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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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Polarised to Pyramidal Training Intensity Distribution: The Principle of Specificity is Key

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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: Training zone demarcation using the classic three zone model.

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.).

Figure 2: The typical heart rate intensity distribution of a 2 km rowing race. 24% at low intensity (it takes time for HR to rise), 34% at a moderate intensity (still rising) and 42% at a high intensity.

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).

Figure 3: Time in Zone 70.3 Taupo bike (top: 2 hr 14 min) and run (bottom: 1 hr 18 min). Bike includes 2% low intensity, 72% moderate intensity and 26% high intensity. Comparatively, running includes 0% at low intensity, 54% at moderate intensity and 46% at high intensity.

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)

Figure 4: Time in Zone for full ironman (2017 Ironman NZ) bike (top: 4 hr 58 min) and run (bottom: 2 hr 55 min). Bike includes 25% at low intensity, 74% at moderate intensity and 0.2% at high intensity. Comparatively, running includes 4% at low intensity and 96% at moderate intensity and 0% at high intensity.

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: 1 week of training (7 January until 13 January). 64% <LT1, 25% LT1-LT2 and 11% >LT2

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.

 

References

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

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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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