An Experimental Knee Joint Effusion Does Not Affect Plasma Catecholamine Concentration

Abstract

2073 Knee joint effusion results in quadriceps inhibition and is accompanied by increased excitability in the soleus musculature. In order to develop an intervention that is successful in returning the musculature to a normal state we must understand the neuroendocrine processes involved in the arthrogenic muscle response seen following knee joint effusion. PURPOSE: To determine if an experimental knee joint effusion results in an increase in plasma epinephrine and norepinephrine levels. METHODS: 10 healthy, physically active volunteers were admitted to the hospital on 2 separate occasions, during one admission subjects had their knees injected with 60mL of sterile saline and in the other admission they did not. Ten mL of blood was drawn and reflex measurements were elicited and recorded at 5 measurement intervals: baseline, post needle stick, post lidocaine, 25 minutes post effusion, and 45 minutes post effusion. Measurements obtained during the control admission were protocol matched to the effusion condition. Soleus Hmax, Mmax, plasma epinephrine and norepinephrine levels were measured. A mixed effects model ANOVA for repeated measures was used for each dependent variable. RESULTS: Hmax during the effusion admission was smaller at baseline compared with measures taken post needle stick (P = .015), 25 minutes (P< 0.0001) and 45 minutes (P < 0.0001) post knee joint effusion. Hmax was greater at 25 minutes and 45 minutes post effusion when compared with measures taken post needle stick and post lidocaine (P< 0.0001). No differences were noted for the H-reflex during the control admission. Norepinephrine and epinephrine levels did not change during the effusion of the control admission (P<0.05). CONCLUSION: We suggest that the facilitation seen in the soleus following knee joint effusion results from stimulation of joint mechanoreceptors and removal of descending spinal and supraspinal inhibition and is not the result of an increased sympathetic response. Supported in part by a grant from the National Institutes of Health to the University of Virginia General Clinical Research Center, number M01RR00847.