I feel that during my 5-1-5 my limiter was on respiratory side (main limiter was VL) and during FTP was on cardiac side?
Yes welcome in the personnel kitchen.
In all out loads as mentioned , you load the full team. So you will first overload the real limiter. But as it is a race or a highly motivated workout you still keep going as you have the option to survive by using compensators. Now earlier than later the compensator have enough as well and will finally limit your high performance. You now can quit or you have to slow done, as the priority is the O2 hierarchic or pyramid.
Lets go through the picture which may start to make sense.
In a race or hard training based on performance you load the TEAM. You get the end result of the teams needs and performance. That's it.
You miss for example when rower no 2 started to loose the optimal strokes per minute he now just keeps the stroke rate but no power any more on the oar.
In a physiological assessment or workout you try to find who in the team start to push the limitation.
Now 2 main options. Just stopped there and work individual with this rowers to get up his stroke rate and let the three other work on a higher stroke rate as they are hold back from the no 2 .
So as all have to stop by stroke rate 40 only No2 may perhaps improve, but as well may be overloaded. The other three really will get worse , as they never really push their own limitation So split to boat work individual till No2 is able to get back to contribute to the team. In case of specific stroke rate workouts.
Or change so he can go faster with different options still in the same boat.
So in an all workout like your FTP or race you overlook the limiter and hope for help from the compensators.
If your limiter is a vital system like respiration in COPD or cardiac limiter like after a heart attack , than you will have no real compensator, as you will shut down the loco motor muscles first.
Now you look above and you can see why the tHb is so crucial when we look at NIRS. SmO2 is great but we need the combination and the connection in physiological terms to understand the reactions. So top athletes have one additional gear, ob nice we start protecting the vital pO2 systems reaction. Blood volume shift.
Are the arms and legs in competition for cardiac output?
Secher NH, Volianitis S.
The Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, Denmark.
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.
[PubMed - indexed for MEDLINE]
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,
(3) Department of Biomedical Sciences, Panum Institute, 2200 Copenhagen N,
(4) Department of Exercise Science, Concordia University, Montreal, Quebec, CanadaJ.A.L. Calbet
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.
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.
- 1The Copenhagen Muscle Research Centre, Rigshospitalet, Tagensvei, Denmark.
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.
And to give the flowers where they belong. Hunter already over 200 years back postulate the pointedout that blood will go where it is needed.
So here our idea in a picture
a ) First we have to survive. You see Cannons idea and our idea on who to back this up and what equipment we used .
now look this idea below.
So in a race you end up on the top asking all to contribute no mater how efficient and good it is just try to hold on the performance.
In a physiological training you decide who you like to integrate in a workout and why.
No speculation to your case:
Driven by a performance based training program you learned perfectly to achieve the performance goal. In the route to the goal you always needed the VL and no matter finally what you do he is ready to help as soon you are on the bike.
Problem he has to do most of the load.
he knows that the body learned that and what ever you do you push him to the limit and in some cases may ask one or the other muscle group or systems to step in.
This is in survival mode you add other potential muscles used in cycling.
Unusual situation and you create a lot of CO2 as many of this muscles now are not very efficient in delivery but even worse in utilization.
Your H + is going out of balance.
H + is not a reason of f ailed muscle contraction as so many believe. You can add H + and you can have a low pH it does not interfere with muscle contraction or power production. This is another reason why lactate can not en used as an indirect feedbag on a too low pH Here below one of many great studies in that direction.
Muscle Nerve. 1993 Jan;16(1):91-8.
Dissociation of [H+] from fatigue in human muscle detected by high time resolution 31P-NMR.
Degroot M1, Massie BM, Boska M, Gober J, Miller RG, Weiner MW.
- 1Magnetic Resonance Unit, Veterans Administrative Medical Center, San Francisco, CA 94121.
Previous in vivo studies of skeletal muscle fatigue have demonstrated significant relationships between the decline of muscular force and changes in muscle metabolism. However, these studies performed measurements over relatively long time intervals or during steady state exercise, thereby obscuring rapid metabolic changes occurring at the onset of exercise and recovery. To overcome these limitations, fatigue of human calf musculature during sustained isometric foot plantar flexion was quantified continuously as the decline in maximal voluntary contraction force (MVC), while concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), intracellular free hydrogen ion (H+), and monovalent phosphate (H2PO4-) were simultaneously measured at 2-second intervals by 31P nuclear magnetic resonance.
The first major finding was that [H+], which has been thought to be a mediator of muscle fatigue, actually declined during the first 10 seconds of exercise when force was declining and rose immediately postexercise, when force partially recovered.
Second, the correlations of [H+], [H2PO4-] and Pi with MVC during the first minute of exercise were determined to be curvilinear and not linear as previously suggested. Furthermore, using either a linear or curvilinear regression model, [H2PO4-] and Pi demonstrated a closer correlation to MVC than [H+] during the first minute of exercise. Thus, these results reveal nuances in the relationships of MVC to metabolites previously undetected by low time-resolution measurements. These findings suggest that during sustained isometric exercise, rising [H+] is not likely to be the sole mechanism of muscle fatigue and are consistent with the view that a rise of Pi or [H2PO4-] is a major causation factor in force reduction.
This leaves us with the idea back to survival ( energy or O2.)
If we can not deliver O2 we have a problem. So even though high H + or low pH may not reduce muscle strength they inhibit O 2 supply ( O2 dissociation curve. ) so we have O2 but it is not bio available.) this creates the dilemma for any body who believes they can use lactate and SmO2 to find what ever they try to find.
We can have a drop in SmO2 but as well a drop in lactate.
We can have a drop in SmO2 but an increase in lactate . we can have an increase in SmO2 and a drop in lactate and we can have a increase in SmO 2 and an increase in lactate. Now you us a systemic lactate testing idea with a punctual NIRS feedback and we can keep dreaming .
Now VL runs into trouble , you keep going you already create some H + in the perfect and super hard working VL . You add a long time unwilling RF or Hamstrings guy in it. Not yet ready to contribute and early limitation in delivery ( vascularisation but as well in utilization ( mitochondria density ) but a person trained to push the pyramid. So you shut down delivery due to cardiac and respiratory limitation now and you try to shift some blood . After a hard race you immediately shift first from one not priority area to priority area in case you have to go once more and vital systems did not yet recovered.
The integration of non trained leg muscles adds to the pH and H + dilemma . The O2 disscurve shifts more to the right. Still O2 there but not bio availability. Bad loading in the lungs to the blood, High CO2 and you reach your respiratory limitation which finally create a problem for your cardiac systems . So FTP end tHb drop due to cardiac limitation as you after the load open too many blood vessels. CO can not keep central venous BP and you will create a protective vasoconstriction.
If this does not works you will get dizzy. You can sustain that somewhat by not stopping immediately so your muscle compression will help to maintain the BP easier.
Why in a race the first three rarely collapse . They keep going to celebrate. The worst collapse is always the 4 th in a race ??? Exceptions are sports , where the whole body is involved ( Rowing cross country skiing and triathlon WHY ?? Even winners often collapse.
Have fun to read swenglish.