Does It Hurt?

Pain is more complex than scrunching thousands of interactions into one glorified number from 0 to 10. There’s not a single healthcare professional or strength coach (or anyone) that doesn’t deal with pain. With so many professionals treating pain, how can it be so difficult to define? In the patient/client’s eyes, treatment is rendered ineffective if pain fails to resolve. Pain is as much a grueling burden as an elusive mystery.

Whether it be a chronic or acute condition, every human being is designed to endure pain—your survival depends on it. Acceptance and appreciation of this attribute is a step in the right direction in understanding your pain.

Is pain a life sentence? According to respected pain science expert, David Butler, the answer is NO.

Our body has an innumerable amount of pain sensors that flicker at the mere thought of pain. These sensors, which are microscopic proteins made inside neurons, are replaced every few days. Good news for a chronic pain sufferer. The pain sensor manufacturing rate can also decrease or increase based on the body’s perceived threat status.

So if these sensors don’t last long and the rate of production varies, why is chronic pain so…chronic?

“Ignition nodes,” a term coined by Butler, are areas of the brain that are essentially hijacked by the presence of pain. Normally, these cortical tissues are devoted to other qualities such as emotion, movement, memory, and sensation. But when chronic pain is the culprit, it reroutes the electrical signaling of the nervous system to be more devoted to the pain experience. Survival is of foremost importance, not remembering if you forgot to close the garage door. That throbbing ice pick in your shoulder is a little more important than your leaf blower getting stolen.

So are people that are hurting in a bad mood because they are simply in pain or because their brain is being robbed of “good mood real estate?” Probably a little of both.

A “danger” memory is placed within the cells by planting a number of excitatory sensors around the danger messenger neuron. These sensors open longer each time they are activated. Aches that hurt will ultimately hurt more—a term known as hyperalgesia. Otherwise, pain that remains constant will no longer be enough to continually set off the alarm system. Basically, sensitivity to the pain increases to allow for the perception of pain to remain relatively stable.

Neurons also have the capacity to weave complex webs of pain “highways.” Neurons can potentially grow toward the “danger” signal up to 30% of its original length and activate other areas to cause pain. Also, MRI imaging has verified brain structural adaptations associated with chronic pain.

Chronic pain really just becomes a sensitivity game whose electrical pathways can be accessed more readily the more often traveled even if the stimulus (tissue damage) is not present.

Agonizing pain with no further tissue damage? That’s correct.

And this is where the pain experience becomes VERY gray.

Visualizing movement has been documented to cause swelling and more pain in the hurting area. Thoughts have even been shown to increase pain.

Fear and anxiety can flood your cells with hormones having a strong affinity for these meticulously placed excitatory sensors created by the “danger” messenger neuron. Emotion acts as the volume knob to your pain tune.

So if your thoughts and emotions are inseparable from pain, how can you explain all the current research of asymptomatic structural injuries documented with diagnostic imaging? I’m sure these people have “bad days” or some form of anxiety to ignite the pain experience. Being in an MRI tube is enough to make anyone’s back hurt.

This could be because pain fails to manifest itself if the injury is gradual enough to not set off the body’s alarm system. Threat perception is completely different when you herniate a disc over the course of 20 years compared the one time you “threw out” your back moving a friend’s couch.

In the latter instance, your body has managed to localize the danger and begin to stick adrenergic receptors around the site like a set of James Bond proxy mines. The slightest trigger can cause an explosion of pain.

Never see it coming.

Herniating a disc over 20 years is like watching grass grow, your body’s defense system doesn’t care! When you are in a high anxiety situation, the excited biochemical molecules that blast through the cells of your body aren’t being sucked in by these carefully placed receptors because they are NOT there!

It is important that everyone becomes educated on their own pain experience. What exercises are a risk to your specific injury? What social situations trigger your pain? Is performing painful movements with perfect technique actually hurting you? Does getting stung by a bee hurt more because you stepped on a hive as a kid?

Each person’s dynamic pain surveillance system must be based on a biopsychosocial model. Chase the threat (whatever this may be) and have the courtesy to understand that each person is the sole owner of their pain.

Just because you tore your hip labrum back in 1957 when acetabular labrums were “new” doesn’t mean you know “how it feels.”

Take inventory of your pain.

What causes it?

Long formal engagements, pistol squats, wearing a swimsuit, thinking about throwing a ball, lack of sleep…the list can go on forever.

What makes it better?

Diaphragmatic breathing, watching a movie, running, seasonal changes, etc.

Answering these two questions alone could put you on the road to relief.

References

Butler, D., and L. Moseley. Explain Pain. Adelaide: Noigroup, 2003.

Dameron, TB. “Bucket handle tear of acetabular labrum accompanying posterior dislocation of the hip.” J Bone Joint Surgery 41A (1959): 131-34.

Devor, M and Z. Seltzer. “Pathophysiology of damaged nerves in relation to chronic pain. ” Textbook of Pain. Edinburgh: Churchill Livingstone, 2005.

Doubell, TP, RJ Mannion, and CJ Woolf. “The dorsal horn: state dependent sensory processing, plasticity and the generation of pain.” Textbook of Pain. Edinburgh: Churchill Livingstone, 2005.

Edwards, FA, “Dancing dendrites.” Nature 394 (1998): 129-30.

Kendall, NAS, SJ Linton, and CJ Main. Guide to assessing psychosocial yellow flags in acute low back pain: risk factors for long term disability and work loss. Wellington: Accident Rehabilitation & Compensation Insurance Corporation of New Zealand, 1997.

Moseley, GL. “Imagined movements cause pain and swelling in a patient with complex regional pain syndrome. Neurology 62 (2004): 1644.

Price, DD. Psychological Mechanisms of Pain and Analgesia. Seattle: IASP Press, 2000.

Wall, PD, and R Melzack, et al. Textbook of Pain. 5th ed. Edinburgh: Churchill Livingstone, 2005.

The Science of Foam Rolling

Foam rolling has become a mainstream activity in strength and conditioning, rehabilitation, and other related health fields. Clients and patients continue to make claims that they just “simply feel better” when they routinely use self-myofascial release (SMR) strategies. Others claim that foam rolling elicits similar effects to static stretching that will hamper performance if performed prior to a training bout. Little efforts have been made to embark on a scientific rationale related to SMR. What is allegedly happening at the biochemical level? How about bioenergetics?

One statement that everyone can agree on is pressure is absolutely applied to the soft tissue structures being rolled. Applying pressure is adding energy to the tissue colloid. It is well established in physics that this addition of energy is capable of turning a colloid gel into sol. Think of melting cold Jell-O (gel) back into a liquid (sol) by heating it in the microwave. Thus, tissue viscosity has the opportunity to decrease under increasing pressure.

The perpetually changing cytoplasmic matrix can dissolve rapidly upon application of pressure because it is held together with weak bonds. This incredible process harnesses the matrix’s ability to transition from a liquidity substance to a gel substance with mindboggling speed. As pressure is applied, the matrix becomes more like melted Jell-O. As pressure is released, the matrix immediately re-gels. And you thought Instant Pudding was fast.

Stress and lack of body movement can cause the gel to dehydrate, harden, and contract. Applying pressure appears to bring about rapid transformation into a liquid combined with rehydration. As soon as the foam roller is removed, the matrix immediately re-gels.

It seems pointless to go from gel to liquid and then back to gel again. However, the gel isn’t the same. This process transforms the water content, ability to conduct energy, and movement of the targeted tissue. The ground substance becomes more porous, which is a better medium for the diffusion of oxygen, nutrients, and metabolic waste products. It also allows for better diffusion of enzymes and building-blocks involved in metabolic regeneration.

Metabolic waste products and toxins can accumulate in connective tissue that becomes densified or contracted in response to trauma or structural asymmetry. This thickened gel matrix can trap materials electrically by its ample supply of negative charges and mechanically do to the narrower channels between the fibers.

A) A dehydrated gel with trapped particles. B) The application of pressure converts the gel to a sol, releasing trapped particles. C) Ground substance re-gels, but is more porous, open, and hydrated. Photo courtesy of Energy Medicine by James Oschman.

Pressure from the foam roller can potentially release these trapped constituents and be freed into the interstitial fluid before being carried away by the lymphatic system leading to excretion.

Concurrently, pressure to the fascial network can generate piezoelectric fields, which are electrical fields generated when the living cells of the body are compressed or stretched. Each step taken in everyday walking compresses the bones in the legs that generate these electrical fields. Streaming potentials may also be produced by increased blood flow and propulsion of extracellular fluid through the matrix.

These resulting electrical fields can stimulate surrounding cells making fascial changes not limited to the area in contact with the foam roller. However, the angle of application could be correlated with the resulting field’s overall strength. This is a possible reason why foam rolling strategy and direction can yield drastically different energetic results.

Decreased range of motion, poor circulation, and overall lack of movement in specific regions of the body create the potential for these cells to partially become “energetically isolated from the living matrix.” It is possible that manual treatment and SMR have the ability to restore and incorporate these cells back into the network of unrestricted energy flow with increased movement excursions.

A foam roller’s place in strength and conditioning, rehabilitation, or use as a restorative modality is still up for debate and for good reason. Theory is only theory. However, there are growing bodies of knowledge out there that are continually increasing our understanding and reasoning for implementing specific tools to achieve a desired result. Saying foam rolling does nothing is simply not a good enough explanation considering how far the world of science has come.

References

Bassett, C.A.L. “Biological Significance of Piezoelectricity.” Calcified Tissue Research 1 (1968): 252-72.

MacGinitie, L.A. “Streaming and piezoelectric potentials in connective tissues.” Advances in Chemistry Series 250. American Chemical Society, Washington DC , (1995): 125-42.

Marsland D.A., Brown D.E.S. “The effects of pressure on sol-gel equilibria, with special reference to myosin and other protoplasmic gels.” Journal of Cellular and Comparative Physiology 20 (1942): 295-305.

Oschman, J.L. Energy Medicine: The Scientific Basis. Edinburgh: Churchill Livingstone, 2000.

Ratner, S. “The dynamic state of body proteins.” Annals of the New York Academy of Sciences 325 (1979): 189-209.

Reddy N.P., Cochran G., Van B. “Phenomenological theory underlying pressure-time relationship in decubitus ulcer formation.” Federation Proceedings 38 (1979): 1153 (abstract 4885).

Rolf, I.P. Rolfing: The Integration of Human Structures. Dennis-Landman, Santa Monica, 1977.

Schoenheimer, R. “The dynamic state of body constituents.” Cambridge, MA. Harvard University Press, 1942.

Tanaka, T. “Gels.” Scientific American 244 (1981): 124-38.

N=1: Stumbling over Selenium

Last spring, I was pressed for time in food prep and decided to grab a week’s worth of cans of sardines. I randomly decided to do this because Dr. Jonny Bowden’s book, “The 150 Healthiest Foods on Earth,” gave it a red star. For those of you unfamiliar with the book, a red star food is basically like hitting a field multiplier in pinball and opening the gravity well.

Now, what was not expected was a considerable positive change in body composition in one week! I wish I had values before and after the week to quantify the change, but unfortunately I don’t do a 7-site skin fold just prior to bed every day.

My first thought was the benefit from all the healthy omegas in sardines. However, I regularly consume a full spectrum of healthy fats and high quality fish oil on a routine basis, so I wasn’t convinced.

Two weeks after, I decided to double my fish oil intake to determine if the added omegas were the root of such change. One more serving of fish oil was actually more omega 3s than each can of sardines contained. The results…nothing.

Naturally, I did a little homework on sardines. It turns out one can of sardines provide approximately 70 percent of the Daily Value of selenium along with other unbelievable amounts of vitamins and minerals. So I couldn’t just attribute selenium as the absolute cause, but I was going to try to figure out if it was the major component.

I settled on consuming 6 Brazil nuts a day to keep my selenium intake high but still below the tolerable upper intake level (UL) of 400mcg/day. Brazil nuts are not particularly rich in omegas and are the highest source of selenium per ounce of any whole food. My results…another ideal drop in body fat in one week.

I decided to continue with this minor diet alteration of 6 Brazil nuts a day while changing nothing else in my routine diet for 1 month. Over the course of the month, I experienced improved skin, sleep quality, and a noticeable increase in facial hair (finally hit puberty!). I felt more recovered every morning after a deep night’s sleep. I also experienced tingling on the surface of my skin, especially around my nipple region (is that weird), for the first couple weeks that diminished by the end of the month.

Taking note of all these apparent changes, one word came to mind—testosterone.

It just so happens that the testes contain high concentrations of selenium and supplementation has been shown to increase quality and quantity of sperm production in males that have low levels of this mineral. Selenium is also required for testosterone biosynthesis. However, I am unaware of any studies correlating serum testosterone and selenium supplementation in humans.

My annual blood test showed a 213 ng/dL increase in total testosterone where I had been consciously consuming foods high in selenium on a daily basis for an uninterrupted 8 months. I made no other major alterations in diet or lifestyle for the period in between annual lab work. Blood was drawn at the same time of day in a fasted state. Were there other factors at play? I’m sure there were, but I noticed a personal improvement in wellbeing with blood work showing only a major change in testosterone and increase in HDL cholesterol levels.

Taking it a step further, selenium also has the potential to improve regulation of your thyroidal hormone production. T3 production is linked with iodothyronine deiodinase enzymes. These enzymes just so happen to have selenocysteine residue at the active site that accounts for the high catalytic activity of the enzymes. This enhances optimal function of TSH secretion in the pituitary and adaptive thermogenesis in brown adipose tissue. Along with testosterone, thyroidal hormone production could be a possible mechanism of why I saw immediate body fat reduction.

There are too many variables to consider how I responded so well to increasing my selenium intake. An argument could be made that I consume foods that are grown on over-farmed, selenium depleted soils because I do not live in the Dakotas or Nebraska where the soil and diets of these residents appear to be high in selenium.

Although I do not attempt to consciously reduce my carb intake, my routine diet consists of high amounts of fat and protein—sometimes carbohydrates falling as low as 15% of my total caloric intake. Research has shown that diets excessively high in fats and protein have the potential to gradually deplete selenium levels. If you’re like me and don’t plan on giving up large quantities of meat, be aware of the possible interruption in normal selenium status.

The best approach is to get tested and make adjustments accordingly so you aren’t wasting time and money on supplements or diet modification you don’t necessarily need. But if you like to figure things out on your own, you can learn a lot from self-experimentation.

References

Bank IM, Shemie SD, Rosenblatt B, Bernard C, Mackie AS. Sudden cardiac death in association with the ketogenic diet. Pediatr Neuro. 2008, 39(6): 429-31.

Beckett GJ, Arthur JR. Selenium and endocrine systems. J Endocrinol, 2005 184: 455-465.

Bergqvist, A. G. C. Chee, C. M. Lutchka, L. Rychik, J. Stallings, V. A. Selenium Deficiency Associated with Cardiomyopathy: A Complication of the Ketogenic Diet. Epilepsia.
2003, 44: 618-620.

Bowden, Jonny. 150 Healthiest Foods on Earth. Minneapolis: Fair Winds Press, 2007.

Scott R, MacPherson A, Yates RW, Hussain B & Dixon J. The effect of oral selenium supplementation on human sperm motility. British Journal of Urology. 1998, 82: 76–80.

Longnecker MP, Taylor PR, Levander OA, Howe M, Veillon C, McAdam PA, Patterson KY, Holden JM, Stampfer MJ, Morris JS, Willett WC. Selenium in diet, blood, and toenails in relation to human health in a seleniferous area. Am J Clin Nutr. 1991, 53: 1288-94.

Homunculus Training

The homunculus discussed in this article will pertain to the somatosensory cortex. It is located just posterior to the frontal lobe within the parietal lobe. The structure is termed the postcentral gyrus and was discovered by brain surface stimulation performed by a former Princeton University football player named Wilder Penfield.


The basic premise behind this area of the brain is that the majority of the brain tissue is devoted to the most sensory rich areas of the body—the hands, feet, and facial structures. So how can we use this to optimize training? This question has rarely been asked because motor neurons overshadow their forgotten sensory counterparts. It is often forgotten that the perception of your body to turn on more motor units is part of the foundation for moving big weights.

The Hands

The hands are enormous on the sensory homunculus and for good reason. They are at the ends of our upper extremities and used to explore and perceive our environment. For moving heavy weight, they can be one of the best tools to get the job done. The harder an athlete squeezes the bar, the more motor units are signaled to turn on. The hands feel the increased white-knuckling pressure and are prepared to lift a heavy load. More motor units are turning on because your brain is signaling this output. The sensory input is part of what is signaling your brain to create this driving motor mechanism. This is a synergist loop of events. The sensory neurons tell the brain what to do, the brain conveys the message to the motor neurons, and then the sensory neurons gain additional feedback and make adjustments accordingly through this same loop.

Now, I’m not trying to disregard the innate abilities of the motor neurons. When you tell your hands to create maximum grip tension, you are “outputting” contraction to your muscles. However, think of the sensory neurons as your fine-tuning dial that is constantly surveying the quantity and quality of how the body is performing. Sensory neurons are simply converting external stimuli from the environment into internal stimuli. The point being—the two work as a team and are not easily separated.

Great pressure generated in the hands yields great stability in the shoulders. Try this with a client who has a winging scapula. Have them ball up their fingers in a tight fist and squeeze and observe their scapula suction to their rib cage like a vacuum. I remember reading awhile back that Dan John claimed that the baseball players he trained no longer had shoulder problems when they started doing heavy carries. It’s interesting to consider that when his athletes fatigued they could feel their hands sliding off the handle and would instinctively tighten their grip as a correction. The carry is self-limiting for shoulder stability because when you lose grip and thus shoulder stability, you lose the weight. Without perception, there is no correction.

The Feet

Although not as large as the hands on the sensory homunculus, the feet still have a large portion of brain tissue devoted to them relative to their physical size. Most people’s thighs are physically bigger than their feet (I hope), but the opposite is true on the sensory homunculus.

Homunculus Robbery

The feet can be used in much of the same way as the hands to create pressure to signal more muscle recruitment. While the hands squeeze, the feet push. As more of the surface of the foot is driven into the floor, more motor units are signaled to turn on based on the perception of increased pressure. You’ve just manufactured your own high stability environment.

When you squat/deadlift, consciously push hard into the floor to prime the nervous system for the task. If you’re having trouble with single-leg work, do the same. A foot partially in contact with the floor doesn’t fair well for stability with a couple hundred pound body above.

It’s reasonable to assume that the Vibram wearers that instantly become pain-free just immediately restore perception. A perfect example of less is more. Although their knee may have hurt, their brain previously didn’t understand that they could use their feet to help stabilize. I would think the dynamic and neurological rich foot is a little better at stabilizing than a hinge joint with slight rotation capabilities.

The Eyes

This one is simple. The body follows the eyes. When you are at the bottom of a squat, you should be looking up to obtain a desirable vestibular effect. The eyes provide sensory feedback as to where they want the body to go—which is hopefully up.

I am not suggesting to lift your head/chin in the upward direction as you will lose stability, but to only look up with your eyes. The eyes supply the sensory input that automatically creates a neuromuscular output. No thinking needed. The topic of why you should keep your chin tucked will be expanded upon in a future article.

The Mouth

This is a fairly overlooked area that has the potential to yield more total body stability. The mouth is incredibly oversized as illustrated on the sensory homunculus. A large proportion of the postcentral gyrus is devoted to such a physically small structure.

If we can figure out how to tap into this potential, this could mean a greater degree of lifting stability. Try this out for me, throw a quick jab or hook. Notice that your mouth remains closed. Now do the same thing with your mouth open. Notice the stability difference. It is reflexive to close your mouth during a punch to pressurize your abdomen for a brief moment.

So how do we use this for training? I’m not quite sure yet. Obviously, you should be pressurizing your abdomen with air before big lifts with your mouth closed, but there is more to the mouth than lips closed. I have begun toying around with a mouth guard to allow me to clinch my teeth hard without damage. With the mouth closed and the teeth clinched hard, you are creating a perception that the ensuing task will need maximum motor recruitment. A clenched jaw stimulates a stable cranium. A stable cranium stimulates a stable spine. A stable spine reduces energy leak and maximizes lower to upper body force transfer while minimizing risk of injury.

The tongue could also come into play by firmly pushing it against the anterior portion of the palate. However, this technique may be unsuccessful because it could turn into a game of “turn this muscle on” as opposed to the more instinctive behavior of tight lips and a clenched jaw. Further expansion of this topic is definitely warranted.

Conclusion

I think creating perception is overlooked and underappreciated. Pressure on our feet, hands, and in our mouth matters. No one is yet to figure out how to consciously tap into the huge motor recruitment it takes for a mother (who is completely untrained) to lift a car that her child is under. Who knows, maybe it is safer that we don’t know how. But the possibility is still out there because people have done extraordinary things when a life or death situation demands it.

You’re not optimizing your performance or safety if you are benching with loose hands, letting the bar roll down your fingers during a set of RDLs, and flopping on the edges of your feet during single-leg work. Stability is the name of the game to effectively utilize strength. Use your brains incredible perceptual capacity to your advantage. Strength limitation is often not a lack of muscle tissue. Train your brain to take the governor off of your engine.

Give your body an environmental reason and it will give you a result.