|
|
|
|
Originally Posted by soxmuscle
delayed on-set muscle strain.
|
|
Originally Posted by Squaggleboggin
Delayed onset muscle soreness, unless I'm mistaken.
|
|
Originally Posted by The13ig13adWolf
it happens...however DOMS isn't an indicator of a successful workout.
|
|
Originally Posted by JoeR.
ive heard this before, explain to me how it isnt an indicator of a good workout? Just the function of being sore, means your body has taken some slight muscle tissue micro tears right? So explain to me HOW your statement makes sense.
|
|
Originally Posted by JoeR.
Just the function of being sore, means your body has taken some slight muscle tissue micro tears right?
|
|
Originally Posted by LAM
the soreness general associated from DOMS is more likely attributed to a disturbance in calcium homeostasis than from micro trauma(s) of skeletal tissues
|
|
Originally Posted by CowPimp
I've never read a conclusive study on the subject. It seems to me that the real cause behind DOMS is still up in the air. Do you have a link to the study, or source, where you read that?
|
|
Originally Posted by CowPimp
I've never read a conclusive study on the subject. It seems to me that the real cause behind DOMS is still up in the air. Do you have a link to the study, or source, where you read that?
|
|
Originally Posted by LAM
you are right there is nothing definitive on the subject of the exact causes of DOMS however there are some very good theory's.
#1. FG fibers fatigue due to depletion of CP and glycogen and/or accumulation of H+. With continued activation, ATP levels fall causing rigor or high stiffness. Subsequent mechanical stretch of stiff fibers breaks desmin #2. FG fibers fatigue due to depletion of CP and glycogen and/or accumulation of H+. With continued activation, ATP levels fall causing loss of calcium homeostasis. SR and mitochondria both use ATP to sequester Ca++. Elevated Ca++ level activates calpain proteases which specifically degrade desmin filaments. if you can find Clarkson and Sayers 1999, McArdle et al 1996 or Chleboun et al 1998, Stauber 1996 there is some good info in them |
|
Originally Posted by CowPimp
Interesting. Although isn't degrading or breaking of desmin filaments really just some form of microtrauma?
|
|
Originally Posted by LAM
yup...that's why DOMS has to be caused by serveral things. desmin filaments break during every day activities (walking for example) and we don't get DOMS from it
|
|
Originally Posted by alexvega
i went to university
the biochemistry say, the when a muscle pass from anerobic work to anaerobic, is when the productions of lactic acid happens. thanks |
|
Originally Posted by CowPimp
The buildup occurs during a process called lactic acid fermentation. It is a process that allows NADH to be converted to NAD+ via a redox reaction with pryuvate and recycled in glycolysis, which subsequently allows more ATP to be produced via subtrate-level phosphorylation. The end product is something called lactate. Which is actually an ionized for of lactic acid.
|