Early quadriceps strength loss after total knee arthroplasty - The contributions of muscle atrophy and failure of voluntary muscle activation

Department of Physical Therapy, 301 McKinly Laboratory, University of Delaware, Newark, Deleware 19716, USA.
The Journal of Bone and Joint Surgery (Impact Factor: 5.28). 05/2005; 87(5):1047-53. DOI: 10.2106/JBJS.D.01992
Source: PubMed


While total knee arthroplasty reduces pain and provides a functional range of motion of the knee, quadriceps weakness and reduced functional capacity typically are still present one year after surgery. The purpose of the present investigation was to determine the role of failure of voluntary muscle activation and muscle atrophy in the early loss of quadriceps strength after surgery.
Twenty patients with unilateral knee osteoarthritis were tested an average of ten days before and twenty-seven days after primary total knee arthroplasty. Quadriceps strength and voluntary muscle activation were measured with use of a burst-superimposition technique in which a supramaximal burst of electrical stimulation is superimposed on a maximum voluntary isometric contraction. Maximal quadriceps cross-sectional area was assessed with use of magnetic resonance imaging.
Postoperatively, quadriceps strength was decreased by 62%, voluntary activation was decreased by 17%, and maximal cross-sectional area was decreased by 10% in comparison with the preoperative values; these differences were significant (p < 0.01). Collectively, failure of voluntary muscle activation and atrophy explained 85% of the loss of quadriceps strength (p < 0.001). Multiple linear regression analysis revealed that failure of voluntary activation contributed nearly twice as much as atrophy did to the loss of quadriceps strength. The severity of knee pain with muscle contraction did not change significantly compared with the preoperative level (p = 0.31). Changes in knee pain during strength-testing did not account for a significant amount of the change in voluntary activation (p = 0.14).
Patients who are managed with total knee arthroplasty have profound impairment of quadriceps strength one month after surgery. This impairment is predominantly due to failure of voluntary muscle activation, and it is also influenced, to a lesser degree, by muscle atrophy. Knee pain with muscle contraction played a surprisingly small role in the reduction of muscle activation.

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Available from: Lynn Snyder-Mackler, Dec 17, 2014
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    • "Based on this, we thought that tourniquet use would add to the effect of the surgical trauma on changing afferent signalling to the CNS, whereby efferent activation of the quadriceps muscle would be further reduced. Reduced efferent activation of the quadriceps muscle — known as central activation deficits or arthrogenic muscle inhibition — [15] [23] is well known shortly following TKA [13] [24]. The neural mechanisms are not fully understood, but it has been attributed, at least in part, to alter afferent feedback from the operated knee joint due to swelling, inflammation, pain, and damage to joint afferent [15] [23]. "
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    ABSTRACT: Background: Thigh tourniquet is commonly used in total knee arthroplasty (TKA) but may contribute to pain and muscle damage. Consequently, the reduction in knee-extension strength after TKA may be caused by quadriceps muscle ischaemia underneath the cuff. Aim: To examine if not using a thigh tourniquet during surgery was more effective than using a thigh tourniquet in preserving knee-extension strength 48 h after fast-track TKA. Methods: A total of 64 patients undergoing TKA were randomized (1:1) to the use of tourniquet (T-group) or no tourniquet (NT-group). In the T-group the tourniquet cuff pressure was based on the patient's systolic pressure and a margin of 100 mm Hg. It was inflated immediately before surgery and deflated as soon as surgery ended. The primary outcome was the change in knee-extension strength from pre-surgery to 48 h after surgery (primary end point). Secondary outcomes were pain, nausea, length of hospital stay (LOS) and periarticular swelling. Results: Knee-extension strength 48 h after surgery was substantially reduced by about 90% in both groups, with no statistically significant difference between groups (mean difference 1.5 N/kg, 95% CI 1.3-1.6). Among the secondary outcomes, the T-group had less bleeding during surgery (56 vs. 182 mL, P<0.01) compared with the NT-group. There was no difference in postoperative haemoglobin levels, pain, nausea, LOS or periarticular swelling between the groups. Conclusion: Not using a thigh tourniquet during surgery was not superior in preserving knee-extension strength at the primary endpoint 48 h after fast-track TKA, compared to using a tourniquet.
    Full-text · Article · Dec 2014 · The Knee
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    • "Despite the fact that the patients enter a fast-track or enhanced peri-operative recovery program [2], they loose, on average, 80% knee-extension strength over the 2–3 days of their hospitalization [3]. It is the most pronounced acute loss of knee-extension strength of any cohort of people who have had knee surgery [4], and is caused by failure of the central nervous system (CNS) to activate the quadriceps muscle [5], [6] – known as arthrogenic quadriceps muscle inhibition [7]. "
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    ABSTRACT: Loading and contraction failure (muscular exhaustion) are strength training variables known to influence neural activation of the exercising muscle in healthy subjects, which may help reduce neural inhibition of the quadriceps muscle following total knee arthroplasty (TKA). It is unknown how these exercise variables influence knee pain after TKA. To investigate the effect of loading and contraction failure on knee pain during strength training, shortly following TKA. Cross-sectional study. Consecutive sample of patients from the Copenhagen area, Denmark, receiving a TKA, between November 2012 and April 2013. Seventeen patients, no more than 3 weeks after their TKA. Main outcome measures: In a randomized order, the patients performed 1 set of 4 standardized knee extensions, using relative loads of 8, 14, and 20 repetition maximum (RM), and ended with 1 single set to contraction failure (14 RM load). The individual loadings (kilograms) were determined during a familiarization session >72 hours prior. The patients rated their knee pain during each repetition, using a numerical rating scale (0-10). Two patients were lost to follow up. Knee pain increased with increasing load (20 RM: 3.1±2.0 points, 14 RM: 3.5±1.8 points, 8 RM: 4.3±2.5 points, P = 0.006), and repetitions to contraction failure (10% failure: 3.2±1.9 points, 100% failure: 5.4±1.6 points, P<0.001). Resting knee pain 60 seconds after the final repetition (2.7±2.4 points) was not different from that recorded before strength training (2.7±1.8 points, P = 0.88). Both loading and repetitions performed to contraction failure during knee- extension strength-training, increased post-operative knee pain during strength training implemented shortly following TKA. However, only the increase in pain during repetitions to contraction failure exceeded that defined as clinically relevant, and was very short-lived. NCT01729520.
    Full-text · Article · Mar 2014 · PLoS ONE
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    • "Despite success as a treatment of osteoarthritis TKA leaves patients with persistent muscle atrophy and loss of function. Muscle atrophy of the knee extensors is responsible for the majority of functional deficit 1–3 years post-TKA (Meier et al. 2009) by inhibiting balance (Moxley Scarborough et al. 1999), reducing functional mobility (Brown et al. 1995; Mizner et al. 2005c), and increasing the risk of falls (Moreland et al. 2004). "
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    ABSTRACT: Total knee arthroplasty (TKA) is the most common remediation for knee pain from osteoarthritis (OA) and is performed 650,000 annually in the U.S. A tourniquet is commonly used during TKA which causes ischemia and reperfusion (I/R) to the lower limb but the effects of I/R on muscle are not fully understood. Previous reports suggest upregulation of cell-stress and catabolism and downregulation of markers of cap-dependent translation during and after TKA. I/R has also been shown to cause endoplasmic reticulum (ER) stress and induce the unfolded protein response (UPR). We hypothesized that the UPR would be activated in response to ER stress during TKA. We obtained muscle biopsies from the vastus lateralis at baseline, before TKA; at maximal ischemia, prior to tourniquet deflation; and during reperfusion in the operating room. Phosphorylation of 4E-BP1 and AKT decreased during ischemia (-28%, p < .05; -20%, p < .05 respectively) along with an increase in eIF2α phosphorylation (64%, p < .05) suggesting decreased translation initiation. Cleaved ATF6 protein increased in ischemia (39%, p = .056) but returned to baseline during reperfusion. CASP3 activation increased during reperfusion compared to baseline (23%, p < .05). XBP1 splicing assays revealed an increase in spliced transcript during ischemia (31%, p < .05) which diminished during reperfusion. These results suggest that in response to I/R during TKA all three branches of the ER stress response are activated.
    Full-text · Article · Aug 2013
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