Intraneural blood flow

[BB]

Brian posed this on another thread and it never got addressed before the topic shifted.

when looking at intraneural blood flow, is there any correlation to increasing aerobic capacity and increaed vascularity of neural tissue? Do diseases including diabetes (glycolisization of hemoglobin leading the neuropathies), and atheroslcerosis, which causes decrease blood flow in the small capillary beds, do the same to intraneural blood flow? What role may physical activity, not necessarily structured physical activity like a gym program, but movement for movements sake that maintains metabolic and cardiovascular health also enhance the "health" of the nervous tissue?

Hope you don't mind my moving it here Brian, but I thought it might get more attention that way.

To start I'll just post a link to Barrett's essay on Apaptive Potential. (http://www.barrettdorko.com/articles/adaptive.htm) I think that is a good starting place.

[Barrett Dorko]

Cory,

I'm surprised that this post hasn't generated any replies. Perhpas it is my unique position as a workshop insturctor that has made me more sensitive to this issue, but I think it's an important one.

A few weeks ago after I had spoken for about twenty minutes the air conditioning clicked on in the large ballroom I had been assigned. Moving with the precision of a school of fish, a dozen students shfted uncomfortably and began doing all they could to cover up. "Frantic" would be too harsh a description of their movement but all were distinctly concerned about what this slight change in their environment would soon mean. I asked, and all but two admitted that they commonly suffer from disabling discomfort - and I simply didn't believe the two that denied it.

This sympathetic dominance common to the abnormal neurodynamic is, I think, a key factor in the ongoing problem and reversing it in some fashion is essential for recovery. The drill is this: feet apart, diaphragmatic breathing (even when not exercising), regular self-correction. Add to that aerobic activity and you've got a program bound to help. Finding an exercise regimen that doesn't simultaneously aggravate the mechanical deformation unique to each of us can be a challenge, of course, but I've met many who have done it.

Their history includes this: "I'm okay as long as I work out hard no less than 4-5 times each week. If I miss a couple of workouts I really start to hurt."

Predictably, these are slim women (98% of my students, so this may be a biased view) who dress quite warmly even when in a warm room. At least, it's warm to me.

I'd have to conclude that they're getting some blood flow into the involved nervous tissue simply by contracting the adjacent muscle repeatedly. The problem is that it won't stay there. Correction (ideomotion) seems a better option for pain relief.

[Brian Bettendorf]

Cory,

I've held off on trying to elicit any thoughts on my original question because I found that as I read through the old threads that the answer - or least my own ideas on an answer could be found. I haven't read through the threads enough yet, but I'm getting some ideas.

I agree with you that the concept of adaptive potential applies and felt I was getting a better handle on this until I quickly reviewed the article by Roosterman that Diane posted the other week on the skin. That alone has been enough reading. I think this issue, like many, is complex. Disease states and pain can be caused/promoted by external and internal events, lifestyle choices and genetics.

As Barrett mentioned, aerobic exercise in some cases may be a palliative means by which people deal with pain/dysfunction. When is exercise (we'll stick with aerobic) protective and no longer palliative? These slim women Barrett mentioned probably all exercise and by all measures (BP, aerobic capacity, BMI, cholesterol) are healthy, yet they hurt. Can we really consider them healthy?

Dose-response relationships for the prevention and treatment of many disease states exist. Outside of the mechanical and chemical effects aerobic exercise has on the heart, arteries, .... is there a dose-response relationship to optimize autonomic control. Cardiac variability, the influence of the sympathetic and parasympathetic nervous system on heart rate, shows greater variability in healthy individuals. Lack a heart rate variability has been show to be a predictor of mortality. If we think specifically about the ectoderm now, does anyone have any ideas on how a "healthy" or "unhealthy" ectoderm would influence say cardiovascular adaptations to aerobic exercise that move beyond the palliative kind?

My original thought was that aerobic exercise would over the long-term increase capillary density around the nervous tissue, just as it does the muscular tissue. Some good novel activity for the brain, and aerobic exercise for the nerve.

[EricM]

Brian your last post really got me thinking. This link (http://jap.physiology.org/cgi/reprint/97/3/1119) has some interesting information though my quick lit search was unable to find anything specifically discussing ectodermal adaptations to aerobic exercise. Diane you must have posted something on the microcirculation by now :) Do you know where it might be?
In the past I have wondered about the effects of aerobic exercise on neural tissue and I would agree that there must be some combination of stress to the nervous system with adaptive physiological responses to mitigate the effects of that stress, making it less susceptible to repeated exposure to the stressor. Angiogenesis would be one such response.
And what of adaptive changes in the mesoderm in response to aerobic exercise? To some extent these changes must be present to enhance the health and survival of the ectoderm; are there any negative effects as well?


eric

[Jon Newman]

About 1 year ago we had a discussion at NOI related to this. These were the thoughts of people back then

microcirculation (http://www.noigroup.com/cgi-bin/ubbcgi/ultimatebb.cgi?ubb=get_topic;f=5;t=000196#000000) <--A trick I learned from Eric M. as you can see if you read through that thread.

Maybe some of the McKenzie-anados would be interested in this study

Spine. 2003 Jan 1;28(1):85-90.

Intraoperative measurements of nerve root blood flow during discectomy for lumbar disc herniation.

Hida S, Naito M, Kubo M.

STUDY DESIGN: Nerve root blood flow was intraoperatively measured before and after discectomy for lumbar disc herniation and compared with clinical features. OBJECTIVE: To investigate the relation between nerve root blood flow changes and symptoms associated with lumbar disc herniation. SUMMARY OF BACKGROUND DATA: Several authors have reported that recovery of intraneural blood flow, which restores the supply of oxygen and other nutrients to the nerve tissue, is strongly related to the rapid improvement of nerve function after discectomy for lumbar disc herniation. However, no previous study has quantitatively assessed blood flow in the human nerve root. METHODS: Nerve root blood flow was monitored in 21 patients with lumbar disc herniation using laser Doppler flowmetry (ALF 21 N; ADVANCE, Tokyo, Japan) during discectomy. Possible correlations were investigated between the blood flow rates and the following clinical features: age, duration of sciatica, presence or absence of neurologic deficits, latency to pain relief, and morphology of herniated discs. RESULTS: The blood flow rate in 16 patients who reported immediate relief after discectomy was much greater than in 5 patients whose pain was not relieved immediately after surgery (141% 8%, = 0.0364). The increase in the blood flow rate after discectomy was five times greater in patients with neurologic deficits than in patients without neurologic deficits (158% 36%, = 0.0638). CONCLUSIONS: The results of the current study suggest that immediate relief from pain and resolution of neurologic deficits soon after surgery are the result of early recovery from nerve root ischemia after discectomy, and that ischemia caused by mechanical nerve root compression is mainly related to the mechanisms underlying sciatic pain production and neurologic deficits.

and lastly, an article that pertains to exercise and pain relief

J Psychosom Res. 2004 Oct;57(4):391-8.

Comment in: J Psychosom Res. 2005 Apr;58(4):389-90.

The effect of brief exercise cessation on pain, fatigue, and mood symptom development in healthy, fit individuals.

Glass JM, Lyden AK, Petzke F, Stein P, Whalen G, Ambrose K, Chrousos G, Clauw DJ.

OBJECTIVE: Abnormalities of the biological stress response (hypothalamic-pituitary-adrenal axis and the autonomic nervous system) have been identified in both fibromyalgia (FM) and chronic fatigue syndrome (CFS). Although these changes have been considered to be partly responsible for symptom expression, we examine an alternative hypothesis that these HPA and autonomic changes can be found in subsets of healthy individuals in the general population who may be at risk of developing these conditions. Exposure to "stressors" (e.g., infections, trauma, etc.) may lead to symptom expression (pain, fatigue, and other somatic symptoms) in part by precipitating lifestyle changes. In particular, we focus on the effect of deprivation of routine aerobic exercise on the development of somatic symptoms. METHODS: Eighteen regularly exercising (>/=4 h/week) asymptomatic, healthy adults refrained from physical activity for 1 week. We predicted that a subset of these individuals would develop symptoms of FM/CFS with exercise deprivation, and this manuscript focuses on the baseline HPA axis, immune, and autonomic function measures that may predict the development of symptoms. RESULTS: Eight of the subjects reported a 10% increase in one or more symptoms (pain, fatigue, mood) after 1 week of exercise deprivation. These symptomatic subjects had lower HPA axis (baseline cortisol prior to VO2max testing), immune (NK cell responsiveness to venipuncture), and autonomic function (measured by heart rate variability) at baseline (prior to cessation of exercise) when compared to the subjects who did not develop symptoms. CONCLUSIONS: A subset of subjects developed symptoms of pain, fatigue, or mood changes after exercise deprivation. This cohort was different from the individuals who did not develop symptoms in baseline measures of HPA axis, immune, and autonomic function. We speculate that a subset of healthy individuals who have hypoactive function of the biological stress response systems unknowingly exercise regularly to augment the function of these systems and thus suppress symptoms. These individuals may be at risk for developing chronic multisymptom illnesses (CMIs) (e.g., FM or CFS among others) when a "stressor" leads to lifestyle changes that disrupt regular exercise.

[Diane]

Diane you must have posted something on the microcirculation by now Do you know where it might be?
I'm busy with the Jänig book, which is full of great stuff on circulation and its central control; anything I've posted on that will be either in the Beast Within folder or in the In Sipnal AcCordance folder. (Another ambition is to bring the embryology of the vascular system to here sometime.. even though vasculature is mesoderm, there are bound to be big overlaps with ectoderm in that the ectoderm builds it as it needs it in order to feed itself oxygen.)

About microcirculation of nerves, go read Butler's first book, mobilization of the nervous system. The entire first chunk is all about this topic. A world within a world. He pulled up all kinds of stuff and put it together, PNS, cord and brain are dealt with separately, anatomy and physiology of each of the three main levels and all the transition zones. Shacklock's book has quite a bit on this too, endoneurial swelling etc., especially as it pertains to diabetes, etc., vasculature destroying diseases that result in neuropathies.

Thanks for putting that NOI thread back up Jon, I'd forgotten about that..

[Diane]

I've been ruminating about these thin women: Their history includes this: "I'm okay as long as I work out hard no less than 4-5 times each week. If I miss a couple of workouts I really start to hurt."

Predictably, these are slim women (98% of my students, so this may be a biased view) who dress quite warmly even when in a warm room. At least, it's warm to me.
And: These slim women Barrett mentioned probably all exercise and by all measures (BP, aerobic capacity, BMI, cholesterol) are healthy, yet they hurt. Can we really consider them healthy?
And: If we think specifically about the ectoderm now, does anyone have any ideas on how a "healthy" or "unhealthy" ectoderm would influence say cardiovascular adaptations to aerobic exercise that move beyond the palliative kind?

I've got some speculations in no apparent order.

1. I suspect the nervous system (any of its 3 kinds of motor output systems, somatic, autonomic, and neuroendocrine) would "learn" to expect and even crave whatever it was "taught" or repeatedly exposed to daily or almost daily. Exercise can be just as addictive as any other sort of behavior/input. I can even see this happening to the point of them feeling they can't be warm unless they DO move. It would be more a form of neural learning or inadvertent operant conditioning than an abnormal neurodynamic, probably..

2. The thin-ness.. usually the more the ratio of surface area to volume, the more heat-dissipative will be the organism, a completely passive effect. So, yes, these thinnies will get colder quicker. I wouldn't blame that on their nervous system so much as I'd blame it on their being good ectomorphic entropy producers.

3. You'd think they'd stay warmer than they do, though, by having a higher metabolic rate from all the exercise. But.. the other thing is, usually they are very careful with their intake, eat low fat diets etc., if not be outright bulimic, because they are terrified of looking fat. So they really are too lean, perhaps, to be able to stay warm, go into temperature deficit easily.

4. The other thing is hormonal cycling. Take a system that is stressed by not taking in enough calories to stay "thick" and then overexercising to raise a metabolic rate up (tuning up the mitochondrial burners), and then add a wide hormonal load on top.. there will be times when said organism not only feels crankier emotionally, it will likely feel crankier (more sensitive, less ability to adapt to ambient temperature) physically too.

5. What about the abs? Usually the thinnies are very over ab-trained and rarely let their abs relax in public enough to breathe normally.

6. They probably aren't optimally comfortable or content but they are probably healthy. In general, mammals that undereat or are underfed have greater longevity and less "disease".

There's hope for the thinnies. CBT can help them let go of rigid control of their bodies (and everyone elses' bodies if they are therapists..), and when they reach menopause, and have survived the thermostat problems involved, they'll be warmer for quite awhile before they start to feel cold again. ;)

[Barrett Dorko]

Diane,

I can't disagree, but you're going to have to explain what "CBT" is. You use this type of abbreviation a lot.

There is a "perfect storm" of influences here, all of them contributing to persistent cooling. Often however, if I'm given a few minutes to work specifically with these subjects in standing their sense of warming will rise dramatically and universally, indicating that the mechanical irritation to the nervous tissue is a major factor not only to their pain but to their sympathetic dominance.

I think, I'm pretty sure.

I have the sense that many suffering like this sit in the back and display a timidity that, to me, is astonishing in a professional working with the public. I'll admit I might be way off on that, but I can't deny entirely my common and repeated experience.

[Diane]

Barrett,
CBT = cognitive behavioral therapy