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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