I juts finished a call with a interesting institution who like to do some studies on blood flow and activities besides using Doppler. They had some accepted questions on tHb and its value to be used as a trend in blood flow. There are as so often assumption in tHb = Blood flow or we discussed a while back blood volume under the NIRS tested area. Now one of the discussion points as, that studies show , that when we start any activity we immediately creates a energy ( O2 ) demand which immediately will trigger a vasodilatation. The where skeptical about my info on tHb drop. that when we start a new load like in a 5/1/5 or any activity, that the tHb drop; is an indication of a reduced blood volume or flow under the NIRS as it should actually show up as a vasodilatation so tHb up. . So I am not sure, whether I convinced them , that there is a battle between different reactions but the fastest reaction will be a mechanical reaction so muscle compression before we have the local metabolic triggered vasodilatation and the even slower increase in CO for an additional option to increase blood flow.
. So I sent them this article to have a little bit of an accepted back up for the tHb trend.
Now as you will see the back up is not great as they talk about elevation of blood flow, when in fact we have a mechanical compression and if you use NIRS/MOXY fix it on a biceps and so on and you easy can create all three mechanical tHb reactions from tHb drop due to compression, tHb increase due to venous outflow restriction and flat tHb due to free flow or no flow.
. The free flow, no flow can be separated when you before you create a arterial occlusion go slowly over compression venous occlusion ( pooling ) to arterial occlusion . Thna let go and you have a tHb drop due to pooling out flwo back to base lione flow.
Where as in a free flow you have no change really in tHb downwards during a release of an activity but rather an increase due to the missing compression now and the often still slightly higher CO.
Am J Physiol. 1998 Jan;274(1 Pt 2):H314-22.
Muscle blood flow at onset of dynamic exercise in humans.
Rådegran G1, Saltin B.
To evaluate the temporal relationship between blood flow, blood pressure, and muscle contractions, we continuously measured femoral arterial inflow with ultrasound Doppler at onset of passive exercise and voluntary, one-legged, dynamic knee-extensor exercise in humans. Blood velocity and inflow increased (P < 0.006) with the first relaxation of passive and voluntary exercise, whereas the arterial-venous pressure difference was unaltered [P = not significant (NS)]. During steady-state exercise, and with arterial pressure as a superimposed influence, blood velocity was affected by the muscle pump, peaking (P < 0.001) at approximately 2.5 +/- 0.3 m/s as the relaxation coincided with peak systolic arterial blood pressure; blood velocity decreased (P < 0.001) to 44.2 +/- 8.6 and 28.5 +/- 5.5% of peak velocity at the second dicrotic and diastolic blood pressure notches, respectively. Mechanical hindrance occurred (P < 0.001) during the contraction phase at blood pressures less than or equal to that at the second dicrotic notch. The increase in blood flow (Q) was characterized by a one-component (approximately 15% of peak power output), two-component (approximately 40-70% of peak power output), or three-component exponential model (> or = 75% of peak power output), where Q(t) = Qpassive + delta Q1.[1 - e-(t - TD1/tau 1)]+ delta Q2.[1 - e-(t - TD2/tau 2)]+ delta Q3.[1 - e-(t - TD3/tau 3)]; Qpassive, the blood flow during passive leg movement, equals 1.17 +/- 0.11 l/min; TD is the onset latency; tau is the time constant; delta Q is the magnitude of blood flow rise; and subscripts 1-3 refer to the first, second, and third components of the exponential model, respectively. The time to reach 50% of the difference between passive and voluntary asymptotic blood flow was approximately 2.2-8.9 s. The blood flow leveled off after approximately 10-150 s, related to the power outputs. It is concluded that the elevation in blood flow with the first duty cycle(s) is due to muscle mechanical factors, but vasodilators initiate a more potent amplification within the second to fourth contraction.