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juergfeldmann

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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.

R├ądegran G1, Saltin B.

Author information

Abstract

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.

 

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