New study sheds light on the connection between stress and heart disease

A new study in the journal Biological Psychiatry has identified a link between chronic stress and heart disease, and you may not be surprised to learn that this link is inflammation.  The study looked at activity in a part of the brain that helps to regulate emotion called the dorsal anterior cingulate cortex(dACC) and levels of inflammation in the body.  The researchers found that increased activation of the dACC led to higher levels of the inflammatory molecule IL-6 and these higher levels of IL-6 corresponded with more plaque accumulation on artery walls.  Let's take a look at what all of this means.

To fully understand what this means, we first have to discuss something that is regulated by the dACC called cognitive reappraisal.  Cognitive reappraisal is a method of regulating the emotional response to stimuli.  If this sounds familiar, it's very similar to what one tries to achieve while practicing mindfulness meditation.  The problem is, cognitive reappraisal can be either positive or negative.  If a stimulus causes enhanced activation of the dACC but this emotion does not make it to the amygdala to generate an emotional response, that's a positive thing.  If a stimulus continually activates the dACC but also activates the amygdala constantly, that leads to a constant emotional response and chronic stress.

In this study, they found that constantly reappraising a stressful situation caused increased activity in the dACC which increased inflammation.  Since this area of the brain helps control many autonomic processes, it's not surprising that activation of this area of the brain can modulate the immune response.  Furthermore, the dACC is associated with anxiety and OCD-type behaviors in so much that severing the area has been shown to benefit people with OCD not responsive to medications(1).

Obviously you shouldn't severe your dACC, but this study points to the importance of reducing stress and letting things go to reduce heart disease risk.  The increased level of IL-6, an inflammatory cytokine highly associated with heart disease and Type 2 diabetes, is likely a large player in the relationship between stress and health.  In my next blog, I'll go over some of the physical warning signs that you may be experiencing chronic stress.

The 2am low carb wake up call...

As the Paleo diet becomes more popular and people give it a whirl, it's important to understand that many early versions that were low carb presented problems for some people, especially people who were training hard in exercise modalities that primarily use glucose for fuel such as Crossfit.  One of the more common experiences under this scenario is waking up between 2am-4am, often times with heavy heart pounding.  This phenomenon can be explained and potentially remedied using what we know about blood glucose regulation and what I went over in my last 2 blogs found here and here on allowing the intestine to help the liver with blood glucose regulation.

Now, there is a simple fix, eat more carbohydrates; and you should probably do this over the long term anyway if you are training hard.  There is a solution that you can use during short term low-carb dieting to lose weight or if you want to stick to a low carb diet over longer periods.  But first, let's take a look at what may be happening to wake you up.

The modern Western diet, being high in carbohydrate and low in fiber, relies heavily upon the liver to regulate blood glucose levels.  While it is pretty good at doing it's job, not providing carbohydrates to help it do it's job can make blood glucose regulation difficult.  To help your liver keep pace, glucagon and epinepherine levels rise in the blood to communicate to the liver that it needs to release some of the glucose it stores as glycogen, provided it has stored up enough glycogen from the carbohydrates you consume and made enough glycogen from non-carbohydrate sources.  But what happens if there is not enough glycogen stored in the liver to keep blood glucose above the critical level?

When you are up and moving around, muscles break down glucose in to lactate that the liver can use to make glucose via a process called the Cori cycle.  This likely contributes to blood glucose regulation while you are awake.  The interesting thing here is that epinepherine, more commonly known as adrenaline, causes muscle to break down glucose in to lactate and activates the Cori cycle(1).  As you may know as well, adrenaline also rapidly increases heart rate and the force of contraction of the heart.  Could the 2am low carb wake up call be due to blood glucose levels dipping too low and the adrenals correcting this issue by secreting epinepherine?  This could certainly explain why people get woken up and experience a pounding heart.  If this is the case, there is a simple correction that should remedy the situation.  Remove some of the burden of blood glucose regulation on the liver by allowing the intestine to participate.  In other words, increase your fiber intake.

Most Americans get less than 20g of fiber per day and a person who is undertaking a low carbohydrate diet likely gets less if they are avoiding vegetables.  Bumping this number up to 60g or more could potentially help a person who wishes to maintain a low carbohydrate diet not have to worry about large drops in blood glucose.  Optimally the fiber would come directly from the diet, but you could also take a fiber or resistant starch supplement to get your daily fiber intake up.  Many people are taking Bob's Red Mill unmodified potato starch as a supplement to increase fiber intake, just start with a low dose and space out your intake throughout the day to prevent gas.  You can work up to 4 tbsp per day which adds approximately 32g of resistant starch/fiber per day.

It may take a while to see significant improvements, especially in people who may not have a large amount of bacteria that ferment fiber/resistant starch in to the short chained fatty acids that help the intestine participate in blood glucose regulation.  Be persistent and, most of all, pay attention to what your body is telling you.  Gas tends to be a good thing, but if it becomes painful or smells putrid you may have to take it slower.

Evolution and diabetes part 2: Blood glucose regulation by ancestral humans

In my last blog I went over a study that casts some doubt on the notion that the liver is critical for blood glucose control.  In this study, they found that mice who had their liver blocked from contributing to blood glucose control adapted by shifting that duty over to the kidneys and intestine(1).  The assumption that the liver is king as far as blood glucose control is a fairly widely held concept due to the fact that it can store 100g of glucose and produce glucose from non-carbohydrate sources.  The problem arises when you take in to account that easy access to carbohydrates is a fairly recent phenomenon.  Taken together with other scientific evidence, it appears that the intestine should likely play a larger role in blood glucose regulation than it does today, and the modern diet prevents this from happening.

In this study the kidneys took on a much larger role in blood glucose regulation during times of fasting as the gene crucial for blood glucose regulation increased in expression.  The intestine also saw an increase in expression of this gene, but the total expression of this gene was 50x greater in the kidney.  These results may understate the importance of the intestine in blood glucose regulation, especially in the non-fasted state.

When you compare the diet of ancestral, pre-agricultural humans to that of today, one glaring difference is the fiber content of the diet.  Today, the average human diet contains less than 20g of fiber per day.  In his book The Story of the Human Body, Dr. Dan Lieberman's assessment of the literature points to the consumption of 100-150g of fiber per day by pre-agricultural humans.  This number is in line with what previous research has shown(2) as well as Jeff Leach's experience living with modern day hunter gatherers.  While the difference in fiber intake may not seem important when you consider humans don't absorb fiber, when you look at what it does to the microbiome and the effect it has on blood glucose regulation you can see that it is likely very important.

When bacteria in the intestine break down fiber, they make short-chain fatty acids(SCFAs), specifically butyrate and propionate.  Both of these SCFAs promote intestinal gluconeogensis in complementary ways(3).  Gluconeogenesis is the generation of blood glucose from non-carbohydrate sources and it allows the intestine to participate in blood glucose regulation through the fermentation of fiber by bacteria in the gut.  Interesingly, when gluconeogenesis is shut off in the intestine, all of the metabolic benefits of a high fiber diet are lost despite having a similar microbiome.  So, in a population where people consume low amounts of fiber, the intestine likely has a negligible role in regulating blood glucose.  Ironically, in this population, blood glucose tends to run high.  In a population where fiber is consumed in large quantities, the intestine likely takes on a much larger role in regulating blood glucose.  In this population, blood glucose tends to remain low.  This is not the only piece of the puzzle, however.

There is another issue that arises when bacteria in the intestine don't ferment fiber in to butyrate.  Butyrate is the fuel of choice for cells of the colon(4), but they are able to metabolize glucose as well.  A problem occurs when there isn't enough butyrate for the cells of the colon(Colonocytes), they must rely on glucose as a source of energy(4, 5).  When colonocytes are provided enough butyrate, they break it down in to the ketone beta-hydroxybutyrate which can be further broken down for energy.  When there isn't enough butyrate, they are forced to metabolize glucose which colonocytes break down in to lactate.  Colonocytes cannot metabolize lactate so it is sent to the liver to undergo gluconeogenesis.  In a mouse model of colitis, this is how colonocytes metabolize energy(5).  Unfortunately, glucose is unable to provide enough energy for efficient  gastrointestinal function in this manner(4).

In addition to having an effect on gluconeogenesis by the intestine, SCFAs also stimulate secretion of a hormone called glucagon-like peptide 1(GLP-1)(6).  GLP-1 has several roles in the body, but of interest to our discussion is it's role in insulin and glucagon secretion.  Insulin lowers blood glucose by causing cells to take it in while glucagon causes blood glucose to increase by increasing gluconeogenesis in the liver, kidney and intestine as well as causing those organs to release glucose.  GLP-1 stimulates insulin secretion in a glucose dependent manner, when glucose levels are high GLP-1 stimulates more insulin than when glucose levels are low while it causes glucagon levels to fall independent of glucose levels.  It is worthy to note that carbohydrate consumption also causes GLP-1 to be secreted, but since carbohydrate consumption will cause blood glucose levels to rise, it will cause more insulin secretion than one would see going the fiber route.

People with Type 2 diabetes tend to have a large amount of insulin in their blood, but their cells don't respond to it because they have become resistant.  This causes their blood glucose to run high because insulin can't do it's job of lowering blood glucose.  Since glucagon increases blood glucose and runs high in Type 2 diabetics, it is believed that lowering glucagon levels can help correct the high blood glucose levels associated with the disease.  Metformin, the Type 2 diabetes medicine of choice, works by causing the liver to make less glucose, which causes the same effect as lowering glucagon.  GLP-1 and drugs that mimic it accomplish the same thing, are being used as pharmaceutical therapies, and the result is lower blood glucose levels(7, 8).

The positive effect of administering GLP-1 to improve blood glucose regulation brings up a few interesting questions.  Is the intestine a more important component of blood glucose regulation than we give it credit for?  Is bacterial fermentation of fiber in to butyrate the first step in blood glucose regulation given how important it likely was for blood glucose regulation in ancestral humans?  Finally, is administering pharmaceutical GLP-1 merely restoring an ancient signal from the intestine to the liver saying, "I have your back" with regard to gluconeogenesis and blood glucose regulation?  While we are unlikely to find answers to these questions any time soon, it is very interesting that higher fiber intake is very protective against Type 2 diabetes (9, 10, 11, 12).  Furthermore, people with Type diabetes tend to have more disturbances within the digestive tract than healthy people(13, 14) with the most common disturbance being constipation.

Between the evidence provided above and comparisons of the ancestral diet to our modern one, it seems likely that the modern diet may be presenting an environment that causes blood glucose to be regulated in a way that is not efficient for humans.  Our long history of high fiber consumption likely selected for people who were good at using the fermentation of fiber by resident bacteria as the first step of blood glucose regulation that involved the intestine to a much larger degree than it does today.  The modern diet puts a much larger burden on the liver to make and regulate blood glucose due to the high carbohydrate and low fiber content of the diet.  This provides less fuel to allow the intestine to participate in blood glucose regulation and may be a contributing factor to Type 2 diabetes and the increased occurrence of GI disorders associated with the disease.

Evolution, diabetes, and blood glucose regulation

When practiced appropriately, science can shed a lot of light on some pretty powerful concepts in human health.  To date we have unlocked the human genome, developed some novel pharmaceutical interventions for diseases that were once taking a large toll on society, and begun to understand that we are carrying along an exponentially larger number of bacteria that have a dramatic impact on the way we function.  However, many of the health concerns we see today are not being addressed in the appropriate manner.  Comparing the use of a pharmaceutical drug to no treatment, or placebo, makes perfect sense when you are dealing with a bacterial or viral pathogen, but does it really make sense when the true problem is a poor lifestyle?

When performing science, you are not really trying to prove anything, you are trying to disprove the null hypothesis.  The null hypothesis is the default position, and in the instance of a pharmaceutical intervention against a pathogen it typically means giving some of the subjects a placebo pill to simulate not doing anything.  The problem is, at this point, there is a very large lifestyle component to the vast majority of diseases we are seeing today.  This includes cardiovascular disease, some types of cancer, Alzheimer's, and the topic of this blog, Type 2 diabetes.  If we know that a poor lifestyle largely contributes to these diseases, should the default position be taking a placebo pill and calling it a day, or would it make more sense to have the default condition be changing those lifestyle habits that cause the disease?  I suppose that depends on how you look at what the pharmaceutical intervention is trying to accomplish.

Let's be honest, I've worked in the health and wellness field for 18 years.  When someone is told they need to change their lifestyle or a disease they have is going to progress and they choose not to, they really aren't looking for a solution.  What they are looking for is something that will allow them to continue their poor lifestyle while preventing the damage that their lifestyle causes.  If this is what we are testing for with pharmaceutical interventions for these lifestyle diseases, it only makes sense to have the null hypothesis be the condition where the damage stops.  In other words, the null hypothesis should be the lifestyle that causes no more damage.  That way, when we compare the pharmaceutical intervention to the proper lifestyle group, we have an idea to what extent the drug is actually subsidizing the poor behavior.  When you compare the pharmaceutical drug to doing absolutely nothing other than taking a sugar pill, what would you expect to happen?  The drug will come out looking like it's the cure for something that it's not, which gives the false impression that the person has nothing to worry about.

So what lifestyle should be this default position?  Since these lifestyle diseases are prevalent in Western society, it makes no sense to have the null hypothesis be based on the lifestyle of Westerners.  However, these diseases are not at all prevalent in modern day hunter gatherers who live a lifestyle more in line with the one we spent most of our time evolving under.  This has led many to believe that the null hypothesis, the default lifestyle condition to test against, should be identical to the one we evolved under.

This poses a major problem.  The vast majority of our science has been conducted during a time when the Western lifestyle has been the default condition because that has been the default condition since clinical research has become prominent.  An easy way to understand this is that we have come up with RDAs for nutrients in human health, but these RDAs are only relevant under a Western lifestyle because a Western lifestyle is the condition under which they were tested.  So it is improper to say that the RDA for Vitamin C is the amount of Vitamin C one needs to prevent scurvy.  The proper way to phrase what the science actually shows is that the RDA for Vitamin C is the amount of Vitamin C one living a Western lifestyle during the time of testing needs to prevent scurvy.

Assuming the way we currently do things as it pertains to lifestyle is the default condition can also lead us down the wrong path when we are looking at how our body works.  It has been assumed that the liver is the primary site of blood glucose regulation.  However, this may not actually be the case, it could be that the liver is the primary site of blood glucose regulation in those living a Western lifestyle.  A study looking at blood glucose regulation in mice has shed some light on why this may be the case.

In order to better understand how blood glucose is regulated, researchers studied mice who were unable to regulate blood glucose via the liver.  The liver is considered to be critical in blood glucose regulation, without it we cannot stabilize blood glucose.  As the story goes, we eat carbohydrates that turn in to glucose, the liver stores that glucose and releases it during fasting, and when we are completely fasted, the liver makes glucose from non-carbohydrate food sources.

In the fed state during the study, blood glucose levels were identical between normal mice and mice that were unable to use their liver to regulate blood glucose.  During the fasted state, blood glucose levels dropped initially and ketones went up, but within 30 hours both groups of mice had the same blood glucose level as genetic expression changed in the kidneys and intestine to favor blood glucose regulation by those organs in the absence of the liver(1).  It is important to note that while blood glucose levels were lower in the mice who relied on the kidneys and intestines for glucose production, blood glucose never reached a critical state as the kidneys and intestines utilized ketones for approximately 50% of their energy and were able to provide enough glucose for survival.  In addition, this study found that the kidneys and intestine make glucose out of the amino acid glutamine while the liver uses alanine and lactate.

While it may not seem like this study has any real world relevance since most humans have functioning livers, it does highlight that the liver is not absolutely necessary for blood glucose regulation.  The liver is certainly a large player in blood glucose regulation as it can store approximately 100g of glucose and is capable of making glucose from other sources, but the assumption that the optimal way to regulate blood glucose is through consumption of carbohydrate and storage in the liver is flawed.  At this point we really don't know for sure how to optimally regulate blood glucose, but if we look at some key aspects of the ancestral diet some doubt creeps in.

In my next blog we'll take a look at how blood glucose may have been regulated by ancestral humans and how the drastic change in the way we regulate blood glucose now may be contributing to the increased prevalence of Type 2 diabetes.

Part 2

Evolution, physical activity, and human health

The chronic diseases we see today are often the result of poor lifestyle choices.  Cardiovascular disease, Type 2 diabetes, obesity, cancer, arthritis, depression, and Alzheimer's disease are all considered normal parts of the aging process and are often called diseases of aging.  The problem is, when you look at "less civilized" cultures, particularly modern day hunter gatherers, these diseases either don't exist or are insignificant even in older members.  This has caused many to postulate that the Western lifestyle may be a significant factor in the prevalence of these diseases.

In 2002, Booth wrote a paper going over exercise and gene expression(1).  This paper is a classic in the evolutionary medicine arena because it shined a light on the effect of exercise on gene expression and proposed the theory that genes expressed as a result of physical activity would promote disease in a person who doesn't meet the necessary threshold to activate these genes.  In other words, the lifestyle diseases that are often attributed to aging may be, at least partially, from a deficiency in physical activity.

 

Booth's primary focus was on the notion that physical activity increased muscle mass and fuel utilization, improved cardiovascular function, and improved cellular insulin sensitivity while physical inactivity did the opposite.  Given that lower muscle mass, poor cardiovascular function, and poor insulin sensitivity are either seen in or associated with most of the lifestyle diseases seen in Western culture, it is fair to say that all of these factors may play a role in the relationship between Western disease and physical inactivity.  However, current research adds more to the story.

A review from 2010 discussed the relationship between inactivity and an overly sensitive stress response(2).  Recently, the author of that study was able to identify the physiological change in the brain that come with high levels of physical inactivity.  He found that physical inactivity causes a re-wiring in the rat brain.  Specifically, it causes a more dispersive branching of neurons in the rostral ventrolateral medulla(RVLM), an area of the brain that helps control the stress response(3).  The researchers believe this increased branching is what causes the neurons in the RVLM to be more responsive to stress in physically inactive rats.  While this study has not been repeated in humans, it bears to note that increased sensitivity of the stress response, also called increased sympathetic tone, is also found in many of the lifestyle diseases mentioned above and sedentary behavior is also strongly associated with these diseases(4, 5, 6, 7) and the low grade inflammation that accompanies them(8, 9).

There are other avenues within inactivity physiology that apply to health and are worth mentioning.  During aerobic metabolism, reactive oxygen species(ROS), or free radicals, are continuously generated(10).  Free radicals are molecules with an unpaired electron that serve vital roles in cellular function, but react with healthy molecules within the body and cause oxidative stress when not held in check.  Oxidative stress occurs when free radical generation outpaces the ability of the body's antioxidant defense systems to deal with free radicals.  The body's antioxidant pathways donate electrons to free radicals and help keep free radicals at a healthy level.  As I mentioned in this previous blog, prolonged sitting causes changes in genetic expression that reduce antioxidant and anti-inflammatory pathways and reduce insulin sensitivity.  This would increase oxidative stress which is another physiological factor associated with lifestyle diseases.  In addition, increased oxidative stress leads to higher levels of inflammation which are also associated with these diseases.

Some people attempt to head off oxidative stress by taking antioxidants supplements.  The problem with this is that when supplemental antioxidants are taken and they meet up with a free radical, they donate an electron to the free radical which makes the former antioxidant a free radical, albeit a weaker one.  The antioxidants generated by the body's antioxidant defense system, particularly glutathione, are able to donate electrons to free radicals as well as recharge antioxidants that become free radicals as a result of donating an electron.  This makes the body's antioxidant defense system far more powerful than any antioxidant you can take orally.

What makes this avenue of inactivity physiology particularly interesting is that recent evidence has shown that the average daily energy expenditure of Hadza hunter gatherers is the same as Westerners when controlled for body size despite the physical activity level of the Hadza being greater(11).  Since a person at rest is primarily utilizing aerobic metabolism, it is safe to assume that both groups are either generating the same number of free radicals or the Westerners are generating more based on their larger size alone.  On top of this, the increased level of sedentary behavior associated with the Western lifestyle could potentially induce higher levels of oxidative stress through a reduction in antioxidant gene expression while the physically active lifestyle of the Hadza may promote health by keeping free radical levels at an appropriate level.  Since the Western lifestyle diseases discussed earlier are also associated with high levels of oxidative stress and hunter gatherers like the Hadza rarely experience them, it makes you wonder if shutting down these pathways contributes to the Western lifestyle diseases.  In other words, a deficiency in physical activity may in fact be a strong contributor to the lifestyle diseases that are prevalent in Western cultures for many physiological reasons.

The bacteria in your gut: Your "flexible" genes

Your microbiome, the community of bacteria that live within and on you, has become a hot area of research recently.  This bacteria lives on your skin, in your mouth, all throughout your digestive tract, and basically in any nook or cranny you have.  The bacteria that reside in the digestive tract perform a host of functions for their...well...host.  They help train the immune system, help with mineral absorption, help breakdown things we cannot break down, and make short-chained fatty acids that help keep our digestive tract in tip-top shape.  Many health problems are associated with the composition of bacteria you have in your gut including obesity, Type 2 diabetes, arthritis, IBS/IBD, Crohn's disease, Celiac disease, anxiety/depression, autism, and many others.  This has led researchers to seek out what a healthy microbiome is so that we can manipulate it to promote health.

 

The many ecosystems that make up your microbiome

The Human Microbiome Project was undertaken to take a glimpse at the microbiome of those in Western society while researchers are also taking a look at modern day hunter gatherers to get a glimpse at how our microbiome may have evolved with us.  One of the more notable findings in hunter gatherers is that they tend to have a much more diverse microbiome than those of us in Western society.  Over the course of the last month, more information has been uncovered looking at both the Western population as well a modern day hunter gatherers.

Researchers from the Human Microbiome Project have analyzed microbiome samples from 300 people and determined that, based on current data, there is no single healthy microbiome.  Based on all of the data to date, healthy people can have a wide range of different microbiomes(1).  Several lifestyle factors such as if you were born by C-section, whether you were breast fed, or past antibiotic usage can impact the microbiome in your GI tract while gender can affect the microbiome in different body sites.  Each person has a signature microbiome that is representative of the environment they grew up in and the lifestyle that they have lived.  In fact, lifestyle has a huge impact on the make up of your microbiome, as seen by a recent study looking at Hadza hunter-gatherers.

In the study, researchers found that even people who live in the same environment, which essentially means they are exposed to the same types of bacteria, have different communities that live alongside, and inside, them.  Hadza men and women differ greatly in the composition of their microbiome, due primarily to the fact that men tend to hunt game and collect honey while the women gather primarily plant foods(2).  While the food is shared, the men tend to snack on more of the foods that they collect while the women tend to snack on more of the foods that they collect.  So despite eating the same foods, even just a small change in the percentage of the foods consumed can significantly change the microbiome.  This makes sense because they eat what you eat but don't absorb.  Plant materials, high in fibrous material that humans cannot digest, provide substrate for bacteria living in the colon.  The colon harbors the largest percentage of bacteria in the digestive tract by far.

Hadza chicks, scarfing fries and discussing the latest Real Housewives of Tanzania episode

One interesting aspect of this study is that the Hadza had a large number of bacterial species that are associated with disease in Western populations and low levels of bacteria that are associated with health. Despite having what one would consider a less than ideal microbiome based on what our research shows, the Hadza don't experience IBS/IBD like we do.  This reinforces the notion that there is not a single healthy microbiome, and points to the total collection of bacterial species that make up your microbiome as being important, not the presence of specific species.

A third study followed a group of people called Hutterites for a year.  Hutterites more closely resemble the Amish in that they are exposed to technology such as medical care, exposure to vehicle exhaust, and electricity.  The Hutterite share a communal lifestyle so they have a very similar microbiome between members.  While this similarity between the microbiome of members of the group remains stable throughout the year, the microbiome of the entire tribe changes with the seasons as the availability of food changes(3).  As the seasons change, so does the microbiome of the tribe as the types of foods they consume changes with their availability.

This study, coupled with this other study(4) that showed that extreme shifts in diet can begin drastically changing the microbiome within hours, paints the microbiome as a shiftable genome that helps the host adapt to the changing environment.  In fact, the number of genes within the microbiome of an individual outnumbers the number of genes that they possess in your cells by an order of 100 to 1, maybe even more.  Western medicine has placed such a large emphasis on how strongly genetic factors play in the many diseases we see, yet until recently has ignored the fact that most of the genes that will have an impact on the many biological functions that go on within the human body are directly influenced by diet and lifestyle. 

While research in the microbiome is in it's infancy, it's great that we are directing so much attention towards it.  Studying the microbiome will likely be the next big step in understanding human health and function.  It is also likely necessary to undo some of the damage we may have done with some of our current medical(Antibiotics) and social(extreme hygiene) practices.  This is not to say that these practices aren't necessary or are bad, merely that understanding them and the way they impact our microbiome more thoroughly will only improve their effectiveness.

Introductory Stretching Video

In my last video blog I illustrated how I foam roll at the beginning of my workouts or when I feel my muscles feel like they are getting tight.  In this second video, I go over my stretching routine that follows the foam rolling routine.  For someone who hasn't exercised in a long time, or someone who has lived a sedentary life where they haven't exercised before, this 3 part program is likely where you will start.  The purpose of the entire program is to physically prepare your body for a more active lifestyle and to prevent some of the injuries that often occur in people who have never exercised before that begin an exercise program.

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Next Thursday I will go over the activation and mobility portion of my program.