Effects of unloading on skeletal muscle mass and function in man

Detta är en avhandling från Stockholm : Karolinska Institutet, false

Sammanfattning: An experimental human model of skeletal muscle unloading of one lower limb and confined bedrest wereemployed to quantitate the adaptive responses to 10 days, 4 or 6 wk of unloading in healthy humans onquadricep skeletal muscle mass and function. Muscle cross-sectional area (CSA) was assessed using tomographic imaging (CT, MRI). Fiber CSA, typeand capillarization and myosin heavy chain (MyHC) composition were determined in biopsy specimens fromm. vastus lateralis. Enzyme activity of citrate synthase (CS) and phosphofructokinase (PFK) was analyzed.Strength (peak torque), force-velocity characteristics along with electromyographic (EMG) activity and workcapacity were assessed during maximal voluntary knee extension. Peak torque decreased uniformly across velocities and mode of action by 13% after 10 d and 16-22% after 4wk unilateral unloading and by 25-30% after 6 wk bedrest. Four wk unloading reduced (17%) work capacityand increased fatigability of exercise comprising three bouts of 30 knee extensions. Thigh muscle mass decreased by 7% after 4 wk of unilateral unloading and by 11% after 37 days bedrest.The atrophy was more pronounced in the knee extensor (14%) than in adductor (9%) or knee flexor (p>0.05;7%) muscles, suggesting a hierarchy related to weight-bearing activity. Peak torque/knee extensor CSAdecreased (13%) in response to 6 wk bedrest suggesting atrophy not to fully account for the loss in strength. Muscle fiber CSA decreased by 18% after 37 days bedrest but not (p>0.05; 10%) after 4 wk unloading.Type l/type 11 fiber CSA showed no change. Nor did type I or type 11 fiber percentage change. MyHCcomposition was unaltered after bedrest. Capillaries per fiber or area were unaltered after 4 wk unloading. CSbut not PFK activity decreased. Single-fiber analysis in 3 individuals showed a decrease in force-generatingcapacity per cross-sectional area (specific tension) after bedrest. No change occurred in maximum shorteningvelocity of pooled single fibers. Neural drive, as reflected in EMG activity, was unaltered after 10 d unloading but decreased (19%) after 6wk bedrest. EMG activity at a constant submaximal load, increased after 10 d unloading (25%) and 6 wkbedrest (44%), suggesting decreased electromechanical efficiency. Four days of weight-bearing recovery normalized strength following short term (10 d) unloadmg while halfof the strength loss was recaptured following 4 wk unloading. Seven wk of free reambulation normalizedmuscle CSA while work capacity was still decreased (7%) following unilateral unloading and strength (7%)was reduced following bedrest. The time required to normalize muscle strength, thus, seems to increase withduration of unloading. A rapid recovery in strength was a consistent finding during the first days ofreambulation. The loss in strength and work capacity was about 5% weekly during the first month of unloading. About twothirds of the loss in muscle function can be accounted for by muscle atrophy. Although neural drive appearedto be reduced a decrease in skeletal muscle force-generating capacity of muscle, e.g., decreased specifictension of muscle must in part be responsible for the impaired muscle function seen after prolonged unloading.Key words: Atrophy, bedrest, concentric and isometric and eccentric muscle actions, disuse,electromyography, fatigue, fiber types and size, humans, inactivity, maximal voluntary force, recovery,skeletal muscle cross-sectional area, strength, suspension, tomographic imagingISBN 91-628-1962-3

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