doolee wrote:Here is the exact post so you don't have to go by faith!
During exercise, there is a localized build-up of metabolic waste products within muscle tissue that ultimately results in intracellular acidosis (which is due to ATP hydrolysis NOT "lactic acid"). Since hydrogen and potassium exist in an electrophysiological axis between the intracellular and extracellular environment, the excess hydrogen ions produced through repeated muscular contraction force potassium into the intracellular space while the H+ ions simultaneously move into the interstitium (*think of it as a H+-K+ antiporter). The resultant hypokalemic state hyperpolarizes the membrane which lowers the resting membrane potential as well as relaxing arterioles due to lower intracellular calcium levels, resulting in vasodilation.
Since caffeine has the capacity to enhance the exodus of calcium from the sarcoplasmic reticulum after an action potential (calcium release from the SR in smooth muscle is calcium dependent), if you remove the initial impetus for calcium release (due to cellular hyperpolarization), you remove the potentiality for smooth muscle contraction (vasoconstriction). Furthermore, since caffeine also acts as a PDEI, the only possible end-state would be vasodilation.
Also by PinchTheBear (simplified explanation and separate mechanism)
PDE5I ---> less enzyme to catalyze cGMP hydrolysis, more vasodilation.
This entire thread is proof positive The Blueprint has attracted the very BEST minds in the game!!!
Not since Avant Lab's board of many years ago, have I ever seen such educated, balanced and well articulated posts.
So proud of you, you/gals, this board and mutual sharing, learning and growing going on here!!
doolee wrote:Here is the exact post so you don't have to go by faith!
During exercise, there is a localized build-up of metabolic waste products within muscle tissue that ultimately results in intracellular acidosis (which is due to ATP hydrolysis NOT "lactic acid"). Since hydrogen and potassium exist in an electrophysiological axis between the intracellular and extracellular environment, the excess hydrogen ions produced through repeated muscular contraction force potassium into the intracellular space while the H+ ions simultaneously move into the interstitium (*think of it as a H+-K+ antiporter). The resultant hypokalemic state hyperpolarizes the membrane which lowers the resting membrane potential as well as relaxing arterioles due to lower intracellular calcium levels, resulting in vasodilation.
Since caffeine has the capacity to enhance the exodus of calcium from the sarcoplasmic reticulum after an action potential (calcium release from the SR in smooth muscle is calcium dependent), if you remove the initial impetus for calcium release (due to cellular hyperpolarization), you remove the potentiality for smooth muscle contraction (vasoconstriction). Furthermore, since caffeine also acts as a PDEI, the only possible end-state would be vasodilation.
Also by PinchTheBear (simplified explanation and separate mechanism)
PDE5I ---> less enzyme to catalyze cGMP hydrolysis, more vasodilation.
Interesting, what did he say about the caffeine dosage if anything?
haha np for the post. I know some people are just interested in the mechanisms.
There was no suggested caffeine dose. I would just use a moderate amount as 200+mg was seen to be ergogenic in many studies. Of course, too much caffeine (probably 500+?) would just worsen your lifts due to over stimulation of CNS. Would be a fun lifting session though!
