Fascia May Contribute to Delayed Onset Muscle Soreness

Unpleasant muscle soreness often arises after performing exercises that are new, that have not been performed in a long time, or that include a large volume of eccentric contraction (muscle contracting/shortening against its lengthening, as when you lower yourself down from the top of a pull-up). In many cases, the pain from these exercises does not appear immediately, but surfaces a day or two later, giving rise to the term Delayed Onset Muscle Soreness (DOMS). Once DOMS has set in, pain occurs whenever the affected muscle is moved, stretched or pressed. A variety of prior studies have looked at DOMS and damage to the muscle fibers was a fairly consistent observation. However, the specific areas within the muscle that were found to be damaged and the presence of inflammation has not been consistent among studies. Therefore, many researchers believe we are missing part of the picture. In a recent study by Lau et al. (2015), findings suggest that DOMS may result more from fascia damage than muscle damage.

The Takehome: Delayed onset muscle soreness is generally attributed to muscle damage, but fascia, connective tissue that separates, encloses and supports muscle, might also be important. This study could not immediately look at muscle and fascia’s contribution to delayed onset muscle soreness (DOMS), though. The authors first had to find an external (non-invasive) readout for DOMS that could be linked to a more precise readout which targets a specific tissue type. They found that pressure pain threshold (pain from pressing on the affected muscle) correlated with electrical pain threshold (EPT) read via a needle inserted into specific tissues. Therefore EPT was used to see which tissue (muscle or fascia) was more sensitive to pain after eccentric exercise that resulted in DOMS. The authors observed that changes in pain from pressing the muscle correlated with changes in electrical pain thresholds in the fascia, but not in the muscle itself. In addition, as time progressed after exercise, fascia tended to be more sensitive to this electrical stimulation (maintaining a lower pain threshold) than the muscle. The study is a pairing of associations and correlations, but the authors present a lot of data to support the relevance of their model and don’t over-interpret their results. Their findings suggest that fascia is a greater contributor to pain from DOMS that muscle, but fascia and muscle are intricately linked, so more research is needed to see if the two are truly independent.
Experimental Design:

  • 10 Men (ages 22-28) with no resistance training of upper arm for the past 6 months.
  • 2 exercise bouts (separated by 4 weeks) were performed.
  • Exercise was 10 sets of 6 isokinetic (constant speed) eccentric elbow flexor contractions on a dynanometer.
  • Elbows were forcibly extended from 60 degrees by the machine while subjects tried to maximally resist the extension.
  • Indirect markers of muscle damage were voluntary isometric contraction torque (MVC), range of motion of the elbow joint (ROM), muscle soreness assessed by visual analogue scale (VAS), pressure pain threshold (PPT), and electrical pain threshold (EPT). Markers were assessed before, after, and 1-5 days after exercise.
  • Tissues examined were: biceps brachii fascia (BBF), biceps brachii muscle (BBM), and brachialis fascia (BF).


  • Muscle damage markers were, as expected for repeated bouts of eccentric exercise, less prominent after the 2nd bout of eccentric exercise than after the 1st (e.g., VAS increased after both bouts and PPT and decreased after both bouts, but the magnitudes were smaller for the second bouts as compared to the first).
  • A comparison of BBF, BBM, and BF indicated that after the initial bout of exercise, electrical pain threshold decreased (pain tolerance worsened) more in the fascia (BBF, BF) than in the muscle (BBM).
  • There was a significant correlation between electrical pain threshold (EPT) and physical pain threshold (PPT) of both the BBF and BF 1 and 2 days after the first exercise bout. This correlation was not present for the muscle itself.


  • Women were not included in the study, so sex-differences cannot be accounted for.
  • Life-history of arm training (particularly eccentric work) was not accounted for in the study and might yield different results if training history were different (extensive training vs no training).
  • Of all the markers for damage/pain, only EPT can be measured separately on fascia or muscle. All other markers are a readout of fascia and muscle combined.
  • Cause and effect cannot be conclusively established in this type of study as there was no way to separately damage the muscle and fascia.

Science for Fitness is a Top Fitness Blog of 2015

It’s always great to get some outside recognition. Science for Fitness made it onto two Top Fitness Blogs of 2015. One is by Wealthy Gorilla and the other is by the Institute for the Psychology of Eating. Click on the images below to see the full lists:

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Find Your Basal Metabolic Rate – Count Your Calories

In addition to questions about training and general health, I receive a lot of questions about nutrition. It’s a complicated topic because everyone is at a different place with respect to what they are eating, what they can eat (i.e., food intolerances), and how they need to eat in order to achieve their goals. As with anything, the more work one puts into their nutrition, the more they can get out of it. Depending on where you are at, adjusting when you eat and what you eat can go a long way. But over time this might not be enough. And if you goals change, your nutrition will likely have to change as well. These types of changes are hard to make if you have no idea how much you have been eating and no idea how much of that food was carbohydrates, fats and protein.

For many, there comes a time when the total amount of food (as represented by calories) and the ratio of the “macros” (the carbohydrates, fats, and proteins) in their food becomes important. It can manifest with those who are just starting out for the first time and aren’t seeing the expected “beginner gains” from training and eating well. It can also be for those more advanced who want to optimize their training or because they are trying to dial in their body composition. Let’s take an example from my own training.

I’m one of those tall, thin types (ectomorph) who tend to have a naturally high metabolism (I burn through food at a very high rate even when not training). I also seem to have genetics that makes it very hard for me to gain fat even if I stop training. While this is great for staying lean, it makes it very hard to gain muscle mass through training. Because my body is wired this way, I need to eat a LOT when I am trying to bulk up in a strength cycle, and the easy approach is to just eat and eat – basically everything in sight. In this way, I make sure I’m getting enough calories (energy) to fuel muscle growth. I estimated how much food this was at one point and it was generally over 4000 calories. Beyond this I didn’t need to do much counting. Eating everything in sight worked well. I went from 180lbs to 200lbs (my body fat went form about 6% to 10%).

After my most recent strength cycle, I went back to CrossFit and added in some bodybuilding accessory work for my upper body (which is much weaker than my lower body). The goal was to get a little bigger, but largely drop my fat percentage back down – I typically carry around 6% when I’m not doing strength. So, what I did is switch my eating back to 3 meals a day (largely Paleo) and have 1-2 snacks interspersed. It worked. I got a little bigger and my fat percentage dropped. However, CrossFit is very quantitative. It’s about measuring and tracking your performance and what I noticed is that I wasn’t performing well in many of the workouts. I was getting drained very quickly, often in the warm-ups. In one session I stopped and had a protein shake, whereupon I felt 100% better. It was then I realized I wasn’t eating optimally.

I decided to sit down and calculate how many calories I was taking in at each meal, along with how many carbohydrates, fats and proteins were in each meal. On a typical day I was taking in around 2100 calories. As a reduction from 4000 calories (in my strength cycle), this was a huge drop. In addition, most of the calories were coming from protein and fat; there were relatively few carbohydrates. This is all seemed a bit off, but how is one to know for sure? It’s a fairly complicated question and the answer depends on what your specific goals are, but a great staring point is to calculate your basal metabolic rate (BMR) and then estimate the number of calories you need based on that. The process starts with the Harris-Benedict equation. The original version (from the old studies in the 1900s) is as follows:

Harris Benedict

There have been a number of revisions to the equation over the years. A popular one is as follows:

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I use a slightly different version than this one, but its similar enough. There are also a lot of online BMR calculators that will do all the work for you. Once you calculate your BMR from one of these equations/online calculators, you can estimate calorie needs by multiplying your BMR by a number that estimates your activity level:

Calorie Intake

And there you have a rough estimation of the total calories you should be taking in each day in order to *maintain* your body weight. For me, I should have been taking in 3400 calories to maintain. To drop fat I could have reduced the calories a bit from there and I would have dropped my fat percentage back down gradually. At 2500 calories per day I was dropping fat very fast, but at the expense of having very little energy. It took tremendous effort to train during each session. Part of the problem was not having enough food in general, but another problem was the ratios of my macros were off. I wasn’t consuming enough carbohydrates to help me get through my training. What these different ratios should be is beyond the scope of this article, but it’s important to keep in mind that after assessing calorie intake, the balance of your macros is the next factor to consider.

The Takehome: Although not everyone needs to count their calories and find their BMR, if you aren’t achieving your goals, or if you’ve been training for a while and have never counted your calories, it’s a worthwhile endeavor. At least do it once. See roughly where you should be at and then figure out how much, on average you are eating. If you are serious about your health and training goals, more calculations might be needed such as the balance of macros and the timing of those macros (meals) relative to training. If you would like to arrange one of these more detailed assessments, or if you have general questions, I am happy to help – just drop me a line.


The Origins of “Don’t Squat Below Parallel!”

Today many are accustomed to performing squats below parallel during their training, but there are still those who remember the old days when it was very common for both trainers and doctors to say that squatting below parallel is dangerous for your knees. Recently, I was asked by several of my clients to explain how this notion came about. I wanted to get as much detail as I could, so I did some digging. It turns out that the credit for the notion that squatting below parallel is dangerous goes to Dr. Klein from the University of Texas. The study at the heart of it all is his 1961 paper in the J. Assoc. Phys. Ment. Rehabil. entitled “The Deep Squat Exercise Utilized in Weight Training For Athletics and Its Effects on the Ligaments of the Knee.”

The Takehome: As usual, the study details are listed below. If you have read this section in any of my other article reviews, you will notice some striking differences. The main difference is that I had a very hard time figuring out what was measured in the study. The methods used aren’t explained. Not being able to understand or recreate the technique(s) used for measurement is a massive problem. Publishing such a study today would be impossible. There are numerous other problems including statistics being unclear and data being tossed in the Conclusions section of the article. As if all this weren’t reason enough to dismiss the article outright (it certainly is), in the closing portion of the article the author admits his techniques for measurement are subjective and says that one needs to just trust him. That, my friends, is not science.


Experimental Design:

  • The study is concerned with squatting during weight training (squats where a weight is lifted up and down).
  • Initially 64 human cadaver knee ligaments (medial, lateral, anterior cruciate (ACL), and posterior cruciate (PCL) were examined in different positions (standing, partial squat, deep squat). Cadaver measurements were made for ligament lengths before and after being pushed into a deep squat.
  • 128 live humans were examined including competitive Weightlifters at the Pan-American Games (all had practiced deep squats) and compared to 386 “Control” humans who were from beginning Weightlifting classes, basketball classes, and gymnastics classes (none had performed any deep squat exercises with weights).
  • The standard orthopedic tests were used to determine ligament status (?…stability??).
  • Data from 95 paratroopers are placed in the conclusions section. Measurements were conducted as for the other groups and paratroopers were compared to the same Control group.


  • The author states that, by looking at all the cadaveric group data, the medial and lateral ligaments are exposed to an abnormal stretch effect in a deep squat.
  • For the Weightlifter/Control Group comparison, the lateral ligament was exposed to a greater stretch than the medial ligament in the deep squat group.
  • In addition, 19.4 % more right lateral ligaments were unstable than right medial ligaments and 12 % more left lateral ligaments unstable than left lateral ligaments.
  • Deep squatters (Weightlifters) had 56% greater medial ligament instability in the right leg and 58% more in the left leg, as compared to Controls.
  • Data from paratroopers showed no differences in ligaments when comparing their right and left legs, but overall their ligaments were weaker than those of the Control Group.


  • The review of literature in the beginning discusses how the knee bones and ligaments behave in weighted squats, but this is not referenced – it doesn’t point to any actual studies.
  • After measuring the “stretch” (difference in length for the ligaments above parallel and deep squat), the author states that, by looking at all the group data, the medial and lateral ligaments are exposed to an abnormal stretch effect in a deep squat. There is no justification for what a normal stretch would be.
  • The Control group isn’t a proper Control group. It is mixed with individuals of different ages, sports backgrounds, and training histories. Further, the deep squatting group is a collection of competitive Weightlifters who are invariably pushing their bodies to extremes in a variety of ways to win medals. This population is not indicative of individuals that would squat for health and fitness.
  • The Chi-Square test is used to determine if groups are different, but in this case the participants in the Weightlifter and Control groups are so different on so many levels that we cannot say these differences are due solely to deep squats.
  • The p-values to indicate statistical significance are unclear as worded. Typically [p] being above 0.1 and 0.5 (as indicated in the study) would indicate no statistical difference for the Weightlifter/Control comparisons.
  • The author indicates standard orthopedic tests to indicate ligament status, but the reader has no idea what those tests are and is left to guess that the status is stability. But how is this stability defined/judged? Bill Starr (author of The Strongest Shall Survive: Strength Training for Football) dug deeper into this on his own and found that the test involved pressing into the ligaments (often paining the participants). There was no procedure to insure equal amounts of pressing among participants, nor any work to indicate that this pressing was a good measure of stability.
  • The x-rays indicating abnormal external rotation are very difficult to read.
  • A major problem lies in the author’s perspective on science. He writes” Realizing the testing procedures used in the study were subjective tests, one has to accept the fact that an experienced tester [the author] is capable of demonstrating the evidence of stability or instability of ligaments with relative ease.” This equates to saying, the testing methods I used are subjective, so you will just have to trust me – I’m a professional. The author then goes on to say, “…one should also discount the factor of causal relationship as a chance relationship because of the medical writings related to the problem of ligament stability and instability as based on the specific movement in question.” This equates to him saying, you have to take the relationship I found as causal and not just random chance because others have written about this issue and have raised these concerns/theories. Neither of these viewpoints is scientifically sound.

How I Program for CrossFit

-1I wrote an in-depth article for the CrossFit Solace blog covering CrossFit programming, with specific emphasis on how I create programming for CrossFit classes in the context of the other classes we offer at Solace (e.g., Gymnastics, Strength, Weightlifting, Mobility, etc.). You can read the full article HERE.


Joining the Hylete Train Team

I have added a “Gear” section to my Product Recommendations Page and the first addition is the clothing company Hylete. Hylete was founded on three principles: 1) Train to push yourself both physically and mentally, 2) Compete so as to improve yourself, as well as those around you and 3) Live to be healthy in mind, body, and soul. I couldn’t agree more. Even better is that they make great products. It took me a while to find a company whose clothing line I felt comfortable training in, but better late than never. I am also happy to report that I am officially part of the Hylete Train Team which means I am part of a group of trainers/coaches who promote the company and encourage others to train with Hylete. This gets my followers some perks – just click on any Hylete link on my site, create a free account, and use promo code (TRT90UF1W) to get 20% off your next purchase.


Book Review – Lean Habits


I was sent a free copy of the book Lean Habits by Georgie Fear. Georgie is a registered dietician and professional nutrition coach who co-founded www.onebyonenutrition.com. Georgie has a lot of experience working with clients, helping them achieve their weight loss goals and this book is a road-map to undertaking the challenge yourself.

Who The Book Is For: This book is targeted towards individuals that want to eat healthier and/or lose weight, but are struggling with the processes necessary for those changes. Very often people are eating the wrong foods, eating the wrong quantity of foods, unable to control the timing of their foods, unable to deal with food cravings, unable to separate emotional attachment to foods, and so on. For these people, just telling them where they need to be isn’t enough – they need a progression to get them there.

What The Book Gives You: This book gives you 16 habits that will improve your nutrition and enable you to reduce your body fat if you are overweight. Some habits include, minimizing liquid calories, eating the right amount of fat, shaping your social and physical environment, getting enough sleep. Each habit is presented with an explanation of why it is important (incorporating scientific studies where appropriate), as well as one or more progressions to help make that habit become truly second nature.

Where the Book Excels: This book excels in targeting a specific group of individuals. For those that are very far from a healthy lifestyle, specific, gradual changes are needed. Taking the wrong steps, or going too fast can set them back. This book explains how to improve your eating habits step-by-step, recognizing that the time process may be different for everyone. This book also excels in explaining the science of why things do or do not work. It’s done in a way that is accessible to the average reader, but references are given for those science-minded individuals like myself. Not nearly enough books on exercise and nutrition cite the studies they reference, so I was very pleased with how this was handled.

Areas for Improvement: There is very little I would improve about this book. This is largely because the audience is very clear. The book isn’t targeted to everyone trying to lose weight, so the focus is dialed in. One improvement I would have made is to put numerical references after each study that was cited in the text so it could easily be found in the references section at the end. Also, as the book progresses, a number of studies are mentioned, but authors and journals are not given (only the science), so one has to scan the reference list in the back (which is alphabetical by author) and figure out which study it was based on solely from the description of the science given in the text.

My Final Recommendation: This is a book I plan to keep in my personal library, so if you are someone who has been struggling with the proper behavior for healthy eating habits/weight loss, or if you train such individuals, I would definitely recommend this book.


Paleo Challenge Seminar at CrossFit Solace

Last Thursday I kicked off the CrossFit Solace 2015 “Prelude to Summer” Paleo Challenge with a mini talk on the Paleo diet. It was about 30 minutes and I briefly went over the history of the Paleo diet along with why certain items are excluded (diary, grains, legumes, sugar). Where possible, I presented the science that addressed these aspects of exclusion. In the future, I plan to put together a full, more comprehensive talk on the diet. In the meantime, you can check out a clip from my talk by watching the instagram video below:

Coach/Dr. Hayden @scienceforfitness laying down the paleo law… @crossfitsolace #paleo #crossfit #diet #fitness

A video posted by Chad McDonald (@chadjmcdonald) on


Artificial Sweeteners Can Promote Glucose Intolerance

The movement away from sugar and towards non-caloric artificial sweeteners (NAS), began over a century ago after recognizing that 1) large amounts of calories could lead to obesity and likely a variety of other health problems, and 2) that large amounts of sugar adversely affected hormone levels (in particular insulin), which could also lead to obesity and a variety of other health problems. Thus, consumers looked to NAS as a way to continue to eat sweet foods and beverages while protecting their health. However, research is beginning to indicate that NAS may not be as harmless as we had hoped.

I posted previously about an interesting study in rats, which examined examined the effects of NAS in diet. The results were fascinating as many of the problems we know to arise from over-consumption of sugar, were also found after consuming the artificial sweetener. If you haven’t read my review, it’s worth a read. Recently, another study was published on NAS, this time by Suez and coworkers. Suez et al., 2014 was conducted in both mice and humans.

The Takehome: Glucose intolerance (high levels of blood sugar), often a precursor to Type 2 Diabetes, has been linked to cardiovascular disease, muscle loss, and a variety of other health problems. In this study, the authors found that the commercial non-caloric artificial sweeteners (NAS) saccharine, sucralose, and aspartame all caused mice to develop glucose intolerance. Further examination of saccharine alone (which had the greatest effect of the three), revealed that this intolerance was associated with a change in gut microbiota (bacteria) populations. Fecal matter with these altered microbiota could be transplanted into healthy mice and cause them to become glucose intolerant. In humans, increased consumption of foods with NAS was correlated (a questionnaire-based study) with impaired glucose tolerance and also an alteration of gut microbiota. Finally, ingesting NAS-continaing foods for 1 week was enough time to show reduced glucose tolerance in some, though not all, humans. In these affected humans, microbiota populations were, as expected, altered, though differently than in mice. Nevertheless, when this fecal material from humans was transplanted into healthy mice, the mice developed glucose intolerance. The results of this study indicate that artificial sweeteners don’t give us a free pass to eat without consequence. Although artificial sweeteners do not raise insulin, there appears to be another route by which they can disrupt blood glucose levels, and that is through modification of the bacterial populations that live in our digestive tract. The bacteria in our digestive tract don’t only affect the processing of sugars and artificial sweeteners as highlighted in this study. In fact, they play many other roles in maintaining our health, so it’s quite possible that consumption of artificial sweeteners may negatively impact our health in even more ways than we have yet to realize.

The Experiment:

  • 10-week (young adult) C57/BL6 mice were given one of three NAS in their drinking water: commercial saccharin, sucralose, or aspartame. Control mice were given either water or water with glucose or sucrose. Note: commercial NAS typically contain large amounts of glucose (~95%) and only small amounts of the artificial sweetener (~5%). The investigators matches these ratios.
  • Fecal mibcrobiota composition was assessed in mice through rRNA gene sequencing.
  • Fecal matter was removed from mice and cultured in tissue culture dishes to examine direct effects of NAS on microbiota growth.
  • The effect of NAS in humans (381 non-diabetic males and females, mean age of 43 years old) was assessed through a food frequency questionnaire.
  • 7 humans (5 males, 2 females) who do not normally consume NAS were given NAS-containing foods (at the FDA’s maximal acceptable daily intake levels) for 1 week, after which glucose intolerance and gut microbiota were assessed.

The Results:

  • After 11 weeks, the three groups that drank commercial NAS all had marked glucose intolerance (higher than normal blood sugar levels).
  • The greatest intolerance was found in mice who consumed commercial saccharine.
  • In mice who were on a high-fat diet (to simulate obesity), glucose intolerance from commercial saccharine ingestion was greater than from glucose ingestion.
  • As with commercial saccharine, a lower dose (FDA acceptable daily intake adjusted to mouse) of pure saccharine, also resulted in glucose intolerance in mice on a high fat diet.
  • Fasting serum insulin levels and insulin tolerance were similar in all mouse groups, regardless of diet.
  • Mice drinking saccharine had a fecal microbiota profile different from their starting profiles and from the profile of all control groups (including a group that drank glucose). Profile differences were present even in mice that were on a high fat diet.
  • Gene pathway analysis indicated that the microbiota profile in saccharine-fed mice had gene profiles for enhanced sugar breakdown/fermentation activity. These profiles were previously associated with obesity in mice and humans; overabundance of Bacteroides and under-abundance of Clostridiales.
  • Fecal matter isolated from mice and treated with pure saccharine yielded similar shifts in the microbiota profile and transplanting this altered fecal material into normal mice resulted in their developing glucose intolerance.
  • In humans, NAS consumption was significantly correlated with higher fasting blood glucose, glycosylated hemoglobin (indicates higher than normal levels of blood glucose), and higher glucose intolerance (as measured by a glucose tolerance test).
  • In humans, NAS consumption was significantly correlated with differences in microbiota profiles.
  • In 7 humans given NAS-containing food for 1 week, all developed a poorer glucose tolerance as compared to before they started consuming NAS-containing foods.
  • Fecal material from humans who consumed NAS-containing food for 1 week and developed impaired glucose tolerance was transplanted into healthy mice and resulted in these mice developing glucose intolerance.

The Limitations:

  • Although very often a good model for humans, mice are not humans, so differences may exist where the initial mouse data is concerned. However, the pairing of human data with mouse data in this study makes this much less of a limitation.
  • After seeing the greatest glucose intolerance effect from saccharine, the authors do not further examine effects/mechanisms in mice using sucralose or aspartame. We therefore do not know if the different sweeteners behave any differently beyond impairing glucose tolerance.
  • Insulin levels appear to be unaffected by NAS (as expected), so the exact mechanism of intolerance remains somewhat unclear. We know gut microbiota are involved, but not exactly how.
  • Food questionnaires are noted for being inaccurate as participant reporting is often inaccurate despite the participants’ best efforts.
  • In humans, the microbiota profile differences resulting from NAS were not identical to those found in mice and were also different human-to-human. This suggests that the effects may vary substantially from person-to-person.
  • The human study where NAS-containing foods were consumed had a very low sample size and an unequal distribution of men and women. This would generally be considered “preliminary” data that could be used to support a larger study.
  • In the human study where NAS-containing foods were consumed, the types of NAS consumed were variable, so any differences among them could not be examined.

Video Post – Clip from “Health & Fitness During Aging” Seminar at UCONN

Below is a video clip from my recent seminar at UCONN. The audience was older and the seminar therefore dealt with health and fitness during aging. It examined, from a scientific perspective, the theme of death and rebirth at the organ and tissue level and how these processes are influenced by modifiable lifestyle factors such as nutrition (calories, fat, carbohydrates, salt) and activity (walking, running, weight training). For more information on my seminars, click the Seminar tab on the menu.


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