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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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• 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.
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• 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.
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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.

Hello triplanar thinkers!

For those wondering, the picture is relevant because it shows a technique not often considered for the condition treated:  keeping a severed hand alive by grafting it to the patient’s ankle, then later replanting the hand back on his arm. 

The conclusion of my story about Don didn’t involve any external fixators, but the treatment that he needed might surprise some of you.  To review, Don was the patient with left shoulder bicipital tendinosis whom I treated in part I (link) with the “gold standard” conservative orthopedic approach and part II (link) with the according postoperative approach as a good therapist has been trained to.  As mentioned, I outline this case to review the path that is so very accepted and yet, in my experience since I began training with PRI, not the most effective.  Don’s story concludes below:

Don returned to clinic 8 months after discharge with a new diagnosis of left shoulder pain with the remarks on the script “MRI negative” and “eval and treat.”  This is generally understood as physician lingo for “I have no idea what to do now…good luck with all that.” 

Upon evaluation, Don reported that these left shoulder symptoms started about 2-3 months after we discharged him from PT intervention in spite of his persistence with his HEP and “it was all back to the starting point three months later.”  He still tested as a bilateral brachial chain patient with a PEC pattern, again was positive with impingement tests—Hawkins-kennedy, empty can, Neer sign.  He was frustrated, unable to work in his wood shop or play his accordion for more than 10 minutes without severe pain.  At this point, the patient and I discussed that fact that I had let him down to a degree because I wanted to take a different approach before surgery, but didn’t want to irritate Don or his referral source.  He understood, accepted my apology and we moved forward.

During the first 3 visits, we established that his bilateral brachial chain pattern and according left shoulder dysfunction was not the root of his dysfunction, but rather the manifestation of a “bottom up” pelvis patient whose primary difficulty was in maintaining frontal plane position of his pelvis. 

The key to Don’s left shoulder function?  Right posterior inlet inhibition of his pelvis.  During the seven visits we treated Don using a PRI approach after the gold standard of orthopedic medicine and orthopedic physical therapy had failed to maintain his shoulder function for more than 3 months, his symptoms resolved.  He left the clinic a reciprocal, alternating, smiling woodshop athlete with bilateral HADLT tests of 4/5 at 72 years of age, “tickled” that he could play his accordion as long as he wanted without pain for the first time since before he first went to see the doctor more than two years prior.  Don is in occasional contact for the past 6 months with no return of symptoms, lots of activity and happy thoughts. 

Six-month follow-up with no return of symptoms after the rest of my conservative clinical skills, an appropriate surgery and present day gold-standard postoperative care was unsuccessful.  These are the types of outcomes that keep my passion for this science alive and accelerating.  Moreover, these are the types of patient successes that remind me to be gentle but bold about intervention that I know clinically to be the most effective tool I have in the entire tool chest.

Clearly, each patient is different, and no, I have not seen a consistent correlation over time between the diagnosis of left shoulder bicipital tendinosis and the need for right posterior inlet inhibition.  The objective tests guided me to find the appropriate treatment, not my innate ability to hear the pelvis or shoulder speak to me. 

The point here is not to create a case study for anyone to memorize to use in the future for that one seemingly random patient.  Rather, I hope that the take home is that there is a chance that this gentleman didn’t need as much intervention as he ended up having.  And, even in the face of the “old school” telling you exactly what they want from PT intervention, the risk is worth the reward if one can just take the first three or four visits to break down barriers to a different way of approaching an age-old mechanical dysfunction of a “shoulder.”

Thank you for reading, perhaps you can save a few visits for a few of your patients by way of my experience with Don.   My best to you!

Jess

I have the benefit of being associated with some outstanding thinkers and PRI practitioners.  Whenever and wherever we get together, conversation eventually drifts toward discussion of PRI principles and application.  One of our greatest challenges has been to unravel the foundations from which Ron Hruska evolved the Postural Restoration Institute system of evaluation and treatment that we all utilize with such great success. 

The following are just a couple of questions that we have posed and our attempts to reach conclusions and greater understanding.  If anything it may stimulate some thought and initiate some discussion.

What are we actually measuring when we place a patient on the treatment table and perform our PRI testing algorithm and what is our goal for treatment?

I clearly recall a conversation over lunch between Eric Oetter, Mike Robertson, and myself during the PRI Pelvis Restoration course at the Cantrell Center for Physical Therapy and Wellness. We were discussing the concepts of adaptive capacity, adaptive potential, movement variability, what we are actually measuring when evaluating a patient on the treatment table, and how this affects performance.  

Our conclusion was that what we are actually measuring as PRI-educated therapists and coaches is the capacity of our client/athlete to adapt to the ever chaotic nature of the environment they are perceiving.  Positive findings during examination such as a positive Adduction Drop Test, limited apical expansion, or loss of shoulder rotation was merely indicative of a human system incapable of demonstrating variability ultimately controlled by the central nervous system.  More specifically an autonomic nervous system shift toward sympathetic dominance.

I was reminded of this PRI lunch after reading a blog post recently that referenced the following study:

http://www.ncbi.nlm.nih.gov/pubmed/24502841

In essence, what the researchers found in the study was that pain-free subjects demonstrated variability in the muscle activity of the erector spinae during a repetitive lifting task and those with low back pain did not demonstrate this variability as well as experiencing increased pain during the task.

The authors’ conclusion was that reduced variability of muscle activity may have important implications for the provocation and recurrence of LBP due to repetitive tasks.

Needless to say, this study is somewhat validating for our discussion group of PRI faithful.

Truth be told, after searching there are many studies that support our lunchtime conclusion; and movement variability as a favorable concept in human function is not a new concept having its foundations in dynamic systems theory. 

From Shumway-Cook and Woollacott’s Motor Control:  Translating Research into Clinical Practice:

“… in dynamic systems theory, variability is not considered to be the result of error, but rather as a necessary condition of optimal function.  Optimal variability provides for flexible, adaptive strategies, allowing adjustment to environmental change, and as such is a central feature of normal movement.”

What the PRI model provides is a non-invasive real-time measurement of system variability determined by autonomic nervous system tone.  While EEG, heart rate variability, or galvanic skin response may be preferred methods to determine autonomic tone, these are not tools commonly used by a practicing physical therapist in a clinical setting or a coach in the training room nor would they be practical. 

The goal of treatment then becomes restoring an optimal level of variability to the system to allow for optimization of behavior and maximization of performance.

We came up with a statement that encompassed our entire discussion that included the influence of variability on pain and performance.  I still have the notes on my iPhone dated 8/24/13: 

“Restoring variability to the human system is the ultimate goal to promote neuroplastic change creating a relatively permanent change in behavior that provides adaptability within the system to cope with variability in the environment.”

In PRI terms, our goal is help a patient achieve neutral (restore variability) and then recruit the appropriate PRI planar families (neuroplastic change to remap the three planes in the brain… Thanks to Zac Cupples!) to restore reciprocal and alternating movement (change behavior to cope with the environment).

How did Ron Hruska arrive at the concept of using simple, common orthopedic tests as effective PRI measurement tools?

As mentioned above, as physical therapists our measurement tools are limited by practicality.  If we look at PRI from a strictly biomechanical perspective, the PRI methodology provides for a low barrier of entry to a PT who has never been exposed to its concepts before.  Myokinematic Restoration looks, sounds, and feels like biomechanical course, but we all know that it is not.  This is a brilliant way to provide understanding to a group with more than a few preconceived notions, right?

While I certainly cannot speak for Ron, and I’m willing to be wrong, I believe there is more to this process, and this came from a conversation I had with Eric Oetter over Sunday breakfast.

From our first day in an introductory PRI course we are shown that asymmetry because of in-utero development and positioning, brain hemispheric dominance, asymmetrical vestibular development, and internal anatomical differences is normal, expected, and predictable.  Determining patterning that represents discord in the system then seems to be impossible until your realize that the skeletal system, is inherently symmetrical.  Therefore there is no better way for a physical therapist to determine the state of the system as a whole than identifying asymmetries or patterns via our typical orthopedic testing.

The brain processes and integrates all sensory inputs, internal and external, and generates behavior, including motor behavior, based on our perceptions with respect to the environment, emotional status, and previous experiences.  I don’t think it’s unreasonable to consider that the ability to produce reciprocal and alternating movement is not only an effective measure of autonomic tone but also a key measurement of overall health.

Bill Hartman, PT

“Its Monday Morning, I’ve just taken my first PRI course and now what do I do and where do I start?”

If you have just taken your first PRI course and you feel a bit overloaded with information, don’t feel alone.  The first time I went to a PRI course, can I tell you I was intrigued, stunned and just a bit intimidated all at the same time?  I didn’t know what the heck I was doing so on Monday morning I had a bunch of people blowing up balloons! (Take the Postural Respiration course and you will know what I mean!)

In fact, the entire body of knowledge of PRI can feel like one big elephant you are trying to digest.  And you know the old question, how do you eat an elephant?  One bite at a time!

The first thing to do is what you learn in every course and that is to breathe and relax. There is a lot information here that needs to sink in over time and you won’t get it all the first time. No one that has taken one of these courses has gotten it all the first time but if a door is opened to your curiosity and caring to learn more you are definitely on the right track!

What helped me in my overwhelm was to create a picture in my mind of some of the basics.  For instance, we aren’t symmetrical and never will be but the point is to manage asymmetries and get neutral. Then, have a simple picture anatomically of the basic asymmetries left and right side and how they affect position and posture thru polyarticular chains.  Remember how the diaphragm is the key player and you have a simple way to describe what you are doing to yourself, patients or clients.  They will be impressed by just a short, and I mean short, description of their anatomy and how it affects them.

On Monday morning, pick one person you feel comfortable with to experiment on.  If you have a colleague that has gone to a course practice with them.   Tell your patient that you just got out of a course and you want to try some powerful tools with them.    If you took a Myokinematics course, practice an abduction drop test and show them one basic exercise.  It is best that you practice that exercise yourself and continue to practice PRI tests and exercises yourself, so you know what it feels like and what to feel when you are in position for facilitation and inhibition.  PRI works best when we are managing our own asymmetries!

Immediately you have knowledge and application of assessment and corrective positioning that is really sophisticated and you have just scratched the surface.  You can build on this by learning a new assessment or two with a new corrective position every day.

Have your manual close.  Refer to it, study it and get a more detailed picture in your mind of how the human body works and how you can be more effective.  This is called building a body of knowledge and it doesn’t happen overnight but you can get results and get excited with just the basics and build on top of them.

If you went to a live seminar, order the home study course and review it a few times.  If you got a home course, go to a live course to interact with the instructor and fellow students.  Pack a bunch of questions in your bag when you go!  If you get a little frustrated with all the information and it doesn’t make sense all at once, then you are a normal human being!  Hang in there.  The good news is that becoming more skilled and competent is satisfying and meaningful and that building a body of knowledge and expanding what you know is just plain fun!   

To summarize part I for those who didn’t see it, I treated a gentleman with biceps tendinosis giving my best efforts to treat within the realm of what the patient and his physician expected.  He was pleased, reported 90% improvement and had met all but one of his functional goals—and I wasn’t content.  I wasn’t content because I hadn’t been bold/confident enough to risk the referral source by advocating for the patient like I had wanted to.  When things had a hitch, I had broached the subject of asymmetry several times, with a discussion of thorax and diaphragm position combined with respiration being key to arthrokinematics and myokinematics of the affected left shoulder briefly.  But the feedback each time was something of the “dang kids and their wide-eyed plans.”  So, I deferred to the ‘gold standard’ treatment of the day for said diagnosis outlined briefly in part I of this story with some PRI principles intertwined the best I could without the patient’s objection.

Three months later, Don arrived for this second round of PT with a diagnosis of left shoulder s/p arthroscopic subacromial decompression with a distal clavicle resection and biceps tenotomy.  His orders were specific to “ROM and strengthening” and he had a firm grip on what he wished to achieve per his physician’s orders.  Though I mentioned that, after the first couple of weeks, it would be wise to treat the cause rather than the symptoms of his left shoulder problem, he only agreed we’d reassess after a few weeks.

I saw him once a week for three weeks and he attained full ROM, felt wondersplendiferous (there is a small reward for whoever first tweets the three root words for this nonsensical term) and he was touting my praises loudly when he arrived at the fourth visit.  No pain, full motion, strong, highly functional at home and with hobbies.

Most of you reading this have been there.  We pray this patient maintains this status and we don’t want to be the bad-news “physical torturist” because sometimes they are functional for a long time this way.  Knowing his reluctance to work outside the realm of he and his surgeon’s normal, I stood down.  He had met all of his goals, he did have functional strength, motion and his goals were met.  I simply reminded him that I had done very little, that there was likely still a root cause of this now-recurring left shoulder dysfunction, not to feel hopeless if it did ever recur, wished him my best and discharged him—physician and patient goals met.  

For now.

I’m interested in your feedback, stories, predictions for part III, anything you'd like to add to this little story so far.  Again, this is outlining a classic case where the road less traveled is a bit risky, and in this case I took the easy way out with some objective data to support my decision. 

Part III coming soon…

Myokinematic Restoration originally scheduled in Spokane, WA, has been moved to Seattle, WA on May 31-June 1st! There are still a handful of seats available, so if you are in the Northwest, be sure to register soon. The early registration rate of $445 has been extended until next Wednesday, May 21st!

Check on the new recent email that has been posted, where James Anderson answers a course attendees questions on the FA Range of Motion charts in the Myokinematic Restoration course manual.

CLICK HERE to read Jame's response, and to check out all the recent email questions in the archives!

Check out this newly released article by Emily Soiney, titled “Taking Yoga to the Next Level-Postural Restoration-Inspired Yoga for the Athlete: The Frontal Plane”. Emily is also busy preparing for the first PRI Integration for Yoga affiliate course which will be held in Portland, OR on September 13-14th! Additional seats have just been opened for this course, so if you are interested in attending be sure to reserve your seat today. CLICK HERE to register!

Jen Poulin will be traveling with her husband, Chris to the UK this summer to share PRI overseas! Pro Sport Physiotherapy in York, England will be hosting Myokinematic Restoration on July 26-27, 2014. Physiotherapist Martin Higgins, along with fitness professional Kevin Duffy will be hosting the course, and space is limited! If you are interested in attending, be sure to sign up soon!

CLICK HERE to register for the course!

Don't miss the opportunity to take the Cervical-Cranio-Mandibular Restoration course taught by Ron Hruska in Richmond, VA on May 17-18th! The early registration deadline is this Friday, and we are still a few registrations short of confirming this course. If you are currently signed up, and want to help make sure this course doesn't get cancelled, phone a friend and invite them to attend the course with you.

CLICK HERE to sign up for the course!