Physiologic and biochemical effects of immobilization on muscle.
Muscle strength rapidly declines during limb immobilization because of a decrease in muscle size and a decrease in tension per unit of muscle cross-sectional area. Muscle fatigability also increases rapidly after limb immobilization. Muscles within limbs fixed by plaster casts have lower levels of resting glycogen and adenosine triphosphate (ATP), a more rapid depletion of muscle glycogen and ATP during work, a greater increase in lactate during work, and a decreased capacity to oxidize fatty acids during work. The greatest loss of absolute muscle mass occurs at the beginning of muscle wasting with subsequent loss of muscle being exponential. A significant decrease in the rate of protein synthesis in muscles is observable at the sixth hour of limb immobilization, which most likely initiates the net loss of muscle protein. A change in the amount of either translational or elongational factor is most likely responsible for the early decrease in this rate of protein synthesis.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002415:Cats; D005221:Fatigue / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D007103:Immobilization; D007333:Insulin Resistance; D007773:Lactates / Q000378:metabolism; D009119:Muscle Contraction; D009132:Muscles / Q000378:metabolism* / Q000502:physiology; D009133:Muscular Atrophy / Q000503:physiopathology; D010084:Oxidation-Reduction; D051381:Rats
D005227:Fatty Acids; D007773:Lactates; D000255:Adenosine Triphosphate