Thanks to Craig's nice track and field example and out discussion ion the recovery section after the second 150 m sprint and the possible reaction due to " gravity " I received 2 emails. They absolutely with their terms argue , that this is a nice study but in now way woudl NIRS pick up this reactions. They believe it is a nice story but not backed up by science.
Well that is where one of the discussion points is. As many time mentioned .
Belief " moves towards religion and needs not facts to claim the " truth. Somewhat different with science.
NIRS is one option to show this facts.
Here some independent information on what we discuss here and as well what Craig's small experiment actually shows.
The more informed readers may start to see how the different physiological reactions can be picked up with NIRS and if we need facts we than can go back to how we started by using VO2 and Physio flow and blood sampling to show how time lag and direct feedback can support each otehr when the physiology is used accordingly. I may show some fun data and the dilemma we had in the past when we " believed" on VO2 and lactate what we tested and forgot that the unseen real is now real with MOXY and the unreal seen is lactate and VO2
Gravitational forces significantly affect venous return, cardiac output, and arterial and venous pressures. ( and therefor tHb and SmO2 ) To illustrate this, consider a person who is lying down and then suddenly stands up. As the person stands, gravity acts on the vascular volume so that blood accumulates in the lower extremities. (Compare the size of veins in the top of your feet while lying down and standing.) Because venous compliance is high and the veins readily expand with blood, most of the blood volume shift occurs in the veins. Therefore, venous volume and pressure becomes very high in the feet and lower limbs when standing. This shift in blood volume decreases thoracic venous blood volume and therefore central venous pressure decreases. This decreases right ventricular filling pressure (preload), leading to a decline in stroke volume by the Frank-Starling mechanism. Left ventricular stroke volume also falls because of reduced pulmonary venous return (decreased left ventricular preload). This causes cardiac output and arterial blood pressure to fall. If arterial pressure falls appreciably upon standing, this is termed orthostatic or postural hypotension.This fall in arterial pressure can reduce cerebral blood flow to the point where a person might experience syncope (fainting).
When a person stands up, baroreceptor reflexes are rapidly activated to restore arterial pressure so that mean arterial pressure normally is not reduced by more than a few mmHg when a person is standing compared to lying down. However, in order to maintain this normal mean arterial pressure, the person who is standing upright has increased systemic vascular resistance (sympathetic mediated), decreased venous compliance (due to sympathetic activation of veins), decreased stroke volume (due to decreased preload), and increased heart rate (baroreceptor-mediated tachycardia). Patients with autonomic nerve dysfunction or hypovolemia will not be able effectively utilize these compensatory mechanisms and therefore will display orthostatic hypotension.
Without the operation of important compensatory mechanisms, standing upright would lead to significant edema in the feet and lower legs in addition to orthostatic hypotension. Venous pooling and reduced venous return are rapidly compensated in a normal individual by neurogenic vasoconstriction of veins, the functioning of venous valves, by muscle pump activity, and by the abdominothoracic pump. When these mechanisms are operating, capillary and venous pressures in the feet will only be elevated by 10-20 mmHg, mean aortic pressure will be maintained, and central venous pressure will be only slightly reduced.
When a person is lying down in a horizontal position, gravity is no longer causing a shift in blood volume from the thoracic compartment to the legs and feet. Therefore, the thoracic (central venous) compartment has increased blood volume compared to standing. This increases preload on the heart, thereby increasing stroke volume, although the resulting increase in cardiac output will be tempered by a reduction in heart rate through vagal activation and sympathetic withdrawal. Sympathetic activation of the systemic vasculature is also reduced, which causes systemic vascular resistance to fall as the resistance vessels dilate.