Science

This year we are offering an optional Interdisciplinary Integration evening series on Thursday, Friday, and Saturday of Advanced Integration. You must be signed up for Advanced Integration to attend these sessions. They will be offered from 5:15-6:30pm each night if you would like to attend. 
Thursday-Dr. Rebecca Hohl and Ron Hruska will present on Dental Occlusion. 


Friday- Dr. Heidi Wise will present on PRI Vision


Saturday- Dr. Paul Coffin will present on Podiatry.

Posted September 17, 2015 at 6:48PM
Categories: Science PRI Vision

Two weeks ago, we travelled to St. Louis, MO for the 66th Annual NATA Clinical Symposia & Expo. Matt and I had a great time meeting nearly 600 Athletic Trainers at our PRI booth. There is a lot of excitement for PRI in the Athletic Training field, especially having Evidence Based Practice (EBP) CEUs for Myokinematic Restoration, and more courses to come!

I also had the opportunity to present at this conference for the first time. The topic of my presentation, "The Influence of Pelvis Position on Hamstring Injuries: To Stretch or To Strengthen" drew around 450 people into the room, with standing room only. For those who were unable to get into my presentation, they will have the opportunity to listen to it on the NATA Online CEU Center in the near future. I have also attached my presentation handouts HERE!

Dan Houglum, MSPT, ATC/L, PRC also presented at this year's conference. The title of Dan's presentation was "Asymmetrical Posture and Common Pain Related Syndromes". He also had a nearly full room, with Athletic Trainer's eager to learn more about PRI. Dan is also willing to share his presentation handouts, which I have attached HERE!

Posted July 9, 2015 at 7:59PM
Categories: Athletics Science

There is a “silver-lining” to nearly every negative situation in which you find yourself.  If you open yourself up, you can find the positives and then use your experience and knowledge gained to help others…hopefully, creating a “greater good” in the universe.  I hope the following story, lessons learned, perspective, and insight are informative.

The aftermath of a very personal health situation brought me in to see Lori Thomsen at the Hruska Clinic.  She took me on as a patient one year ago.   Realizing quickly that I was a candidate for PRI Vision intervention, I was assessed by Ron Hruska and Heidi Wise the same day and prescribed a specific pair of PRI lenses.  I filled the prescription and followed up with Lori the next day. 

Lori guided me through a program consisting of upright exercises.  (Exercises in the Vision program are primarily upright activities, because you are learning how to use the floor to propel yourself forward through all phases of the gait cycle, using the PRI Vision lenses as a tool.)  Coincidentally, at this same time, I was beginning to more fully appreciate the need to get my own clients “on their feet”.  Admittedly, I was designing exercise programming primarily for the supine, side-lying, and all-fours positions.  Having received Lori’s instruction for my own upright activities, I was able to more adeptly implement upright activities with my own clientele, especially when it came to teaching L mid-stance.  I believe I have been able to avoid major pitfalls/setbacks and progress my clients more quickly than I might have, if I had not been a patient of Lori’s.

[Side Note:  It is important to make a distinction between assessing one’s ability to center themselves in L or R mid-stance (as is part of the PRI Vision assessment) versus teaching L mid-stance and other phases of the gait cycle at the appropriate time in one’s rehab/training program.  Assessment does not involve cueing; teaching does.]

The most enlightening piece of information Lori taught me was the use of the quad during mid-stance.  As a member of the PRI faculty, Lori teaches the Pelvis Restoration course.  She frequently refers to her “3 Amigos”: L abdominal wall, L quad, and L hip.  It wasn’t until I was a patient, when she actually took me through the integration of the “3 Amigos” on MY body, that I fully appreciated the quad in L mid-stance.

I think perhaps that the quad is overlooked when teaching L mid-stance, due to overemphasis on the L heel.  Let me try to explain in an admittedly round-about way J 

In L mid-stance you should feel 75-80% of your body weight traveling down into the back half of your foot (mid-arch to center of heel). Your left foot should be firmly planted on the ground without the toes lifting up in front.  I have witnessed individuals lifting their toes or entire forefoot into dorsiflexion when cued to: “find your left heel” or “press down through your left heel” .  I have inadvertently used these types of cues and seen those little toes wiggling around in the shoe, trying to lift up.  Sometimes it helps to have the client go barefoot, so you can see if they are “cheating” with their toes.  “Cheating” with the toes IS cheating, because it is extension. Toe extension kicks on dorsiflexors…kicks on hip flexors…kicks on low back, etc. etc.  (There are certainly those who walk as “heel-diggers”, pulling themselves forward through this entire list of muscles. These are very extended individuals who tend to use their pecs as their abdominals and present with significant FHP.) 

PRI programming accentuates “sensing” or “feeling” your left heel making contact with the ground in mid-stance, because those in LAIC patterns tend to bypass the L heel altogether during the gait cycle.  Their L foot tends to be in constant plantar flexion, so the first part of the foot that hits the ground on heel-strike is the arch or the ball of the foot (late mid-stance to early toe-off phase).  Maybe we take the client/patient through proper heel-strike phase, but in mid-stance, we should be teaching them to merely “sense” or “feel” their left heel vs. “press” or “dig” their left heel.

Back to the quad…  In L mid-stance, the quads should be in an eccentric contraction phase around the knee joint, counter-balancing the eccentric contraction of the hamstrings.  Because the knee is slightly flexed in mid-stance, the quad is on a slight stretch but holding tension, getting prepared for the propulsion phase where the concentric action of the quad takes over (stretch-shortening).  There is a “springiness” to the quad, unless the L foot is not firmly planted or the L hemi-pelvis is anteriorly tilted.   In either of these cases, the quad is acting more concentrically. 

I like the word “springiness”, because it reflects my most recent reflections on mid-stance.  “The first modal peak [of the vertical component of ground reaction forces (GRF)] occurs during the first half of support and characterizes the portion of support when the total body is lowered after foot contact.” (Hamill and Knutzen, Biomechanical Basis of Human Movement).  This is mid-stance. 

When I ask my clients if they “feel” the floor under their feet, sometimes they look at me like I am crazy.  When teaching L mid-stance, I have begun asking them if can “drop” their bodyweight (75-80%) into the L foot and “allow” the L left leg to “accept” that weight.  Now, maybe they can sense some weight, actually the GRF pushing up into their left foot (through the “springy” eccentric quad).  Now they have a point of contact from which to propel forward.  They are not in a constant state of  “pulling” or “lifting” themselves off the floor with vision, jaw, neck, shoulder, low back, and/or gastroc muscles.  [Side note in regards to Cervical Revolution:  all of this “lifting” and “pulling” through the kinetic chain, bottom-up, is to no avail, because ultimately there is gravity crushing down on all of those lifting forces, meeting at the skull and generating cranial compression.]

When you really think about this, walking is hard stuff!!  Each leg has to be able to “accept” 75-80% of your body weight in able to propel forward and not evade this difficult task with the above-listed extensor and pulling muscles. 

Again, back to the quad…  “If you can feel your L quad, Lilla, your L abs should automatically be kicking on”, Lori says during our session.  The quad is one of the markers for integration from the ribcage to the pelvic inlet through the pelvic outlet to the femur. 

I’m in L stance with pelvis rotated left, L foot flat on ground, upper body rotated right, reaching out and down with left arm to facilitate both trunk rotation and thoracic flexion, a bit of thoracic abduction to help find L abs.  I’m doing everything right, but still no abs.  When I “press” down into the ground, as suggested, I am concentrically activating my quad, and it is difficult to posteriorly tilt my pelvis and reach the knees forward.  However, when I think of “dropping” my weight onto my L leg (feeling those GRFs and a “springy” eccentric quad), I can reach my knees forward with posterior pelvic tilt, effectively bringing my pelvis under my ribcage so that they are in a position to access the side abs.  YEAH and whew!

I didn’t mention the third amigo, the L hip (Glute Med), which comes into play in the frontal plane, balancing the forces of the IC Adductor.  I am certainly not downplaying the role of this amigo in L mid-stance!  I only wanted to emphasize the important role of the quad (a muscle that is not given as much “press” in teaching L mid-stance), because Lori’s instruction certainly helped me, both personally and professionally.

Attached are 2 short video demonstrations.

Toe Extension MCS

Quad MCS

Lilla Marhefka, PhD, HFS, CSCS, PRT

Posted April 28, 2015 at 2:11PM
Categories: Videos Clinicians Science

Have you ever struggled to explain to a colleague, patient, family member or friend what the Postural Restoration Institute is? If so, you will love this new video that we have created. While it was a couple years in the making, it turned out great, and kudos to Matt Hornung for finishing up this project over the past few months! Hope you enjoy it!

Posted April 21, 2015 at 8:50PM
Categories: Videos Courses Science

In PRI, we are typically focusing on creating a reciprocal and alternating neuromuscular system. However, our neuromuscular system is connected with all the other systems in our body. There appears to be a coupling between autonomic, central, endocrine, and gastrointestinal systems which, in parallel with our neuromuscular system, are also asymmetrical and rhythmically shifting. “Asymmetry, Lateralization, and Alternating Rhythms of the Human Body” has been broken up into 5 parts describing this phenomenon in addition to the story of how and why our asymmetry came to be. It can also be accessed at on my website where I have written on other various topics that relate to PRI. 

CLICK HERE to read Part 5: "Connecting Ultraradian and Neuromuscular Rhythms of the Human Body"

CLICK HERE to read Part 4: "How Does One Reconcile an Asymmetrical Neuromuscular System?"

CLICK HERE to read Part 3: "How Did Humans Become Asymmetric?"

CLICK HERE to read Part 2: "What Does Asymmetry Provide for a Human Being?” 

CLICK HERE to read Part 1: "The Prevalence of Human Asymmetry and Lateralization"

Posted April 14, 2015 at 1:32PM
Categories: Articles Science

Happy April! And I mean it, that's no Fool's joke.

'Tis the month of Interdisciplinary Integration (better get your spot!), and to celebrate, I wanted to post up a link to a write up on this past December's Advanced Integration course.

It's four parts (one for each day of the course). All parts have all been published, so here is part Ipart IIpart III, and part IV.

Hope this gets your brain gears moving a little like it did mine.

-Lance Goyke

Posted April 1, 2015 at 1:35PM
Categories: Courses Clinicians Science

“It doesn’t matter whether you’re an 80-year-old smoker, a 23-year-old Olympian, or a regular, fit guy-odds are the way you’re breathing right now is flooding your body with stress hormones, compromising your joints and mobility, bottlenecking your energy and undermining your performance in the gym and everyday life. Fourteen times a minute, you become a little weaker and a bit duller.

Hruska is on a mission to change that. Step one is understanding how your body is organized.”

Ron Hruska was recently interviewed by Men’s Health along with Bill Hartman and Neil Rampe discussing Postural Restoration, after Trevor Thieme, Senior Editor for Men's Health attended a Postural Respiration course last year. Topics discussed include: optimal breathing and the typical respiration patterns, asymmetry, PRI in pro baseball, and common compensations that can cause neck, back and joint pain.  

The 90/90 hip lift with balloon was shown as a way to get your diaphragm in a position to work correctly, helping you to breathe appropriately and avoid chronic stress which can increase your risk of dementia by 67%, stroke by 59% and diabetes by 45%.

“You can think of neutrality of being functionally symmetrical- the ability to shift your center of gravity from one side to the other, to breathe efficiently with both lungs, and to maintain position of your true core. “Being neutral helps everything,” says All-Star first baseman Paul Goldschmidt. “When I lift, I’m stronger. When I run, I’m faster. It allows me to fully express my power and speed.”

If you haven't already, go out and grab the April 2015 Men’s Health issue and flip to page 144 to read the article, which they refer to as the "#1 Greatest Health Tip Ever!"

The article that originally appeared in the April issue of Men's Health is now online, you can read it here!

Posted March 25, 2015 at 3:21PM

In PRI, we are typically focusing on creating a reciprocal and alternating neuromuscular system. However, our neuromuscular system is connected with all the other systems in our body. There appears to be a coupling between autonomic, central, endocrine, and gastrointestinal systems which, in parallel with our neuromuscular system, are also asymmetrical and rhythmically shifting. “Asymmetry, Lateralization, and Alternating Rhythms of the Human Body” has been broken up into 5 parts describing this phenomenon in addition to the story of how and why our asymmetry came to be. It can also be accessed at on my website where I have written on other various topics that relate to PRI. 

CLICK HERE to read Part 2: "What Does Asymmetry Provide for a Human Being?” 

CLICK HERE to read Part 1: "The Prevalence of Human Asymmetry and Lateralization"

Posted March 3, 2015 at 1:59AM
Categories: Clinicians Science

Joe Heiler from SportsRehabExpert.com recently featured Mike Cantrell in an audio interview on his website discussing the PRI MyoKinematic Restoration course plus answers some frequently asked questions about the PRI model, hip asymmetries that don't seem to fit a pattern, scoliosis, using a balloon to improve breathing, what type of 90/90 hip lift to use, and a whole lot more. Joe gave us permission to include the MP3 audio file on our website, so CLICK HERE to listen to the hour long interview with Mike!

Also, if you haven't already checked out SportsRehabExpert.com, it is definitely an excellent resource and PRI topics are commonly discussed on this site. Several other interviews have been conducted with Ron Hruska, Julie Blandin, Kevin Neeld, Michael Mullin, Neil Rampe and others discussing PRI in their respective fields! Check it out, if you haven't already!

 

Posted November 21, 2014 at 3:47PM

Author’s Note: This is the second installment in an ongoing series on my blog, Integrative Human Performance, meant to introduce the Postural Restoration Institute and the concepts that it teaches, as well as how we integrate them into training and rehab.  You can view this post in its original format on the blog by clicking here.  If you missed the first installment, you can click here to give that a read in its original format, or click here to read it on the PRI website. In this installment, I’ll take the neurological underpinnings of PRI’s methodology (discussed in Part 1) a bit farther to discuss the biochemical and physiological responses to the different autonomic states. I’ll give a brief insight into the relevance of these responses to muscle activity at the end, and will focus in detail on how that impacts postural and movement patterns in the next couple of installments.

In the last installment, I explained that while on the surface PRI may seem solely concerned with postural and movement dysfunctions, its ultimate goal is to assess a person’s autonomic state and their relative balance of sympathetic and parasympathetic output, as well as the ability to change which division is more dominant in the face of various stimuli.  In this post, I will outline the specific physiological responses that these autonomic subdivisions elicit and detail the mechanisms by which they work.  It is my hope that this explanation will give you a better understanding of how the neurological influences outlined in part one translate to patterns of movement and muscle activity that I will describe in parts three and beyond.

Autonomic Nervous System Function: Mechanisms Responsible for its Effects

As I briefly mentioned in part one, higher brain centers in the limbic system and even the cerebral cortex send information to peripheral effectors via action potentials through efferent neuronal circuits.  These circuits pass through the brainstem, which contains the reticular formation in the pons and medulla.  While in the first post I described how these nerve impulses can impact muscle tone and activity, I only briefly mentioned that they also impact traditional “autonomic functions” such as heart rate and the rate and depth of ventilation.  In fact, the input the brainstem has in cardiorespiratory function is, at least in the sense of direct influence, more profound than its influence on skeletal muscle.  This is made apparent by the fact that the Cardiovascular Control Center (CCC) and the Respiratory Control Center (RCC), which are responsible for regulation of heart and breathing activity, respectively, are both located in the brainstem.

The Cardiovascular Control Center is in the medulla oblongata (cue the obligatory The Waterboyreference). The CCC innervates the heart with parasympathetic fibers via the vagus nerve (which I mentioned briefly in part one) as well as via sympathetic cardiac accelerator nerves.  While cardiomyocytes can spontaneously depolarize and initiate a heartbeat, these autonomic nerves enable the CCC to alter heart function in response to afferent feedback from peripheral chemoreceptors and mechanoreceptors as well as efferent feedforward stimulation via higher brain centers.  At rest, the parasympathetic system predominates and allows for relatively minor changes in heart activity by increasing or decreasing its output.  In other words, the sympathetic system does not appreciably contribute to adjustments to cardiac activity at rest.  The same is actually true of the onset of exercise–the increase in heart rate and contraction force are largely due to the withdrawal of parasympathetic output up to approximately 100 beats per minute, at which point the sympathetic nervous system will increase activity to meet any further increase in demand.

The Respiratory Control Center is also located in the medulla oblongata as well as in the pons.  The most widely-accepted theory behind its function is the Group Pacemaker Hypothesis, which states that there are four distinct regions that are responsible for initiating and regulating the breathing process, two in each of the aforementioned subdivisions of the brainstem.  The Dorsal Respiratory Group (DRG), located in the medulla oblongata, is generally considered to be responsible for initiation of inspiration at rest.  Cells in the Solitary Tract Nucleus propagate signals to the Retrotrapezoid Nucleus, which in turn innervates respiratory muscles like the diaphragm and the external intercostals via the phrenic and intercostal nerves, respectively.  The Ventral Respiratory Group (VRG, also in the medulla oblongata), on the other hand, acts secondarily to the DRG and is generally thought to be active only during forced breathing, like when you exercise.  There is still some debate over this latter point, however, since the preBotzinger Complex, which is located in the Ventral Respiratory Group, has been hypothesized to be the structure primarily responsible for the initiation of spontaneous breathing as well as the generation of the rhythmic pattern of ventilation.  The two other regions involved in the breathing process, the Apneustic Center and the Pneumotaxic Center, are located in the pons.  The Apneustic Centers (there is one on each side of the brainstem) regulate inspiration by influencing the DRG.  Continuous firing of the Apneustic Centers stimulates the DRG, consequently increasing the depth and rate of inhalation.  The Pneumotaxic Centers (also one on each side of the brainstem), in contrast, are innervated by the Vagus Nerve, and upon stimulation inhibit the Apneustic Centers, thus promoting exhalation.  Much like the CCC, the RCC can respond to input from both peripheral chemoreceptors as well as higher brain centers.  It appears that input from higher Central Nervous System structures, such as the hypothalamus and cerebrum, to the Pneumotaxic Centers provides the primary drive for initiation of the respiration cycle, while peripheral sensory feedback fine-tunes the regulation process.  It is possible, however, for normal respiratory cycles to continue in the absence of input from higher brain centers, so long as the damage is done above the level of the pons.  This phenomena is called redundant control, and is a mechanism that increases the likelihood of survival of the organism since multiple systems must fail in order for function to be lost.

One point to highlight with regards to the Respiratory Control Center is that its innervation of the respiratory muscles is via somatic motor neurons, which are not traditionally classified as autonomic in nature despite the fact that those innervating respiratory muscles are largely under involuntary control.  This does not mean, however, that the Autonomic Nervous System has no influence on respiration.  When subcortical structures in the limbic system are activated in response to a perceived threat, it is believed that they can bypass the respiratory centers altogether via extrapyramidal upper motor neuron fibers that innervate the same lower motor neurons that are controlled by the DRG and VRG and are responsible for respiratory muscle activity.  In addition, higher centers can also exert inhibitory effects on the Apneustic and Pneumotaxic Centers.  The inhibition of the Apneustic Centers is apparent when you try to hold your breath as long as you can, since the Vagus Nerve (specifically the Ventral Vagal Complex, or VVC) stimulates the Pneumotaxic Centers, which inhibit the Apneustic Centers.  The result is a suppression of inhalation, although this ability is obviously limited, as evidenced by the fact that you can’t kill yourself by simply holding your breath–you are forced to inhale eventually. (Author’s Note: even though we’re quite confident in this claim, for liability reasons we recommend you don’t test it at home.) Inhibition of the Pneumotaxic Centers, on the other hand, is a result of decreased Ventral Vagal Complex tone and causes an inhibition (or rather a lack of excitation) of the Pneumotaxic Centers.  This, in turn, impairs the Pneumotaxic Centers’ ability to inhibit the Apneustic Centers, which become hyperactive and facilitate an increase in the length and depth of inspiration.  Recall that I mentioned the VVC and its effect on the balance of sympathetic and parasympathetic function in part one of this series.  Be sure to make note of the facilitation of inspiration when the parasympathetic activity of the VVC is diminished, since that will resurface later in this post and in subsequent installments.

The takeaway here is that in addition to potential direct and indirect influences on skeletal muscle, the autonomic nervous system has a profound direct influence over basic autonomic functions such as cardiac and ventilatory activity.  Both the cardiac and respiratory control centers in the brainstem can respond to feedback from peripheral sensory receptors as well as descending input from higher brain centers in anticipation of a threat.  Parasympathetic input to the heart predominates at rest, while a withdrawal of parasympathetic outflow and subsequent increase in sympathetic outflow causes an increase in heart rate and force of contraction.  Parasympathetic input to the respiratory control centers is characterized by an increase in ventral vagal tone, which leads to an increase in the length and depth of expiration secondary to a decrease in the length and depth of inspiration.  Sympathetic input to the respiratory control center is characterized by a decrease in ventral vagal tone, which leads to subsequent increase in the length and depth of inspiration and concomitant decrease in the length and depth of expiration.

Sympathetic Nervous System Activation: The Response to Subcortical Threat Appraisal

In the previous section I established that the autonomic nervous system has considerable control over the function of both the heart and the respiratory muscles.  What I specifically want to examine now is the response that the autonomic nervous system has to perceived threats, and the effect that that response has on cardiorespiratory functions.

Structures of the limbic system (e.g. the amygdala and cingulate gyrus) and some higher centers (e.g. the insula) are responsible for initiating emotional responses and regulating threat appraisal.  When a threat is perceived, multiple responses can be undertaken due to the evolution of the Vagus Nerve in mammals, as explained by Stephen Porges’ Polyvagal Theory.  The most evolutionarily recent response, which correlates with the more evolutionarily recent ventral portion of the Vagus Nerve, is the suppression of sympathetic activity by the Ventral Vagal Complex in favor of prosocial behaviors such as communication and self-calming.  This response is generally the first response in humans, since it is faster due to myelination of the ventral portion of the vagal nerve.  According to the Polyvagal Theory, however, as the threat level increases or persists despite the aforementioned attempts to mitigate it via prosocial behaviors, we tend to decrease ventral vagal tone and “fall back” on more primitive responses.  One such response is the fight-or-flight response, which can occur when the VVC fails to inhibit or attenuate sympathetic output.   As sympathetic output increases, we see a number of physiological effects.

With regards to the autonomic functions discussed previously, cardiorespiratory activity will increase with increased sympathetic outflow.  The cardiac accelerator nerves to the heart will increase their rate of firing and release the catecholamine norepinephrine at the sinoatrial node and ventricles of the heart.  This neurotransmitter activates beta-1 adrenergic receptors in these regions of the heart, which activate G proteins in the cytoplasmic leaflet of the cell membrane.  G proteins in turn activate cyclic AMP (cAMP), an intracellular second messenger molecule that is responsible for activating cellular enzymes like protein kinase A that will, in the case of cardiomyocytes, increase heart rate and force of contraction.  In addition, sympathetic input to the adrenal medulla causes the release of the catecholamine epinephrine  (and to a lesser extent, norepinephrine) into the blood.  Epinephrine (and to a lesser extent, norepinephrine) activates alpha-1 adrenergic receptors in smooth muscle cells lining blood vessels, again activating a G protein in the cytoplasmic leaflet of the cell membrane.  This G protein, in contrast to those associated with beta-2 adrenergic receptors, binds to a membrane-associated enzyme called phopholipase C.  This enzyme cleaves a phospholipid in the cell membrane called phosphatidylinositol into (1) inositol triphosphate, an intracellular signaling molecule that causes calcium ion release from the sarcoplasmic reticulum and thus contraction of the smooth muscle, and (2) diacylglycerol, another intracellular second messenger that is responsible for activating protein kinase C and the subsequent pathways it controls.  The overall result is vasoconstriction of the blood vessels.  In the vasculature that supplies active skeletal muscles, however, alpha-1 adrenergic receptors are inhibited, allowing epinephrine to activate beta-2 adrenergic receptors that promote relaxation of the smooth muscle and vasodilation of blood vessels via the aforementioned cAMP-protein kinase A pathway.  The net result is a reduction of blood flow to inactive skeletal muscles and most visceral organs and an increase in blood flow to active skeletal muscles, hepatocytes, and coronary vasculature to meet the increased metabolic demand that is either present in these cells or that the brain anticipates will be present due to the perception of an immediate threat.

As far as respiration is concerned, as I previously stated subcortical structures of the limbic system can bypass the respiratory centers in the brainstem altogether in the face of a perceived threat via extrapyramidal upper motor neuron fibers that innervate the lower motor neurons responsible for respiratory muscle activity.  An increase in the firing rate of these lower motor neurons leads to an increase in ventilation rate.  In addition, it is important to note that heart and ventilatory function are tied very closely.  Inspiratory activity is related to an increase in heart rate, primarily via a decrease in the rate of time spent in diastole (the phase of relaxation in the cardiac cycle), since the increase in the volume of the thoracic cavity with contraction and depression of the diaphragm decreases the pressure in the cavity.  The heart must respond to the lowered pressure by increasing heart rate to adequately fill the lung vasculature as well as prevent a drop in arterial pressure in the systemic vasculature, since a large quantity of blood is tied up in the pulmonary circuit during inhalation in order to facilitate oxygenation of red blood cells.  Expiration, on the other hand, is related to a decrease in heart rate due to a decrease in the volume of the thoracic cavity when the diaphragm relaxes and ascends and subsequent increase in pressure in the cavity.  The heart responds to the pressure increase by slowing heart rate to limit venous return to the lungs and to prevent an excessive increase in arterial pressure as the large quantity of blood that was just oxygenated leaves the pulmonary circuit and enters the systemic circuit.  Also recall that an increase in sympathetic activity secondary to inhibition of the ventral vagal complex causes an inhibition (or rather a lack of excitation) of the Pneumotaxic Centers in the Respiratory Control Center. This, in turn, impairs the Pneumotaxic Centers’ ability to inhibit the Apneustic Centers, which become hyperactive and facilitate an increase in the length and depth of inspiration.  Relating this to the previously outlined link between heart and ventilatory functions, the increase in heart rate caused by direct sympathetic innervation to the heart is reinforced by increased inspiratory activity caused by decreased ventral vagal tone and inhibition of the Pneumotaxic Centers of the Respiratory Control Center; this is another example of redundant control.

The takeaway is that humans, in addition to other mammals, have the unique ability to respond to a perceived threat by inhibition of sympathetic outflow via the ventral portion of the vagus nerve.  In the face of chronic or a high level of stress, however, ventral vagal tone can decrease and we can regress to the more primal response of increasing sympathetic nervous system activation, i.e. initiate the fight-or-flight response.  In this case, greater sympathetic outflow to the heart will increase its rate and force of contraction, while increases in epinephrine and norepinephrine circulating in the blood will lead to a decrease in blood flow to non-active skeletal muscle and most visceral organs and an increase in blood flow to active skeletal muscle, the liver, and the heart.  Increased firing rate of pathways connecting the limbic system to the motor neurons controlling respiratory muscles causes an increase in overall ventilation rate, while sympathetic input to the respiratory control center secondary to a decrease in ventral vagal tone causes an increase in the depth and length of inspiration and a relative decrease in the depth of length of expiration.

Sympathetic Nervous System Activation: Downstream Effects on Skeletal Muscle 

In the first installment, I described potential direct and indirect mechanisms by which the sympathetic nervous system can potentially influence resting muscle tone via gamma motor neurons innervating muscle spindles and beta-adrenergic receptors that interact with the neuromuscular junction and the sarcoplasmic reticulum.  Earlier in this article, I also described how an increase in sympathetic outflow leads to increased blood flow to active skeletal muscles, decreased blood flow to inactive skeletal muscles, and an increase in the activity of respiratory muscles.  There is one other downstream effect of sympathetic nervous system stimulation on skeletal muscle that I’d like to introduce, and it once again relates to the cardiorespiratory system.  While the ratio of inhalation to exhalation length and depth increases with sympathetic activation, the overall increase in ventilatory rate allows for increased clearance of carbon dioxide, which is a byproduct of cellular metabolism that is produced in greater amounts when metabolic activity in tissues is high.  As you can imagine, this is beneficial during times of exercise or fighting off/fleeing from a threat where metabolic demand of skeletal muscle, liver, and heart tissues will be very high, and thus CO2 accumulation will warrant its clearance.

A problem may arise, however, when sympathetic activation stimulates an increase in ventilatory activity in the absence of significantly increased metabolic demand, as could be the case when the VVC chronically fails to inhibit sympathetic outflow and we become engrained in a sympathetic-dominant state.  This system rigidity and inability to vary autonomic states may still facilitate the clearance of CO2, even if it’s not appreciably accumulating in tissues.  When blood CO2 levels fall even in minuscule amounts, blood pH rises (i.e. it becomes less acidic) and shifts the saturation curve of oxyhemoglobin to the left, a phenomena called the Bohr Effect.  This means that oxyhemoglobin, which is responsible for transporting oxygen to tissues, will have a higher affinity for oxygen at any given partial pressure of oxygen in the bloodstream.  This, in turn, impairs oxyhemoglobin’s ability to unload oxygen to the tissues, including to myoglobin in muscle tissue.  Oxidative metabolism in muscle tissue subsequently suffers, forcing the cells in these tissues to rely heavily on non-oxidative (i.e. anaerobic) metabolism.  Non-oxidative metabolism is insufficient in producing enough ATP for muscle contraction in the long-term, since oxidative metabolism is far more efficient in terms of ATP production.  Lack of ATP renders actin-myosin cross bridges that have formed unable to dissociate, a phenomena that also occurs to an obviously far greater extent in rigor mortis.  The result is a relatively rigid, shortened muscle.  Theoretically, the muscles that would be most affected by this decrease in oxyhemoglobin unloading and subsequent tissue oxygenation would be those  receiving the greatest amount of blood flow due to sympathetic-mediated vasodilation of their blood vessels, which would also be the muscles with the highest metabolic demand and work rate.  Remember that point, since it will resurface in the next couple of installments when I delve into specific patterns of muscle activity and movement.  Also of note is that anaerobic metabolism is inefficient in producing CO2 as a byproduct in comparison to oxidative metabolism.  Thus, a shift from predominately oxidative to anaerobic metabolism via chronic elevated sympathetic tone could have the effect of producing a self-sustaining or even positive feedback loop.

The takeaway here is, as I emphasized in part one, an increase in sympathetic outflow is not inherently bad, but it can cause problems when we are unable to shift out of it and into a more parasympathetic-dominant state. With regards to cardiorespiratory function, increased carbon dioxide clearance due to an increase in ventilation rate during short-term sympathetic activation is absolutely beneficial in ridding the tissues of CO2 that accumulates as a byproduct of metabolic activity.  In the long-term, however, increased clearance of CO2 in the absence of increased metabolic demand can lead to decreased oxygenation of tissues, including skeletal muscle.  The resulting shift in the affected cells from predominately oxidative to glycolytic activity may eventually impair ATP production, which, in the case of skeletal muscle, limits the release of actin-myosin cross bridges.  The net result is that the muscle becomes relatively rigid and shortened.  The muscles most affected by this mechanism are those which receive the greatest blood supply, i.e. the muscles that are doing the most work.

  

Wrapping Up

I know I threw quite a bit at you in this post, so I’m going to stop there for both your sake and mine.  I hope that this post allows you to understand the link between the neurological underpinnings of PRI outlined in the first installment and the biochemical and physiological processes by which these neurological mechanisms affect skeletal muscle.  The next post, in turn, will serve to connect these biochemical and physiological processes to the “big picture” of muscle activity, postural compensations, and movement patterns that PRI emphasizes.

References

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Posted November 16, 2014 at 1:46PM
Categories: Courses Athletics Science
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