Good point.
Remember, that the " shift " of blood or v blood volume is only in action, when the cardiac output is not able to sustain BP. So in the stop period , where we get rid of muscle compression and therefore due to the lag time of CO the rush of blood in the muscles increase, we will see a " cardiac " weakness, when we have not enough pressure to maintain the central BP and than we will have a vasoconstriction. This can be anywhere but is most often , where it is most efficient. The upper body blood flow may be in bikers or for sure in runners much smaller than the huge capillary network in legs so a release in muscle compression in the legs will " suck " a lot of blood in the now open vasodliatated leg region and we will see a vasoconstriction there.
This vasoconstriction can be very local depending on the situation.
We have some great example s from cross-country skiing , where your point is well taken as we see the drop in tHb in the arm muscles when we hit a CO limitation. There is a great point in Dr. Bellars webinar, where he shows , that many MOXY users see a drop in SmO2 and sometimes in tHb in nonpriority muscle.
That is absolutely right and that is what we look for. The question only is , what causes this drop in SmO2 and tHb, when do we see it and than we can make some interpretation on what or where a limitation in that moment is. There are many individual access, where in some it is veyr easy to see and in others we have to add some additional feedback or ideas to it like HR RF to name some easy to use bio markers
Here some interesting topics looking at this direction. As you can see 1877 the topic was already in discussion !!!!!
J. Physiol. (1963), 166, pp. 120-135
Blood FLOW THROUGH ACTIVE AND INACTIVE MUSCLES OF THE FOREARM DURING SUSTAINED HAND-GRIP CONTRACTIONS
BY P. W. HUMPHREYS AsD A. R. LIND
From the National Coal Board Physiology Research
Branch, Department of Human Anatomy, University of Oxford
(Received 4 July 1962)
Despite the vasodilatation which occurs in a muscle during contraction,the full exploitation of this physiological response is hindered by the mechanical compression of the vessels by the contracting muscle (Gaskell, 1877), and its function is presumably thereby impaired. The continuous
mechanical compression of the blood vessels through the active muscle has been generally accepted as the cause of the early onset of fatigue during sustained contractions; the validity of this view may be judged from the values of intramuscular pressure, of 150-300 mm Hg, determined during
maximal isometric contractions of frog muscle (Hill, 1948) and of rabbit muscle (Mazella, 1954). Grant (1938) and Barcroft & Dornhorst (1949) found small increases in the blood flowing through the muscles during both sustained and rhythmic contractions, while in a previous report from this laboratory Clarke, Hellon & Lind (1958) showed that at a tension of 1/3 maximal the increase of blood flow during contractions was greater as muscle temperature increased and could, in fact, be substantial.
Some more updated studies but really no t new.
Are the arms and legs in competition for cardiac output?
Secher NH, Volianitis S.
Source
The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Denmark.
Abstract
Oxygen transport to working skeletal muscles is challenged during whole-body exercise. In general, arm-cranking exercise elicits a maximal oxygen uptake (VO2max) corresponding to approximately 70% of the value reached during leg exercise. However, in arm-trained subjects such as rowers, cross-country skiers, and swimmers, the arm VO2max approaches or surpasses the leg value. Despite this similarity between arm and leg VO2max, when arm exercise is added to leg exercise, VO2max is not markedly elevated, which suggests a central or cardiac limitation. In fact, when intense arm exercise is added to leg exercise, leg blood flow at a given work rate is approximately 10% less than during leg exercise alone. Similarly, when intense leg exercise is added to arm exercise, arm blood flow and muscle oxygenation are reduced by approximately 10%. Such reductions in regional blood flow are mainly attributed to peripheral vasoconstriction induced by the arterial baroreflex to support the prevailing blood pressure. This putative mechanism is also demonstrated when the ability to increase cardiac output is compromised; during exercise, the prevailing blood pressure is established primarily by an increase in cardiac output, but if the contribution of the cardiac output is not sufficient to maintain the preset blood pressure, the arterial baroreflex increases peripheral resistance by augmenting sympathetic activity and restricting blood flow to working skeletal muscles.
PMID:
17019302
[PubMed - indexed for MEDLINE]
Than another nice one
Acta Physiol Scand. 1998 Mar;162(3):421-36.
Skeletal muscle blood flow in humans and its regulation during exercise.
Saltin B1, Rådegran G, Koskolou MD, Roach RC.
Author information
- 1The Copenhagen Muscle Research Centre, Rigshospitalet, Tagensvei, Denmark.
Abstract
Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown.
However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.
Than here one you can combine with a case we showed on inversion reaction.
Noninvasively determined muscle oxygen saturation is an early indicator of central hypovolemia in humans
Babs R. Soller,1 Ye Yang,1 Olusola O. Soyemi,1 Kathy L. Ryan,2 Caroline A. Rickards,2 J. Matthias Walz,1 Stephen O. Heard,1 and Victor A. Convertino2
1Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and 2U. S. Army Institute of Surgical Research, Fort Sam Houston, Texas
Submitted 5 June 2007 ; accepted in final form 13 November 2007
ABSTRACT
Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and fat corrected deep muscle oxygen saturation (SmO2) and pH to standard hemodynamic parameters for early detection of imminent hemodynamic instability. Muscle SmO2 and pH were determined with a novel near infrared spectroscopic (NIRS) technique. Heart rate (HR) was measured continuously via ECG, and arterial blood pressure (BP) and stroke volume (SV) were obtained noninvasively via Finometer and impedance cardiography on a beat-to-beat basis. SmO2 and SV were significantly decreased during the first LBNP level (–15 mmHg), whereas HR and BP were late indicators of impending cardiovascular collapse. SmO2 declined in parallel with SV and inversely with total peripheral resistance, suggesting, in this model, that SmO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand. Spectroscopic determination of SmO2 is noninvasive and continuous, providing an early indication of impending cardiovascular collapse resulting from progressive reduction in central blood volume.
and here one from this group doing many great studies.
Cardiac output, and leg and arm blood flow during
incremental exercise to exhaustion on the cycle ergometer
Jose A. L. Calbet (1,2), Jose Gonzalez-Alonso (2), Jörn W. Helge (2,3),
Hans Søndergaard (2), Thor Munch-Andersen (2), Robert Boushel (3,4), Bengt Saltin (2)
(1) Department of Physical Education. University of Las Palmas de Gran Canaria, Spain
(2) The Copenhagen Muscle Research Centre, Rigshospitalet, 2200 Copenhagen N,
Denmark.
(3) Department of Biomedical Sciences, Panum Institute, 2200 Copenhagen N,
Denmark.
(4) Department of Exercise Science, Concordia University, Montreal, Quebec, CanadaJ.A.L. Calbet
Abstract
To determine central and peripheral haemodynamic responses to upright leg cycling
exercise, nine physically active males underwent measurements of arterial blood
pressure and gases, as well as femoral and subclavian vein blood flows and gases during
incremental exercise to exhaustion (Wmax). Cardiac output (CO) and leg blood flow
(BF) increased in parallel with exercise intensity. In contrast, arm BF remained at 0.8
l.min-1 during submaximal exercise, increasing to 1.2±0.2 l.min-1, at maximal exercise
(P<0.05), when arm O2 extraction reached 73±3%. The leg received a greater
percentage of the CO with exercise intensity, reaching a value close to 70% at 64% of
Wmax, which was maintained until exhaustion. The percentage of CO perfusing the
trunk decreased with exercise intensity to 21% at Wmax, i.e. to ~ 5.5 l.min-1. For a
given local VO2 leg vascular conductance (VC) was 5-6 fold higher than arm VC,
despite marked haemoglobin de-oxygenation in the subclavian vein. At peak exercise
arm VC was not significantly different than at rest. Leg VO2 represented around 84% of
the whole body VO2 at intensities ranging from 38 to 100 % of Wmax. Arm VO2
contributed between 7 and 10% to the whole body VO2. From 20 to 100% of Wmax, the
trunk VO2 (including the gluteus muscles) represented between 14-15% of the whole
body VO2. In summary, vasoconstrictor signals efficiently oppose the vasodilatory
metabolites in the arms suggesting that during whole body exercise in the upright
position blood flow is differentially regulated in the upper and lower extremities.
And here the one I mentioned where there is no problem when we have a muscle copmpression and lower flow as long the intensity is not high .
- Low blood flow at onset of moderate-intensity exercise does not limit muscleoxygenuptake.
PubMed
Nyberg, Michael; Mortensen, Stefan P; Saltin, Bengt; Hellsten, Ylva; Bangsbo, Jens
2010-03-01
The effect of low blood flow at onset of moderate-intensity exercise on the rate of rise in muscle oxygen uptake was examined. Seven male subjects performed a 3.5-min one-legged knee-extensor exercise bout (24 +/- 1 W, mean +/- SD) without (Con) and with (double blockade; DB) arterial infusion of inhibitors of nitric oxide synthase (N(G)-monomethyl-l-arginine) and cyclooxygenase (indomethacin) to inhibit the synthesis of nitric oxide and prostanoids, respectively. Leg blood flow and leg oxygen delivery throughout exercise was 25-50% lower (P < 0.05) in DB compared with Con. Leg oxygen extraction (arteriovenous O(2) difference) was higher (P < 0.05) in DB than in Con (5 s: 127 +/- 3 vs. 56 +/- 4 ml/l), and leg oxygen uptake was not different between Con and DB during exercise. The difference between leg oxygen delivery and leg oxygen uptake was smaller (P < 0.05) during exercise in DB than in Con (5 s: 59 +/- 12 vs. 262 +/- 39 ml/min). The present data demonstrate that muscle blood flow and oxygen delivery can be markedly reduced without affecting muscle oxygen uptake in the initial phase of moderate-intensity exercise, suggesting that blood flow does not limit muscle oxygen uptake at the onset of exercise. Additionally, prostanoids and/or nitric oxide appear to play important roles in elevating skeletal muscle blood flow in the initial phase of exercise. PMID:20089709
There are many many more studies supporting this interesting idea and again is helping us to close the gap between science and practical application.
