This is an interesting thought, but my prediction is that hypertension is likely not the cause of lethargy while on cycle. Here's my reasoning:
1) The heart and circulatory systems are already adapted to maintaining blood flow while overcoming great pressure (assuming the person has been strength training for a period of time prior to the cycle). During a heavy straining movement systolic BP can be 400+, which is much higher than any resting high BP while on cycle. Thus resting hypertension would be very unlikely to occlude blood flow to any significant degree.
2) Endurance athletes who blood dope or use EPO would also greatly increase blood viscosity and they don't report lethargy.
3) The body is extremely good at extracting oxygen from the blood. Even during maximal aerobic exercise aVO2 difference doesn't decrease to any significant degree. Thus it seems unlikely that high resting BP would cause any decrease in oxygen extraction at the tissue level.
4) Systolic BP increases during aerobic exercise even while oxygen consumption is going up. It seems reasonable to assume that elevated BP at rest would not compromise oxygen carrying capacity.
5) It takes a near-full occlusion of a vessel to induce oxygen deprivation at rest, so it seems unlikely a slight rise in BP would occlude flow to the point that oxygen deprivation actually occurs.
6) Hemoglobin reaches near 100% oxygen saturation in the lungs even when blood is moving through very quickly (at heart rates approaching 200), so an increase in blood viscosity and/or BP is likely not going to limit oxygen delivery at this step.
With all that said, I don't know what causes the lethary on cycle. My first instinct would be to examine brain chemistry and neurotransmitter levels. Especially since some people report difficulty sleeping while on cycle with certain compounds. Lethargy combined with difficulty sleeping would suggest some sort of brain chemistry issue.
VERYgood response! However I have some comments,
1) With incr blood pressure, it isnt the short burst of 400mmHg that will do the trick, it is a chronic high BP that does it. The short burst is compensated simply by the elasticity of the blood vessels.
The heart and cirr systems do compensate yes, but it is the fact that it fails to do so. In fact the compensatory mechanisms actually exacerbate the problem and here is how:
SNS compensation
- tachycardia (incr HR), vasoconstriction
Ventricular remodelling
- incr size of ventricles
Hormonal activation
- RAAS, ADH, ANP
Thesesystems are activated when teh body senses that the heart is unable to pump all of the blood volume. As you can see, thee mechanisms, over time, will actaully make things worse, ie, RAAS activation results in aldosterone whicb retains salt leading to water retention.
So, occlusion isnt really the issue here.
See this excellen wiki article. Easy read, quite complete too.
http://en.wikipedia.org/wiki/Heart_failure#Symptoms
See the symptoms and pathophysiology.
2) Endurance atheletes using EPO dont experience lethargy. I thought about this too but teh rfact is polycythemia (incr RBC numbers) does very much induce lethargy. I am just not sure whythose endurance atheletes experience it. Perhaps it is because they use it short term ie, right before their competitions?
http://emedicine.medscape.com/article/205039-overview
Look atthat link, so blood doping woudl be considered secondary polycythmeia. Look at the Sx
3) Yes I agree with you about oxygen extraction. I think I said something incorrect up there. What I mea to say is when you have icr BP, you can get heart failure, resulting in the blood not getting circulated, so less fresh O2 avaiable. But the O2 that is avaiable is extracted just fine yeah.
4) See above
5) Again we are not talking about occlusion
6) Againm see 3). Our concern isnt oxygen saturation at the lungs it is the circulation of RBCs