Dr Delanghe, Waterloo Chiropractor

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keto 1

Welcome to part 2 of the my exploration of very low carb diets for endurance athletes.  My last article provided the basis for understanding this article as it explored how and when our body choses to use fat vs. carbs.  Check it out here.

In this article, I will now explore (1) do low carb diets actually enhance fat metabolism and (2) does that actually makes us faster.

Does VLCD increase fat burning capacity?

Short answer, yes, the body is forced to increase fat use to support the energy needs during exercise. Research clearly shows that after adapting to a keto diet for as little as 3 weeks results in significantly elevated rates of fat oxidation (0.6g/min to 1.5g/min) during exercise. Fat oxidation at moderate intensities (65% VO2max) in elite ultra-endurance athletes on a keto diet contributed 88% of the fuel for exercise verses 56% in athletes consuming high carbohydrate diets. Now, if we remember what we discussed in the last article, we learned that as we increase intensity we increase the amount of carbohydrates burned. This begs the question “will those high fat oxidation rates continue at intense ecercise (80% VO2max)?”. Another study investigated the fuel usage of elite race walkers at 80% VO2max, and they too found that fat oxidation was elevated to the same levels as previous research (1.5g/min).

low carb

Research Outcomes of VLCD and Performance:

The more important question in my mind (and likely yours as well) is “well that is fine and dandy- my body will burn more fat, but what will happen to my performance?!”. We will review some key research studies that have looked at fat adaption diets (high fat diets for 3-7days), keto diets and their effect on performance. The majority of high fat diet adaptation and keto diets find that performance decreased and a handful found they had no-statistically significant effect. Only two articles find a performance benefit.

Keto, Training and Performance

Louise Burke et al. (2017) conducted a large study investigating the effects of a keto diet, chronically high carbohydrate diet or periodised carbohydrate diet on race performance of elite race walkers after a 3 week intervention and training camp. Athletes on the keto diet perceived the training to be significantly more difficult and experienced an inability to complete the exercise training sessions planned. This is a very important point because if an athlete cannot train as hard as they could they won’t see much improvement in their sport.

After the 3 weeks of intense training, the keto group had higher fat oxidation compared to the two high carbohydrate groups. All groups had significant increases in their maximal oxygen uptake (VO2max) as a result of the training. As we discussed in the previous article, burning fat is less efficient and this study clearly demonstrated that at all competition race speeds there was significantly more oxygen used in the keto group and there was no change in the fraction of VO2max at various speeds. The high carbohydrate and periodised carbohydrate groups used less oxygen and were able to keep the same pace at lower fraction of VO2max. In plain English, the two carbohydrate groups improved their running economy and efficiency with the training where the keto group did not reap the benefits of the training because the cost of burning fat is so high.

Lastly, this study compared pre and post training performance walk times in a real 10km race. They found that both carbohydrate groups had a reduction in their time by 5-6% (on average 190s and 124s faster for high carbohydrate and periodised carbohydrate group). There was no improvement in the keto group and on average their times were 23s slower. There was a wide variability in performance for the keto group, ranging from 162s faster to 208s slower, meaning that keto worked for some individuals but not others.

High Fat Diet With Carbohydrate Loading

What if we don’t go into ketosis and we use a fat adaptation strategy + carbohydrate load, best of both worlds right? Havemann et al. (2006) showed that when elite cyclists consumed a high fat diet (68%) for 6 days with 1 day of carbohydrate loading that there was no significant difference in time to complete a 100km simulated bike race compared to a traditional high carbohydrate diet. However, if we look at the time to completion, we find that the high carbohydrate trial was completed on average 3 minutes 44 seconds faster (likely significant in the real world), leading us to believe that on average high carbohydrate diet may be superior to high fat diets. Again, 3 out of 8 racers on the high fat diet did improve their time compared to high carbohydrate diet, demonstrating that there may be some athletes who may respond well to a high fat diet.

More importantly, this research included 1km sprints throughout the ride to simulate a race like situation and found that the power output was significantly lower in the high fat diet group which lead to slower sprint times. Despite having lower power output in the high fat trial, they perceived they were working as hard as they were in the high carbohydrate trial. There was no difference in muscle recruitment during the sprints, meaning the high fat trial worked just as hard as the carbohydrate trial but did not achieve the same results in the sprint performance. The researchers thought that the high fat diet + a carbohydrate loading period would result in glycogen sparing due to increased reliance on fat for fuel, thus improving sprint times as sprinting relies on glucose to provide fuel. This was not the case and it is possible that high fat/fat adaptation diets reduce the ability to effectively burn carbohydrates.

Summary

  • VLCD do result in higher rates of fat oxidation during exercise
  • VLCD may reduce response to training
  • VLCD decreases economy in elite athletes
  • VLCD decreases ability to work at maximal effort which is important when there is change in work intensity- ie running up a hill, breaking away from the pack
  • Most studies show that on average VLCD negatively affect performance in endurance athletes, however there are some that may respond well
  • Remember that VLCD are not the same as training fasted or temporarily low carb diets to train your body to use fat more effectively, as this is an effective training method

In my final article in this series, I will explore the roll of supplements, the keto diet, and how that relates to athletic performance.

References:

Volek JS, Noakes T, Phinney SD. Rethinking fat as a fuel for endurance exercise. Eur J Sport Sci. 2015;15(1):13- 20.

Volek JS, Freidenreich DJ, Saenz C, Kunces LJ, Creighton BC, Bartley JM, Davitt PM, Munoz CX, Anderson JM, Maresh CM, Lee EC, Schuenke MD, Aerni G, Kraemer WJ, Phinney SD. Metabolic Characteristics of keto-adapted ultra –endurance runners. Metabolism. 2016;65(3):100-10.

Burke LM, Ross ML, Garvican-Lewis LA, Welvaert M, Heikura IA, Forbes SG, Mirtschin JG, Cato LE, Strobel N, Sharma AP, Hawley JA. Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers. J. Physiol. 2017;595(9):2785-2807.

Havemann L, West SJ, Goedecke JH, Macdonald IA, Gobson ASC, Noakes TD, Lambert EV. Fat adaptation followed by carbohydrate loading compromises high intensity sprint performance. J. Appl. Physiol. 2006;100: 194-202.

Leckey JJ, Ross ML, Quod M, Hawley JA, Burke LM. Ketone diester ingestion impairs time-trial performance in professional cyclists. Front. Physiol. 2017;8(806).

53650544 - foods high in carbohydrate on rustic wooden background. top view

There has been a burst of social media hype around the idea of using very low carbohydrate (ketogenic or keto) diets for endurance events. The keto diet usually consists of 5-10% of total kcal (~50g or less) from carbohydrates per day, 75% from fat and 10-20% from protein, although there is no set standard of carbohydrate level. In this article I want to talk about how the body uses energy during exercise before we get into the research.

If we look at the stores of energy in the body, we know that our ability to store carbohydrates as glycogen is limited. We can store carbohydrates in our muscles and liver and the more trained an individual is the more they can store, however it is still limited and can only supply about 1500-2000kcal and muscle glycogen is depleted within 1hour of intense exercise. Fat on the other hand is very calorically dense and we can store 65 000 kcals (could fuel about 20 marathons!) in our adipose (fat) tissue and within the muscle. Fat can supply significantly more energy than carbohydrates without supplementation. This diet is seen as attractive because it promotes the idea that we can max out our capacity to burn fat as a fuel while running, reducing the amount of food or energy we need to take on the run. Therefore, it seems logical to adopt a keto diet, max out our ability to burn fat as a fuel, right? Well let’s look at this topic a little deeper.

low carb

 

Understanding Energy Production During Activity

Our body uses two processed to produce energy in the form of adenoside triphosphate (ATP). The first method is anaerobic (without oxygen) and the second is aerobic (with oxygen). There are 3 energy systems that the body uses depending on a few factors, such as intensity, length of event, and availability of oxygen.

(1) Phosphocreatine System

This system is the quickest way to produce energy and is the first system to turn on to crank out ATP. Let’s say as you are reading this article your fire alarm stated to ring, you would immediately jump up and run out the door. In this fight or flight response you are using mostly the phosphocreatine system. It works by taking the phosphocreatine that is stored in the muscles, and through an enzymatic reaction the phosphate is split off and added to adenosine diphosphate to make ATP. This is a very simple reaction, and the body can use this system for about 8-10 seconds before it’s tapped out. This system can recover; it takes about 4 minutes before the system is ready for another intense bout.

(2) Anaerobic glycolysis

This is the second system to turn on to support energy production. To continue with out analogy from above, after our initial jumping and sprinting for the door, after the 8ish seconds our body tends to rely more heavily on the anaerobic glycolysis system. This system uses carbohydrates (glucose) and through a series of steps breaks down 1 glucose molecule into 2 pyruvate molecules. Without oxygen, this pyruvate can be further broken down into lactate and a hydrogen ion and ATP. This system will last about 1-2 minutes. In repeated sprints, such as hockey shifts, research shows that subsequent sprints rely on anaerobic glycolysis to provide 50% of the energy.

(3) Oxidative phosphorylation (Aerobic system)

This system takes a while to get warmed up and to get going once you start exercising. In untrained individuals, it can take a few minutes for this engine to get running fully, but in elite athletes it can fully turn on within about 30-60seconds. In our analogy above, lets say we lived in the country and we needed to go run to the fire station down the road, after our initial sprint and quick getaway, our aerobic system turns on and produces a majority of the energy needed. This system can last forever; at rest we are aerobically oxidizing mostly fats to provide energy for the body at rest.

The aerobic system can burn carbohydrates, fat and protein depending on availability and intensity. Protein used in very small amounts to provide energy for exercise and we wont discuss it further here. I want to discuss the differences between fat and carbohydrate oxidation.

The classic study from Romijn et al. showed that the fuel sources changed depending on the intensity of exercise. They looked at 25% VO2Max, 65% VO2Max and 85% VO2Max. The found that as intensity increased, so did caloric expenditure and the more intense exercise relied more heavily on carbohydrate use. This is because at higher intensity of exercise the fat breakdown and transport into the mitochondria and oxidation rates are too slow to keep up with the energy demands.

pic

Carbohydrate is also the preferred fuel during intense activity as it provides 5.5% more kcal/L of oxygen compared to fat oxidation, meaning it is a more efficient fuel source. Research shows that elite level marathoners fuel use is 85% carbohydrate and 15% fat oxidation.

One thing to note is, you do not only use one system at a time, your aerobic system is always running in the back ground. Think of these systems like dimmer switches, they can be turned up or turned down depending on the situation. For example, if we take a cyclist who is riding on a flat surface, they have their aerobic system pumping out most of the ATP to cover the cost of their cycling. When they hit a hill, there is an increased demand for ATP. The aerobic system take a little while to adjust, and therefore the anaerobic system has to kick in to provide some quick energy, and that means the phosphocreatine system turns on, and the anaerobic glycolytic system turns on to meet the ATP needs of the body.

Key points:

  • Fat is slower to provide energy, and therefore intensity is lower when using fat as a fuel source
  • Fat is less efficient; it uses more oxygen to produce less ATP
  • High burst of exercise- ie the energy change when cycling or running up a hill is usually covered by anaerobic glycolysis which uses glucose (carbohydrate)
  • Most elite athletes run at high %VO2 and burn a large amount of carbohydrates

References:

Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, Wolfe RR. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol. 1993;265:E380-E391.

O’Brien MJ, Viguie CA, Mazzeo RS, et al. Carbohydrate dependence during marathon running. Med Sci Sports Exerc. 1993;25:1009–1017. doi: 10.1249/00005768-199309000-00007

Bosch, AN, Goslin BR, Noakes TD, Dennis SC. Physiological differences between black and white runners during a treadmill marathon. Eur J Appl Physiol. 1990;61:68-72.

training and performance

The days of my protein rambling have almost come to an end! In my last post, I discussed how much protein should be ingested/day and how that protein should be distributed. The article before that discussed whether acute protein consumption before and activity enhances performance.iron sources

In my final article in the protein series, I want to discuss acute protein ingestion related to an acute bout of exercise. This is something that I get asked about all the time at the club: is it important to quickly ingest protein directly after a given activity to enhance recovery from that bout of training?

CLICK HERE to read the rest in the RW Magazine.

VitD

Vit D

By: Stephanie Boville MSc., RD

As the snow and cold weather rolls in, it is often accompanied by the common cold or worse, the flu. Endurance athletes are more at risk of illness, specifically upper respiratory tract infections (URTI) because they often engage in intense training sessions outdoors that often last over an hour and athletes who are overtrained are even more at risk. Studies show that runners training for 96km/week doubled their odds of illness compared to those training only 32km/week and about 40% of marathoners experience an URTI in the 2 months of winter training leading up to a marathon race.

Along with the vigorous training, other factors such as stress, lack of sleep and inadequate nutrition can lead to immune suppression, increasing risk of illness. Being a Registered Dietitian, I would like to explain how vitamin D may help boost your immune function this winter season.

Immune function in athletes:

There are a few reasons why URTI’s are common, although this is not a complete list of all the immunological changes that occur with heavy exercise, it will provide background as to why illness is specific to the upper respiratory system.

  1. Cortisol, a stress hormone, is increased which temporarily suppress the immune system.
  2. Specific biomarkers of inflammation increase and have been linked to immune suppression.
  3. Natural Killer cell (cells that kill viruses) activity is reduced for at least 6 hours by 40-60% following exercise lasting over an hour.
  4. Nasal neutrophil phagocytosis (cells responsible for searching for and destroying bacteria) is decreased
  5. Nasal and salivary Immunoglobuin A (IgA) (antibodies secreted in the saliva which are responsible for protecting the immunity of the respiratory tract) concentration is decreased by 70% for 18h after a 31km race.
  6. Nasal mucociliary transit time is prolonged post marathon race for several days, meaning the movement of foreign particles and bacteria out of the upper respiratory tract and away from the lungs is less efficient.

All of these aspects combined demonstrate that there is possibly a window of increased risk of contracting an URTI after exercise because the immune system is compromised. The last three points demonstrate a few possible reasons to why the upper respiratory tract is so vulnerable, especially because the nose and throat are the first line of defense against pathogens entering the body.

Nutrition and Immunity:

The first point I want to make is that overall adequate nutrition plays a role in maintaining a healthy immune system. If we look at the IOC paper discussing the consequences athletes face when they are in a relative energy deficient state (inadequate overall energy intake), we see that one of the many systems affected is immunity. Therefore, you might want to think again before you try and “shred those Christmas and New Year’s gains” in mid flu season unless absolutely necessary. We need to understand that good dietary basics are necessary to support a healthy immune system before we start to get more specific with our micronutrients.

Vitamin D and Immunity:

There are three studies I want to discuss:

Study 1:

Study 1 was an observational study investigating the effects of vitamin D status on the incidence and immune function during winter training in 239 endurance athletes. They found that being vitamin D deficient resulted in significantly more symptom days and increased symptom severity of URTI when compared to optimal, adequate and inadequate vitamin D levels. They also investigated saliva samples which showed that salivary IgA concentration was significantly reduced in athletes with deficient levels of vitamin D, and that athletes with adequate, inadequate and deficient levels of vitamin D had reduced salivary IgA secretion rates compared to optimal levels. From the information in the paragraphs about we see that one area in common, the salivary IgA. Both exercise and reduced levels of vitamin D results in decreased salivary IgA concentration and secretion rates which suggests that having an optimal levels of vitamin D has an important role to play in maintaining immunity in athletes. Lastly this study found that the antimicrobial peptides in the blood were positively correlated with vitamin D status suggesting that optimal vitamin D may result in better immune function and protection.

One limitations of this study is that it was an observational study and therefore no clear links can be determined whether an intervention with vitamin D supplement in vitamin D deficient athletes will reduce frequency, length and severity of illness. Rather this study concludes that there is an association between reduced vitamin D status and increased illness length and severity along with reductions in immunological markers.

Study 2:

Study 2 investigated the effect of a 2000IU vitamin D supplement on length and severity of URTI in non-athletic adults. They supplemented participants for 12 weeks with Vitamin D or placebo and found no differences in URTI incident or severity. However, there are a few things to consider. First, we know athletes have a higher risk of URTI’s, and therefore the results may not be generalizable to an athletic population. Second, even though there was a significant increase in Vitamin D levels with supplementation it was not enough to get participants to an “optimal” level as set out by study 1 and vitamin D levels may not have been sufficient enough to show changes in immunity. Third, both groups had adequate baseline levels of vitamin D and it could be possible immune function is only compromised at inadequate or deficient levels of vitamin D. Fourth they did not do any salivary or plasma samples and therefore we can not see the immunological changes.

Study 3:

Study 3 investigated the effects of 14 weeks of 5000IU vitamin D3 supplements in 39 athletes on antimicrobial peptides and proteins. They found that the 5000IU dose for 14 weeks was enough to elevate blood levels of vitamin D to optimal levels and that 14 weeks of winter training without supplementation decreased vitamin D levels. 5000 IU of vitamin D per day resulted in significantly higher percent change in antimicrobial peptide concentration compared to placebo and increased the salivary IgA and antimicrobial peptide secretion rates. Therefore, their conclusion was that optimal vitamin D may help up-regulate the systems needed to protect against URTI.

Some limitations of this study include participants started at adequate levels of vitamin D and therefore the changes might underestimate the importance of vitamin D’s effect on immunity and bigger changes might be seen when vitamin D levels start at an inadequate/deficient level. Another limitation to this study is they did not record incidents of URTI and therefore no conclusion could be made as to whether the immunological changes resulted in decreased illness.

Main points:

Research has clearly demonstrated that vitamin D is of critical importance in the bodies immune system however there is more to learn about how vitamin D levels impact the frequency of illness and severity, and at what level is the immune system compromised.

From the studies above we learn that:

  1. Optimal levels of vitamin D increase antibacterial peptides in the blood
  2. Optimal levels increase salivary IgA secretion rates and concentration
  3. Observational studies show that illness severity and length is decreased compared to lower levels of vitamin D.

Because salivary IgA is suppressed after intense exercise and taking vitamin D increases the IgA secretion rate and concentration, this may be one mechanism that optimal vitamin D is used in to protect against upper respiratory tract infections.

Practical application:

Should we be supplementing? Usually my belief is “food first, supplement second”. With that being said, there are few foods that contain high levels of vitamin D. We can make vitamin D from the sun, however we are too far north for adequate sun exposure to make vitamin D this time of year (fall through spring). Even in the summer we may make inadequate amounts of vitamin D from the sun if we wear sunscreen, have dark skin or train inside or early/later in the evening. It is likely a good idea to supplement to make sure you are getting adequate amounts of vitamin D. Not only does it play a role in immunity, but it also helps maintain bone and muscle health, and therefore it is an important nutrient.

How much vitamin D: Health Canada has set the Adequate Intake (AI) level of vitamin D at 600 International Units (IU)/day and the upper limit at 4000 IU/day for most ages with some exceptions. First AI means that there is not sufficient evidence to set a Recommended Dietary Allowance (set to meet the needs of 97-98% of healthy individuals) but the AI is assumed to be adequate. There is debate about the AI for vitamin D as many think this AI is set too low, and people are also supplementing over the upper limit (like in study 3 from above). In the following years this AI could see and increase.

Food Sources: People often think milk is the best source of vitamin D, however 1 cup of milk only provides around 100IU or 1/6 of your daily needs of vitamin D. One of the best sources is actually salmon, which, depending on the kind can provide anywhere between 200-600IU in one 2.5oz serving (the size of a deck of cards).

Supplements: Depending on diet and your current vitamin D status, supplementing with 1000-2000IU is should be enough to give your vitamin D levels a boost and is recommended, especially in the winter.

There are many other tactics athletes can try to maintain and help with increased immune function. If you would like to learn more, book an appointment so we can optimize your nutrition intake to support your health, wellbeing and athletic performance!

Related Article: Does Vitamin C help to prevent the common cold?  Check out Dr. Delanghe’s past article.

Reference:

Nieman, D.C. Exercise effects on systemic immunity. Immunology and Cell Biology. 2000. 78: 496-501.

Gleeson, M. Immunological aspects of sport nutrition. Immunology and Cell Biology. 2016. 94: 117-123.

He, C.S., Handzlik, M., Fraser, W.D., Muhamad, A., Preston, H., Richardson, A., Gleeson, M. Influence of vitamin D status on respiratory infection incidence and immune function during 4 months of winter training in endurance sport athletes. Exerc Immunol Rev. 2013. 19: 86–101.

Li-Ng M., Aloia, J.F., Pollack, S., Cunha B.A., Mikhail, M., Yeh, J., & Berbari N. A randomized controlled trial of Vitamin D3 Supplementation for the prevention of symptomatic upper respiratory tract infections. Epidemiol. Infect. 2009. 137: 1396-1404.

He, C.S., Fraser, W.D., Tang, J., Brown, K., Renwich, S., Rudland-Thomas, J., Teah, J., Tanqueray E., & Gleeson. M. The effects of 14 weeks of vitamin D3 supplementation on antimicrobial peptides and proteins in athletes. Journal of Sports Sciences. 2016. 34: 67-74.

Version 3

We are extremely excited to welcome the newest member of the Delanghe Chiropractic and Health team: Stephanie Boville MSc, RD.

From weight loss and managing osteoarthritis, all the way to sports nutrition, Stephanie will be here to help you conquer any and all of your dietary concerns and goals!  With 6 years of post secondary education, and a strong science/evidence- based approach, only advice based on the BEST available research will be implemented.

No cleanses, magic powders or fad diets and no guessing.

How many grams of carbohydrates will you need to optimize your marathon performance?  Are you getting in enough protein to maintain muscle and enhance performance?  Are you taking in the right foods to decrease the pain and inflammation associated with arthritis?  Stephanie can help you!

What it takes to be an RD:

The process of becoming a registered dietitian is unlike any other designation for those offering advice on diet.  RDs are highly educated and trusted professionals for a reason!

The first step in becoming a dietitian is to complete a 4 year undergraduate degree from an accredited university program.  Once the future dietitian has completed their undergraduate degree, they must apply to an accredited internship program or masters program, which can be very competitive and must be accepted within 3 years of graduating from their undergraduate degree. The internship or masters program require the future dietitian to complete various competencies and log hours working under a certified dietitians. Rotations include public or community health settings, food service, diabetes, inpatient units and outpatient units within the hospital. If that isn’t enough, the dietitian is then required to write a 6 hour regulatory exam to demonstrate their knowledge and competence of being employed as a dietitian before they receive certification. Once the dietitian receives their certification, they are required to submit yearly self directed learning tools to prove to the college that they are committed to continuing their education and improving their skills in their nutrition practice. They are also subjected to randomly being selected for peer and practice assessment where the dietitian is evaluated by both patients and co-workers to assess their work performance and competency. If anything unusual is revealed in these assessments there could be further investigation by the college into the dietitian and action if they are found to be incompetent.  Because of this long road to become a RD, it’s clear why they can be the professionals trusted with your dietary health!

To learn more about Stephanie and her hours, click HERE.

Too book an appointment, call (519)885-4930.

acu

What is Acupuncture?

Modern acupuncture is defined as a therapeutic technique in which sharp, thin needles are inserted into specific points on the body. Mechanical, electrical or physical stimulation is sometimes added to the needle to increase the effect. Needles are inserted into acupuncture points, aka: acupoints which were first established in traditional Chinese medicine.

Classical vs. Anatomical Acupuncture: What’s the difference?

Classical acupuncture is based on Tradition Chinese Medicine (TCM). Ancient Chinese believed that everything in the universe was energy. The philosophy that emerged from this thinking is called Taoism which translates to the energy of the universe. The energy is also referred to as Qi (chi).

Qi consists of two equal and opposing energies, Yin and Yang and is commonly represented by the picture above. The curved line represents movement and dynamic fluid between the 2 energies. They are mutually supportive and interdependent.

It was believed that Qi flows through the body along energy channels (referred to as meridians) and could flow into specific sites aka: acupoints. If Qi was deficient, blocked, or out of balance, symptoms such as pain would appear. Needling these sites relieved the symptoms by unblocking and restoring flow of Qi and re-establishing energy balance in the body.

Anatomical acupuncture was originated by Dr. Joseph Wong in the mid 1970s and bridges the gap between TCM and Western medicine. The acupoints are chosen based on anatomy and physiology.

The main difference between classical and anatomical acupuncture is the paradigm used in the selection of points.

The Points

Early studies show most acupoints are located on or near peripheral nerves. There is no evidence to support the existence of new or special structures under these acupoints, however, histological studies (ie: looking under a microscope) have shown a higher concentration of neural tissue and neuroactive components at acupoints compared to non-acupoints.

Neural tissues are the actual tissues themselves and include nerve endings and sensory receptors. Neuraoactive components are cells that release chemical mediators that can excite or inhibit signals to the brain.

The Neural Acupuncture Unit (NAU)

The NAU is a collection of the neural and neuroactive components surrounding the needle. In the diagram, the NAU is the area within the dotted lines. These tissues would be stimulated by the needle.

What Happens When the Needle is Inserted?

Local Effects

When a needle is inserted, it causes some damage to the issue near the insertion point, which stimulates a chain of biochemical reactions in your body. As a result, your body produces various inflammatory and immune response in the NAU. Basically, it is a micro-injury which does negligible harm to the body while creating a therapeutic response.acu2

Non-local Effects

Without getting too in-depth, the non-local effects involve altering pain signals through receptors in the spinal cord and how they relay messages to the brain. The nerve signals from the local tissue travel to the spinal cord and through complex mechanisms, block the original pain signals from getting to the brain.

Another area of the brain is also involved. The hypothalamus-pituitary complex (don’t have to remember this name!) is also stimulated when a needle is inserted and releases anti-inflammatory chemicals into the bloodstream that can help to reduce pain.

These local and systemic responses help to explain the pain-relieving effects of acupuncture.

In my next article, we’ll look at the effects that acupuncture can have for different injuries!

REFERENCES:

Wang, Kain, White. Acupuncture analgesia: I. The scientific basis. Pain Medicine. 2008

Zhang, Wang, McAlonan. Neural acupuncture unit: A new concept for interpreting effects and mechanisms of acupuncture. Evidence-Based Complementary and Alternative Medicine. 2012

training and performance

Welcome back to another protein-focused edition of Training & Performance! My last article looked at the evidence in support of avoiding protein while you run. Today, I will discuss one of the more common questions I hear at my practice: does protein timing and distribution matter? And should you be consuming protein directly after a workout?

iron sources

Muscle/Protein Physiology

Our muscles are in a constant state of breakdown and renewal. For the average person (depending on factors such as age and level of activity), muscles are broken down and rebuilt at a rate of 1-2%/ day. To help support this renewal, the building blocks of muscle (amino acids) need to be taken in on a regular basis.

While the amino acids we ingest provide the raw material to support that 1-2% renewal rate, that is not all they do. The act of ingesting amino acids also triggers a physiological cascade that signals more muscle growth. So, when the body is being fed amino acids, not only does it have the material for muscle growth, but an anabolic muscle-building state is also put into action!

So it’s no surprise that ingesting protein is important to muscle growth. Now the question is, how much and how frequently do we need to ingest protein to optimize both of these benefits and maximize our gains?

Click HERE to read the rest in the Run Waterloo Magazine.

training and performance

I have written many times(1234)  about the importance of ingesting carbohydrates during a race (if it’s long enough).

I’ve also discussed how taking in other sources of fuel, like protein, is not the best move due to it triggering an increased risk of GI distress. The reason: in part, protein is not absorbed and metabolized as quickly as carbohydrates. Delayed gastric emptying results in water diffusing into your guts and increasing the odds of needing to take a PB-killing washroom break! iron sources

One thing I have heard in response to this tip from patients and athletes at H+P is that IF one is able to handle protein from a GI standpoint, is it worth experimenting with on top of carbohydrates as a fuel source? Is there an additional benefit to taking in protein during a race if it doesn’t bother your stomach? That is what we’ll be looking at with this article.

CLICK HERE to read the rest in the RunWaterloo magazine!

TFL

What is it?!

Overuse injury associated with pain on the outside (lateral) part of the knee

Anatomy

The ITB is a band or sheath of fibrous connective tissue that surrounds the muscles on the outside of the thigh and crosses both the hip and knee joint. It originates from the tensor fascia latae (TFL) and gluteus maximus muscles and then continues down the femur (thigh bone) where it attaches to both the femur and tibia (shin bone) on several bony landmarks.

The function of the IT band is to stabilize the hip and knee as well as limit hip adduction (leg moving towards the midline) and internal rotation of the knee.

Epidemiology and Risk Factors

The knee is the most commonly injured area in runners – accounting for 25-42% of all running injuries. ITBs is the second most common knee injury for runners with patellofemoral pain syndrome being first.

ITBSigns/Symptoms

Runners usually have no exact history of trauma and find that the pain comes on gradually over the outside of the knee during a run. The pain usually appears within a few km of a run and increases in intensity. That same area can also be tender to touch.

Pathophysiology/Etiology

There are a couple theories on the pathophysiology of ITBs.

Some researchers believe that ITB inflammation is a result of excessive friction between the ITB and the boney prominences which occur when the ITB slides over the boney structure and causing inflammation during repetitive movements such as running. Others have argued that rather than the ITB band causing excessive friction, the inflammation is caused by the ITB compressing an area of highly innervated fatty tissue between the IT band and boney prominence

Contributing Factors to Developing ITB Syndrome

The most common factor in developing ITBs is an increase in exercise intensity through mileage, hill training or speed work.

Other reported possible causes which may increase tension in the ITB by altering hip and knee angles include:

  • Downhill running
  • Wearing old shoes
  • Always running on same side of road
  • Leg length discrepancies
  • Excessive pronation of the foot (foot rolling inward)
  • Tight ITB
  • Weakness of glute medius muscle

ITBs and Running Biomechanics

It has been suggested that injuries can manifest as a result of an increase in exercise intensity beyond a threshold level, combined with certain intrinsic factors in athletes.

A recent systematic review looked at biomechanical variables and investigated whether distance runners who suffer from or develop ITBs have different biomechanics than runners who do not develop ITBs.

The evidence shows that it is unlikely that abnormal biomechanics at the foot or shin bone can contribute to increasing tension of the ITB.

The results suggest more is happening at the hip and knee. Runners who eventually develop ITBs have more internal rotation at the knee and greater glut medhip adduction angles during the stance phase of running (when the foot is in contact with the ground) compared to healthy controls.

Some researchers have found that this internal rotation of the knee is due more to an externally rotated femur (thigh bone rotated outside) and suggests this may be due to insufficient activity in the medial rotators of the hip (gluteus medius, gluteus minimus, TFL).

As for muscle strength and endurance, there is currently no evidence to suggest that reduced muscle strength plays a role in ITBs. However, the research is limited because many of the trials give inaccurate impressions of a muscle’s functional strength. Future research is needed to look at the timing of muscle action rather than the magnitude of strength.

Research also suggests that runners with current ITBs tend to have more trunk flexion than healthy controls. It is uncertain whether the increased trunk flexion is due to a tight ITB or if the ITB becomes tight as a consequence of the flexed trunk (aka: the torso leaning forward)

How do we treat it!?

Stay tuned to my next article on the latest evidence for treating and managing ITBs!

References:

Foch et la. Associations b/n IT band injury status and running biomechanics in women. Gait & Posture. 2014.

Louw & Deary. The biomechanical variables involved in the aetiology of iliotibial band syndrome in distance runners – a SR. Physical Therapy in Sport. 2014

iron sources

When it comes to performance, there’s no doubt that nutrition plays a significant role. In the past, I’ve really focused on acute nutrition: what you can do directly before or during your run to be faster (i.e. here).

training and performance

An area I have neglected to focus on is what you should be doing from a nutritional standpoint on an on-going basis to stay healthy and perform at your best. One key area that I see as a recurring problem in my practice and athletes around me is iron deficiency anemia.

Iron has a number of roles in the human body. The most important function is how it is incorporated into hemoglobin and myglobin to facilitate oxygen transportation. If these proteins decline, our ability to transport oxygen to our working muscles also drops, and performance plummets along with it (such as here and here).

CLICK HERE to read more in the RW Magazine

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