Courses

Here is the 2014 weather report for Advanced Integration. Looks like it will be some pretty good weather (by Nebraska standards at least).

Posted December 2, 2014 at 8:03PM
Categories: Courses

We had a fantastic weekend in Scottsdale at Salt River Fields with the staff of The Arizona Diamondbacks and large room full of passionate baseball professionals. A big thanks to Ken, Ryan, Nate, Neil, Andrew and all the rest for making us feel so welcome once again. Your level of professionalism, humility and innovation as an organization continues to amaze me. It was an honor to work together in the development and presentation of this course with one of the most proficient clinicians in performance and advanced biomechanics I've ever met, Allen Gruver, PT, ATC, CSCS, PRC. Since his days as my student intern 14 years ago, Allen has challenged my thinking and helped me analyze the details of the asymmetrical human machine more than just about anyone else.

I was especially grateful for all the first time attendees in this course and the opportunity to present basic PRI principles and also principles of baseball integration to a fresh audience. You are why we developed this material and a big part of why the weekend was so great. Thanks for your interest in PRI and the way we approach the patterned baseball athlete. I hope we can be supportive of your learning process if you choose to take further PRI courses, but hope you feel like you've been given enough material to have success with baseball athletes if you choose not to. It was a great experience developing this material for you guys and rewarding for Allen and I to put something together that has the potential to benefit both the new and the experienced PRI clinician.



 

Posted November 20, 2014 at 7:11PM
Categories: Courses

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

  • Fouad et. al: Assessment of parasympathetic control of heart rate by a noninvasive method. Am J Physiol. June 1984;246(6): 838-842.
  • Yamamoto et. al: Autonomic control of heart rate during exercise studied by heart rate variability spectral analysis. J Appl Physiol. September 1991;71(3): 1136-1142.
  • St-John W & Paton J: Role of pontile mechanisms in the neurogenesis of eupnea. Respire Physiol Neurobiol. November 2004;143(2-3): 321-332.
  • Feldman J & Del Negro C: Looking for inspiration: new perspectives on respiratory rhythm. Nat Rev Neurosci. March 2006;7(3): 232.
  • Lefaucheur J & Lofaso F: Diaphragmatic silent period to transcranial magnetic cortical stimulation for assessing cortical motor control of the diaphragm. Exp Brain Res. October 2002;146(3): 404-409.
  • Ward D & Karan S: Effects of pain and arousal on the control of breathing. J Anesth. 2002;16(3): 216-221.
  • Critchley H et. al: Human cingulate cortex and autonomic control: converging neuroimaging and clinical evidence. Brain. October 2003;126(10): 2139-2152.
  • Sloan et. al: Effect of mental stress throughout the day on cardiac autonomic control. Biol Psychol. March 1994;37(2): 89-99.
  • Porges S: The polyvagal theory: New insights into adaptive reactions of the autonomic nervous system. Cleve Clin J Med. April 2009;76(2): 86-90.
  • Rankin J et. al: The effects of airway pressure on cardiac function in intact dogs and man. Circulation. July 1982;66(1): 108-120.
  • Seals D et. al: Influence of lung volume on sympathetic nerve discharge in normal humans. Circ Res. July 1990;67(1): 130-141.
  • Preiss et. al: Patterning of sympathetic preganglionic neuron firing by the central respiratory drive. Brain Res. April 1975;87(2-3): 363-374.
  • Gotoh F et. al: Cerebral effects of hyperventilation in man. Arch Neurol. 1965;12(4): 410-423.
  • Lum L: Hyperventilation: The tip and the iceberg. J Psychosom Res. 1975;19(5-6): 375-383.
  • Bishop D et. al: Induced metabolic alkalosis affects muscle metabolism and repeated-sprint ability. Med Sci Sports Exerc. May 2004;36(5): 807-813.
  • Hollidge-Horvat M et. al: Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise. Am J Physiol Endocrinol Metab. February 2000;278(2): 316-329.
  • Bellingham A et. al: Regulatory mechanisms of hemoglobin oxygen affinity in acidosis and alkalosis. J Clin Invest. March 1971;50(3): 700-706.
  • Relman A: Metabolic consequences of acid-base disorders. Kidney Int. May 1972;1(5): 347-359.
  • Skinner J & McLellan T: The Transition from Aerobic to Anaerobic Metabolism. Res Q Exerc Sport. March 1980;51(1): 234-248.
  • Howard H et. al: Effects of Chronic Hypoxia on Muscle Enzyme Activities. Int J Sports Med. February 1990;11(1): 10-14.
  • Fitts R: The cross-bridge cycle and skeletal muscle fatigue. J Appl Physiol. February 2008;104(2): 551-558.
  • Iorga B et. al: ATP binding and cross-bridge detachment steps during full Ca²⁺ activation: comparison of myofibril and muscle fibre mechanics by sinusoidal analysis. J Physiol. July 2012;590(14): 3361-3373.
  • Yu L & Brenner B: Structures of actomyosin crossbridges in relaxed and rigor muscle fibers. Biophys J. March 1989;55(3): 441-453.
  • Nelson C & Fitts R: Collective effects of low cell pH and inorganic phosphate on force, velocity, stiffness, and power in rat slow and fast muscle fibers. FASEB J. April 2014;28(1): 1102.7.
Posted November 16, 2014 at 1:46PM
Categories: Courses Athletics Science

I enjoyed a great weekend enhancing performance through the integration of neurologic reference centers in Salem, OR. We looked at the wonderful human system of asymmetrical systems and worked to help lateralize all things toward the left. I also met two wild and crazy Australians, Craig Ambler (the good looking red head) and Mark Barclay (the more mature looking one) all the way from Wagga Wagga, New South Wales. Mark, Craig told me to say both of those things. These guys rented a bright yellow muscle car they could barely control and then struggled to drive on the left side of the car while they negotiated the car down the right side of the road. "How is it that you Americans get away with driving on the wrong side of the road?" "How is it that you Australians get away with driving on the wrong side of the car?" Two Aussies from the rural Outback trying to drive an American Muscle Car on the wrong side of the road. Can you imagine? We thought it fitting that our group picture was taken with these two Aussies who were having a hard time sitting in the left half of a muscle car they could barely control (sounds very Impingement & Instability to me). And Jen Poulin, PT, PRC, I know this story isn't exactly the proverbial "Yellow VW Bug" story you tell so well, but I thought it was great that the muscle car was yellow. And a big thank you to my good friends Raulan Young, MPT, PRC and Tara Osborne, DPT, PRC for coming all the way from Idaho to spend a weekend with PRI Neurology. It was good to have both of you there. And by the way, Craig and Mark, I think we're the ones driving on the wrong side of the road!

Posted November 13, 2014 at 8:01PM
Categories: Courses

Thanks again to Allina Commons in Minneapolis for hosting the Pelvis Restoration course this past weekend. We had 58 course attendees from PTs, DCs, OTR/L, ATC, CSCS, PTAs and PT/PTA students in the room. Despite losing my voice, we had a great weekend! The course participants were awesome with their understanding, questions, and learning a lot of new material. I feel a better understanding of how important the pelvis is in integrating respiration was achieved.

Posted November 11, 2014 at 3:39PM
Categories: Courses

What a great weekend in one of my favorite states, North Carolina teaching the PRI Integration for the Home course! I can't decide if it was the beautiful fall weather or just the beautiful people and that Carolina hospitality that make coming to this area so special. Thank you Craig Kerbo for all your tireless efforts making this course happen and for being such a gracious host. And thank you to my good friend and PRI faculty member, Jen Poulin, PT, PRC for joining me as the lab assistant. We were blessed with a great mix of brand new clinicians and also PRI experienced therapists, including 4 PRC's! The focus was on breathing and alternating reciprocal gait, with special attention given to inhibiting the Left AIC to maximize left stance time and to improve balance to decrease risk of falling. Saturday evening several of us enjoyed a nice evening in downtown Greensboro and were happy to find the statue of General Nathan Greene, because he is likewise focused on maintaining Left AIC inhibition longer in late left stance to optimize his gait.

Posted October 29, 2014 at 6:27PM
Categories: Courses

The cortical, pre-frontal lobe and temporal power that was in the room at this last weekend’s course in Phoenix at East Valley Spine and Sports Medicine was unbelievable!!  The 25 class attendees had close to 200 PRI courses behind them.  Some of them had taken 15 to 16 courses prior to this one.  We rolled through TMCC with constant and consistent integrated thinking that will help with the revisions that will be made for the upcoming Cervical Revolution: An Integrated Approach to the Treatment of Patterned Cervical Rotation, being taught in early 2015. Thank you East Valley Spine and Sports Medicine for a wonderful weekend of cranial “ expansion” and for your ongoing hospitality over the years with all the PRI courses you host!

Posted October 23, 2014 at 10:16PM
Categories: Courses

Author's Note: The following is an article I wrote for my blog, Integrative Human Performance.  I intend to turn it into a three-part series aimed at introducing patients and professionals alike to the basics of PRI.  Click here to view the post in its original format.

An Introduction to the Postural Restoration Institute, Part 1: The Neurological Nature of PRI

If you’ve worked with, talked to, or read articles by myself in the last few years, then you’ve inevitably heard me discuss or reference the Postural Restoration Institute.  While PRI has become quite popular in many circles within the physical therapy and strength and conditioning fields, there are still many practitioners and non-experts alike who have not heard of it or don’t fully understand what it is.  So, I’m going to do my best to introduce PRI, explain why I find it useful, and discuss how I implement it in my programs.  Due to the abundance of information that this entails, I’ve decided to split this into a three-part series; this first installment will cover the history of PRI as well as the neurological foundation on which it is based.

The History of PRI

The Postural Restoration Institute was founded in 1999 in Lincoln, Nebraska by physical therapist Ron Hruska.  Over the course of his clinical experience to that point, Ron had noticed specific patterns in the majority of his patients and found that, despite the varying nature of their issues, a common approach to their treatment often resulted in significant improvement in function.  As a result, he focused on learning about the asymmetrical nature of the human body and how to integrate those imbalances into a treatment program. Thus, the science behind PRI was born. 

But what exactly is PRI? For many, the buzzword “posture” immediately comes to mind.  This is not entirely inaccurate, since assessment of static and dynamic posture and subsequent attempts to restore neutrality are a critical component of the PRI treatment philosophy.  But rather than the be-all-end-all, posture is more of a means to an end for PRI practitioners–it’s a valuable tool for assessing the neurobiological state of the patient.  To sum up a tremendously complex methodology as succinctly as possible, PRI is a treatment approach that assesses the adaptability of the nervous system to various environmental stimuli via autonomic nervous system-mediated muscle activity and movement.  That’s quite a mouthful, so let’s see if I can break it down for you, starting with the structure and function of the autonomic nervous system.

The Autonomic Nervous System: Structure

If you think back to your high school or college anatomy class, you might recall that there are a bunch of subdivisions of the nervous system.  The first subdivision is made up of the Central Nervous System (CNS), which consists of the brain and spinal cord, and the Peripheral Nervous System (PNS), which consists of all of the nerves and ganglia that lie outside of the brain and spinal cord.  Depending on the source, you might see the Peripheral Nervous System then subdivided into sensory and motor divisions, with the Autonomic Nervous System (ANS) being a further subdivision of the latter.  This isn’t entirely accurate, however, since the ANS does contain sensory afferents.  In fact, the parceling of the ANS into the Peripheral Nervous System is also not exactly correct, since the cell bodies for some neurons of the ANS reside in the gray matter of the spinal cord. In addition, the executive control of many of the functions of the ANS belong to the medulla in the brainstem, while regulatory control belongs to other structures of the limbic system. In order to appreciate the wide-ranging physiological effects that the autonomic nervous system has, it is important to understand that there is significant interplay and overlap between it and what are traditionally considered the Somatic Nervous System–the division of the PNS typically associated with voluntary movements of skeletal muscle–and the Central Nervous System.

The Autonomic Nervous System: Function

 

Direct Influences on Skeletal Muscle

In general, the autonomic nervous system monitors and controls visceral functions that are below the level of consciousness, including breathing, heart rate, salivation, perspiration, and pupillary dilation.  Though there is limited evidence of direct modulation of skeletal muscle activity by the autonomic nervous system in humans, there is a much larger body of evidence in experimental animals, such as cats and rabbits. It has been proposed, for example, that thin, unmyelinated sympathetic efferents innervate intrafusal muscle fibers in muscle spindles, which monitor and regulate muscle length and tone. Again, while the bulk of the evidence is in experimental animals, these findings would imply that an increase in sympathetic outflow could affect skeletal muscle tone or length. Furthermore, beta-adrenergic receptors have been confirmed to be present on the sarcolemma of muscle cells.  These receptors have a particularly high affinity for epinephrine (EPI), which is a hormone released by the adrenal medulla following sympathetic nervous system activation by post-ganglionic sympathetic fibers. This presence could have a number of potential effects on skeletal muscle, each of which have varying levels of in vitro and in vivo evidence in animals and humans, including:

-potentiation of the Na+/K+ pump to attenuate fatigue

-augmentation of acetylcholine (ACh) release at the motor end plate

-a positive inotropic effect (an increase in twitch force) due to interaction with ryanodine receptors that increases calcium ion release from the sarcoplasmic reticulum

-a positive lusotropic effect (an increase in relaxation rate) due to interaction with the calcium ion pump inhibitor phospholamban that increases calcium ion reuptake into the sarcoplasmic reticulum

Interestingly, the beta-adrenergic receptors are more densely distributed on Type I muscle fibers than Type II muscle fibers. Coupled with the fact that Type II fibers lack phospholamban, it is possible that the aforementioned effects are more prominent in Type I muscle fibers, which are generally present in higher proportions in anti-gravity postural muscles such as the hamstrings and in lower proportions in hip flexors like the vastes muscles.  This will come into play in later installments of this series when I discuss specific patterns of motor activity described by the PRI model.  The takeaway here is that the autonomic nervous system–specifically the sympathetic division–may exert some degree of direct influence over skeletal muscle, enabling it to augment motor output factors such as muscle tone, muscle length, twitch force, and relaxation rate.

Indirect Effects on Skeletal Muscle

The ANS can also affect skeletal muscle independent of the aforementioned direct mechanisms. Indirect effects are due to closely-tied neural pathways.  Limbic system inputs to the reticular formation in the pons and medulla modulate autonomic function as well as posture and muscle tone via the descending pathways of the reticulospinal tract.  The limbic system is largely responsible for functions dealing with emotion, behavior, motivation, and threat appraisal, which would make sense in the context of its relation to autonomic and muscle function; emotional responses such as fear or arousal are known to affect both autonomic functions (such as blood pressure and ventilation rate) via autonomic ganglia as well as resting muscle tone via gamma motor neurons that innervate the intrafusal muscle fibers of muscle spindles.  The takeaway, then, is that regardless of the strength of the evidence supporting a direct effect of the ANS on skeletal muscle, the ANS undoubtedly influences characteristics of skeletal muscle and motor activity indirectly via subcortical input and reticulospinal pathways in response to emotional or threatening stimuli.  

Subdivisions of the Autonomic Nervous System

The autonomic nervous system itself can be further subdivided into parasympathetic and sympathetic divisions.  The parasympathetic division is usually characterized as responsible for “rest and digest” functions, while the sympathetic division is characterized as responsible for “fight or flight” functions.  While sympathetic activation can generally be thought of as an increase in effector activity and parasympathetic activation can generally be thought of as a decrease in effector activity, this is not always the case.  It is important to note, however, that most organs receive dual innervation by both divisions, which are concomitantly active to varying degrees.  Thus, while someone might be described as being in a “sympathetic state,” that does not mean that the parasympathetic division has been turned off. Rather, it means that the parasympathetic division’s input has been decreased or its associated receptors have been down-regulated or desensitized.

The sympathetic nervous system is known to be activated by stress.  The human body is effectively indiscriminate about the nature of the stress, which means that psychological, emotional, and physical stresses elicit a similar response, although that response may vary in intensity.  While many are quick to demonize sympathetic activity and frame it as detrimental to health, it would be shortsighted to overlook the fact that sympathetic nervous system activation is a normal physiological response that is necessary for our survival.  Problems can arise, however, when the sympathetic nervous system is overstimulated as a result of chronic stress and/or the Ventral Vagal Complex (VVC), a branch of the vagus nerve which is normally responsible for inhibiting sympathetic response in the face of stress, fails to do so.

Much like the sympathetic system, the parasympathetic system is physiologically crucial to our survival, and decreasing its activity secondary to increased activation of the sympathetic system can impair the “rest and digest” functions that are critical to recovery and general physical and mental health.  Thus, if we constantly bombard ourselves with various forms of stress and/or impair the ability of the VVC to regulate sympathetic output, never letting the ratio of autonomic activity return to a state that’s more parasympathetic-dominant, then we are promoting rigidity of the autonomic system, which impairs our ability to adapt to different stressful stimuli.  To put it another way, the VVC acting as a brake on sympathetic output allows us to respond to stresses in a variety of ways; we can respond to a certain stress with self-calming or with social behaviors, or we can respond with the typical fight or flight response.  Failure of the VVC to inhibit defensive neural circuits, however, limits us to a single type of response that is, when chronically activated, extremely costly both physically and mentally.  Using the analogy of a light switch, it’s not that “turning on” the switch is problematic, it’s that being unable to “turn the switch off” can prove to be costly in the long run.

Wrapping Up: Practical Implications

Why should you care about any of this?  With regards to athletes, it’s been said that the best are not the ones who can get “jacked up,” or into a sympathetic-dominant state, the fastest, but rather the ones who can most efficiently switch out of a sympathetic-dominant state and into a more parasympathetic-dominant resting state.  This makes sense logically: if you’re not working, then you should be resting to conserve and restore energy, and an inability of the nervous system to adapt to this change in stimuli or to depress sympathetic activation in the face of stress (via VVC activity) and shift autonomic states can impair this process.  This notion has been bolstered by studies examining the relationship between vagal tone and heart rate variability, which are known to reflect autonomic nervous system activity and have been linked to general health concerns such as cardiovascular disease, hypertension, and depression, as well as fitness-specific concerns such as overtraining or detraining. With regards to the general population, it is possible that this same mechanism is related to the biopsychosocial model of pain. Psychological and social stress has been linked to failure to alleviate conditions involving pain, so it is possible that failure of the VVC complex to mitigate chronic sympathetic activation plays a role. While this has been postulated in the literature, the evidence for this particular relationship in vivo in humans is scant at this point in time.

With the link between the ANS and motor output (primarily via sympathetic influence on skeletal muscle activity) established, I will delve into the specific patterns of activity that PRI describes and how to identify and address them in the next two posts in this series. My goal for this post was to get you to understand that while on the surface PRI methods may seem to address undesirable postural patterns and suboptimal muscle activity, the actual underlying philosophical nature of treatment is to address imbalance in the activity of the nervous system and restore the ability of the ANS to adapt to various environmental stimuli. In the words of PRI practitioner/preacher Mike Cantrell: “PRI is all neuro, all the time.”

 

References

  • Roatta S & Farina D: Sympathetic actions on the skeletal muscle. Exerc Sport Sci Rev. 2010;38(1): 31-35.
  • Passatore M & Roatta S: Influence of sympathetic nervous system on sensorimotor function: whiplash associated disorders (WAD) as a model. Euro J Appl Physiol. 2006;98: 423-449.
  • Santini M & Ibata Y: The fine structure of thin unmyelinated axons within muscle spindles. Brain Research. 1971;33: 289-302.
  • Ondicova K & Mravec B: Multilevel interactions between the sympathetic and parasympathetic nervous systems: a mini-review. Endocr Regul. 2010;44(2): 69-75.
  • Boulton et. al: Effects of contraction intensity on sympathetic nerve activity to active human skeletal muscle. Front Physiol. 2014;5: 194.
  • Birznieks et. al: Modulation of human muscle spindle discharge by arterial pulsations – functional effects and consequences. PLoS one 7.4, 2012.
  • Lynch G & Ryall J: Role of β-adrenoceptor signaling in skeletal muscle: implications for muscle wasting and disease. Physiological Reviews. 2008;88(2): 729-767.
  • Knutson G & Owens E: Active and passive characteristics of muscle tone and their relationship to models of subluxation/joint dysfunction. J Can Chiropr Assoc. 2003;47(4): 269-283.
  • Alvares G et. al: Reduced heart rate variability in social anxiety disorder: associations with gender and symptom severity. PLoS one 8.7, 2013.
Posted October 23, 2014 at 3:00AM
Categories: Courses Athletics

The Portland, OR Pelvis Restoration course was awesome this past weekend! Clinicians appreciated the pelvic inlet and the importance of its position during stance and swing phases of gait. This position is imperative for synchronizing respiratory and pelvic diaphragms....without that can you say neck, shoulder, hip, knee, and foot instability.  Thanks Shine Integrative Physical Therapy for hosting!  Bonus for me?  I got attend a PRI Yoga session. Fabulous!!!  Thanks Emily and Alice.
Thanks course participants for your inquisitive minds and as James says "drinking the PRI kool-aid!"

Posted October 22, 2014 at 10:55PM
Categories: Courses

I am not sure where to begin with this course in review!  First I was blessed to share some extra time in the Big Apple with my husband Chris!  This October, we celebrated 15 years of marriage and it has been an amazing ride. This was my last course of 2014 and only my second Pelvis Restoration course of the year.  I so thoroughly enjoyed teaching the course attendees all about the power of respiration as it relates to the “Diaphragmssss” It was a year of AFIR and Myokinematics, but this past weekend was a nice divergence to the IPER and IsPIRs of the Pelvic Inlet and Outlet.  It was great to help the course attendees connect the dots from Myokinematic Restoration and Postural Respiration with Pelvis Restoration. We had a great time discussing patterns and how it is important to move in and out of patterns through life.  This concept resonated with the entire class!  My class also had a record number of PT students. It is so refreshing to share in their enthusiasm for learning.  Here’s to Brynn from Finish Line Physical Therapy for being a great host. I have made so many new PRI friends this past year and that makes all the sacrifice of travel and being away from my family all worthwhile!  I have enjoyed visiting cities like Boston, Dallas,  Indianapolis, Montreal, Madison, Canton, Pittsburgh, Cary, Tampa Bay, Seattle to name just a few.   Until we meet again #PRINATION, looking forward to taking a seat and a nice winters rest.  See y’all in 2015!

Posted October 22, 2014 at 3:43PM
Categories: Courses
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