Peripheral regulation  therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the myocytes. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract. Management
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McArdles disease
Left ventricular thrombus is a blood clot (thrombus) in the left ventricle of the heart. LVT is a common complication of acute myocardial infarction (AMI). Typically the clot is a mural thrombus, meaning it is on the wall of the ventricle. The primary risk of LVT is the occurrence of cardiac embolism, in which the thrombus detaches from the ventricular wall and travels through the circulation and blocks blood vessels. Blockage can be especially damaging in the heart or brain (stroke). Pathophysiology
LVT occurs most often during the first 2 weeks following AMI. AMI patients most at risk display the 3 characteristics of Virchows triad:

Stagnation of blood
The risk of LVT formation increases as infarction size increases. A larger infarction means a larger area of tissue injury, which may be akinetic or dyskinetic, resulting in stagnation of ventricular blood. Endothelial injury
Monocytes and macrophages play important roles in healing after myocardial infarction. With the absence of monocytes and macrophages, chances of LVT formation are very high. Failure to clear cellular debris from the infarct compromises the endothelial lining of the left ventricle and exposes the damaged tissue to the blood. The response is to build a thrombus composed of fibrin, red blood cells and platelets. Hypercoagulable state
For several days after AMI, the levels of tissue factor and D-dimer, which are involved in coagulation, are high, which increases the risk of LVT formation. LVT may be good for the heart when tissues are severely damaged because it acts to thicken the wall, thus protecting it against rupture.