Research Update--Changes due to eccentric exercise?

Changes due to eccentric exercise?
Some more studies for you! We know that a great way to create a lot of Delayed Onset Muscle Soreness (DOMS) is by eccentric exercise. Again, I am not recommended that you go out of your way to create muscle damage, but it happens and is probably an important step in the hypertrophy (increase in muscle size) process. Now that does not mean that it is always painful, however. Pain is an interpretation in the brain! Below are some brand new studies to shed some light on what is really going on....

(NOTE--the hyperlinks below are all fixed now!)

Sensory and electromyographic mapping during delayed-onset muscle soreness

Authors: Hedayatpour,N.; Falla,D.; Arendt-Nielsen,L.; Farina,D.
Source: Med.Sci.Sports Exerc., 2008, 40, 2, 326-334

Conclusion: "Novel topographical mapping of both surface EMG (Electromyography) and PPT (Pressure-pain thresholds) of the quadriceps showed site-dependent effects of eccentric exercise, probably attributable to variations in the morphological and architectural characteristics of the muscle fibers. Greater manifestations of DOMS (Delayed Onset Muscle Soreness) in the distal region of the quadriceps may indicate a greater susceptibility of this region to further injury after eccentric exercise."

Effects of neuromuscular electrical stimulation of the knee extensor muscles on muscle soreness and different serum parameters in young male athletes: preliminary data

Authors: Zorn,C.; Szekeres,T.; Keilani,M.; Fialka-Moser,V.; Crevenna,R.
Source: Br.J.Sports Med., 2007, 41, 12, 914-916

Conclusions: "Although the changes of blood parameters measured in the present work correspond to those reported in the literature on eccentric strength training, no delayed onset muscle pain could be detected. Further studies should be carried out, also investigating different stimulation protocols in non-trained healthy subjects and in patients with less muscle mass."

Uniform and prolonged changes in blood oxidative stress after muscle-damaging exercise

Authors: Paschalis,V.; Nikolaidis,M.G.; Fatouros,I.G.; Giakas,G.; Koutedakis,Y.; Karatzaferi,C.; Kouretas,D.; Jamurtas,A.Z.
Source: In Vivo, 2007, 21, 5, 877-883

Conclusion: "We believe that muscle-damaging exercise should be viewed as a different challenge compared to non-muscle-damaging exercise with regard to its effects on blood oxidative stress."

Adaptive changes in motor control of rhythmic movement after maximal eccentric actions

Authors: Bottas,R.; Nicol,C.; Komi,P.V.; Linnamo,V.
Source: J.Electromyogr.Kinesiol.

Conclusion: "The present results emphasize the capacity of the neuromuscular system to compensate for prolonged eccentric-induced contractile failure by optimizing antagonistic muscles coordination in a demanding rhythmic task. The underlying compensatory mechanisms could be related to increased sensitization of small diameter muscle nerve endings."

Decreased blood oxidative stress after repeated muscle-damaging exercise

Authors: Nikolaidis,M.G.; Paschalis,V.; Giakas,G.; Fatouros,I.G.; Koutedakis,Y.; Kouretas,D.; Jamurtas,A.Z.
Source: Med.Sci.Sports Exerc., 2007, 39, 7, 1080-1089

Conclusion: "A repeated bout of lengthening contractions attenuated muscle damage and blood oxidative stress compared with the first bout."

Myofibre damage in human skeletal muscle: effects of electrical stimulation versus voluntary contraction

Authors: Crameri,R.M.; Aagaard,P.; Qvortrup,K.; Langberg,H.; Olesen,J.; Kjaer,M.
Source: J.Physiol., 2007, 583, Pt 1, 365-380

Conclusion: "The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extra cellular matrix in the phenomenon of delayed onset of muscle soreness."

Changes in serum cytokines after repeated bouts of downhill running

Authors: Smith,L.L.; McKune,A.J.; Semple,S.J.; Sibanda,E.; Steel,H.; Anderson,R.
Source: Appl.Physiol.Nutr.Metab., 2007, 32, 2, 233-240

Conclusion: "The pro-inflammatory macrophage inflammatory factor-1beta (MIF-1beta) was 18% higher during the 12 h after RUN2. The overall cytokine profile suggests a slight reduction in systemic inflammation after RUN2."

Quantifying delayed-onset muscle soreness: a comparison of unidimensional and multidimensional instrumentation

Authors: Cleather,D.J.; Guthrie,S.R.
Source: J.Sports Sci., 2007, 25, 8, 845-850

Conclusion: "So the findings may be of use to researchers and sports medicine professionals in their deliberations about which instrumentation to use in quantifying DOMS (Delayed Onset Muscle Soreness) and in distinguishing such pain from other, potentially more serious, musculoskeletal damage."

Delayed onset muscle soreness does not alter O2 uptake kinetics during heavy-intensity cycling in humans

Authors: Schneider,D.A.; Berwick,J.P.; Sabapathy,S.; Minahan,C.L.
Source: Int.J.Sports Med., 2007, 28, 7, 550-556

Conclusion: "The change in blood lactate concentration from rest to end-exercise was significantly greater during exercise performed with DOMS (Delayed Onset Muscle Soreness). Eccentric exercise causing a moderate degree of DOMS (Delayed Onset Muscle Soreness) does not appear to impact upon the mechanisms mediating phase II or the slow component of O2 uptake kinetics."

Research Update Part 1-Techniques to reduce delayed-onset muscle soreness

Have you ever wondered how you can increase your ability to recover from a hard training session? Does contrast therapy work? Stretching? Supplements?

Below are some brand new, cutting edge studies on ways to possibly reduced DOMS (delayed onset muscle soreness)--you know, that feeling you get after starting a new training program or doing a new exercise. Usually it peaks within 24-48 hours afterwards.

I don't think your goal should be to actively seak out muscle soreness per say; but your goal should be to keep increasing your performance in the gym each time. A simple way is to

1) add more weight

2) add more reps

3) add more sets

4) more sets and more reps = more volume (work done)

5) increase the density (amount of work done in a set period of time).

Most people only focus on #1.

Here are the studies! Any questions, let me know.

Rock on

Mike N

Techniques to reduce delayed-onset muscle soreness

Elimination of delayed-onset muscle soreness by pre-resistance cardioacceleration before each set

Authors: Davis,W.J.; Wood,D.T.; Andrews,R.G.; Elkind,L.M.; Davis,W.B.
Source: J.Strength Cond Res., 2008, 22, 1, 212-225

Conclusion: "Aerobic cardioacceleration immediately before each set of resistance exercises therefore rapidly eliminates DOMS (Delayed Onset Muscle Soreness) during vigorous progressive resistance training in athletes."

Effect of hydrotherapy on the signs and symptoms of delayed onset muscle soreness

Authors: Vaile,J.; Halson,S.; Gill,N.; Dawson,B.
Source: Eur.J.Appl.Physiol., 2008, 102, 4, 447-455

Conclusion: "Overall, CWI (Cold Water Immersion) and CWT (Cold Water Therapy) were found to be effective in reducing the physiological and functional deficits associated with DOMS (Delayed Onset Muscle Soreness), including improved recovery of isometric force and dynamic power and a reduction in localised oedema. While HWI (Hot Water Immersion) was effective in the recovery of isometric force, it was ineffective for recovery of all other markers compared to PAS. (Passive Recovery)"

Ice-water immersion and delayed-onset muscle soreness: a randomised controlled trial

Authors: Sellwood,K.L.; Brukner,P.; Williams,D.; Nicol,A.; Hinman,R.
Source: Br.J.Sports Med., 2007, 41, 6, 392-397

Conclusion: "The protocol of ice-water immersion used in this study was ineffectual in minimising markers of DOMS (Delayed Onset Muscle Soreness) in untrained individuals. This study challenges the wide use of this intervention as a recovery strategy by athletes."

Stretching to prevent or reduce muscle soreness after exercise

Authors: Herbert,R.D.; de Noronha,M.
Source: Cochrane Database Syst.Rev., 2007, (4), 4, CD004577

Conclusion: "The evidence derived from mainly laboratory-based studies of stretching indicate that muscle stretching does not reduce delayed-onset muscle soreness in young healthy adults."

A light load eccentric exercise confers protection against a subsequent bout of more demanding eccentric exercise

Authors: Lavender,A.P.; Nosaka,K.
Source: J.Sci.Med.Sport,

Conclusion: "The results suggest that the 10% ECC (Eccentric Exercise) induced some protection against a subsequent bout of 40% ECC (Eccentric Exercise) performed 2 days later. It appears that the light eccentric exercise preconditioned the muscles for exposure to the subsequent damaging eccentric exercise bout."

Effects of a protease supplement on eccentric exercise-induced markers of delayed-onset muscle soreness and muscle damage

Authors: Beck,T.W.; Housh,T.J.; Johnson,G.O.; Schmidt,R.J.; Housh,D.J.; Coburn,J.W.; Malek,M.H.; Mielke,M.
Source: J.Strength Cond Res., 2007, 21, 3, 661-667

Conclusion: "The findings provided initial evidence that the protease supplement may be useful for reducing strength loss immediately after eccentric exercise and for aiding in short-term strength recovery. The protease supplement had no effect, however, on the perception of pain associated with DOMS (Delayed Onset Muscle Soreness) or the blood markers of muscle damage."

The effect of contrast water therapy on symptoms of delayed onset muscle soreness

Authors: Vaile,J.M.; Gill,N.D.; Blazevich,A.J.
Source: J.Strength Cond Res., 2007, 21, 3, 697-702

Conclusion: "The CWT (Cold Water Therapy) seems to be effective in reducing and improving the recovery of functional deficiencies that result from DOMS (Delayed Onset Muscle Soreness), as opposed to passive recovery."

Effect of NSAID on muscle injury and oxidative stress

Authors: McAnulty,S.; McAnulty,L.; Nieman,D.; Morrow,J.; Dumke,C.; Henson,D.
Source: Int.J.Sports Med., 2007, 28, 11, 909-915

Conclusion: "The findings indicate caution should be used when consuming nonsteroidal anti-inflammatory drugs during ultra distance events."

Warm-up reduces delayed onset muscle soreness but cool-down does not: a randomised controlled trial

Authors: Law,R.Y.; Herbert,R.D.
Source: Aust.J.Physiother., 2007, 53, 2, 91-95

Conclusion: "Warm-up performed immediately prior to unaccustomed eccentric exercise produces small reductions in delayed-onset muscle soreness but cool-down performed after exercise does not."

Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage

Authors: Davis,J.M.; Murphy,E.A.; Carmichael,M.D.; Zielinski,M.R.; Groschwitz,C.M.; Brown,A.S.; Gangemi,J.D.; Ghaffar,A.; Mayer,E.P.
Source: Am.J.Physiol.Regul.Integr.Comp.Physiol., 2007, 292, 6, R2168-73

Conclusion: "The results support the hypothesis that curcumin can reduce inflammation and offset some of the performance deficits associated with eccentric exercise-induced muscle damage."

Pre-emptive Analgescis--what is he talking about now?

Z Health R Phase Certification in MN this weekend!
Just a heads up for anyone that is one the fence, that the R Phase Cert is here this weekend! There is currently an awesome group of people signed up and it will be a blast! I will be there all day Sat and Sun and I am sure I will learn new stuff again even though this will be my third time through the first 3 days. Basics are best!

The Pain Train Continues
If you missed the last post on pain, see the one before this and check it out. Below is another guest post from Nicole Nelson in relation to pain. Ok, so I am biased since she is my sister, but the information is great and there is a bit about how it relates to Z Health and movement towards the end also. She is currently at the U of MN working on her advanced degree to be a certified registered nurse anesthetists (CRNA)--those people that put you as close to death as possible during a procedure and make sure you come back too!

Pre-Emptive Analgescis

by Nicole Nelson, RN

Chronic pain affects millions of people in the world today. As an anesthesia provider it is crucial to know how to adequately treat pain in a multi dimensional approach. One way anesthesia providers may decrease post operative pain is by giving pre-emptive analgesics. Decreasing pain at the spinal level is a good approach to both acute and chronic pain. Research of the pain pathways is complex and new thinking has shown that it is a multi sensory system according to the neuromatrix of pain (Mosely, G. 2003).

Pain can be difficult to define since everyone perceives and experiences pain differently. According to the definition by Morgan, Mikhail and Murray, pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage (Morgan, Mikhail, & Murray 2006). Pain is categorized as either acute or chronic. Post operative pain is considered acute pain and is usually due to nociceptive stimulus. Chronic pain on the other hand is when acute pain fails to be resolved from either abnormal healing or inadequate treatment. Chronic pain may be nociceptive, neuropathic or mixed (Morgan, Mikhail and Murray 2006). A recent article by Weiss, Vanderlin and Hietpas states that chronic pain is the nation's leading cause in adult disability (Weiss, M., Vanderlin, D., Hietpas, J. 2007).

Physiologic pain pathways can be very complex and only a brief overview will be provided here. When a pain receptor is stimulated it travels to the CNS by two neurons known as either A-delta or C nerve fibers. The A-delta fibers are large in diameter, fast conducting myelinated fibers which transmit "first" pain experienced as sharp, prickling and injurious ( Kelly, D., Ahmad, M., Brull, S. 2001). The C fibers are small in diameter, slower conducting unmyelinated fibers that are responsible for "second" pain experienced as dull, aching and visceral type ( Kelly, D., Ahmad, M., Brull, S. 2001). The sensory neurons then travel to the spinal cord and synapse with second order neurons located in the dorsal horn. The second order neurons then travel either up the spinothalamic tract or ipsilateral spinal pathway to the thalamus. Once the impulse arrives in the thalamus it is sent to other CNS centers such as the somatosensory cortex. These higher centers are responsible for the perception of pain and the emotional components that accompany it (Kelly, D., Ahmad, M., Brull, S. 2001). In the sensory pathway there are four distinct steps in the transmission of painful stimulus known as: transduction, transmission, modulation and perception. It important to understand each area since each step is a potential target for analgesic therapy. Transduction is a process where nociceptors respond selectively to noxious stimuli and convert chemical, mechanical or thermal energy at the site of the stimulus into neural impulses (Kelly, D., Ahmad, M., Brull, S. 2001). The intensity of the impulse arriving in the dorsal horn depends on how much excitatory or inhibitory transmitter is released. Transmission occurs once the signal has arrived in the dorsal horn and where it synapses depends if the signal is coming from an A-delta or C nerve fiber. The A-delta neurons synapse in laminae I, II and V, and the C fibers in laminae I and II (Widmaier, E., Raff, H., Strang, K. 2006). Neurotransmitters are released and can cause changes in the excitability of the cell. In addition to causing increased excitability to the cells, repeated noxious stimulation of the dorsal horn may result in an increase in the number of neurons in laminae I and II whose nuclei express C-fos protein, a protein thought to be involved in the memory of pain ( Kelly, D., Ahmad, M., Brull, S. 2001). This is one area in which preemptive analgesic such as morphine could decrease the number of cells expressing C fos protein. The next step in the sensory pathway is known as perception. This step involves the impulse leaving the dorsal horn and traveling up to the thalamus then on to the somatosensory cortex. Analgesic therapy has traditionally targeted the pain perception component of the analgesic pathway (Kelly, D., Ahmad, M., Brull, S. 2001). By understanding each concept in the pain pathway it allows providers to use several different analgesic agents which each act on a specific area in the pain pathway.

As stated earlier, treatment of either acute or chronic pain involves a multi-dimensional approach. Preemptive analgesic may be one way to treat acute pain before it can trigger long-term neuronal changes leading to chronic pain. Some of the neuronal changes in chronic pain involve a term known as "wind up" that occurs when the initial pain stimulus goes on too long and the NMDA receptors become sensitized (Kelly, D., Ahmad, M., Brull, S., 2001). This then triggers a cascade of events that leads to CNS hypersensitization. This process can lead to a long line of complications from pain such as hyperalgesia, non-pain nerves begin to fire and carry pain messages, the threshold of opiod receptors is increased, sensitivity to catecholamines is lowered and the pain fields spread to adjacent neurons in the spinal cord (Copstead, L,. Banasik, J. 2005). The long line of complications and neural changes that occur from chronic pain only reinforces why acute pain should be treated aggressively. As researchers develop a better understanding of acute pain mechanisms it has been shown in clinical trials that preemptive analgesic could benefit the patient with decreased postoperative pain, decreased hospital stays and improved overall satisfaction of care (Turan, A.,White, P., Karamanlioglu, B., Pamukcu, Z. 2007). Preemptive analgesia is defined as analgesia given before the initiation of nociceptive stimulus (Pyati & Gan, 2007). There still remains a lot of controversy over preemptive analgesia. A recent review of literature by Pyati and Gan in 2007 demonstrated that around 40% of studies showed a beneficial effect (reduction in pain and analgesic consumption) of pre-incision analgesia as opposed to analgesic administration after surgical incision ( Pyati & Gan, 2007). There are many factors that play a role in preemptive analgesia such as which drug is given, dosage and duration of medication and the exact time that the medication was given preoperatively. Gabapentin is just one of many medications a provider could give as a preemptive analgesic. Gabapentin has primarily been given as an anticonvulsant but it is also used extensively in the treatment of neuropathic pain. It works primarily on voltage dependent calcium channels, resulting in postsynaptic inhibition of calcium influx and which will reduce presynaptic excitatory neurotransmitter release (Pyati & Gan, 2007). Research has now shown gabapentin is helpful in reducing the central neuronal sensitization that occurs in postoperative pain (Turan, A., White, P., Karamanlioglu, B., Pamukcu, Z. 2007). In one particular study by Pyati and Gan in 2007 demonstrated a reduction in morphine consumption post operatively by 32% when 3 grams gabapentin was administered before and during the first 24 hours after abdominal hysterectomy (Pyati & Gan, 2007). In another study with inflammatory pain, gabapentin was shown to reduce hyperalgesia and inhibit C-fiber response to noxious stimuli by modulating both central and peripheral nociceptive response (Turan, A., White, P., Karamanlioglu, B., Pamukcu, Z. 2007). Lastly in a study by Turan, White, Karamanlioglu and Pamukcu in 2007 it showed the effects of tourniquet pain from a total knee surgery. Gabapentin decreased postoperative pain as much as 50% in the controlled group (Turan, A., White, P., Karamanlioglu, B., Pamukcu, Z. 2007).

Preemptive analgesic is the first step in controlling acute post surgical pain and including ideas evolved from the pain neuromatrix may be an insight into controlling chronic pain. The pain neuromatrix was developed over a decade ago by Melzack and Wall (Moseley, 2003). Melzack and Wall developed the ideas in the pain neuromatrix on the bases that pain is produced by the brain when it receives neuronal signals that danger to body tissues exists and that there needs to be an action (Mosely, 2003). There are four basic concepts within the neuromatrix. The first concept is that pain is produced by the brain (Mosely, 2003). The second concept is that pain is produced when the brain perceives that danger to body tissues exists and action is required (Mosely, 2003). Third concept consists that pain is part of the survival system, any threat, can be interpreted as pain (Mosely, 2003). The last concept is that pain is individual (Mosely, 2003). In traditional ideas of pain it is perceive that pain is caused by a physical injury. The main difference between traditional ideas and the neuromatrix is that pain can be caused by a physical injury but pain can also be stimulated within the body by either a noxious or non-noxious threat. Acute pain is generally well understood but chronic pain syndromes, which are often characterized by severe pain associated with little or no discernible injury or pathology, remain a mystery (Melzack 2003). Melzack states, "chronic pain is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology. A great study by Onodera, Shirai, Miyamoto and Genbun in 2003 looked at the density and distribution of neural endings in rabbit lumbar facet joints after anterior spinal fusion and to evaluate the effects of intervertebral immobilization. The author states, "These results suggest that immobilization of the intervertebral segment causes a reduction in the number of mechanoreceptors in the facet joint capsules because of the reduction in mechanical stimulation. Moreover, in the upper adjacent facet joint there may be neural sprouting caused by nociceptive stimulation" (Onodera, Shirai, Miyamoto and Genbun 2003). One simple way to apply this idea is to think about when you accidentally burn your finger on a hot stove. According to the ideas in the neuromatrix the actual pain is considered an action signal so you pull your hand away to decrease the threat, then you might franticly wave your hand around to decrease the pain by increasing mechanoreceptor stimulation. Another example is to apply other systems such as the Z Health Performance System to the neuromatrix. Z Health uses joint mobility exercises to increase mechanoreceptor stimulation and therefore potentially reduce chronic or acute pain.

The ideas involving pain physiology are very complex. Preemptive analgesic may be just one way of many to help prevent acute postoperative pain. Using a multi sensory system such as the neuromatrix of pain could be another way to treat chronic pain and trigger new non-painful neural pathways. Including all the concepts in pain physiology and add the ideas of the neuromatrix may lead to a new way of thinking on how to treat acute and chronic pain in the near future.

References

Copstead, L., Banasik, J. (2005). Pathophysiology 3^rd edition. St. Louis: Elsevier Saunders

Kelly, D., Ahmad, M., Brull, S. (2001). Preemptive analgesia I: physiological pathways and pharmacological modalities. Regional Anesthesia and Pain, 48(10), 1000-1010.

Melzack, R. Pain and the neuromatrix in the brain. Department of Psychology, McGrill University, Montreal, Canada. rmelzack@ego.psych.mcgill.ca

Morgan, E., Mikhail, M., Murray, M. (2006). Clinical Anesthesiology. New York: Lange Medical Books/McGraw hill.

Moseley, G. (2003). A pain neuromatrix approach to patients with chronic pain. Manual Therapy

Onodera, T., Shirai, Y., Miyamoto, M., Genbun, Y. (2003). Effects of anterior lumbar spinal fusion on the distribution of nerve endings and mechanoreceptors in the rabbit facet joint. Journal Orthopedic Science, 8(4), 567-576.

Pyati, S., Gan, T. (2007). Perioperative Pain Management. CNS Drugs, 21(3), 185-211.

Turan, A., White, P., Karamanlioglu, B., Pamukcu, Z. (2006). Premedication with Gabapentin: The Effect on Tourniquet Pain and Quality of Intravenous Regional Anesthesia. Brief Report-International Anesthesia Research Society, 104(1), 97-101.

Weiss, M., Vanderlin, D., Hietpas, J. (2007). Controlling Chronic Pain in the Workplace- Nerve Stimulation and Intrathecal Drug Delivery Systems. Continuing Education, 55(11), 463-467.

Widmaier, E., Raff, H., Strang, K. (2006). Vander's Human Physiology. New York: McGraw Hill.

Pain Perception and the Neuromatrix--Guest Blog by Katelin Bigelow

Another guest blog for you on a new look at pain by Katie Bigelow. This is based on a growing body of evidence and neuroscience regarding how to view pain.

Katie is a Z Health trainer level 3 trainer in GA and look for more excellent info from her in the next few years. . If you are in that area, I would highly recommend that you drop here at line at this email. kbigelo AT emory DOT edu

Take it away Katie!

Pain Perception and the Neuromatrix

By: Katelin Bigelow

Introduction

Pain is a sensory output from the nervous system that has eluded scientists for many years. It is not clearly understood why pain can act as both a survival mechanism and a debilitating disorder in individuals. The mechanisms of how pain works in the brain and the significance of each structure and its affects on pain perception continues to be studied. Understanding the function of the basic structure of the nervous system, the neuron, has allowed for increased knowledge in how the signal begins and travels to the brain. Many aspects of the neural signaling pathway have been studied on how a stimulus reaches the brain, but it is what occurs in the brain that is least understood. This article will review the definition of pain, the structure and function of the neuron, the neural pathway a stimulus must travel, and the neuromatrix theory of pain in the brain.

What is Pain?

The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage (International Association for the Study of Pain 2007). Pain is a survival response that signals threat to the body resulting in an action signal being released and physical movement away from the harmful stimulus. As the International Association for the Study of Pain states, pain can be caused by a sensory or emotional stimulus. Pain does not have to come directly from a physical threat as it can be emotional or spiritual, but it is perceived as a danger by the brain. Thus any stimulus is painful if the brain interprets it as threatening to its survival. The amount of pain experienced does not directly relate to the amount of tissue damage sustained (Butler and Moseley 2003). Chronic pain may occur without any significant tissue damage, or with pain that is out of proportion to the amount of tissue damage suffered. The brain may not even receive the message that the threat is gone and continue to send the action signal of pain to the body.

Pain’s danger signal is a multi-system output event that can create changes throughout the entire body to meet the needs of any threat. Pain decreases cognitive accuracy and negatively influences memory, attention, and focus at the time of the event. Pain alters nervous system activity and modifies immune system activity usually reducing its functional capacity. Visuomotor systems are activated by painful stimuli as well as physiologic motor systems, which aid in the escape of the threat, promoting safety and survival. (Cobb 2007).

Neuron Structure

A neuron or nerve cell is the specific type of cell found only in the nervous system. A neuron contains sensory, chemical, thermal, electrical and other receptors that send and receive information to and from other cells in the body. A neuron’s receptors are the first to receive information regarding initial harmful stimuli. A nerve cell contains the same basic organelles as other cells in an organism. These organelles and their characteristic features of the cell allow the neuron to maintain plasticity and rapid responsiveness to environmental conditions (Lambert and Kinsley 2005). In addition to the organelles located in the soma, the neuron structure also contains dendrites and an axon. Dendrites are branching fibers that extend from the neuron cell body and retrieve information from surrounding neurons and cells. Dendrites increase the surface area of the neuron with branch-like extensions known as dendritic spines. Dendritic spines also increase communication between the surrounding cells. The axon of a neuron is a cylindrical extension of the cell body coming from the opposite side of the neuron’s dendrites. The axon of a neuron projects information out to surrounding cells via the action potential. Action potential is created when the threshold of positively charged particles is reached inside the cell and an electrical impulse is released to surrounding cells (Butler and Moseley 2003). The axon of a neuron can also have myelin sheath surrounding it to aid in protection and the speed at which signals are sent. The neuron’s distinctive structure as shown in Figure 1 from the National Institute on Drug Abuse allows for information to travel rapidly and efficiently throughout the nervous system. The nervous system governs all other body systems and maintaining homeostasis.

Figure 1

Neuron Structure

Neural Signal Pathway

The neural signal pathway describes the process of how a stimulus, painful or otherwise, is initiated and travels up to the brain where processing and output occur. A painful stimulus first occurs when the receptor site of a nocioreceptor or pain receptor on a neuron receives an activation signal. This causes the neuron to fire and send information via the axon to the peripheral nerve fibers, which become larger and larger as the message becomes closer and closer until the spinal nerve is formed (Wilkinson et al., 1994). The peripheral nerve fibers branch and send the message into the dorsal and ventral roots. The information then enters into the meninges on its way to spinal cord. The pain signal then travels into and up the spinal cord towards the brainstem. Once the brain receives the stimulus it then determines whether or not it is threatening. The threatening information enters clusters of nodes responsible for sensation, movement, emotions, and memory where the information is expressed. There is no pain center in the brain; instead there are many structures throughout the brain that play a role in the expression of pain. There is a specific pattern, theorized as the neurosignature by Dr. Ron Melzack that is responsible for painful output (Melzack 2001). The brain structures that are thought to be involved in the pattern are shown in Table 1, along with their functions. These brain structures play a role in processing the stimulus, and are responsible for the final output that is received as pain. The output travels back down the neural pathway to the area that initially received the threatening stimulus, and the individual responds with action and movement.

Table 1

Brain Structures and Functions Involved in Pain Neurosignature

Structure	Function
Premotor/Motor Cortes	Organize and prepare to initiate movements.
Cingulate Cortex	Focus and concentration.
Prefrontal Cortex	Memory and decision-making.
Amygdala	Addiction, fear, and the condition of fear.
Sensory Cortex	Sensory information.
Hypothalamus/Thalamus	Autonomic nervous system regulation, motivation, and stress response.
Cerebellum	Movement and cognition.
Hippocampus	Memory, spacial cognition, and fear conditioning.

Pain Neuromatrix in the Brain

The model of the neuromatrix of pain in the brain theorizes that pain is a multidimensional experience produced by patterns of nerve impulses. These patterns, called neurosignatures, are triggered by sensory or emotional stimulus that can be noxious or non-noxious. Pain is a warning signal produced by the brain when any danger is perceived. The pain neuromatrix seeks to explain the complex neural network involved in the interpretation of a stimulus and the resulting output. An individual’s neuromatrix is genetically determined and modified by the constant sensory experiences received from the environment (Melzack 2001).

The pain neuromatrix has four major components that determine the sensory output of pain. The first component is the input of stimulus from the surrounding environment that allows for bodily awareness and a sense of self. Second, the input travels up the neural pathway to the brain where it is processed and integrated to become a characteristic pattern, known as the neurosignature (Melzack 2001). The neurosigniture is imprinted into the brain’s neuromatrix as major sensory events are interpreted. The third component is the process of converting the patterns created by the neurosignature into self-awareness, which is accessed through the virtual body. The virtual body and the primary somatosensory homunculus are the most well known for spatial representation of both the internal and external physical environment. Both are significant in the conversion of neurosignature to awareness (Moseley 2003). The fourth component to the pain neuromatrix in the brain is the output stimulus of pain. The virtual body aids the brain in sending the pain signal to the most relevant body part that will result in action/movement and thus ensure survival.

Chronic pain has an added complexity to the activity of the pain neuromatrix. Chronic pain contributes two inter-dependent mechanisms, 1) nociceptive and 2) non-nociceptive mechanisms. Both increase the conviction of the nervous system that body tissue is in danger resulting in an increase of activity in the pain neuromatrix. Nociceptive mechanisms include immune system related dysfunction that stimulates nocioreceptors in the body’s tissues. The non-nocioceptive mechanism includes a cognitive-evaluative aspect. The increased neuromatrix activity results in the repetitive cycling of the given neurosigniture, which constantly produces a painful output regardless of any actual danger to the body’s tissue. (Moseley 2003).

Another factor in chronic pain is the stress the individual experiences. Pain disrupts regulatory systems throughout the body. Stress is produced to return the body back to homeostasis and thus also is important to pain. Stress is a biological system and like pain is activated by any threat to the biological homeostasis, psychological stability and the body-self image (Ader and Cohen 1993). When any significant traumatic event occurs in the body, cortisol is released. Cortisol is an essential hormone and responsible for producing and maintaining high levels of glucose for immediate response after any injury, threat, or emergency (Melzack 2001). While cortisol is meant to aid in the immediate survival process it can have adverse effects if it is constantly being released over long periods of time, like with chronic pain. Sustained cortisol release over extended periods of time can cause weakness, fatigue, decalcification of bone, and suppress the immune system (Woolf 2007). Prolonged immune suppression may diminish gradually and give way to excessive immune response. Sensitization of inflammatory cells can result in reducing the nocioceptor threshold and increasing the responsiveness of the immune system (Woolf 2007). The immune system’s attack on its own body’s tissue might produce autoimmune diseases that are chronic pain syndromes (Melzack 2001).

Conclusion

The pain and neuromatrix in the brain theory offers a paradigm shift for how pain is interpreted by the nervous system. Any stimulus coming from the receptors of a neuron can be perceived by the brain as pain regardless of whether body tissue damage is actually occurring. All pain is created and processed in the neuromatrix of the brain and is a result of the brain’s perception of the given event. There is no specific location in the brain where pain is located; rather it is affected by multiple structures and their functions. Pain is also individual and dependent upon a person’s genetics, experiences, emotional status, stress levels, and environmental factors. A better understanding of the pain neuromatrix will help advance our knowledge and ability to cope with pain.

References

Ader, R., and N. Cohen. “Psychoneuroimmunology: Conditioning and Stress.” Annual Review of Psychology, 1993, vol. 44, pp. 53-85.

Butler, D.S., and G.L. Moseley. Explain Pain. Adelaide, South Australia: Noigroup Publishers, 2003.

Cobb, W. E. “The T-Phase Approach to Pain & Performance Barriers.” T Phase Manual, 2007 pp. 1-5.

[IASP] International Association for the Study of Pain. 2007, Dec. 13. IASP home page. . Accessed Dec. 13, 2007.

Lambert, K., and C.H. Kinsley. Clinical Neuroscience; The Neurobiological Foundations of Mental Health. New York: Worth Publishers, 2005.

Melzack, R. “Pain and the Neuromatrix in the Brain.” Journal of Dental Education, 2001, vol. 65, pp. 1378-1382.

Moseley, G.L. “A Pain Neuromatrix Approach to patients with Chronic Pain.” Manual Therapy, 2003, vol. 8, pp. 130-140.

[NIDA] National Institute on Drug Abuse. 2006, Nov. 2. NIDA home page. . Accessed Dec. 13, 2007.

Wilkinson, S. V., M.T. Neary, R.O. Jones, and K.F. Sunchein. “The Neuroanatomy of Pain.” Pain Management, 1994, vol. 11, pp. 1-13.

Woolf, C.J., and Q. Ma. “Nocioceptors-Noxious Stimulus Detectors.” Neuron, 2007, vol. 55, pp. 353-364.

Z Health S Phase Wrap Up

S Phase Wrap Up!

S Phase is the Unfair Advantage!

Below are my comments/thoughts on it. Remember, these are MY interpretations of the course and events and may or may not be the same as Dr. Cobb. When possible, I have put quotes around exact quotes.

For a brief overview, also check out my first post on it here

No one is really taught to be an athlete

Mental note to myself-work on motivating clients/athletes to earn the basic R Phase drills and that it gets even more fun! R Phase is just the beginning

Use can start to see immobility after only 2 weeks of little to no movement

"There is really no true focus on high-level athletic skill development for 98% of our culture" UNTIL NOW!

"Movement is a skill and skills are trainable."

One of the basic movements we learned was the plyo step, or a fast step back to go forward. This was a debate recently on the Strength Coach podcast also. Check out episdo #9 here

Athletic development is a LONG TERM process! Even the best athletes with great parents (read:genetics), correct coaching and training, motivation, etc still take YEARS to reach a very high level. Nobody really wants to hear this in today's "fix me now" society. Ben Johnson, drugs aside, worked for almost 10 years with elite sprint coach Charlie Francis before he broke any records (ref conversation Aaron S)

Visual information from the eyes is of huge importance! 20/20 vision is not enough! If your are eyes are sending your brain "bad" info, you are screwed for starters! We learned different assessments and fixes for them! Remember, the eyes are controlled by muscles and muscles can be trained.

We saw some video of a football player running sprints before and after just visual work and the difference was amazing!

Working with a metronome really gives you an idea of speed and forces you to work outside your comfort zone. I think mine may have a horrible "accident" soon.

"People only see what they are prepared to see" --- Ralph Waldo Emerson

I will have a post on this at some point, but the more I learn, the more I "see". If I can't fix it or do anything with it, I will not even "see" it. The explanation of this is probably related to the reticular filter in the brain. A little part of the brain that decides what info to let in and what to keep out. Click here for some quick further reading on it.

Want to do things you never thought you could do? I can help! Email me or see this link for info.

Depending on your eye alignment, you may fall asleep while reading because it is so taxing on the eyes or the opposite is that you may be ADHD like if you are the other extreme. Again, this probably can be corrected if the eyes are the source of the issue.

There is a good reason why there are some basic eye drills on the Neuro Warm Up 1 and 2 (you can pick up a copy at the link on the upper right here).

Movement
Reviewed the static athletic ready stance (weight on the inside).
Reviewed the three point sprint stance
Reviewed the 4 point stance
Practiced movements (pivots, crossover, t-step, plyo step, hip turn) to transition from any direction--forward, backward, lateral and angular

Plyometrics
Classic plyos
1) eccentric component (muscle lengthening)
2) amortisation (no change in muscle length per say, going from eccentric to concentric)
3) concentric (muscle contraction)

Goal is to increase RATE of force production, so max force in min time

Eccentric component and range of motion (number of joints involved) are probably the most important components

Given the above info, plyos should be QUIET not loud.

Life is plyometric, so this applies to EVERYONE! Last time I checked, I did not see any fall in slow motion, so everyone needs to work up to be able to do some form of "plyos" (again, progression is key)

Linear Speed
Sprinting!
This was actually FUN! I can honestly say this was the first time that running at a higher speed was actually fun and felt good. More work to do of course, but it was great.

Combos
Everything can be combined, including the visual work.

Overall it was a great time and I am already looking forward to going back to S Phase again

Any questions, let me know.
Rock on
Mike N

Jammed Joints and Muscular Weakness--Stability and Mobility

Question of the week "What is Z Health and how do these goofy looking exercises help me?"

Answer
I think the main influence of the Z Health drills is to remove the "neurologic brakes"

"Jammed joints create muscular weakness."--Dr Cobb

If I injure my elbow, neurologically my body will start to shut down the muscles that cross my elbow (triceps, biceps, etc) in an effort to protect my body and reduce the risk of further damage. My body is trying really hard to protect itself which is pretty smart!

Now if that joint is not brought back up to 100% mobility, my body still has some "neurologically braking" going on, thus performance is not optimal. At some level, my body thinks that there still is an issue in my elbow and will be shutting down the muscles to some degree.

If that make sense, lets go even further in that the NS (nervous system) connects ALL the joints, so ANY joint that is not back to 100% mobility is going to dampen performance! Yes, that is a leap, but it makes logical sense (and I've seen it happen many times). So far, every chronic shoulder issue that I've helped someone with, I have yet to do anything with their shoulder! Most of the time it is the opposite foot/ankle, opposite hip, thoracic, or same side wrist. The body moves as a whole (hopefully or else you have some problems), so ALL the joints must be working optimally.

It is true that many times issues will follow the back force transmission line (think of your body as a big X where the force from your RIGHT foot can end up in your LEFT hand and LEFT jaw/face) , but not always. This is the reason to evaluate EACH drill that is performed. Physiology is messy, so you want to assess, not guess.

If you are interested in a custom Z Health session, email me and check out this link.

Stability vs Mobility
Further down the rabbit hole, here is something that I've thinking a lot about for awhile now regarding stability vs mobility.

I think we need to train mobility in order to get any stiffness or stability! This was the end point of my whole mobility in the low back rant (it recently ran at Diesel Crew also, so thanks to Smitty for doing that).

Watch babies/kids--they have tons of mobility and then they LEARN stability. Frankie Faires likes the word "coordination" and I will agree with that so put another way "Stability is just coordination". People are making this too complicated. Yikes, I think I just said others are making it too complicated. I better write down this event.

I actually heard Gray Cook say something similar to this awhile back on the Strength Coach Podcast, so that was pretty cool since he is a bright dude. He is on most episodes of the Strength Coach Podcast, so check it out at this link. You can also search for it in itunes.

Comments?
Mike N

Dr. Lonnie Lowery on Nutrition and Inflammation-Special Guest Blog Post

Special Guest Blog Post from Dr. Lonnie Lowery on Nutrition and Inflammation

It is my honor to present some notes that Dr. Lonnie Lowery took from a Feb 2008 research workshop featuring NIH-sponsored list of heavy hitters that occurred in Chicago, IL on Nutrition and Inflammation.

In case you have been living under a rock, Dr. Lonnie Lowery is a nutrition professor, former competitive bodybuilder and Exercise Physiologist living in the Midwest. He is also a writer for www.t-mag.net so go there and check out his excellent articles. The good doctor is a wealth of information and walks the walk.

Dr. Lowery can be contacted through Charles Staley's site. He also does monthly conference calls with a new topic each month. I've been on the calls and they are really well done, so drop Charles Staley a line if you want in on them.

The following is pretty detailed, but excellent, cutting edge information!

Why Should You Care?

Inflammation is proposed to be at the root of many issues from muscle growth (hypertrophy), healing, to cardiac issues. Even most cardiologists I talked to a few years back admit that the main benefit to statin drugs is probably their modification of inflammation in the body and perhaps their effect on cholesterol is more of a "side effect".

So sit back and let Dr. Lowery enlighten us with some brand new research! Take it away Doc!

Dr. Lonnie Lowery on Nutrition and Inflammation

Talk #1: Nutrition and Age-Associated Inflammation: Implications for Disease

The first talk was done by a legend in the field of inflammation and nutrition: Simin Meydani. As a DVM, PhD, perhaps I should refer to her as "doctor, doctor" Medydani. (And I thought I spent too much time in school!) You may not find the title of her talk especially exciting (unless you're middle-aged like me, with a growing interest in overall health) so I'll serve up a whole bunch of key points and spike it with some data of my own:

• Excessive macrophage (an aggressive white blood cell type) activity and decreased T-cell (a different white cell type) activity leads to more and more inflammation and less resistance to infection as we age. An increase in prostaglandin E2 (PGE2) is obvious in old versus young rodents, for example. I sometimes think of PGE2 as inflammation itself. The end result is increased risk of coronary heart disease, Alzheimer's, osteoporosis, increased infections and even cancer. Ugh.
• Inflammatory cytokines like interleukin-6 and TNF-alpha increase the enzyme that makes more prostaglandin E2. You might care because exercise, especially the eccentric type, is known to be a consistent, albeit brief, inducer of IL-6.

• We'll see more on exercise in the next talk.
• Low antioxidant status (low glutathione presence) leads to more ceramide in the body. Ceramide leads to more creation of prostaglandin E2, so this is not good. Strength athletes enduring hard training don't need to struggle with excess inflammation. Keep up your antioxidant defenses.
• Vitamin E corrects and decreases PGE2 levels in old mice by interfering with the enzyme that makes it.
• 200 I.U. of vitamin E is better than either 60 I.U. or 800 I.U. among human elderly. Their antibody response to an immune challenge is improved at this dose. Some minor effect among the young was also noted.
• A huge variability in subject responses to vitamin E is due to genetic differences. (Intellectual people have loved to say "gene polymorphisms" for years… say it with me: "g-e-n-e p-o-l-y-m-o-r-p-h-i-s-m-s". Don't you feel smarter?
• Calorie restriction of 30% below needs but not 10% below needs results in lower PGE2, which appears to be one mechanism by which lifespan is lengthened. Interestingly, both levels of restriction improve clinical responses to immune challenge (in this case a delayed-type hypersensitivity reaction).
• Low-fat, high fish (oil) intakes lead to lower interleukin-6 production. That could lead to less inflammation and less catabolism in the body. Low-fat, low-fish intakes do not offer the same benefits.
• Over a three month period, 1.5g EPA combined with 1.0g DHA and a couple hundred I.U. of vitamin E strengthened immune response to a skin challenge as noted above. This is interesting since adding vitamin E interferes rather than helps in some studies investigating fish oil.
• Aggressive macrophages infiltrate fatty tissue, leading to inflammation via interleukin-6, interleukin-1 beta and TNF alpha. And I thought these little guys were a pain regarding muscle recovery! More on this later.

Talk #2: Molecular Basis of Inflammation: Relationships between Catabolic Cytokines, Hormones, and Energy Balance

As a weight lifter and not just a person looking for healthy aging, this lecture rocked. Here are the goods:
• A 154 pound (70 kg) man will eat 50 tons of food in his lifetime. He'll use 10 million liters of oxygen to burn it and he'll regulate his day-to-day intake to within one percent. (That's great but it's still plus or minus 10,000 kcal per year, or about three pounds of fat, which could explain the slow creep of body weight many guys experience as they age.)
• Depending on race, 16-28% of men in the U.S. have metabolic syndrome (high blood pressure, insulin resistance, central obesity, low HDL cholesterol and high blood triglycerides). Inflammation is an underlying factor. Imagine, one of the next four guys you meet is an inflamed metabolic train wreck!
• The biochemical pathways of leptin and insulin interact to help determine how fat you are, among other things.
• The mechanism linking energy balance and muscle size has been described/ explained in more detail in a 2007 paper by Nader and colleagues (Nature Medicine 13: 1016-19). This finally gives key insights as to why eating extra kcal and not just protein is so important to muscle size.
• Individuals with rheumatoid arthritis have faster metabolic rates, 25% lower muscle protein synthesis, less body cell mass and 36% less strength thanks to pro-inflammatory tumor necrosis factor (TNF-alpha) and friends. Further, their physical activity levels drop as they unconsciously compensate for the hyped metabolism. Harsh.
• The immune system is a huge player in muscle mass. Just as IL-1, IL-6, and TNF are catabolic, conversely IL-15 and IGF-1/ MGF are anabolic. ('Course you may already know this.)
• In the aged, inflammatory IL-6 actually predicts all-cause mortality. If you think inflammation is no big deal, I hope you learn better before you're old!
• Young or old, IL-6 rises by six hours after exercise (confirms my data in graph above)
• Blockade of the "marijuana receptor" has received attention as a potential way to give obese subjects the "un-munchies". Unfortunately for hopeful dieters, this approach also leads to anti-euphoric effects like nightmares and depression.
• As I understand it, a company named Acceleron is making a drug called Activin that blocks myostatin. The speaker said human trials begin next year. Whoa.
• Combined testosterone plus GH replacement is getting some spanking new 2008 attention. In truth, many competitive bodybuilders could've told these researchers how this works 20 years ago.
• The immune system can determine energy and protein balance. Resistance exercise is the "natural way to entrain these pathways" while pharmaceutical approaches to harnessing the benefits of exercise are still in their infancy.
---Dr. Lonnie Lowery

Lonnie Lowery is a nutrition professor, former competitive bodybuilder and Exercise Physiologist living in the Midwest

Z Health S Phase Update I

Greetings from sunny AZ! Just wanted to do a super fast Z Health Update on S Phase!

S stands for Sports Phase, so it is time for athletic movement! Whoo ha.
The basis of Z Health is the 9S model

Strength
Stamina
Skill
Sustenance (nutrition)
Suppleness (flexibility/mobility)
Structure
Spirit
Style
Speed

Think of all of those coming off of the athlete in the middle. The job of the coach/trainer to infuse each of those qualities into the athlete to make them better. This may change during each training session! How many qualities do most strength coaches/personal trainers work on during a session/season even?

VISION
A key component to elite performance is vision. Not just your visual acuity (how well can you see the eye chart in the docs office), but beyond that.

We go over many different types of vision such as
Dynamic Visual Acuity
Eye Tracking
Eye Focus/Accommodation
Peripheral Vision
Vergence Flexibility and Stamina
Imagery
Sequencing
Eye-hand and Eye-foot Coordination

So vision is beyond just an eye chart! Think of all the great players like Michael Jordan, Wayne Gretzky, Walter Payton, etc and all of them are described as having great vision. Many times the greats were NOT the best in the weight room. Performance on the field is what matters.

Remember that your eyes are controlled by MUSCLES, therefore, vision can be TRAINED. I have never been able to figure out why most people, even at a very high level, NEVER talk about this fact??

Most Olympic athletes have not even done visual training. We are primarily visual creatures and the nervous system's highest priority (most of the time) is visual. So this has HUGE applications to sport and pain relief!

This also means that if you sucked at any ball sports now or when you were growing up (my hand is up), you probably have a vision issue and many many times IT CAN BE CORRECTED! Trust me, I know first hand the difference is jaw dropping. You will actually ENJOY sports!

Athletics should be a LIFE LONG activity, and the true promise of Z Health is that it can elevate almost anyone to an extremely high level at virtually ANY age! Life does not end a 30, 40, 50 or even beyond 60 years of age!
But, like all things, you need to put your time and reps in and no one will ever do that for you. Then again, was anything that gave a huge sense of accomplishment ever easy?

Movement Training (aka Speed training)
There a trend now for speed camps and speed work galore. Yep, athletes need to be fast, but most of it is not speed in a linear sense (e.g straight line). They need to be taught how to move and do transitions from one position to the next.

The reason R Phase and I Phase are before S Phase is that they teach all the basic movements that are integrated even further in S Phase. To use a language analogy, if you want to learn Spanish, you need to learn the alphabet (letters--R Phase) first. Next put them into words (I Phase--integrated movements) and then sentences (S Phase--larger/gross movements). Without a good foundation, you will have bad movement but it just be a little faster.

Think of putting a larger engine (more muscle) into a car with a bad alignment--no good! You could even argue that with a bigger engine, you are on a path to tear yourself apart even FASTER!

Again, QUALITY over QUANTITY.

So far it has been great and there are still 2 more days to go! Can't wait!

Any questions, let me know.
Rock on
Mike N

Z Health Interview, S Phase, Research, USAPL Results

Greetings! I am off to AZ for Z Health Level III (S Phase) where the S stands for “sports” training tomorrow! Whoo ha! Can’t wait. I will get a report up here once I am back or possibly while I am down there. Time will be at a premium since I have a Biostats II exam 9 hours after I get off my flight back to MN here. Wish me luck!

In the meantime, TONS of great stuff today! Research, USAPL meet results, Z Health testimonial and an interview done with yours truly.

Z Health Interview

I was recently interviewed for the Z Health newsletter, which was a true honor. I have published it below also if you are not on the Z Health list. If you want to sign up to the Z Health newsletter, click here

Z-Health Evolution: Interview with Mike T. Nelson

We interviewed Mike T. Nelson, MS, CSCS. Mike is a PhD student in Kinesiology, RKC, and Z-Health Level 1, 2, & 4 certified trainer, who shared with us how he found Z-Health, as well as his personal evolution.

Mike, what brought you to Z-Health?

I was in Charles Staley's coaching group, and some of the lifters were saying that they felt better and were breaking PRs (personal records) after doing Z-Health, so I got the R-Phase DVD. I started waving my limbs around to it like a bird having an epileptic seizure, and began feeling better and movement was easier. I now know that the "bird approach" probably wasn't best –and that precision is key. But, as Dr. Cobb says, even Z done badly is better than not doing it at all.

Clearly you have advanced from there, so what were your next steps?

In June 2006 Brad Nelson (no relation) arranged for Dr. Cobb to come to town for some private sessions. I remember Dr. Cobb doing a muscle test on my left hamstring, and it was horribly weak. He had me do some elbow circles, and I thought he was out of his mind. I could not believe I was paying big money for this -- he knew I had a hamstring issue. When he retested my hamstring, it tested strong and I had no cramping. I was astounded.

I ended up paying on the spot for R-Phase training that fall. To be honest, I had no idea what I had signed up for, but thought if I could learn HALF of what I had observed by the end of certification, I would be thrilled.

That sounds like quite an experience. How did R-Phase go?

At the time I went to Arizona for the first weekend of R-Phase, I was physically a mess. Training was taking its toll on me; after doing heavy deadlifts it was almost impossible to wash my face in the sink the next morning since I could not bend at the waist without lots of pain. On bad days, my WARM-UPS ALONE were taking me close to an hour – and that was just to get to the point where I could actually start my "work out". By the time I went back to Arizona for the R-Phase second weekend, I was doing the drills with more precision, and the results were much, much better. While I had left the first weekend feeling great, by the time I got back to Arizona again I was pretty messed up. I remember asking Dr. Cobb at dinner one night, "If you were me and you know what you know, what would you do?" His response was basically to walk off the plank, give it a shot 100%, and see what happens. I realized that I was on a short path to driving myself into the ground, so what did I have to lose?

And what DID you do? Did you actually start over?

I emailed Brad Nelson, who was already R-Phase certified, and asked for his help on relearning all my exercise technique. Basically, I was not using the correct technique and adding WAY too much tension to compensate. Most of my lifts were "technically" correct, but there was a better and more efficient way. So I started doing deadlifts with the bar only, and then with only 135 lbs, for several weeks. That was a huge blow to the ego, but I stayed the course. I felt great, and my lower back was also feeling pretty good now. There was more work to do, but progress is always good!

In March, I opted to do the Tactical Strength Challenge and ended up pulling 365 lbs, even though my heaviest deadlift during training was only 225 lbs. It's amazing what happens when your body is more efficient! I woke up the next day and felt tired, but my movement was not in the hopper and soreness was very minimal. Washing my face in the sink was easy and pain-free! Life was great.

That is really impressive that you were willing to just start over like that. Can you give me just a bit of a sneak peek into the I-Phase (Level 2) and T-Phase (Level 4) Certifications?

I-Phase is where you integrate movement and work with the visual and vestibular (inner ear balance) systems. It was incredible--visual and vestibular input can have profound effects on movement. Everything was starting to make sense. Z-Health was not just mobility drills, it was a system for ALL movement, based upon how the body takes in information – proprioceptive (joint info), visual (eye movements), and vestibular (inner ear input). Brad Nelson summed it up well when he said, "R-Phase is a great tool; I-Phase is the whole tool SHED".

T-Phase work involves lots of hands-on work from soft tissue to lymph to cranial work. Since much more learning takes place when you do something under your own active control, we also learned how to do ACTIVE work to follow up on all the hands-on passive work. I also realized that Z-Health is not just a system -- it is a complete way of dealing with movement on virtually any issue. Just like R-Phase, everything is tested, so you know if you made good changes or not. That is when I fully began to understand how to look at movement and potential solutions just at a glance.

Thank you so much for your time. We look forward to catching up with you again after S-Phase!

You can learn more about Mike at www.miketnelson.blogspot.com or www.miketnelson.com.

USAPL Results

Wanted to a give a HUGE shout out to the following for doing the USAPL meet held here at the Press a few weeks back. It takes some huge cajones to walk up in front of a large crowd of people wearing just a wrestling singlet (which if you are guy looks like you are carrying grapes int the wrong place) and perform strength feats on command! My hats off to EVERYONE that competed. A special shout to the following

Joe Warpeha
Fawn Friday
Maura Shuttleworth
Anna White
Steve Reishus
Tony Williams
Jacob Chatterton

There is a great write up of the meet at The Minnesota Power Pages

A very cool testimonial from Fawn Friday also and Z Health and her deadlift.

This is a true story. After missing 281 pounds at the Minnesota State Open powerlifting Competition, I asked Mike Nelson (who came as a spectator) for a quick Z adjustment. He tested my hamstrings and glute medius. Neither were firing as well as they should. Toe pulls and ankle tilts with visual adjustment, corrected both muscle groups. I went back to pull the 281lbs on my next attempt! Setting the Minnesota Record for raw Deadlift at 123lb class!

~Fawn Friday

Thanks again Mike!

Blog family update
I have added more blogs to the blog role call on the right. Be sure to check these out

Awesome training info from Steve at his blog, complete with lots of videos! I predict even more great things to come from his blog Steve's blog

I met Aaron (with Steve and others) recently at the NSCA Minnesota conference. We were chatting afterwards about training and Z Health. Aaron is really bright guy and very passionate, so be sure to check out this blog. Aaron's blog

If you are interested in a review of the NSCA state conference, check out Aaron’s review here

Sean Schniederjan is a big KB guy and has been able to join us for the infamous Friday Night Deadlift Party at the Press and on his first time showing up pulled 405! Nice work!! Check out his blog at The Russian Kettlebell Room

It is a true honor to be able to exchange info with everyone!

Research Update!
More research than you can shake a stick at

Funny research

Using heart cells, researchers create a beating heart
Results from a recent experiment may represent breakthrough for regenerative medicine.

My comments--I was able to take a Muscle Physiology class where the lead researcher was a guest speaker. Truly amazing advance!!

I’m a Powerlifter by Chip Conrad from EliteFTS

Excellent article by Chip Conrad!!

Weight Lifting and Aortic Dissection: More Evidence for a Connection

Carbs and Cardio Bunnies--Low Carb and Endurance Performance?

Can you really have optimal endurance performance while on a ketogenic (very very low carb) diet? Most would say--heck no; but this research study says otherwise.