases, and given the increasing number of conditions that are being attributed to gut bacteria, the risk might just be too great given our level of understanding.

The bottom line: the future looks promising

So what’s the take home message? The microbiome is an exciting area of research, and undoubtedly will lead to treatments for a number of diseases in the future.

As it stands, our understanding is largely based on observational data – a case of correlation, rather than causation. But many people are confident causation is there, we just need the definitive proof.

In the meantime, the best thing we can do to feed our hungry bugs is to increase the amount of fibre in our diets and reduce unnecessary antibiotic use. The good news is that a lot of people are getting excited, and the gut microbiome is no longer the playground of just the microbiologists. Gut scientists, lung scientists and neuroscientists are all getting in on the action, and these collaborations are rapidly increasingly our knowledge of how the bacteria in our bowels are affecting our health. The time for the microbiome to really show its potential grows ever closer.

1 https://www.bbc.co.uk/programmes/b09zgykv

2 http://www.bbc.co.uk/news/health-43674270


Early to bed and early to rise… makes a teen healthy, wealthy and wise? (Part 2)

By Gaby Illingworth, Rachel Sharman & Russell Foster; @OxTeensleep, @gabyillingwort1, @DrRachelSharman, @OxSCNi

To the possible dismay of parents hoping to start the family day bright and early, teenagers hit the hay and wake up at increasingly later times during adolescence – a delay of between one and three hours compared to pre-pubertal children.

Teenagers struggle to fall asleep early but still need to wake up for lessons during the school week, which contributes to a reduction in time spent asleep. At the weekend, the morning hours may well be spent snoozing to “catch-up” on lost Zzz’s.

In 2015, the National Sleep Foundation recommended that teenagers, aged 14 to 17 years, should be getting eight to ten hours of sleep a night. However, across the globe, teenagers are routinely not getting enough sleep, with older adolescents more likely to have insufficient weekday sleep than early adolescents. One of the consequences of insufficient sleep is that sleepiness during the day is common in this age group.

Sleep researchers have suggested some mechanisms behind this change in teenagers’ sleep timing.

How teenagers become owls: slower clocks, increased light sensitivity, or decreased sleep pressure

Although we don’t know why adolescent sleep changes, we do know that changes occur in the two processes which govern sleep – the circadian rhythm and sleep/wake homeostat. (Catch up on these two concepts in our previous post.)

The teenage biological clock has been proposed to run more slowly at this age, driving their sleep timing later, meaning their chronotype becomes more owl-like.


From DIVA007 on Flickr

Another suggestion is that their biological clock might be more sensitive to light in the evening (delaying sleep) and less sensitive in the morning (making them wake up later).

Adolescent sleep pressure is also thought to accumulate more slowly during the day, making them less tired when they reach the evening.

Jetlag without leaving the country

We know what jetlag feels like when we travel across time zones. Our internal time takes a while to adjust to the new external time.


Teenagers experience something similar with ‘social jetlag’: when their internal time (chronotype) is misaligned with social time (school commitments). At the weekend, they are more likely to be able to sleep according to their chronotype than during the school week. This misalignment of sleep/wake timing has been shown to associate with poorer cognitive functioning.

To blame the bright screens or not?

Teenagers’ lack of sleep is not all down to physiology. They, just like adults, may be engaging in behaviour that isn’t conducive to sleeping well.

The effect of light exposure on sleep has received increasing attention with the proliferation of electronic device use in recent years. However, the results are mixed.

One study on young adults asked individuals to read an e-book at maximum intensity under dim room light for around 4 hours (18:00–22:00) before bedtime on five consecutive evenings, whilst the control group read a printed book.

While the study concluded that those that read the e-book took longer to fall asleep, had lower morning alertness, and a delay of the circadian clock compared to reading a printed book, the effects were relatively small. Those participants who read e-books took only 10 minutes longer to fall asleep (Chang et al., 2015).


As a result, some caution needs to be exercised when the press reports that reading an e-book before bed has unintended biological consequences that may negatively affect performance, health, and safety.

Nevertheless, the impact of using electronic devices prior to sleep does seem to be important. In a large US survey, adolescents were shown to have increased the time spent using electronic media devices from 2009 to 2015.

This was correlated with a decline in sleep duration (Twenge et al., 2017), and light from such devices has been blamed. Such studies have encouraged the use of in-built or downloadable applications that can dim the brightness of screens and/or reduce the light emitted.

Light interventions are now being considered as a tool for adolescents experiencing difficulties with sleep, including reducing their exposure to evening light and increasing morning light to advance the clock to a time more suited for school.

Unfortunately, the evidence showing that such interventions can be helpful is lacking. Furthermore, it is important to stress that game use, social media, and watching TV are all likely to be cognitively arousing so teens may simply feel like staying up when they use electronic media devices.

As a result, disentangling the light effects versus the alerting effects of devices is complex and awaits good experimental studies.

Highly caffeinated



From Austin Kirk on Flickr

Caffeine is a stimulant with a half-life of approximately six hours in healthy adults (meaning that half of it is broken down in our bodies in six hours). It works by preventing the molecule adenosine, which promotes sleep, from having its effect in the brain, thus promoting wakefulness.

Teenagers are advised to consume no more than 100mg of caffeine per day, yet highly-caffeinated energy drinks are popular among teens. Many energy drinks contain higher caffeine levels than 100mg in a single can. Consuming caffeine later in the evening, or consuming it excessively throughout the day may be another contributory factor to delayed sleep.

Correspondingly, the National Sleep Foundation 2006 ‘Sleep in America’ poll found that adolescents who drank two or more caffeinated beverages each day were more likely to have insufficient sleep on school nights, and think they have a sleep problem, than those who drank one beverage or fewer.

We don’t need no early morning classes

School-based interventions are now underway that aim to improve teenage sleep. Sleep education programmes inform teenagers about the lifestyle factors that may be affecting their sleep and how they can improve sleep hygiene.

There is also a movement to delay school start times to better suit the adolescent clock by giving teenagers the opportunity to sleep at hours more aligned with their chronotype and reduce their social jetlag.

Given all the research, one could suggest that “early to bed, later to rise, may help the teen be healthy, wealthy and wise” would be a better amendment to the age-old quote for our average teenager.


Chang, A.M., Aeschbach, D., Duffy, J.F. and Czeisler, C.A., 2015. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proceedings of the National Academy of Sciences112(4), pp.1232-1237.

Twenge, J.M., Krizan, Z. and Hisler, G., 2017. Decreases in self-reported sleep duration among US adolescents 2009–2015 and association with new media screen time. Sleep medicine39, pp.47-53.

Early to bed and early to rise… makes a teen healthy, wealthy and wise? (Part 1)

By Gaby Illingworth, Rachel Sharman & Russell Foster; @OxTeensleep, @gabyillingwort1, @DrRachelSharman, @OxSCNi

Teenagers are well-known for routinely staying up late and then having a long lie-in. Sometimes this is put down to laziness or their transition from childhood into ‘Kevin the Teenager’.

However, there are biological reasons which help explain why teenagers are late to bed and late to rise, and why they might not actually be getting enough sleep to make them healthy, wealthy, and wise.

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Created by Matteo Farinella

Sleep matters. A wealth of evidence supports the importance of sleep for our physical, mental, and emotional functioning. Insufficient sleep has been linked to problems with attention, creativity, memory and academic performance, as well as increased impulsivity, and difficulties with mood regulation.

Sleep: a double-act

Sleep is driven by two processes working in tandem: the circadian rhythm and the drive for sleep (sleep homeostat).

The circadian rhythm is a roughly 24-hour cycle of changes in physiology and behaviour, generated inside our bodies. These rhythms come from certain genes being turned on and off (called clock genes) in almost all cells throughout the body. The master clock, (the suprachiasmatic nucleus in the brain), coordinates the rhythms within these cellular clocks.

The second system involves a balancing (homeostatic) process. Put simply, the longer you have been awake, the greater the need for sleep will become. The drive for sleep is thought to stem from a build-up of various chemicals (in the brain) while we are awake. For example, adenosine is a building block of our body’s energy currency (ATP), so it builds up as a consequence of energy use in the brain. Adenosine inhibits wake-promoting neurons and stimulates sleep-promoting neurons. As we sleep, adenosine is cleared and sleep pressure reduces.

Sometimes the two systems oppose each other. For example, we would feel very sleepy mid-afternoon due to increasing sleep pressure if it were not for the circadian drive for wakefulness.


Sleep occurs when the circadian drive for wakefulness ends and the drive for sleep kicks in. Then when the ‘sleep debt’ you have accumulated during the day has been re-paid (and so sleep pressure is reduced), and the circadian drive for wakefulness is sufficiently strong, we wake up.

Why some people don’t like mornings

Some of us love to burn the midnight oil, while others schedule in regular morning runs. The technical term for your preferred sleep/wake timing is chronotype, what we colloquially refer to as being an owl or a lark. You are owl if your biological clock runs slower and a lark if it runs faster.

We don’t run on 24 hours

While our day runs on 24 hours, for most of us, our internal clocks don’t. Therefore, our internal clock needs to be adjusted daily by external time cues such as light intensity. The master biological clock receives light signals direct from cells in the retina, which are most sensitive to blue light.

Dusk triggers the production of melatonin (the ‘vampire hormone’). Although not a sleep-inducing hormone, melatonin serves as a cue for rest in humans, with levels increasing as we approach sleep and remaining high during the course of the night.

In contrast, dawn light suppresses melatonin levels. The circadian clock responds differently to light depending on the timing of exposure, so that morning light advances the clock (making us get up earlier) and evening light delays the clock (making us get up later the next day).

As well as playing a role in sleep regulation via the circadian clock, light affects how alert you feel. You may have noticed that bright light increases your alertness, so relatively bright light before bedtime will increase the likelihood that you will feel sleepier later.


Stay tuned for next week’s blog about how changes in these systems affect teenage sleep.

Sleep across the animal kingdom

By Kimberley Whitehead, University College London

As creatures that spend a glorious one third of our lives asleep, we might be quick to assume that all animals on earth sleep.  Do they, and if so, how can we actually tell?

To understand the mechanisms of sleep and wakefulness better, physiologists often study animals. This is because their nervous systems are simpler, but still share similarities with ours. For example in animals with fewer genes involved in sleep, such as flies, it is easier to understand genetic effects. In the case of the zebrafish, life is made easier for neuroscientists who use this species because the fish is transparent when young, so the brain is visible and can be imaged in a living fish! However, if scientists study a fly or a fish, how can we tell that they’re asleep, especially if they don’t have eyelids?

Before we can look at differences in sleep between species, we first need to define criteria of sleep that we can apply to even simple animals. Firstly, sleep has to be reversible! If somebody was unconscious and couldn’t ever be roused, that would be a coma state, rather than sleep. Secondly, arousal threshold – i.e. what it would take to get a response – has to be increased during sleep, compared to wakefulness. For example, a cat will let you put all sorts of objects on it while sleeping, which it never would have tolerated when awake! Thirdly, sleep tends to happen at certain times of day, and in certain positions or situations: for us a nice comfy bed, for fish at the bottom of the tank.

In addition to these behavioural differences, if sleep is a distinct state from full consciousness, we would expect brain activity to differ. It turns out that indeed, even in flies, there is a difference in brainwaves between wakefulness and sleep. Brainwaves reduce in size as we fall asleep. Humans then go through cycles in which brainwaves get bigger and slower as sleep deepens whereas this is not apparent in flies for example.


Monica Folgueira and Steve Wilson, Wellcome Collection

Not only does sleep differ from wakefulness, it also varies across our lifespan. The sleep-specific brainwaves of adults are not present in baby rodents and humans. This suggests that sleep in early life may differ from sleep in adults.

Young animals also sleep much more. This extensive sleep in early life might be important for learning; baby flies deprived of sleep don’t learn how to find an appropriate mate. In mammals, there is some evidence that the twitchy movements babies have during sleep might help them to learn how to sense their environment.

Not only is sleep different in early life, it also differs in later life. In the elderly, changes in sleep patterns are seen across the whole animal kingdom. In both flies and humans, their sleep becomes more fragmented and elderly humans are more likely to report sleep problems than young adults.


Robert Hindges, Wellcome Collection

Understanding the criteria of what defines sleep, and the normal changes in sleep across the lifespan, paves the way to understand sleep disorders, such as narcolepsy. The brain circuits involved in narcolepsy are the same between zebrafish and humans. This offers exciting opportunities to understand these circuits better, because they’re so much easier to manipulate in fish. Aside from diseases which primarily affect sleep – like narcolepsy – many neurological disorders eventually affect sleep. This means that researchers using animal models can use sleep as a marker of overall brain health or degeneration.

Since there are ways to tell whether even simple animals are asleep, research about sleep across the animal kingdom can offer fresh insights into the million dollar questions of why we sleep, and what causes sleep problems.

This blog is based on a recent public engagement event at the Grant Museum of Zoology, put on by University College London and The Physiological Society. Surrounded by weird and wonderful pickled and stuffed animals, sleep scientists from University College London studying flies (James Jepson), zebrafish (Jason Rihel) and humans (me – Kimberley Whitehead) each brought a different angle to the discussion.

Follow these links to learn more about the research done by:

The Ultra Cycle Diaries – The Finish Line

by Daniel Brayson, King’s College London, @DrDanBrayson

Having never attempted anything like the Transcontinental Race before, my expectation ahead of the race was to complete it before the cut-off time, which was set at 15 days and 2 hours. In the very early stages of the race, I rode quite conservatively knowing that to finish within this time was critical for my sense of achievement. However, I very quickly realised I was capable of much more. I arrived at the first checkpoint in around 60th position, which surprised me. I then arrived at all the remaining checkpoints in higher positions than the previous one and was placed somewhere in the 30’s for the final checkpoint on the Transfagarasan highway in Romania.

The last hurdle

Approximately 1000 kilometres from the finish line in Meteora, I was in a good position to make a late charge for a top 30 position and I set about the task gamely. I rode through the remaining portion of Romania and a short section through Bulgaria into Serbia. Feeling hardened from the first 75% of the race I felt my performance improving rather than declining and set about three substantial climbs in northern Serbia with a certain amount of gusto and swagger. Temperatures were fierce, up into the 40°Cs, but I felt I had acclimatised to these by now and in my mind I was conquering these hills with no problems, better than any I had attempted previously at the height of the midday sun. Having capacity for only 1750 ml of water and a broken smartphone, I found myself rationing water as I couldn’t know when the next opportunity to resupply would arrive. I made up for it when I had the opportunity and guzzled litres at service stations but as it turns out, the damage had been done. Later that evening, when the sun had disappeared below the horizon and temperatures had dropped to the point it was “cool,” I started to suffer. I felt hot and restricted in my clothes despite the cool evening breeze; I became irritated by my clothes to the extent that I removed my jersey and rode shirtless for a while. After a little while longer, my feet felt hot and irritated too, so I took them out of my cleats and rode on top of those. Then suddenly my legs went completely: I’d hit a wall, pedalling felt like I was sitting on a ledge mixing cement with my feet, and I was overcome with delirium. I stopped at a service station and slept in a secluded area covered in pinecones for the night. I was so out of it I hadn’t noticed the pinecones at first, and stirred from sleep a few hours later to find myself cursing them wildly. At this point, I intended to crack on, but as I stood up I felt a wave of nausea overcome me, so I figured I needed more rest.


In the morning, I ‘soft pedalled’ (rode slowly) for about 100 kilometres, at which point I came face to face with a steep hill at 1pm. Again, the temperature was up in the 40°Cs. With no obvious signs of shade on the sides of the road I looked around, feeling dejected. I had been riding next to a river and noticed locals frolicking in their bathers. I found a small quiet area and immersed myself, fully clothed, in a shallow part of the river and remained there in state of semi-consciousness for almost 4 hours. When the mid-afternoon sun was less fearsome I rode another 40 kilometres to the nearest town and holed-up in hotel for the next 8 hours. At this point, I could not stomach any solid food, and realised I was suffering at the hands of the extreme temperatures and heat exhaustion.

Lessons from the Transcontinental Race

At the time, I felt that I had not ridden at the right times of day in order to avoid the heat, and this point comes through as in my video diary. Now, as I reflect, I know that I couldn’t have ridden at night since I can’t suppress the urge to sleep then (remember response inhibition?) The logistics of trying to reverse my body clock in preparation for a race whilst performing a demanding vocation would be insurmountable. My feeling now is that I should have been better prepared to ride in the heat. Principally, I should have addressed two issues. Firstly acclimation: I should have trained for the heat. I didn’t, because being British I am not often enough exposed to extreme heat to actually appreciate the effects it has on human physiology and performance – and to believe these temperatures actually exist! However, training for heat has been shown to potentially benefit overall performance, not just performance in the heat, so if there is any chance of high environmental temperatures it is worth undertaking heat training regardless. Secondly, I should have allowed a greater carrying capacity for water and fluids. This was perhaps the biggest flaw in my preparation. At times I should definitely have been carrying at least 3 litres, if not more! I paid the price for this and by the time I had recovered I had to re-align my expectations back to finishing before the cut-off. So with the intention of managing my workload carefully, I gingerly clambered aboard my bike and set off for the finish line.


The finish line

After a calamitous final section in which I suffered a terminal failure of my rear tyre, I walked the final 7 kilometres, in suffocating heat, and arrived at the finish line in Kalabaka, Greece, in a foul and dispirited mood. I was robbed of the glory of rolling across the finish line, triumphant and fulfilled. Nevertheless, I had finished and I had finished 12 hours before the cut-off. On the lack of glory at the finish my final thought as I left Kalabaka to return to the UK was, ‘there’s always next time’.

The Ultra Cycle Diaries – Nutrition

By Daniel Brayson, King’s College London, @DrDanBrayson

In cycling very long distances as fast as possible, ultra-endurance cyclists use an extraordinary amount of energy. Replenishing these energy stores is critical for racers to maintain performance and stay competitive. To achieve this, riders do not simply settle for 3 square meals per day, or even 3 big meals a day, which would simply not be enough! Instead, we eat more frequently, and because we do not want to stop too often, this means eating whilst riding: “grazing on the go,” as it is affectionately referred to amongst cyclists. This involves eating an array of convenient snacks ranging from the healthy – bananas, oranges and kiwi fuits – to the energy packed goodness of carbohydrate and fibre rich wholegrain bars, nuts for fat replenishment, all the way through to the downright despicable: chocolate bars, Peperami and lots of jelly sweets. Did I mention ice cream? There was a bit of that too. The overriding consensus amongst riders is that a calorie is a calorie no matter where it comes from, and you take all you can get!

Fatigue 2

Biting more than you can use

Although it is intuitive to think that you need to eat a lot more to compete in these races, there is a limit to how much energy a human can take on board. Take the example of carbohydrates. The limit to how much carbohydrate can enter the bloodstream is dictated by a clever transporter system between our gut and our circulation. The ‘problem’ with this system, from the point of view of an ultra-racer, is that it can only transfer approximately 60 grams of carbs per hour from the gut to the bloodstream, maybe up to 90 at a push. In an ultra event, racers are likely to use much more. On top of this, this transport relies on an adequate blood supply to the gut to deliver energy to the system and facilitate it’s function. However, when cycling most of our blood supply is directed to the muscles because they are using so much energy. This can make this transport system slower and less effective and may lead to “gastrointestinal distress” – tummy ache to you and me! This is a common problem for ultra-cyclists, but it is even more common in ultra-runners, probably because of there is more jumbling up and down in the tummy, which I think is the technical terminology…

Measuring the loss of energy stores

If the human body is in a state where it can’t take on as much energy as it uses, it is likely there will be a net loss of energy stores in the body; this has actually been shown in a couple of studies which examined ultra cyclists. However, the magnitude of this deficit is up for debate. One study showed that it could be as much as 8000 calories per day, whilst another derived that it was a more conservative 1500 calories. This discrepancy is likely due to the fact that these studies chose very different methods of measurement. To add to these studies I attempted to use yet another type of measurement to see if I could determine my ‘energy status’ during the Transcontinental Race. I opted for measuring circulating glucose (sugar) and lipids (fats) by pricking my finger and then using an everyday device that a diabetic might use to monitor their blood sugar. Simple.

Or perhaps not. I found that when I measured glucose, cholesterol and triglycerides, values were usually either the same as or higher than the resting values that I measured before the race, which goes against the hypothesis that I would be suffering from an energy deficit, and the data generated by previous studies. I can think of a number of mitigating circumstances. Firstly, I had devised a plan to take measurements pre- and post-meal. Yet, it quickly became obvious that I would rarely find myself in a pre- or post-meal state, because I ate so often. Timing of measurements was therefore erratic at best. Also, continually lancing my fingertips became a painful burden: my fingers were wounded and bruised for most of the time I was racing. Eventually, I decided it was too much of a hindrance, especially as my chances of finishing the race were already jeopardised by heat-induced illness. Heat also affected my appetite and ability to adequately digest: I was nearly re-acquainted with more than one meal towards the end of the race and spent the last two days eating nothing but ice-lollies.

In case you needed reminding, this was no walk in the park! Come back next week to find out if the ice-lollies got me over the line!

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