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To: techdiver@opal.com
Subject: physiology behind questions
From: jolieb@gr*.ci*.up*.ed* (Jolie Bookspan)
Date: Fri, 6 May 94 01:16:11 EDT
More physiology behind the recent questions:

  > I told the University's Diving Safety Officer about this and he 
  > thought it was due to what he called 'blood pooling'. As I was 
  > decending head down and kicking strongly, the blood vessels in 
  > my head constricted to ensure an adequate blood supply to my 
  > legs.  

Don't worry, the brain and heart are spared vasoconstriction during 
flow redistributions with exercise. 

At rest the majority of blood flows to the viscera (guts), heart, and 
brain, with only 15-20% of total systemic flow distributed to muscle. 
During exercise, blood flow redistributes - most to muscle. Flow 
to active muscle may increase by up to 15 times and more but not at 
expense of brain. Blood flow to spleen and kidneys reduces from 
about 2.8 liters per minute to about 500 ml during maximal exercise. 
(This renal hypoxia is the spur for more red blood cell production, 
one of the reasons exercise is beneficial and improves physical 
condition.... Erythropoietin, the kidney hormone behind this, is for 
another story). Muscle blood flow during submaximal exercise is 
lower in athletically fit than untrained people (but higher, 
considerably, during maximal exercise. Much is involved - that's for 
another story.)

   > When I went head-up
   > the combination of constricted vessels and gravity caused a low
   > blood pressure condition in my head, causing (along with the 
   > depth) the extreme narcosis.  Does this sound reasonable ...

Blood flow and its distribution underwater are not much affected 
by posture. The effect of gravity is reduced underwater (gravity is 
not reduced, just its effect due to buoyancy). In one experiment we 
did at the Biokinetics Research Lab at Temple U and reported in 
Undersea Biomedical Research (1991 I think - I have to look it up - 
it's not listed in Medline) we measured blood volume changes with 
different postures. Large effect in the air due to gravity. But not 
underwater. Blood floats out of the lower limbs regardless of posture
similar to the effect observed in spacecraft during microgravity.

   > it is possible that a reduced venous return to the right side 
   > of the heart could cause a transient drop in cardiac output 
   > that could reduce blood flow via the carotids to the brain.

Exercise increases venous return (venous return is blood in veins 
returning to the heart). The skeletal muscle pumping action in 
vessels in working muscle, and the movement of breathing, increase 
venous pressure and facilitate venous return. Immersion also greatly 
increases venous return because blood floats from the lower limbs 
into the thorax. This volume redistribution is one of the main reasons 
behind both the dive reflex (heart rate reflexively decreases with 
increased venous return) and immersion diuresis, which is why you 
have to pee when immersed - a multivariable regulatory response to 
normalize increased thoracic volume - by helpfully showing some the 
way out.

   > Also, blood flow wouldn't have to stop entirely to result in a 
   > buildup of CO2 in the tissues - it would just have to slow enough 
   > that CO2 is not eliminated from the tissues at rate equal to or 
   > exceeding its production by metabolism.

It's not the FLOW of blood that determines removal of CO2.

   > It seems to me ... 
   > the oxygen concetration at an inspired PPO2 of 2 ATM is high 
   > enough above"normal" that it would lead to a vascular 
   > constriction effect that could only be countered by proportionally  
   > high CO2 concentrations (i.e., CO2...
   > Yes? No? Maybe?

O2 is a vasoconstrictor. A good thing. Too much O2 is Not Good - your 
body works to prevent too much reaching the brain - not always 
successfully, but that is another story - physiology (and 
physiologists) always have another story. 

O2 is only one of many vasoconstrictors. CO2 is only one of many 
vasodilators. Your body continually varies vessel caliber size, all day 
all night. Size is mainly controlled by vessel smooth muscle degree of 
contraction. This degree of contraction is governed by a variety of 
excitatory and inhibitory stimuli, not just O2 and CO2 but hydrogen 
ions (H+), potassium ions (K+), hormones, pH, and metabolites like 
lactic acid. Moreover, response depends on location in the body - for 
example, smooth muscle of brain arterioles are sensitive to CO2 but 
not motor nerve stimulus. Arterioles in the skin overlying the skull 
are little affected by CO2, and greatly affected by motor nerves. 
There's lots going on - can't draw conclusions from blind assessment 
of one part of your elephant. 

  > I have heard that the popping noise may be due to the creation of 
  > a low pressure area in the joint, which cavitates a bubble out of 
  > solution in the fluid of the joint. 

There are several ways a joint produces a popping noise. Gas coming 
out of solution is one, similar to propellers cavitating bubbles. The 
April 1994 issue of SkinDiver magazine explained exactly that 
question in the regular Scuba Fitness column. The column is 
unrelated and unaffected by any editorial policy of the magazine and 
the fitness column is often worth reading if I say so myself. If you 
can't find it, I'll post the gist here.

Mr. Pyle - Thanks for your thanks. We recently exchanged posts on 
CompuServe, and I enjoy hearing about your diving.

Mr. Crea - Hello again. You asked me to remind you about the dive 
medicine workshop at Dive Philadelphia. If you can, keep 14-16 Oct 
1994 open. Will post you privately.

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