A new blog post has been a long time coming (we’ve been busy!; me doing some training, work and the addition of a little girl and Prof writing a book), and with Ironman NZ behind us for another year, it’s given me the chance to write something I’ve been wanting to express for some time.
I love a bit of social media interaction. Whilst I’m not the most vocal, I do enjoy keeping an eye on the latest hot topics in the world of endurance sports and Ironman Triathlon. Over the past few months or so, “polarized training” has become a real buzz word in the triathlon training world. Particularly Ironman. But is this really the best way to train when considering an event like Ironman? Here is a spin on it from Plews and Prof.
Training intensity distribution and polarised training
When we refer to training intensity distribution (TID), we are talking about how much of the time we spend in low, moderate and high training intensity zones.
Figure 1 shows a great illustration of the zones we’re talking about from the father on the topic for us, Professor Stephen Seiler, which I’ll use throughout this essay. Have a read of his 2009 paper if you want to really geek out. In a nutshell, there are generally two main models of TID that have dominated the literature. These are namely the polarised (1) and the threshold (2) models of training. The polarised model was first described within the training performed by the East German system from 1970-80, whereby a high volume of low-intensity training appeared balanced against regular application of high-intensity training bouts (~90% to >100% VO2max). This was partially confirmed in 2004 by Fiskerstrand & Seiler (1), who showed a “polarized” pattern of training also when they explained the training and performance characteristics of 28 international Norwegian rowers developing across the years 1970-2001. This polarised model is said to be described as performing about 75-80% of your training at a low intensity (<2 mM blood lactate), 5% at threshold intensity (~4 mM blood lactate), and 15-20% at high intensity (>4 mM blood lactate) (3). This training organization contrasts the classic threshold model (~57% low intensity, 43% threshold, 0% high-intensity (4)) of endurance training, whereby large volumes of mid-zone threshold work is thought to be optimal (2). This former study on world class international rowers provided evidence to support the importance of the polarized training model for endurance athletes striving to be the best in the world, and subsequently has been largely adopted by athletes across many endurance sports. (5,6)
Iron distances races: Racing in the black hole
What’s very interesting about the polarized training method as it relates to Ironman, is that most of the research has been carried out in sports where race pace intensity is above the second (“anaerobic”) threshold. Sports like rowing 7 for example, (where much of the TID research has been done), is closer to VO2max intensity. To illustrate, Figure 2 shows an example of the typical intensity breakdown over a 2 km rowing race (split into the three-zone model), where the majority of time spent during the 6-8 min race is above the heart rate associated with the anaerobic threshold. Even in a cycling road race there would be substantial amounts of time spent in the low intensity bandwidth (below the first aerobic threshold, whilst sat in the peloton), alongside shorter times spent above the second threshold (closing gaps, making breaks etc.).
Comparatively, the intensity distribution of Ironman racing is vastly different, with most of the time being spent in the moderate intensity bandwidth. Figure 3 shows my HR distribution during the Taupo 70.3 event in December 2017. From this, its clear that most of the ~4h race duration is spent at a moderate exercise intensity. To take this a step further, we can look at my race for Ironman New Zealand 2017, where there is even more time spent in the moderate intensity heart rate bandwidth (Figure 4).
When looking at Figures 3 and 4, keep in mind that the moderate intensity training bandwidth is quite large (145-160 b.min-1 cycling and 150-165 b.min-1 running). The Ironman distance mostly happens in the low end of this bracket (average and max HR for bike and run respectively = 145/157 and 151/163 b.min-1) while the 70.3 distance occurs near the top (154/161 and 164/176 b.min-1)
Pyramidal Model of Training Intensity Distribution
More recently, a number of retrospective studies have put forth another model of TID for cycling, (8) running, (9) and triathlon, (10) termed the “pyramidal” model. Here, most training is still carried out at low intensity, however there are decreasing proportions of threshold and high-intensity training performed. This is a model less discussed that many might not be familiar with. Indeed, we often assume that an athlete who is not polarized in their TID must be in the “threshold” model by default. However, published research has revealed this middle-ground model that we need to appreciate.
Exact defining percentage breakdowns of the Pyramidal model have yet to be clearly established, however this general implies ~25-30% and 5-10% of TID at moderate and high intensity training levels, respectively, with the balance being low intensity training (50-70%). (3) As such, within the pyramidal model of TID, we expect to see less training time at a low and high training intensity, and more time at moderate training intensity. From a specificity standpoint, this middle ground training is much closer to the demands of ironman racing (Figures 3 and 4). Thus, when race day approaches, and training sessions become more “specific” and closer to race intensity, it stands to reason that perhaps the Pyramidal model may particularly suit long course triathletes.
Figure 5, shows my TID during one week in the month of January 2018 (competition phase) before the New Zealand National Middle-Distance Champs. As we can see, my TID certainly fell in line with the Pyramidal model.
Take home points
For Ironman distance racing, or any sport preparation for that matter, we have to consider the principle of specificity. For Ironman, as we are still working in an aerobic event, building aerobic endurance is of key importance. Thus, however you’re skinning it in your Ironman training, a fundamental principle needs to be an aerobic foundation. Ideally, we should be working within a range of TID, that span across the polarized (80/20) and pyramidal (60/40) models, depending on the phase of the training cycle. For example, early season training might look more polarized, while pyramidal may appear to form, as we get closer to racing.
One final point, it that we must also acknowledge the role of athlete health (11) and the stress that training places on the autonomic nervous system (12,13) when substantial amounts of training time are performed above VT1. Thus, future research may want to consider describing the optimal durations of pyramidal and polarized training phases in the diets of Ironman athletes.
1. Fiskerstrand A, Seiler KS. Training and performance characteristics among Norwegian international rowers 1970-2001. Scand J Med Sci Sports 2004;14:303-10.
2. Seiler S. What is best practice for training intensity and duration distribution in endurance athletes? Int J Sports Physiol Perform 2010;5:276-91.
3. Stoggl TL, Sperlich B. The training intensity distribution among well-trained and elite endurance athletes. Front Physiol 2015;6:295.
4. Neal CM, Hunter AM, Brennan L, et al. Six weeks of a polarized training-intensity distribution leads to greater physiological and performance adaptations than a threshold model in trained cyclists. J Appl Physiol (1985) 2013;114:461-71.
5. Laursen PB. Training for intense exercise performance: high-intensity or high-volume training? Scand J Med Sci Sports 2010;20 1-10.
6. Seiler KS, Kjerland GO. Quantifying training intensity distribution in elite endurance athletes: is there evidence for an “optimal” distribution? Scand J Med Sci Sports 2006;16:49-56.
7. Plews D, Laursen PB. Training intensity distribution over a four-year cycle in Olympic champion rowers: different roads lead to Rio. International Journal of Sports Physiology and Performance 2017;In Press.
8. Lucia A, Hoyos J, Pardo J, Chicharro JL. Metabolic and neuromuscular adaptations to endurance training in professional cyclists: a longitudinal study. Jpn J Physiol 2000;50:381-8.
9. Esteve-Lanao J, San Juan AF, Earnest CP, Foster C, Lucia A. How do endurance runners actually train? Relationship with competition performance. Med Sci Sports Exerc 2005;37:496-504.
10. Neal CM, Hunter AM, Galloway SD. A 6-month analysis of training-intensity distribution and physiological adaptation in Ironman triathletes. J Sports Sci 2011;29:1515-23.
11. Maffetone PB, Laursen PB. Athletes: Fit but Unhealthy? Sports Med Open 2015;2:24.
12. Plews DJ, Laursen PB, Kilding AE, Buchheit M. Heart-rate variability and training-intensity distribution in elite rowers. Int J Sports Physiol Perform 2014;9:1026-32.
13. Seiler S, Haugen O, Kuffel E. Autonomic recovery after exercise in trained athletes: intensity and duration effects. Med Sci Sports Exerc 2007;39:1366-73
Runners’ Toenail Problems: Do Triathletes Even Need Nails?
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.
Women Are Naturally More Fit Than Men, Study Shows
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.”
Materials provided by University of Waterloo. Note: Content may be edited for style and length.
- 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
Should Triathletes Get Regular Heart Tests and Should You Care About Myocardial Fibrosis?
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 isn’t 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:
- 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.
How Exercise Enhances The Brain – Benefits For The Busy Triathlete
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:
- Exercise only
- Exercise and cognitive training (combined)
- 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.
Stop the Watts – Are You Missing the Point?
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!
Fat Could Make you Faster, Science Says
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?
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).
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.
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.
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.
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).
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.
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.
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.
Our study brings forth a number of points we need to consider.
- 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.
- 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.
- 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
- Well-trained and recreationally trained athletes performed a HIT session with similar levels of RPE, blood lactate, and carbohydrate oxidation.
- Well-trained runners oxidized nearly three times more fat than recreationally trained athletes during their HIT session.
- 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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