Discussion
During exercise, damage to the sarcolemma can lead to loss of force production and skeletal muscle failure (1,2). It’s this loss of integrity which causes a disruption in the somatic nervous systems ability to effectively communicate with the muscle (3). Typically, this is caused by heavy loads during the eccentric motion (lengthening) of muscle tissue (4). Even if you have enough energy per se the inability of the somatic nervous system to communication with your muscles can limit excitation-contraction coupling (4-6).
As you can probably infer, maintaining the structural integrity the sacolemma (plasma membrane) plays an essential role in acheiving maximal stimulation and withstanding neuromuscular fatigue. Aplodan (creatinol-o-phospate) reduces Ca2+ overload and Mg2+ depletion but more importantly reduces creatine phosphokinase (CPK) loss across the plasma membrane (7). CPK is an essential enyzme in the anaerobic production of ATP from phosphocreatine. Obviously, limiting it’s loss through an enhanced sarcolemmal membrane is another way Aplodan can improve exercise performance.
I’m going to end today’s discussion here. In summary, it’s necessary to maintain sarcolemmal integrity in a two fold manner. One, this allows the somatic nervous system to continue to communicate with muscle cells to delay neuromuscular fatigue which can limit excitation-contraction coupling. Secondly, Aplodan helps reduce the loss of the ever important CPK enzyme responsible for anearobic energy production with respect to phospocreatine. Honestly, I can’t wait to add creatine back into my stack to fully utilize the power the studies which imply Aplodan is a strong exercise performance aide.
I guess tomorrow we will discuss excitation-contraction coupling and it’s effect on quantul summation/recruitent of skeletal muscle fibers. This will hopefully paint a picture as to why it’s important to stimulate as many muscle fibers as possible before failure and how neuromuscular fatigue can limit this process.
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