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Jan Van Berkel: The Fat Adapted Healthy Athlete

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High levels of visceral fat, that is the fat we carry around our organs, is a well-known marker of health decay. Our athlete Jan Van Berkel experienced substantial reductions in visceral fat (339 g to 166 g) after making a few key changes in behaviour. These adjustments coincided with large improvements in both health and performance, and just last week he recorded a personal best time in the South African Ironman (5th professional). Carry on reading to learn how he achieved this, and what it means to become a “F.A.H-lete”, or fat-adapted, healthy athlete.

The first major Ironman of the season for Plews and Prof athletes turned out to be a good one at Ironman South Africa (IMSA). With 4th and 5th places, and two personal best times from Kyle Buckingham and Jan Van Berkel (JVB). Both athletes delivered stellar performances on the day and were thrilled with their results.

I (Plews) have been working with JVB since November last year. We started out working more on a consultancy basis, but since the new year have moved towards a coach-athlete relationship. JVB has been a pleasure to work with, and his result in IMSA was well deserved after a lot of hard work in training.

He managed to achieve this result even after training through a very cold winter in Switzerland, with limited biking and ability to train outdoors. As many of us know, including Prof up in Canada, that isn’t easy!

When JVB and I first started working together, as with all athletes we work with, we begin with a battery of tests to establish some baseline parameters and monitor progress. One of the tests we used for JVB was a DEXA scan.

 

What is a DEXA scan?

DEXA stands for Dual-energy X-ray absorptiometry and is considered to be the gold standard tool for measuring body composition and bone mineral density. DEXA achieves this by using two X-ray beams of different energy levels, which are scanned up and down the body. When these different energy level photons pass through tissues, they slow at rates related to their elemental composition, and the unique elemental profiles of bone, fat, and non-bone lean tissue allow for visualization and determination of each tissue type.

In JVB’s case, we were interested in establishing baseline measures of his body composition, and specifically having a look at his level of fat mass relative to lean mass.

 

What is visceral fat and why is it more important than subcutaneous fat?

Visceral fat is excess intra-abdominal adipose tissue accumulation. In other words, it’s the fat that we can’t see, stored deep underneath the skin, rather than the subcutaneous fat that is more apparent to us on the outside of our body. The visceral (internal) fat is more of a gel-like fat that wraps around major organs, such as the liver, pancreas and kidneys. Having high levels of visceral fat has even led to a new term, called skinny-fat, referring to those who are thin on the outside, but fat on the inside. As you will discover, although some might not like it, it’s healthier to be thin on the inside and fat on the outside, although neither are that great.

Visceral fat is especially dangerous because these fat cells contribute to the way your body operates. Visceral fat is considered toxic and provokes inflammatory pathways. Such inflammation drives more fat deposition and interferes with the body’s normal hormonal functions. These changes can influence changes in appetite, fat gain, mood and brain function.

The Data

 

The DEXA scan data from JVB’s Test 1 and Test 2 (4 months apart) are shown above. To keep things simple, I have just included visceral fat and total body fat percentage. Visceral fat was cut nearly in half, going from 339 g to 166 g. As well, total body fat percentage was lowered from 12.6% to 8.3%.

Getting into science: how is this possible?

The changes in JVB’s visceral fat are quite remarkable, especially in an already lean elite athlete. From the outset, we should acknowledge that we don’t know exactly what mechanisms are responsible for the changes at this stage. However, using some guiding principles of physiology, we can make some reasonable assumptions. We would also like to give a massive thanks to our colleague Alessandro Ferretti for offering insights on the data as well.

After a lifetime of consuming the typical high carbohydrate diet prescribed to most endurance athletes, JVB likely had developed a mild to moderate level of insulin resistance (IR). Talking with Alessandro, who works with several high-level athletes, he’s noticed a relationship between competition level and IR; the higher the level, the more pronounced the IR problem. We have observed similar. The problem is, when we measure Hemoglobin A1c (HBA1c; aggregate blood glucose over 3 months, a marker of pre-diabetic state), we often get a false-negative result (i.e., no sign of any problem here). High training loads of course lower the blood glucose level, and we get lower HBA1c values over the long-term. While HBA1c values give us the false-negative result, morning fasted BG levels are likely to be raised.

We know that high blood glucose levels drive inflammation, and inflammation drives fat deposition. Typically, the inflammation will be magnified in a localized manner around both the gut and liver. In an athlete like Jan, who has very low levels of muscle fat and overall adiposity, a high(er) fat deposition around the organs can still be present as shown, as they remain inflamed due likely to IR and/or additional factors.

In endurance athletes undergoing high training loads (such as professional Ironman athletes), inflammation can be high, regardless of any IR, simply due to a chronically high training load. That, alongside a higher carbohydrate diet, means that inflammation never gets its chance to subside, even during periods of rest. We can assume that would be the case due to the link between training load, chronic glucocorticoid activation, inflammation and visceral fat deposition. Inflammation also appears to favor visceral over subcutaneous fat, meaning subcutaneous fat is the last place for inflammation to subside. Thus, fat remains hidden on the inside, as it was in JVB.

Another factor involved in excessive inflammation, is that typically when we gain fat, we increase the number of fat cells (adipocytes). However, in such localized areas, rather than increasing the number of adipocytes, there seems to be an over-stretching of adipocyte fat deposition. This results in fat cells stretching over normal size, initiating a further inflammatory response that compounds the problem. Importantly, more inflammation under a high carbohydrate diet with IR, means more fat deposition around the organs.

When we consider all the above, high levels of visceral fat in some elite athletes may be apparent irrespective of any insulin resistance. This is due jointly to

  1. the exercise-induced inflammation alongside diets that are high in refined carbohydrates
  2. to the preference of inflammation to remain around the organs and
  3. to the overstretch/inflammation reaction that occurs when fat deposition around the organs is increased

Jan Van Berkel and Low Carb High Fat approach: how did it work?

So by now, the question I guess everyone is asking is: “how and why did JVB see such changes?” Very simply, a complete switch over to a low carbohydrate (CHO)/high fat (LCHF). JVB was very diligent in his diet, and didn’t take any shortcuts. Low carb for him was generally Ketonix device, and was able to ride for >4 hr. from fasted without any carbohydrate supplementation or the feeling of hunger. This is something he was previously unable to do.

 

 

JVB’s lower carb diet would likely have caused a cascade of events to occur. First, the diet allowed him to achieve a low and stable (non-fluctuating) blood glucose level. Second, he became more metabolically flexible. Improvements in metabolic flexibility resulted in an increase in the energy production derived from fat and ketones, which reduced the energy derived from external carbohydrate sources. Additionally, the reduction in blood glucose would have directly influenced his levels of inflammation, particularly around the organs. With visceral fat deposition reduced, the liver no longer has to work as hard to convert excess blood glucose into fat. As well, the shift in energy metabolism towards fat and ketones, means the cost of producing energy becomes lower, and reactive oxygen species (ROS) production is reduced. Less damage and inflammation during Jan’s training also occurs at the same energy equivalent. This again reduces the total inflammatory load and visceral fat deposition.

Due to the above mentioned factors, Jan Van Berkel achieved a massive 49% reduction in visceral fat.

Take home points

What is important here is that JVB had substantial improvements in his health by going away from the conventional high carb diet prescribed to most professional athletes. This occurred in concert with substantial improvements in his performance, which is difficult to argue against. Improvement in performance and health. As we’ve spoken on previously, fitness and health are NOT the same thing, and athletes with the wrong guidance can be even less healthy than your everyday working man or woman.

In the above case with Jan, a change in his diet may have played the pivotal role. However, in situations where athletes undergo chronic high-intensity training, the pivotal player may be the high-intensity exercise. Nevertheless, both are likely have an important part to play as previously discussed. The fat adapted healthy athlete is one who ticks both boxes, taking a holistic approach towards performance, health and longevity.

Having been involved in elite competitve triathlon from a very early age, the area of performance and individual improvement has always intrigued me. As I've grown and gone through various experiments on myself and in the lab, I've realised that much of what we've been taught is false.

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Runners’ Toenail Problems: Do Triathletes Even Need Nails?

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Quick summary: If you’ve spent a lot of time training for triathlons, you may have experienced problems like black, thickened, or ingrown toenails. You may have lost toenails now and then as well. These issues affect the big toe most of all. Some runners and triathletes avoid these problems by having them surgically removed. Is that a smart idea? Do you really need your toenails?

Causes of toenail problems for triathletes

  • Ingrown toenails are caused by repeated stress that drives the toenail into the soft flesh of the toe, combined with growth of either the toenail or the skin of the toe. This can cause a lot of pain and a few visits to the doctor.
  • Black toenails are caused by repeated contact between the toenail and the shoe. This causes bleeding, and it may turn the toenail black. The blood can cause the toenail to separate from the toe, opening you up to bacterial and fungal infections before another toenail grows in its place.
  • Permanent toenail thickening occurs when damage to the root, or “matrix”, of the nail causes it to become deformed. The nail will grow according to the new shape of the root. It will often grow thicker and look grey or yellow, like a fungal infection. This condition is permanent and can harm your triathlon performance.

What happens if you have your toenails surgically removed?

The flesh underneath your toenails is very sensitive. However, if you have your toenails removed, the flesh normally grows thicker, tougher, and far less sensitive. If you have cosmetic concerns, you can add nail polish to this area. People won’t be able to tell the difference unless they’re near you. The doctor will use either a laser or a chemical, and the procedure is painless.

On the other hand, there are some people whose toes won’t create that protective layer of skin. You could be one of them. The only way to find out is to have your nails removed.

The verdict: Whether you have toenails or not won’t affect your running ability. An ingrown toenail will until you have it treated. A permanently thickened nail will also affect your speed and endurance, and that’s not treatable.

Your two options are prevention and surgery. As a triathlete, you’re going to have cosmetic issues. That’s just a fact. If you’re not into the idea of surgical removal, there are some steps you can take to minimize damage to your toenails.

  • Wear the correct size shoes. A shoe that fits well will prevent all the microtrauma that can cause bleeding under the nails.
  • Keep the nails well trimmed. If they’re even a little bit too long, they can cause shoe-related trauma on the inclines and declines.
  • Use skin lubricant. This will prevent a lot of soreness, bruising, and other problems caused by accumulated trauma. This is a method Dr Christopher Seglar, a San Francisco sports medicine podiatrist and triathlete, uses on long runs of 30 kilometres or more. His toes are fine on shorter runs. However, if you train a lot, you may want to use skin lubricant for those, too.

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Women Are Naturally More Fit Than Men, Study Shows

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Quick oxygen uptake places less strain on the body’s cells and is considered an important measure of aerobic fitness.

“The findings are contrary to the popular assumption that men’s bodies are more naturally athletic,” said Thomas Beltrame, lead author on the study.

The study compared oxygen uptake and muscle oxygen extraction between 18 young men and women of similar age and weight during treadmill exercise. Women consistently outperformed men with around 30 percent faster oxygen handling throughout the body.

“We found that women’s muscles extract oxygen from the blood faster, which, scientifically speaking, indicates a superior aerobic system,” said Richard Hughson, a professor in the Faculty of Applied Health Sciences, and Schlegel Research Chair in Vascular Aging and Brain Health at Waterloo.

By processing oxygen faster, women are less likely to accumulate molecules linked with muscle fatigue, effort perception and poor athletic performance.

“While we don’t know why women have faster oxygen uptake, this study shakes up conventional wisdom,” said Beltrame. “It could change the way we approach assessment and athletic training down the road.”

Story Source:

Materials provided by University of Waterloo. Note: Content may be edited for style and length.


Journal Reference:

  1. Thomas Beltrame, Rodrigo Villar, Richard L. Hughson. Sex differences in the oxygen delivery, extraction, and uptake during moderate-walking exercise transition. Applied Physiology, Nutrition, and Metabolism, 2017; 42 (9): 994 DOI: 10.1139/apnm-2017-0097

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Should Triathletes Get Regular Heart Tests and Should You Care About Myocardial Fibrosis?

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Are triathletes at risk of myocardial fibrosis? New evidence has shown triathletes may be at increased risk of myocardial fibrosis (MF); a nasty condition where scarred or fibrotic tissue replaces heart muscle cells. A recent study out of Germany looked at 55 men and 30 women and found a clear link between MF and male triathletes.

While the study has limitations, it did make us wonder about how triathlon can adversely affect the heart.

Why you should care about myocardial fibrosis

‘Myocardial fibrosis (MF) is a common phenomenon in the late stages of diverse cardiac diseases and is a predictive factor for sudden cardiac death,’ says an article by Freek et al in 2016.

So in other words, MF can kill you. But how?

Myocardial fibrosis can cause arrhythmia; a sometimes fatal abnormal heartbeat pattern. Whether the arrhythmia has caused your heart to beat too fast, too slow, too irregularly or too early; if you suffer from arrhythmia, you’re in trouble.

How does this study say triathlon causes myocardial fibrosis?

During high intensity, endurance events, systolic blood pressure increases. This increase may result in a greater myocardial mass, which may put an athlete at a higher risk of myocarditis; inflammation of the heart muscle.

If the heart becomes inflamed due to exercise often enough, it is believed it can lead to the heart replacing muscle with fibrotic tissue that isnt as spongy, responsive or powerful as normal heart tissue known as myocardial fibrosis.

How did they prove myocardial fibrosis?

The study used a contrast and examined it under MRI. Evidence of myocardial fibrosis was apparent in the left ventricle — the heart’s main pumping chamber — in 10 of 55 of the men, or 18 percent, but in none of the women.

Why don’t the women have myocardial fibrosis?

“Comparison of the sport’s history showed that females had a tendency to complete shorter distances compared to male triathletes. This supports the concept that blood pressure and race distances could have an impact on the formation of myocardial fibrosis,” said study leader Dr Starekova.

Sorry Dr, but we all know this isn’t true for female Ironman competitors who compete and train over massive distances. This seems to point to the fact the scientists really don’t know why more men were at risk than women.

Has myocardial fibrosis caused death in endurance athletes before?

Yes. One study showed the results of a post-mortem cardiac exam performed on a marathon runner who died suddenly. It found his death was caused by enlargement of his left ventricle and myocardial fibrosis. In this case, it was a series of fatal arrhythmias or irregular heartbeats that caused the sudden death of the athlete.

“Life-long, repetitive bouts of arduous physical activity resulted in the fibrous replacement of the myocardium, causing a pathological substrate for the propagation of fatal arrhythmias,” was the official summary.

In other words? The marathon runner’s heart had become stiffer, which lead to an irregular heartbeat that caused death.

Another study looked at the hearts of 51 healthy male Ironman athletes to see if any changes occurred. They found:

  • Those who trained at higher volumes had larger left ventricles
  • Those with significantly larger left ventricles (chambers of the heart) also had greater blood pressure at an aerobic or anaerobic threshold.

They recommended these athletes (who experienced higher blood pressure) should undertake interventions to prevent stiffening of the heart or MF.

Does triathlon definitely cause myocardial fibrosis?

No. The study only looked at 85 subjects which is definitely not enough to make solid conclusions, especially considering contrasting evidence.

A number of studies have disputed the link between triathlon and MF. Leschik and Spelsberg said, “The idea of exercise-induced cardiac disease was suggested by Heidbüchel and LaGerche but the data are controversial.”

In some athletes, studies have found left ventricular hypertrophy and myocardial fibrosis which causes arrhythmia, but in many others, these abnormalities were absent.

Should you be worried about your heart?

Despite all studies concluding further research is needed, we do know a few things:

Key Messages

  • Triathlon can cause changes in your heart and CAN cause MF
  • Triathlon can lead to cardiac arrest in men > 60 years old
  • Risk probability in ambitious triathletes >35 years old is high, so cardiac testing may be important
  • Those most at risk of developing cardiac changes (men training at large volumes) should be identified early through testing
  • Triathletes experience significant peaks in blood pressure and changes to their left ventricles are recommended to undertake a prevention program
  • Ideal training dosages that prevent cardiac changes from occurring is not yet known, but there may be a tipping point of systolic blood pressure that leads to MF

While the new study out of Germany does have some compelling evidence, the study group was small, and there is no cause for alarm. The recommendations that young pros should be screened may be of value though and could be something handy to remember for coaches of young, keen athletes.

 

 

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How Exercise Enhances The Brain – Benefits For The Busy Triathlete

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We all know exercise is good for our health, but new science tells us exercise is great for our brains too. Scientists have proven exercise can improve memory and learning in animals, but a new study out of Canada proves humans can improve memory and brain activity thanks to high-intensity exercise.

Previous studies showed exercise promotes ‘Miracle Gro’ for the brain

Last year, scientists at New York University’s Langone Medical Center decided to look at the impact of exercise on the brains of mice. They placed healthy mice into two groups; group one had a running wheel in their cage, while group two had no wheel. After a month in the cages, the scientists looked at the differences between the mice’s brains.

The exercise group showed higher levels of B.D.N.F, which is a protein some scientists label as ‘Miracle-Gro’ for the brain. This snazzy protein helps neurones grow and strengthens synapses which are the ways nerve impulses signal to each other.

Exercise ‘switches on’ a healthy brain protein

B.D.N.F is produced by a gene that occurs in all mice but was largely concealed in sedentary mice.

For those chubby mice that sat around all day, there was a thick barrier of molecules that surrounded this gene preventing it from being switched on.

In contrast, in the sporty mice, the barrier was flimsy, allowing the gene to switch on, producing more B.D.N.F to promote brain health and improve learning and memory.

If you’re getting lost in the acronyms, don’t worry; the key takeaway is that exercising improves your brain’s function overall.

Those findings are fairly general though, so new scientists wanted to look at memory improvements in humans.

New evidence shows memory improvement thanks to exercise

A new study in the Journal of Cognitive Neuroscience looks at how high-intensity exercise effects the memories of a group of ninety-five college students.

Scientists divided the students into three groups:

  1. Exercise only
  2. Exercise and cognitive training (combined)
  3. No exercise or cognitive training (control)

The exercise comprised of 20 minutes of high-intensity interval training at the university’s physiology lab three-times per week. High intensity was chosen as it a very “strong physical stimulus” which was thought to create the most cardiovascular change in young people.

What is brain training?

If you’re wondering what cognitive training is, you’re not the only one. In this study, scientists used general mental training consisting of memorising similar faces, then matching correct faces as they appeared randomly on a computer screen.

Why faces? The memory required to recognise and memorise details on the human face is a very specific, yet important type of memory. It was just one type of memory that could have been measured in the study.

What did they find after 6 weeks?

  • Everyone who exercised enjoyed better fitness (obviously…)
  • Almost everyone who exercised performed better on the memory test, including quickly differentiating between similar objects despite this not being part of the brain training
  • Those who’s fitness improved the most, experienced greatest memory enhancements

Biggest improvements in fitness saw other improvements

  • Individuals who enjoyed the greatest fitness improvements from the training also had higher levels of neural growth factors.
  • Those who enjoyed the biggest increase in fitness also enjoyed improvements in high-interference memory performance.

“In effect, more fitness resulted in stronger memories,” says Jennifer Heisz, an assistant professor at McMaster University who led the study. “The brain training adds to that effect, even for a type of memory that was not part of the training,” Heiz told The New York Times.

No fitness improvements show little memory improvement

In contrast, those who had the smallest improvements in fitness also had only slight improvements in memory. Dr Heisz thinks this may be because the exercise may have been too intense for these individuals. “It’s possible that they would have developed a better response with different and perhaps more-moderate exercise,” Heisz says.

How you can have better memory

It’s simple; add some memory tasks to your workouts before and after getting sweaty. “I would suggest memorising the details of a painting or landscape” — or perhaps a loved one’s face — before or after each workout, Heisz says. “It could provide broader memory benefits all around.”

Benefits for the busy triathlete

If you’re a busy triathlete juggling home life, your social life, training and work; this study proves you can enjoy benefits across multiple areas in your life by combining your efforts. Add a bit of mental stimulation before and after a workout, and you’ll feed your brain. Both studies prove this will not only enhance memory but also strengthen your brain as a whole.

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Stop the Watts – Are You Missing the Point?

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A good friend of mine is obsessed with data. He would argue it’s a healthy obsession and suggests data is critical and closely linked to improved performance in sport. While I appreciate that quality data can assist, my cycling and past in triathlon exploits have been driven by a healthy understanding of self before data.

Having had the pleasure of training with legends of triathlon such as Jason Shortis, I learned and adopted methods based on gut feel and listening to the mind and body. Tools for measuring performance have certainly advanced quickly in recent years and I’m gradually converting to smart trainers and the world of Zwift.

The real data nuts out there will even argue that measure of fatigue, sleep and emotions etc can be tracked. It’s certainly has been interesting to observe the switch from ‘old school’ training methods towards scientifically backed training and racing methods.

But are we missing the bigger picture?

When did you last ride without a Garmin or cycling computer? Perhaps it’s your cycling friends that frantically upload images to socials in chase of likes? It seems we’re more concerned about how doughnuts look on Instagram rather than the conversation held with friends while eating the doughnut.

Whether you’re directly or indirectly involved in this behaviour, Adam Alter suggests we need to ‘demetricate’ during exercise. What does demetricate mean? No, it’s not getting rid of the metric system in this particular context. Demetricating (might be making up words now) is about getting back to the enjoyment of exercise and putting data or screens aside, even if it’s for a session or two each week.
A keen runner himself, Adam is an academic and author who predominantly focuses on judgment and decision-making and social psychology. He was first introduced to demetricating during exercise by a friend that places tape over his watch when running. The intent of this is to get back to the joys, feeling, and emotions of running… being in the moment.

The benefits of demetricating, or reducing screen time are overwhelming. During the past few weeks, my data-loving friend and I have partaken in a little experiment whereby we can’t use a phone, cycling computers or smart watches to measure our activity. We took it another level and installed free apps such as Moment and Quality Time to track and restrict phone usage.

The results were outstanding, yet not surprising. Improved relationships, better conversations, decreased anxiety and a greater sense of happiness just to name a few. The best bit of this trial? Since introducing some tech and screen time back into exercise, my watts have improved!

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Fat Could Make you Faster, Science Says

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We took a stab at debunking one myth – dehydration and exercise and performance. Time to take a swing at another. Fat burning at high exercise intensity.

To steal a phrase from our New Zealand colleagues, WTF? (What The Fat)!?

Our question: could fat burning be more critical for high-intensity performance than previously thought?

Background

Physiologists have long known that fat fuels us at rest and even for low to moderate exercise intensities. Beyond this point, however, we’ve been told that fat’s contribution diminishes towards negligible values as exercise approaches maximum levels – when we’re in the ‘red zone’.

The classic textbook shot here (below) for reference. This is what we teach and learn.

For high-intensity exercise performance, it makes sense that carbohydrate oxidation is essential. Put simply, we get a higher rate of ATP (energy) per unit of oxygen uptake per unit of time. More energy means better performance capacity.

The question: is fat oxidation at high exercise intensity really negligible? Does it actually turn off? Does it play a negligible role for athletes competing in short (<8min) high-intensity Olympic-type sports?

To answer, we need to get at more detail to understand the issues. As a starting point, I’ve shown Figure 1 from Jeukendrup & Wallace (2005), which takes various studies to show nicely the different factors (training status, exercise mode, gender and diet) that influence the relative degree of carb and fat oxidation with exercise intensity (x-axes).

The most important point that we usually take from these examples is that which is shown from the textbook example above; that calculated fat oxidation becomes negligible at high exercise intensities, reaching zero it seems once exercise intensity reaches values ranging from 75-90% of VO2max. Right at the spot where most athletes need to compete.

Is that really the case? Is it all about carbohydrates for high-intensity exercise, or is it possible that fat oxidation could also be important? How do we begin to get insight into the question?

If you want to follow what we’ve done in the forthcoming study, we need to dive into more detail.

Indirect Calorimetry Substrate Estimates

Substrate oxidation (carb and fat burning) is estimated using gas exchange measurements from a metabolic cart (right) and stoichiometric equation calculations. This technique, known as indirect calorimetry, is thought to be the gold standard technique for measuring this.

Let’s take a basic look at how it is calculated.

Inside the cells of the body needing energy, we know that the reactions converting the substrates carbohydrate (glucose) and fat (palmitate).
Glucose oxidisation:

 

 

Palmitate (fat) oxidisation:

 

 

We’ll skip a few details to get to the heart of the matter, but basically, because the oxidation of those substrates have different O2 and CO2 inputs and outputs, it winds up that the CO2 you exhale relative to the O2 you take in, gives us a ratio (VCO2/VO2) number from our metabolic cart data ranging from 0.70 to 1.00, termed the RQ (respiratory quotient), or RER (respiratory exchange ratio). When that ratio number reads 0.70, it tells us we are burning pure fat. When it reads 1.00, it tells us we are burning pure carbohydrate. So by using this method, we can estimate the relative quantities of carbohydrate and fat being oxidized at a given exercise intensity. That’s how the various graphs above shown by Jeukendrup & Wallace (2005) are being calculated.

Limitations

But this estimation has one important limitation related to the current topic. While it’s mentioned in the Jeukendrup & Wallace paper and others, I don’t believe this point has been well-discussed or researched to date. The point is this: When we exceed our threshold intensity (maximal lactate steady state), a shift in acid-base balance occurs. With increased required carb burning (anaerobic glycolysis), lactate accumulation in the contracting muscle moves into the blood and increases the acid content [H+] (likely related to that burn you feel with hard exercise), which is buffered predominantly by the main buffer in your blood, bicarbonate [HCO3-] (see schematic from Marieb, 2009). This excess (non-oxidative) CO2 is then added to the total VCO2, making our VCO2 amount larger than it would have been had the acid not been added to the mix when we crossed the threshold.

The regulation of this buffering system and its various players are shown.

 

How does the Acid Load Affect the RQ and Carb/Fat Determination with Exercise?

As you’ve probably gathered, the higher lactic acid-induced production of CO2 [through HCO3- buffering] has a large influence on the calculation of carbohydrate and fat oxidation. It creates an overestimation of the carb burning amount and an underestimation of the fat burning. The estimation of fat use with these equations goes so low in fact that it often becomes zero, and then negative. Of course, we can’t report a negative number, so scientists typically present their data up to the point where it becomes zero, and not beyond. See again those Jeukendrup & Wallace (2005) examples above.

Given these challenges, the contribution of fat metabolism to energy demand during high-intensity exercise is less studied.

Our Study

What did we do? Or more accurately, what did our Norwegian colleagues that ran the study do? The details are for all to read in our recently published open access BMJ article. This research group, Ken Hetlelid, Eva Herold, and Stephen Seiler, took nine well-trained male runners with big engines (VO2max 71 ± 5 ml/kg/min) and compared their substrate oxidation responses during interval training with nine recreationally trained runners (VO2max 55 ± 5 ml/kg/min).

Methods

The recreational runners were active in a variety of sports, performing endurance-type training 2-4 times per week, while the well-trained running group included regional level distance runners and national level orienteers training 6 to 10 sessions per week. All runners were using typical western diets (relatively high carb).

Both groups of runners performed a high-intensity interval training (HIT) session, and indirect calorimetry, as described, along with heart rate, blood lactate and rating of perceived exertion (RPE) were measured. The HIT session, performed on a treadmill up a 5% gradient, was self-paced and consisted of six, 4-min work bouts separated by 2-min recovery periods.

Results

Both groups of runners performed the HIT session at the same level of RPE and blood lactate level. That means generally that the effort felt the same for both groups. The self-paced HIT session was, of course, run faster for the well-trained guys (15 vs. 11 km/h roughly), and that difference in running speed (figure right) was explained by higher absolute and relative oxygen uptake levels (figure below), and calculated energy expenditure. You’d expect that.

 

But if we dig a bit deeper, let’s uncover WHY it was faster, and WHY the well-trained guys were able to get at more energy. Check out the data below.

 

Here’s why…

It wasn’t the carbohydrate oxidation. That was identical in both groups (unclear; right), just like its end product (lactate) was.

It was the fat…

The fat oxidation, at those high exercise intensities, was nearly 3 times greater in the well-trained runners compared to the recreationally trained (right and above figures). It wasn’t zero, or negligible, as we are often told, but in fact accounted for 33% of the total energy expenditure in the well-trained guys over the sequence of high-intensity intervals.

Not only was fat oxidation 3 times greater – Fat oxidation at high intensity looks like it was the key discriminating factor explaining performance in the interval set between the two groups. It was the main why. Something happened with training it seemed to allow more fat oxidation at high exercise intensities.

 

 

The new findings didn’t end there…

Fat oxidation didn’t just explain HIT performance. It also explained VO2max – that gold standard marker of fitness and performance we often hear about. When we lined up all the subjects in the study and compared their VO2max with their average carbohydrate and fat oxidation rates during the HIT session, it was the average fat oxidation rate during the HIT session that very highly explained VO2max. Carbohydrate rate, though unclear, actually trended the opposite direction.

Considerations

Our study brings forth a number of points we need to consider.

  1. Typical less trained response. First observation. Check out the fat oxidation line for both groups of runners as they progress through their interval session. Notice how the less trained group has the typical response we see reported (typical volunteer subject group doing university degrees). Notice their negative fat oxidation values, especially during the recovery phases, as bicarb buffers the sugar-burning acid release. But certainly a different response for our better fat burning well-trained guys.
  2. Underestimation, not an overestimation of fat oxidation. Recall the bicarb issue previously mentioned. That blood buffer creates its bias towards the overestimation of carbohydrate oxidation and the underestimation of fat oxidation. So fat oxidation at the muscle level is likely higher than what we report here. You can’t say our study is not valid because of the bicarb issue – it biases our estimates in favour of carbs, not fat.
  3. Self-paced HIT session vs. completely all out. It’s important to appreciate that we have a self-paced intermittent high-intensity exercise situation, and not a near all-out 2K rowing race that might be performed at an even higher exercise intensity. So our situation gives us more potential for greater fat utilization. Both groups performed their prescribed intervals just above the second ventilatory turn point (VT2) identified during preliminary testing. But this is a high intensity right around the range that many scientific spokespersons (usually supported by an industry we all love) are claiming no benefit of fat oxidation.

But no benefit? Negligible?

To us, it doesn’t make much sense that fat oxidation would become zero at high exercise intensities. I remember giving first-year lectures in my days and we often started with a video called “All systems go”. Its not the most exciting piece of work, but can be seen here.

 

The gist of the video was that all energy systems contribute to ATP production all the time. In this example, we were talking the ATP-PC system, anaerobic glycolysis, and the aerobic system. Not on and off like a light switch, but all on in different proportions, at different times. Likewise, isn’t it logical to think that the lipolytic (fat) system would still be functioning in the background to contribute to ATP provision during high-intensity exercise as needed? Our study, albeit just one, suggests this may be the key factor that changes with training status.

Why does our Study Matter?

Interpretation of science to date has been that carbohydrate oxidation dominates and is the only substrate of importance for high-intensity exercise. Practice in nutrition logically follows. As an example, we recently attended the ECSS Congress and watched a Gatorade-spokesperson tell us that fat metabolism at high exercise intensity is not discussed, because “it doesn’t play a role during high-intensity exercise”. Let’s hope our study is the beginning of further work in this area.

To summarise, the new findings from our study are

  1. Well-trained and recreationally trained athletes performed a HIT session with similar levels of RPE, blood lactate, and carbohydrate oxidation.
  2. Well-trained runners oxidized nearly three times more fat than recreationally trained athletes during their HIT session.
  3. Fitness (i.e., VO2max) and the capacity to perform high-intensity intermittent work was mostly explained by the higher fat oxidation rates at high-intensity.

In our next post, we’ll talk about why it makes sense that fat oxidative capacity at high exercise intensity should be a key high-intensity performance factor.

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