Why the study?
Does major abdominal surgery cause intrinsic muscular defects that account for postoperative fatigue?
Does major abdominal surgery cause intrinsic muscular defects that account for postoperative fatigue?
Postoperative fatigue following major abdominal surgery appears to be driven by central fatigue rather than intrinsic muscular defects.
Postoperative fatigue after major abdominal surgery may be centrally mediated; hypothesis-generating for central over peripheral mechanisms in recovery.
We attempted to define the site of muscle action accounting for the apparent muscle weakness occurring with postoperative fatigue. A model of the normal pathway of muscle contraction is presented. A series of studies, designed to separate the elements of the pathway, was performed on 38 patients undergoing major abdominal surgery. Central fatigue was measured with Christensen's analogue, voluntary strength by grip strength, perceived effort by grading the difficulty of a set work load, involuntary muscle function by ulnar nerve stimulation, and muscle bulk represented by total body nitrogen, measured by in vivo neuron activation analysis. Fatigue increased for the first 2 weeks after operation, was back to pre-operative levels within 1 month, and improved further at 3 months. Grip strength fell after operation and returned to pre-operative levels within 3 months. Perceived effort rose after operation and returned to pre-operative levels by 3 months. Involuntary muscle function was unaffected by operation. Similarly, total body nitrogen fell in the first 2 weeks after operation but was improved on baseline levels at 3 months. However, there was no consistent correlation between the movement patterns of any of the muscle parameters and fatigue. The results suggest that fatigue after surgery is not accompanied by any muscular defect, and that the apparent muscular weakness is probably a secondary phenomenon to the central fatigue.
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Schroeder et al. (1991) studied this question.
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