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Low Blood Volume


Sam_ci
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Increased Levels of Circulating Vasodilators - Stewart, Khan and Spence and now Shibao propose the orthostatic intolerance found in some CFS patients is not due to ANS abnormalities but to increased levels of vasoactive products.

Vasoactive products are able to alter how the vasculature – the blood vessels – function. As the first two papers on orthostatic tolerance on this website demonstrated POTS patients appear to have disturbed blood vessel functioning (inappropriately increased or decreased vasoconstriction). Several researchers have believed this is likely due to autonomic nervous system dysfunction but these Stewart, Khan and Spence don’t think so.

Read more: http://phoenixrising.me/research-2/the-perils-of-standing-orthostatic-intolerance-and-chronic-fatigue-syndrome-mecfs-i-the-evidence/the-perils-of-standing-orthostatic-intolerance-in-chronic-fatigue-syndrome-mecfs-iii-possible-causes

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The problem with internet information is that it is dated. Infact this is quoting an article from around 2002 if Im correct.

Low blood volume in POTS:

1. increased ang ii (measure serum levels of angiotensin II)

2. net deficiency (increased or more likely reduced sympathetic outflow to the kidney and or being investigated - impaired dopamine activity)

3. impaired dopamine salt handling (tenative - being investigated)

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Would the net deficiency theory, link into what is coming out of the sports medicine at the moment I read an article by a Professor Tim Noakes which got me thinking about the whole deconditioning thing again!

http://www.pponline.co.uk/encyc/how-physiological-biochemical-and-neural-systems-influence-your-training-and-competition-performance-152

The muscle recruitment: (central fatigue) model

The argument

This model proposes that it is not the rate at which either oxygen or fuel are supplied to muscle that limits its performance but rather the processes involved in skeletal muscle recruitment (activation), excitation and contraction. It suggests that the brain concentration of the neurotransmitter serotonin, and possibly others including dopamine and acetylcholine, alters the neural impulses from the brain to the exercising muscles to reduce skeletal muscle activation - the actual mass of muscle that is active during any exercise. Alternatively, fatigue may be induced by inhibitory reflexes arising from the exercising muscles and feeding back to the spinal chord.

The evidence

A number of studies have shown that manipulating central nervous system neurotransmitter concen-trations, particularly by increasing dopamine and reducing serotonin, can enhance exercise performance, and vice versa. There is also direct evidence for reduced central nervous system drive to muscle after fatiguing muscle contractions.

I have already described the clear evidence that fatigue at high altitude is caused by reduced activation of exercising muscles by the central nervous system and that a central 'governor' must be involved in causing fatigue when liver glycogen stores are depleted. It is also likely that heat-induced fatigue is controlled by the central nervous system, as it cannot be explained by any other model. In all these cases, reduced central activation of muscle would function as a protective mechanism to prevent organ damage.

A contrasting finding that electrical activity within the skeletal muscles actually rises during exercise at a constant workload is usually inter-preted as evidence for increased activation by the central nervous system to compensate for a prog-ressive failure of muscle fibre contractile function.

But competitive athletes do not work at a constant rate. And our own studies of prolonged exercise, including bouts of self-chosen high-intensity work, show a progressive reduction in power output during successive bouts of high intensity exercise. This response is very strongly suggestive of central rather than peripheral fatigue. The fact that a relatively small percentage of the available muscle mass (perhaps as little as a maximum of 40%) is ever recruited, even during maximal exercise, remains a perplexing enigma. And proponents of any model of peripheral limitations for exercise performance need to explain why the body does not recruit all its available muscle mass to produce the necessary force under varying exercise conditions as so-called 'peripheral fatigue' develops.

An alternative view

I have argued that a reduced central activation of the exercising muscles may be necessary to protect humans under specific conditions. I believe these control mechanisms are necessary to prevent the following potentially dangerous developments:

* myocardial ischaemia during high-intensity exercise;

* muscle ATP depletion and rigor during high intensity exercise;

* myocardial ischaemia or cerebral hypoxia during exercise at altitude;

* falling blood pressure during exercise in patients with chronic heart failure;

* heatstroke during prolonged exercise in the heat;

* brain damage from hypoglycaemia during prolonged exercise, when liver glycogen stores are depleted.

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