How To Train Your Bacteria!

Bacteria and our relationship with them go back to the origins of life on this planet. Without them we would simply not be here today! The microbes that live in and on us outnumber our own cells by a staggering 10 to 1. It’s a perfect example of biological symbiosis, two organisms living in mutual harmony, well not always harmonious and when it does go awry then our health takes a nosedive.

Microbiome-in-Numbers-1.jpgOur genetics, the human genome has made a life-long partnership with the microorganisms that call us home, otherwise known as the microbiome. This partnership of genome and microbiome has navigated us through precipitous environmental changes, most recently the Ice Age. Could our genome have achieved this alone? No, absolutely not. Our microbiome serves as a first line of defence against environmental aggressors, pathogens, toxins and stressors. But, that’s not the only thing it does; it mediates our immune response, it provides essential molecules that our own host cells are unable to produce and it provides a small amount of energy in the form of short-chain fatty acids. Put simply, without our microbiome we would have perished long ago.

If we wish to improve our health we really need to understand the relationship between our genome and microbiome and learn how they combine to navigate a healthy path through a changing and challenging environment. One of the biggest physiological changes of human evolution over the past few million years has been the increase in the size of our brains.

brain-sizeThe brain is our most metabolically active and demanding organ taking up to 25% of our daily energy and this rises to 70% in babies and young children. This explains why babies come packaged with so much body fat, they simply have to have a secure source of energy to fuel the rapid development of their brains. No other species in the animal kingdom is born with so much body fat. This hungry brain drove an appetite for energy-dense food, primarily fat from large animals. When we hunted these larger animals to extinction we needed to adapt to more fleet-footed prey which required higher cognitive function and hence an increase in brain size. It was this exquisite interplay between increasing energy demand and increasing food scarcity that fuelled the increase in brain size. This also led to a dependence on fat especially from animals and this in turn led to a decrease in the size of our large colon whilst also increasing the size of our small intestine so that we could extract the energy from food more quickly. Over time the energy contribution from the large colon decreased however its protective function was maintained.

It could be argued that many of today’s modern diseases arise from an imbalance or dysbiosis in the gut and this has come about by eating foods that disrupt the capacity of our bacterial communities to protect us. Agricultural foods such as wheat and dairy and industrial foods such as refined flour, sugar and oils have decimated the bacterial communities within our gut. We are not adapted to consume foods that arose with farming only 10,000 years ago and in evolutionary terms this is a mere blip. Therefore, if you avoid these foods your microbiome will repay you in better health and well being. Therefore, the bottom line on training your bacteria is to avoid feeding them foods they are not adapted to eat and stick to energy-dense nutrient-dense natural whole-foods.



Increasing Meat Consumption, Good or Bad!

This BBC article reveals how meat consumption increases with increased GDP however don’t be fooled into thinking that increased meat consumption is the cause of modern diseases as many would have you believe.
When examining population data (which is not always the most reliable anyway!) there is more association between diets rich in refined carbs and increased disease outcomes than there is with meat. Animal-sourced proteins (eggs, fish, dairy, meat, etc) are by far the richest source of nutrient-dense foods on the planet, that’s why we evolved to eat them!
Final food for thought. Why spend hours foraging/grazing on plant foods when you can get all the energy and nutrients you need from animals for a much lower investment in both time & energy?

Smart-choice homo-sapien!

Protein Power


This is a great article explaining our fundamental need for protein. It’s geared towards a low-carb or ketogenic diet however it can be equally applied to other dietary approaches. It’s well supported with evidence from scientific studies which are referenced at the end of the article.

The minimum recommendations are 1.2g per kg of lean body mass per day. A person weighing 70kg with a lean body mass of 60kg would therefore need 72g (60 x 1.2) of protein per day. Protein need increases with activity so if you exercise a lot then your need for protein will be higher. The main takeaway is to ensure you’re getting enough protein every day.

For personalised dietary advice on protein please contact Exeter Nutrition (,, Skype: Exeter Nutrition)

Media Meddling + Political Self-Interest = Dodgy Dietary Advice

This is a great example of how Governments can manipulate the media for their own agenda. This was the headline story on a recent BBC’s article, its main message being that ‘moderate’ carbohydrate consumption is associated with lower all-cause mortality which just so happens to coincide with current dietary advice both in the US and UK. Great, so we can safely carry on eating according to current guidelines? No, not at all, let’s dig a little deeper and we can begin to distil the real motive behind this headline and I will argue that it is more about protecting US national interest than it is about improving our health and well-being.

First, this ‘large’ epidemiological study was published by The National Institutes of Health (NIH), a department of the U.S. Health Ministry and all of its researchers were American. Contrast this with the PURE study which is referenced in the introduction of the American study. PURE was composed of many more researchers from six different countries and funded by organisations from 10 different countries. Secondly, lets look at the scale of the studies; 15,428 participants from 4 different US communities were involved in the US study whereas PURE reported results from 135,335 participants drawn from over 600 communities and 18 countries. The PURE study dwarfs the American study in both scale (a factor of 9) and breadth (>600 communities vs. 4, 18 countries vs. 1). I would argue that the PURE study is more relevant from a dietary perspective as it more accurately reflects current dietary patterns (2003-2013) as opposed to the American study which covers a period much further back in time (1987 to 2017).

So, lets look at the primary outcome of both studies, which is all-cause mortality. In the American study, there were a total of 6,283 deaths which averages out at 251 deaths per annum over the 25 year period compared to 5,796 deaths in PURE which averages out at 580 deaths per annum, however, the PURE study was much bigger by a factor of 8.772 (135,335 participants/15,428 participants). When we take account of this size difference the outcome is striking, 580 deaths per annum in PURE versus 2,201 deaths in the American study. This means that the risk of all-cause mortality is nearly quadrupled in the American study relative to the PURE cohort!!

So, when you look behind the headlines the results are very revealing. Following an American diet which is heavy on refined carbohydrates (such as sugar & flour), processed convenience foods and cheap processed seed oils (canola, sunflower, vegetable, etc) will quadruple your risk of all-cause mortality relative to the diets of the 18 countries that make up the PURE study. The main takeaway from headlines such as this is to view them with a heavy dollop of scepticism and investigate them carefully. The current dietary recommendations are failing to reverse a growing global wave of obesity, type 2 diabetes, cardiovascular diseases, cancer and dementia. I would argue that this study is all about protecting the interests of an American political and economic elite and has absolutely nothing to do with serving the health interests of individual citizens especially American citizens. As for general dietary advice stick to whole natural foods and avoid anything with a label on it!! For specific dietary advice contact Exeter Nutrition (,

Not Too Much, Not Too Little, Just Right, The Goldilocks Approach To Training


As we train we accumulate stress, however, if we do this too quickly or accumulate too much then this can lead to overtraining, illness and injury. Training Peaks provides a means of measuring training stress by workout or time period and can provide insights into fatigue, form and fitness.

In Training Peaks, training stress score (TSS) is represented as longer term fatigue accumulation or Chronic Training Load (CTL) and shorter term fatigue accumulation or Acute Training Load (ATL). The balance between short and long term fatigue is referred to as Training Stress Balance (TSB). CTL, ATL and TSB are presented together in the Performance Management Chart (PMC). The PMC is an incredibly powerful tool for planning, monitoring and adjusting training however it’s not always that straight forward to understand.

In trying to better understand PMC it helps to think of stress as money, ATL as a current account and CTL as savings.

When we train we accumulate stress which is drawn from our current account or ATL. If we take out too much money too quickly then we leave ourselves financially exposed or from a training stress perspective, physiologically exposed. Therefore, we need to manage our short term training program in the same way we manage our current accounts, that is, not going overdrawn too often or too deeply. CTL represents our longer term financial position or fitness. The more we deposit and the less we take away the more our savings accumulate.

TSB represents a balance between our longer term financial health or fitness and our current financial position or level of fatigue/form. The more our current account is cash positive (TSB >0) the better able we are to manage a range of financial purchases. If we are cash negative (TSB <0) then purchases will weaken our current account. The more savings we have accumulated the better able we are to cover near term financial debits.

As with money we need to adopt a strategy to grow or build fitness so that it’s accumulation longer term affords more choice and flexibility in the near term. Therefore, training stress can be thought of in the same way as money in that we need to handle it with respect and plan carefully for its accumulation. We need to monitor it closely to ensure it is accumulating in line with our goals. It also pays to stay abreast of the latest strategies or opportunities that may deliver greater returns on our existing capital.

Each time we train we draw down on current account or ATL reserves. Are we spending our money wisely, are we drawing down too quickly, or are we increasing our longer term financial exposure by excessive spending in the short term? Our financial or fitness outlook will depend on time, our initial capital outlay, and the financial or fitness strategy we adopt.

As with financial investment, it pays to play the long game. Invest in smaller regular deposits or sessions and avoid expensive outlays that eat into both short and longer term financial reserves. Not too much training, not too little but just right. PMC will help you determine your Goldilocks training strategy.

Can HIIT Really Improve Bike Performance?



High Intensity Interval Training or HIIT is an exercise protocol that is often touted as a time-efficient method of training. But, how effective is it and what does it involve? In an effort to answer these questions a search of the scientific literature was undertaken for evidence of its benefits. Most of them point to quite impressive performance and health improvements (Sloth et al 2013) and one study in particular by Gibala et al (2006) examined their benefits against more traditional endurance training. The headline from this study was that six sessions of HIIT completed over two weeks yielded the same or slightly better performance gains as two weeks of traditional endurance training. It’s a fascinating study and one that is worth delving into for a better understanding of the benefits of HIIT.

In the Gibala study, two groups of eight healthy individuals were assigned either a HIIT or traditional endurance exercise protocol. The HIIT protocol was a Sprint Interval Training (SIT) session which consisted of repeated 30-s “all-out” efforts on a cycle ergometer. Subjects were encouraged to pedal as fast as possible throughout the 30s test. This was followed by a 4-min recovery period cycling at low cadence and against light resistance. The sessions were performed three times a week on alternate days (i.e., Monday, Wednesday, Friday) over 14 days. The number of intervals for each session from one through to six were as follows: 4,4,5,5,6,7. In contrast the control group were assigned six sessions of 90-120 minutes of continuous endurance cycling (ET) at 65% VO2peak.

TrainingProtocolGibala2006 copy

The results from the study with respect to changes in exercise performance following training were impressive:

  • The time required to complete a 750 kJ time trial (approx 25 miles) decreased by 10.1% and 7.5% in the SIT and ET groups, respectively. This translates to an average reduction from 61 minutes to 55 minutes for the SIT group


  • There was an increase in mean power output during the 750 kJ time trial from 212 ± 17 to 234 ± 16 watts in the SIT group and from 199 ± 13 to 212 ± 12 watts in the ET group
  • The time required to complete the 50 kJ test decreased by 4.1% in the SIT group (Post: 113 ± 6 vs Pre: 117 ± 6 s) and 3.5% in the ET group (Post: 122 ± 10 vs Pre: 115 ± 9 s)
  • The mean power output during 50 kJ time trial increased from 435 ± 23 to 453 ± 25 watts in the SIT group and 416 ± 39 to 433 ± 40 watts in the ET group

The results for both protocols indicate the benefits of exercise, however, and this is really important the benefits of SIT arose from a total training volume significantly lower (~90%) than traditional endurance training (∼630 versus ∼6500 kJ). These data demonstrate that SIT is a time-efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance comparable to endurance training.

For further information please click on the references below, the second of which reviews emerging evidence from recent studies into HIIT.


Gibala M et al (2006) Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance. J Physiol 575:3;901–911

Sloth M et al (2013) Effects of sprint interval training on VO2max and aerobic exercise performance: A systematic review and meta-analysis. Scandinavian Journal of Medicine and Science in Sports 23:6











Lipid Metabolism & Its Dynamic Response to Exercise – Part 2

In part 1 we introduced the topic of lipid metabolism and its potential to improve exercise performance. Lipids represent the biggest reservoir of stored energy in the body and at low to moderate exercise intensity they are the main fuel type, however, it does beg the intriguing question as to why fat burning or fat oxidation falls off quite dramatically at higher intensities. Our aim in this series is to explore the latest scientific literature to find out how we may extend our fat oxidation capability (that is, how efficiently we burn fat) for longer and at higher intensities and thereby improve exercise performance.

Lipid Reserves & Distribution

So, first up, let’s take a look at Table 1 to see how our lipid reserves are distributed around the body.

Table 1. Characteristics of fatty acid and TG metabolism compared in adipose tissue, skeletal muscle and liver (Frayn et al 2006)
  Adipose tissue Skeletal muscle (at rest) Liver
Input LP–TG ~ 45 g/day NEFA ~ 20 g/day NEFA ~ 20 g/day
  NEFA ~ 5 g/day LP–TG ~ 10 g/day Remnant-LP–TG ~ 25 g/day
      DNL ~ 1 g/day
Stimulation of uptake Feeding/insulin Fasting (high NEFA supply) Exercise Delivery
Typical whole-body TG store 15 kg 300 g 100 g
Half-life of store 250 days 24 h 100 h
Lipolysis of TG store HSL-stimulated lipolysis HSL? Unknown
  ATGL – basal lipolysis    
  MGL – monoacylglycerol hydrolysis    
Releases mainly NEFA into plasma FA for oxidation FAs re-esterified in ER and released as VLDL-TG
Quantitative data involve some estimates and should be taken as representative only. ER, endoplasmic reticulum; FA, fatty acids; LP, lipoprotein; MGL, monoacylglycerol lipase; TG, triacylglycerol; DNL, De Novo Lipogenesis

We can immediately see that adipose tissue at approximately 15kg is by far the largest reservoir of lipids. Adipose tissue is found mainly on the upper body, particularly around the stomach. The other two areas where lipids can be found are skeletal muscle and the liver. What we need to understand is that these stores are very active. Lipids are in a constant state of flux moving between adipose tissue, liver and muscles which we shall now examine in more detail.

Lipid Exchange & Cycling

The continual flow of NEFA and TG between adipose, muscles and the liver is illustrated in Figure 2. The turnover of plasma NEFA is rapid with a half-life of only 4-5 minutes (Frayn et al 2006). Dietary fat is broken down into TG and packaged in lipoproteins known as chylomicrons in the small intestine. Chylomicrons, which have a short half-life of around 5 minutes, deliver TG to tissue expressing the enzyme, lipoprotein lipase (LPL) which is found in adipose tissue, cardiac and skeletal muscle.


Figure 2. Lipid exchanges between gut, adipose tissue, skeletal muscle and liver. Note that adipose tissue LPL also releases NEFA into the plasma, making further fatty acids available for uptake by muscle and liver. ER, endoplasmic reticulum; FA, fatty acids; Ox, β-oxidation. (Frayn et al 2006)

In the fed state, LPL is upregulated at adipose tissue by the action of insulin and this leads to storage of TG and a consequent reduction in circulating NEFA. In contrast, NEFA circulation increases during the fasted state thereby providing a readily available source of energy for those tissues such as cardiac and skeletal muscle that demand it.

Frayn et al (2006) estimate that chylomicrons release up to 2/3 of their TG-payload, before making their way to the liver with the remainder (approx. 20g per day). Remnant chylomicrons and TG along with NEFA are recycled in the liver and released in very low-density lipoproteins (VLDL), which have a half-life of approximately 5 days (Table 1). Apolipoproteins and cholesterol are important constructs in the cargo-carrying structure of lipoproteins and as TG is extracted from VLDL’s their proportion or density steadily increases and VLDL’s transition to low density lipoproteins (LDL’s). NEFA’s bound to albumin or TG packaged within lipoproteins form part of a TG-NEFA cycle between adipose, liver and muscles and the flux of this cycle is determined by dietary inputs and other factors which we will examine.

So, how does this TG-NEFA cycling or flux respond to exercise? Let’s take a look.

The Dynamic Response of TG-NEFA Cycling to Exercise

A well-designed study by Wolfe et al (1990) serves as a useful introduction into the normal functioning of the TG-NEFA cycle. The investigators utilised tracer-isotopes in five healthy volunteers to accurately track the movement of NEFA as they appear and disappear within the changing flux of the TG-NEFA cycle in response to exercise.

Screen Shot 2017-04-19 at 16.10.09

Figure 3. Percent re-esterification of fatty acids made available via triglyceride hydrolysis (Wolfe 1990)

During rest up to 70% of NEFA are re-esterified (Figure 3), however, this reduces down to 25% within the first 30 minutes of exercise. Another dramatic shift in NEFA flux is seen at the end of exercise when re-esterification rises above its pre-exercise level to 90%. During rest a high proportion (over 70%) of NEFA are re-esterified; this constant cycling means the body is primed to respond rapidly to fluctuating energy requirements as illustrated in this study when re-esterification drops to 25% following the start of exercise. This means fatty acids can be delivered quickly for oxidation by working tissues. The authors estimate the energy cost of this cycling as less than 2% of total energy expenditure at rest and this drops to below 0.5% during exercise. They argue that ‘the benefit afforded by a high rate of TG-NEFA cycling at rest in terms of regulation of substrate availability is thus accomplished economically in terms of overall energy expenditure.’

Upregulation of TG Hydrolysis to Meet Increasing Energy Demand

At the same time that NEFA re-esterification is reduced, TG hydrolysis (that is the breakdown of TG to release NEFA) is tripled (Figure 4).

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Figure 4. Rate of appearance (Ra) of glycerol and NEFA at rest, in exercise, and in recovery (Wolfe 1990)

Figure 5 below illustrates how TG hydrolysis combined with reduced NEFA re-esterification serves to amplify the total pool of NEFA made available for oxidation. This ensures lipid energy supply keeps well ahead of energy demand, even at higher intensities. This begs an intriguing question; if fatty acid supply is not impeded at higher intensity why is fatty oxidation reduced. In other words, there is plenty of fuel, why is it not being used. If we can answer this question, then we begin to identify a clear opportunity to improve performance, so that we can exercise for longer at a higher intensity using fat as our main fuel source.

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Figure 5. Comparison of rate of appearance of NEFA (o) with total fatty acid oxidation (o) as determined by indirect calorimetry (Wolfe 1990)

The authors conclude that ‘TG-NEFA plays an important role in enabling a rapid response of fatty acid metabolism to major changes in energy metabolism’ which is evidently the case in the five healthy individuals studied. This study illustrates unequivocally the dynamic nature of TG-NEFA in response to exercise.

In part 3 we’ll be looking at how we can optimise our fat burning capability for performance.


1        Frayn KN, Williams CM, Arner P. (1996) Are plasma non-esterified fatty acid concentrations a risk marker for coronary heart disease and other chronic diseases? Clin. Sci. 90:243–53

2        Frayn KN (2010) Metabolic Regulation: A Human Perspective, 3rd Edition; Wiley-Blackwell

3        Frayn KN. Adipose tissue as a buffer for daily lipid flux. (2002) Diabetologia; 45:1201-1210

4        Frayn KN,  Arner P,  Yki-Järvinen H (2006) Fatty acid metabolism in adipose tissue, muscle and liver in health and disease. Essays in Biochemistry; Chapter7:4289-103


5    Wolfe RR, Klein S, Carraro F, Weber JM (1990) Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. American Journal of Physiology; 0193-1849/90