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Experimental Knee Pain Reduces Muscle Strength
The Journal of Pain, Vol 12, No 4 (April), 2011: pp 460-467 Available online at www.sciencedirect.com
Experimental Knee Pain Reduces Muscle Strength Marius Henriksen,* Sara Rosager,* Jens Aaboe,* Thomas Graven-Nielsen,y and Henning Bliddal*,y * Clinical Motor Function Laboratory, The Parker Institute, Frederiksberg Hospital, Frederiksberg, Denmark. y Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.
Abstract: Pain is the principal symptom in knee pathologies and reduced muscle strength is a common observation among knee patients. However, the relationship between knee joint pain and muscle strength remains to be clarified. This study aimed at investigating the changes in knee muscle strength following experimental knee pain in healthy volunteers, and if these changes were associated with the pain intensities. In a crossover study, 18 healthy subjects were tested on 2 different days. Using an isokinetic dynamometer, maximal muscle strength in knee extension and flexion was measured at angular velocities 0, 60, 120, and 180 degrees/second, before, during, and after experimental pain induced by injections of hypertonic saline into the infrapatellar fat pad. On a separate day, isotonic saline injections were used as control condition. The pain intensity was assessed on a 0- to 100-mm visual analogue scale. Knee pain reduced the muscle strength by 5 to 15% compared to the control conditions (P < .001) in both knee extension and flexion at all angular velocities. The reduction in muscle strength was positively correlated to the pain intensity. Experimental knee pain significantly reduced knee extension and flexion muscle strength indicating a generalized muscle inhibition augmented by higher pain intensities. Perspective: This study showed that knee joint pain has a significant impact on muscle function. The findings provide evidence of a direct inhibition of muscle function by joint pain, implying that rehabilitative strengthening exercises may be antagonized by joint pain. ª 2011 by the American Pain Society Key words: Knee pain, muscle strength, physical function, exercise.
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nee pain is the cardinal symptom in knee osteoarthritis (OA), and reduced knee muscle strength is common among these patients.3,21 Pain reduction and restoration of muscle function are thus primary goals in the treatment of knee OA and in fact there is ample evidence that muscle strengthening exercises result in improvements in pain.3 Structurally knee OA is characterized by cartilage loss, joint contractures, deformities, and laxity, yet the pathogenesis of knee OA is generally unknown. Impaired muscle function is suspected to play a pathogenetic role in the structural degeneration of the knee joint,32 Received May 5, 2010; Revised September 8, 2010; Accepted September 26, 2010. Supported by grants from The Oak Foundation and The Association of Danish Physiotherapists Research Foundation, and The Association of Danish Physiotherapists Practice Foundation. The authors have no conflicts of interest regarding this article. Address reprint requests to Marius Henriksen, PT, PhD, Clinical Motor Function Laboratory, The Parker Institute, Frederiksberg Hospital, Ndr. Fasanvej 57, DK-2000 Frederiksberg C, Denmark. E-mail: marius. [email protected] 1526-5900/$36.00 ª 2011 by the American Pain Society doi:10.1016/j.jpain.2010.10.004
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and exercise may be beneficial for articular cartilage.30 Many of the structural changes are progressive with disease severity.22 While pain traditionally is weakly correlated to radiographical knee OA severity,5,8 a recent large cohort study has shown the opposite,27 and other structural changes, such as quantification of synovitis by means of magnetic resonance imaging techniques, show better correlations to pain.1,19 Knee pain has been shown to alter many aspects of motor function, including the dynamics of walking16 and muscle coordination,20,41 and reduced muscle function is suggested to be involved in structural disease progression.32 Thus, adaptations in muscle function due to pain could be a possible source for development of the structural changes. However, the isolated effects of knee pain on muscle strength are unknown. The multiple changes associated with knee OA may introduce unwanted variability in muscle function assessments. By consequence, it is difficult to assess the isolated effects of pain on muscle function in a patient population. Experimental techniques to induce pain in healthy subjects are thus advantageous in this respect. A harmless technique inducing reversible, localized
Henriksen et al pain in the infrapatellar fat pad of the knee has been used in experimental studies2,16,20,41 allowing assessments of pain adaptations in the muscle function. The infrapatellar fat pad is a source of pain in knee osteoarthritis,1,19 and injections of hypertonic saline into the fat pad with a medial approach produce antero-medial knee pain with similar qualities as clinical pain in the anterior knee.2 Strategies for physical therapy treatment and prevention of knee OA pain are mainly empirical, and a better understanding of underlying sensory-motor mechanisms would be 1 step forward towards optimizing therapy. The purpose of this study was to assess the effects of experimental infrapatellar fat pad pain on maximal isometric and isokinetic knee extensor and flexor muscle strength in healthy subjects. We hypothesized that experimental infrapatellar fat pad pain reduced knee extensor and flexor muscle strength and that reductions in muscle strength would be associated with the pain intensity.
Methods Subjects Healthy subjects (9 females and 9 males) with no history of musculoskeletal problems gave voluntary written informed consent to participate in the study. Their mean age was 26.5 years (SD 6.8), mean height was 1.75 m (SD .13) and mean body mass was 62.0 kg (SD 4.2). The study was approved by the ethics committee for the Capitol Region of Denmark (j. no. H-C-2007-0053).
Protocol The study was designed as a crossover study with each subject tested on 2 days separated by at least 1 week. During a test day, 3 series of muscle-strength tests were performed. Series 1 and 2 were separated by a 5-minute break, during which the subjects rested. Immediately before the second series, an intra-articular saline injection was given in the infrapatellar fat pad. The saline solution was either hypertonic or isotonic for the painful and control conditions, respectively. On a single test day only 1 type of saline solution was injected according to the randomization process: The order of the saline solution injections was allocated using an envelope based randomization technique allowing equal numbers of subjects starting with isotonic and hypertonic saline, respectively. After the second muscle-strength assessment series, a 20-minute break was held to ensure that any pain had vanished before the third series of musclestrength assessments. The person performing the muscle-strength measurement (SR) was blinded to the randomization. All subjects were informed about the study design and that they would receive 1 painful injection and one nonpainful control injection, but the subjects were blinded to the order of injections.
Muscle-Strength Measurements Before the muscle-strength measurements, the subjects warmed up by 15 minutes of submaximal cycling
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on a bicycle ergometer. The subjects’ right knees were determined to be the test knee. The maximal muscle strength was measured using an isokinetic dynamometer (Biodex System 3, pro set; Biodex Medical Systems Inc, Shirley, NY). The subjects were seated comfortably in the dynamometer, and strapped to the chair with nonelastic shoulder straps and a body belt. The dynamometer axis of rotation was aligned with the axis of knee flexion and extension that was assumed to pass through the medial and lateral femoral epicondyles. The distal part of the subject’s right leg was held against the dynamometer with a cuff around the ankle. The patients were asked to extend and flex their knee in a 0 to 90 degrees range of motion with maximal effort and force, and loud verbal encouragement was given during the tests, as well as visual feedback from the dynamometer computer monitor. Muscle-strength measurements were done isometrically at 60-degrees knee flexion and isokinetically at 60, 120, and 180 degrees/second in both knee extension and flexion. Three repetitions in each direction at each angular velocity were performed with short breaks between each angular velocity in which the dynamometer settings were changed and the subjects scored their pain intensities. The order of angular velocities was fixed with the isometric measurement first followed by measurements at 60, 120, and 180 degrees/ second. From each muscle-strength test series, 3 peak torque values from each direction (knee extension and flexion) and each angular velocity (isometric, 60, 120, and 180 degrees/second) were extracted, yielding a total of 24 peak torque values per test series (Pre, During, Recovery). All values were used in the statistical analysis, ie, no averaging was done.
Experimental Knee Pain Pain was induced by injections of sterile hypertonic saline (5.8% solution) into the infrapatellar fat pad of the subjects’ right knees. Sterile isotonic saline (.9% solution) injections were given as nonpainful control. The saline injections were bolus injections of 1 mL, and were given ultrasound-guided to ensure correct placement of the bolus in the middle of the fat pad, directly behind the patellar tendon. Injections were directed at 45 with a medial approach in a posterior-lateral direction using a .4 mm needle (27G) mounted on a 1-mL syringe. The subjects rated the pain intensities after every muscle-strength testing at each angular velocity using a 100-mm visual analogue scale (VAS) with extremes being 0 mm (‘‘no pain’’) and 100 mm (‘‘worst imaginable pain’’).
Statistics Data are presented as mean 6 standard error of the mean (SE). For the analysis of the effects of experimental pain on muscle strength, a mixed linear model was applied using the SAS software (SAS Institute, Cary, NC). All observations were used and each direction (knee flexion and extension) was analyzed separately. The analyses focused on the fixed effects analyses analyzing whether there was an interaction between time (3 levels:
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Pre, During, and Recovery), saline (2 levels: Hypertonic and isotonic), and angular velocity (4 levels: 0, 60, 120, and 180 degrees/second), including each factor as main effects and their corresponding double interactions in the model with gender as a covariate and a random effect for subject. Any statistically significant interactions were broken down post hoc by exploring the pairwise differences comparing hypertonic to isotonic saline injections at times = Pre, During and Recovery measurements, respectively. To analyze the association between pain intensities and reductions in muscle strength, the relative changes in peak torque from the average Pre measurement (expressed as %) to the measurements during pain (hypertonic saline injections) were calculated for each subject, with positive values reflecting muscle-strength reductions. A mixed linear model was applied analyzing the main effects of pain intensity and angular velocity, including the interaction, on the relative change in muscle strength. For each angular velocity, the mixed model produced a best-fit linear regression equation, from which the slopes (beta coefficients) were extracted. To assess if the slopes were significantly different from 0, a T score (beta coefficient divided by standard error) was computed and a Student’s two-tailed t-test was applied. Statistical significance was accepted at P < .05.
Results One female subject was excluded during the data acquisition because of an error in the saline allocation resulting in two hypertonic saline injections given to the subject.
Pain Intensity Hypertonic saline injections effectively induced knee pain compared to isotonic saline injections (P < .0001 [time saline interaction]; post hoc: P < .0001 [hypertonic versus isotonic at time = During]). The VAS scores were similar across angular velocities as seen by a nonsignificant triple time saline angular velocity interaction (P = .41). Average pain intensities following hypertonic saline injection (ie, During pain) pooled across directions (extension and flexion) are shown in Fig 1. The average pain intensity following hypertonic saline injections, pooled across angular velocities and directions, was 32.0 mm (95% confidence interval 29.2 to 34.9 mm). At Baseline and Recovery measurements and During the control condition (ie, following isotonic saline injections) no subjects reported any pain (ie, 0 6 0 mm).
Knee Pain and Muscle Strength
Figure 1. Average (6SE) pain intensity data recorded on a 100-mm visual analogue scale during the muscle-strength tests before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). Muscle strength was measured isometrically, and isokinetically at 60 degrees/second, 120 degrees/second, and 180 degrees/second. There were no significant differences in pain intensity scores across angular velocities. Please note that the pain recordings at baseline (pre) and recovery all were 0 mm (SE 0).
P < .0001; 60 degrees/second: –15.1% 6 1.7%, P < .0001; 120 degrees/second: –14.1% 6 1.8%, P < .0001; 180 degrees/second: –9.8% 6 1.9%, P < .0001; Fig 2). At the pain Recovery measurements, the knee extension peak torques returned to Pre measurement levels, except the isometric and 60 degrees/second peak torques that were reduced by –5.8% 6 1.8% (post hoc: P = .001) and –6.3% 6 1.6% (post hoc: P = .0001), respectively, compared to the control Recovery measurement (Fig 2). In knee flexion, there was a significant effect of pain (hypertonic saline) on muscle strength (P < .0001 [time saline interaction]), and the effect was different across angular velocities (P = .035 [time saline angular velocity interaction]; Fig 3). During pain, the isometric peak torques and the 60 and 120 degrees/second isokinetic peak torques were reduced compared to the
Muscle Strength In knee extension, there was a significant effect of pain (hypertonic saline) on muscle strength (P < .0001 [time saline interaction]), and the effect of pain on muscle strength was independent of the angular velocity (P = .37 [time saline angular velocity interaction]; Fig 2). During pain, the peak torque was reduced at all angular velocities compared to during the nonpainful control condition (post hoc: isometric: –15.0% 6 1.8%,
Figure 2. Average (6SE) knee extension maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second, before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). *P < .001.
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Linear Relationships Between Pain Intensity and Reductions in Muscle Strength at Different Angular Velocities in Knee Extension and Flexion and Pooled Across All Velocities
Table 1.
PAIN
Figure 3. Average (6SE) knee flexion maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second, before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). *P < .0001. control condition (post hoc: isometric: –7.5% 6 1.7%, P < .0001; 60 degrees/second: –11.4% 6 2.0% P < .0001; 120 degrees/second: –5.3% 6 1.8% P = .0004; Fig 3). The difference in peak torques at 180 degrees/second isokinetic did not reach statistical significance (post hoc hypertonic versus isotonic at time = During: P = .08). At the pain Recovery measurements, the peak torques returned to Pre measurement levels, except the isometric knee flexion peak torque that was reduced by –7.9% 6 1.5% compared to the control Recovery measurement (post hoc: P < .0001; Fig 3).
Relative Reductions in Muscle Strength Associated With the Pain Intensity In both knee extension and flexion, the relative change in muscle strength due to pain was the same across angular velocities (extension: P = .57 and flexion: P = .90 [pain angular velocity interactions]). There was a significant association between pain intensities and relative change in muscle strength in both directions (extension: P = .0004 [pain intensity main effect] and flexion: P = .0041 [pain intensity main effect]). The relative muscle-strength change was not associated with angular velocities (extension: P =.73 [angular velocity main effect] and flexion: P = .57 [angular velocity main effect]). The estimated slopes from the mixed linear regression equations showed that at all angular velocities in both knee extension and flexion, the pain intensity was positively related to reductions in muscle strength, ie, higher pain intensity led to larger muscle-strength reduction (Table 1). The relationships between pain intensity and relative reductions in muscle strength are illustrated in Figs 4 and 5.
Discussion This is the first study to investigate the isolated effects of experimentally induced knee joint pain on muscle strength assessed across different angular velocities.
MUSCLE STRENGTH VARIABLES
P FOR INTERACTION
Knee extension Isometric 60 degrees/second 120 degrees/second 180 degrees/second Pooled Knee flexion Isometric 60 degrees/second 120 degrees/second 180 degrees/second Pooled
.2703
SLOPE (SE)
P FOR SLOPE
R2
.51 (.15) .53 (.13) .40 (.13) .31 (.11) .39 (.09)
.0007 <.0001 .0024 .0039 .0001
.09 .15 .09 .08 .24
.52 (.15) .41 (.13) –.42 (.13) .32 (.11) .38 (.10)
.0010 .0027 .0025 .0053 .0004
.08 .09 .09 .07 .21
.5715
Abbreviation: SE, standard error. NOTE. The linear relationships are presented as best linear fit regression slopes (beta-coefficients). P for interaction values represent the pain angular velocity interactions indicating if the relationships (slopes) are different across angular velocities. P for slope values represent beta-coefficients tested against 0, indicating if the relationship is significantly negative or positive. A positive slope value indicates that with higher pain intensities the reduction in muscle strength caused by knee pain increases. R2 values indicate the amount of variation in muscle strength reduction that can be explained by pain intensities.
The reduction comprised both knee extension and flexion muscle strength and the reductions were correlated positively with pain intensity. These effects were similar across angular velocities. Muscle weakness is a well-accepted impairment in knee osteoarthritis, with patients being reported 20 to 40% weaker than healthy controls.3 The source of weakness is important to consider because it will determine how muscle strength is restored. In the present study, experimental knee joint pain reduced the muscle strength by 5 to 15%, which indicates that pain is a significant source of muscle weakness in knee osteoarthritis patients. Joint pain may be elicited from a number of structures, including the infrapatellar fat pad, which has nociceptive innervation4 and is a source of clinical pain.19 Saline-induced pain in the infrapatellar fat pad has been shown to cause changes in knee joint dynamics during level walking and quadriceps muscle coordination during stair walking consistent with clinical observations,16,20 which suggests that knee pain affects central nervous mechanisms, as previously demonstrated using experimental muscle pain.12 The nociceptive-motor interaction occurs at numerous levels in the nervous system, yet little is known about the reflexive pathways between joint nociceptors and the motor neurons. Motor neurons receive input from joint nociceptors31 and reflex discharges can be elicited by stimulation of articular nerves or joint receptors.38 Accordingly, quadriceps coordination and motor neuron recruitment have been shown to be altered by experimental pain in the
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Knee Pain and Muscle Strength
Figure 4. Scatter plots of pain intensities versus relative reductions in knee extension maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second during pain together with the best fit linear regression lines (solid) with 95% confidence interval (dashed lines). Pain intensities are scored on a 100-mm visual analog scale (VAS) with 0 representing no pain and 100 worst imaginable pain. Positive values on the y-axis represent MVC reductions in % from baseline measurements. Please note that each subject is represented by 3 data points.
infrapatellar fat pad.20,41 The present study challenges physiological concepts based on reflex recordings in animal studies, generally describing excitatory influences of joint afferents on motor neuron activity.10,24,43 In contrast, the motor neuron reflexes have been shown to be inhibited during experimental joint inflammation in cats,15 although this change needed time to develop. To the best of our knowledge, there are no studies investigating the reflex patterns during experimental knee pain in humans, but the present study indicates an inhibitory effect of knee joint pain on muscle activation. The sustained muscle inhibition postpain during isometric and slow angular velocities indicates that the immediate adaptive response to knee joint pain in muscle strength is not unadapted when the nociceptive input has vanished, but is maintained for at least 20 minutes postpain. This is in accordance with previous observations showing that pain inhibition of muscle function still occurs when the pain is no longer present.9,17,18,33,35 A postpain inhibition can be of either peripheral or central origin, but the underlying mechanisms are unknown. While the muscle inhibition during conscious pain perception can be considered as an appropriate protective response, the sustained inhibition beyond conscious pain perception may represent an inappropriate adaptation. This might contribute to a development of chronic disability.
Our results show that stronger pain intensities led to stronger muscle-strength inhibition. However, despite significant slopes, the relatively low R2 values indicate that the majority of variability in muscle-strength reductions is not explained by pain intensity. This may be due to the subjective nature of pain and the mismatch between conscious pain sensation and neural activity caused by nociceptive stimuli.25 Nevertheless, the pooled slopes indicate that with each mm increase in pain intensity, the muscle strength is reduced by approximately .4 % compared to the baseline measurements. This may have profound consequences in that pain intensities of 30 mm and above are not unusual in knee OA patients. Such pain intensity corresponds to a reduction in muscle strength of approximately 12%. These findings corroborate the negative correlation between pain and quadriceps muscle strength observed cross-sectionally among knee OA patients.34 Knee extension torque is solely produced by the quadriceps muscle, and knee flexion torque is predominantly attributed to the hamstrings, although the gastrocnemius muscle also functions as a knee flexor.23 While we have no data to evaluate the individual muscle inhibitions, it is possible that both hamstring and gastrocnemius muscles are inhibited by knee pain, indicating a generalized muscle inhibition augmented by higher pain intensities. The inhibition of muscle strength was not caused by mechanical stimulation of the fat pad
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Figure 5. Scatter plots of pain intensities versus relative reductions in knee flexion maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second during pain together with the best fit linear regression lines (solid) with 95% confidence interval (dashed lines). Pain intensities are scored on a 100-mm visual analog scale (VAS) with 0 representing no pain and 100 worst imaginable pain. Positive values on the y-axis represent MVC reductions in % from baseline measurements. Please note that each subject is represented by 3 data points.
because no effects were observed during the isotonic saline injections of the same saline volume. Also, the volumes injected were small (1 mL), and it has previously been shown that quadriceps inhibition only occurs at increased intraarticular pressure induced by experimental joint effusion of more than 20 mL.39 A limitation to this study is that experimental pain is acute and transient, and does not necessarily reproduce clinical or chronic knee pain, and the association between experimental pain and changes in muscle strength cannot directly be transferred to clinical conditions. However, for obvious reasons, it is not possible to induce chronic pain experimentally in human experiments. Nevertheless, patients with knee pathologies have reduced muscle strength,6,7,11,21,26 and knee pain is negatively correlated to quadriceps muscle strength in knee osteoarthritis patients.34 It has been suggested that reduced quadriceps muscle strength precedes development of symptomatic (ie, painful) as well as radiographic knee osteoarthritis.36,37 Indeed, the present study indicates that reduced muscle strength in knee OA, and other painful knee joint conditions, is not exclusively due to inactivity or disuse, but that the pain intensity itself reduces the muscle strength. If reduced muscle strength plays a role in knee OA progression, as indicated by Segal et al,32 then knee pain in the early disease stages may accelerate the degenerative processes via muscular inhibition.
The clinical importance of this is that patients with painful knee joint conditions may be caught in a vicious circle of pain, decreased level of activity, and increasing muscle weakness as a pain-avoidance strategy.14 Other patients may adopt a pain-endurance strategy and maintain their level of activity in spite of pain.13 Pain endurance will not necessarily be associated with muscle-strength preservation because many activities of daily living can be performed with significant muscle inhibition. An example is sustained walking ability in spite of considerable quadriceps inhibition.40 Thus, pain endurers may also be caught in a vicious circle, yet with increased risks of overload/overuse and accelerated disease progression. Likewise, pain avoiders may also be at risk of accelerated progression as inactivity is related to both muscle weakness29 and joint degeneration.42 Accordingly, patients should be encouraged to exercise within a therapeutic window to maintain or increase muscle strength despite pain, although the beneficial range of exercise—even with pain—is not established. While there is ample evidence of clinical effects of strengthening exercises on strength, pain, function, and quality of life,28 there is a risk of overuse to be considered in the individual exercise prescription. The dose-response relationship between exercise and pain remains to be clarified together with the risk-benefit relationship of pain relief (eg, nonpharmacological techniques or medication) used in this context.
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The magnitude of strength gain achieved with exercises varies considerably from 5 to 71% with numerous factors, including training intensity, specificity, and patient compliance as suggested sources of variation.3 However, this study suggests that a gain in muscle strength may be antagonized by knee pain due to the reduced maximal contraction capacity, leading to smaller stimuli of the neuromuscular system during exercise. On the other hand, therapeutic exercises for knee osteoarthritis are performed at submaximal contraction levels (usually 60 to 80% of the 1-repetition maximum), and the inhibitory role of joint pain on submaximal muscle contractions is not known. Although increased muscle strength by itself may have positive effects on clinical
knee pain, even light pain relief during the course of an exercise regime might enhance the gain in muscle strength and thus speed up the rehabilitation, and amplify the long-term clinical effects of exercise on knee osteoarthritis pain. In conclusion, experimental knee pain significantly reduced knee extension and flexion muscle strength, both isometrically and isokinetically in healthy subjects. The reduction in muscle strength was positively correlated to the pain intensity. This suggests that knee joint pain induces a widespread muscle strength inhibition across muscles and angular velocities that can be modulated by pain intensity. These mechanisms may have strong impact on efficiency of rehabilitation of symptomatic knee OA patients.
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25. Merskey H, Bonica JJ, Carmon A, Dubner R, Kerr FWL, Lindblom U, Mumford JM, Nathan PW, Nordenbos W, Pagni CA, Renear MJ, Sternbach RA, Sunderland SS: Pain terms: A list with definitions and notes on usage. Recommended by the IASP Subcommittee on Taxonomy. Pain 6: 249, 1979 26. Messier SP, Loeser RF, Hoover JL, Semble EL, Wise CM: Osteoarthritis of the knee: Effects on gait, strength, and flexibility. Arch Phys Med Rehabil 73:29-36, 1992 27. Neogi T, Felson D, Niu J, Nevitt M, Lewis CE, Aliabadi P, Sack B, Torner J, Bradley L, Zhang Y: Association between radiographic features of knee osteoarthritis and pain: Results from two cohort studies. BMJ 339:b2844, 2009 28. Pelland L, Brosseau L, Wells G, Macleay L, Lambert J, Lamothe C, Robinson V, Tugwell P: Efficacy of strengthening exercises for osteoarthritis (Part I): A meta-analysis. Phys Ther Rev 9:77-108, 2004 29. Rantanen T, Guralnik JM, Sakari-Rantala R, Leveille S, Simonsick EM, Ling S, Fried LP: Disability, physical activity, and muscle strength in older women: The Women’s Health and Aging Study. Arch Phys Med Rehabil 80: 130-135, 1999 30. Roos EM, Dahlberg L: Positive effects of moderate exercise on glycosaminoglycan content in knee cartilage: A four-month, randomized, controlled trial in patients at risk of osteoarthritis. Arthritis Rheum 52:3507-3514, 2005
35. Slater H, Arendt-Nielsen L, Wright A, Graven-Nielsen T: Experimental deep tissue pain in wrist extensors–a model of lateral epicondylalgia. Eur J Pain 7:277-288, 2003 36. Slemenda C, Brandt KD, Heilman DK, Mazzuca S, Braunstein EM, Katz BP, Wolinsky FD: Quadriceps weakness and osteoarthritis of the knee. Ann Intern Med 127:97-104, 1997 37. Slemenda C, Heilman DK, Brandt KD, Katz BP, Mazzuca SA, Braunstein EM, Byrd D: Reduced quadriceps strength relative to body weight: A risk factor for knee osteoarthritis in women? Arthritis Rheum 41:1951-1959, 1998 38. Solomonow M, Krogsgaard M: Sensorimotor control of knee stability. A review. Scand J Med Sci Sports 11:64-80, 2001 39. Spencer JD, Hayes KC, Alexander IJ: Knee joint effusion and quadriceps reflex inhibition in man. Arch Phys Med Rehabil 65:171-177, 1984 40. Torry MR, Decker MJ, Viola RW, O’Connor DD, Steadman JR: Intra-articular knee joint effusion induces quadriceps avoidance gait patterns. Clin Biomech 15: 147-159, 2000 41. Tucker KJ, Hodges PW: Motoneurone recruitment is altered with pain induced in non-muscular tissue. Pain 141: 151-155, 2008
31. Schaible HG, Grubb BD: Afferent and spinal mechanisms of joint pain. Pain 55:5-54, 1993
42. Vanwanseele B, Lucchinetti E, Stussi E: The effects of immobilization on the characteristics of articular cartilage: Current concepts and future directions. Osteoarthr Cartil 10:408-419, 2002
32. Segal NA, Glass NA, Torner J, Yang M, Felson DT, Sharma L, Nevitt M, Lewis CE: Quadriceps weakness predicts risk for knee joint space narrowing in women in the MOST cohort. Osteoarthr Cartil 18:769-775, 2010
43. Woolf CJ, Wall PD: Relative effectiveness of C primary afferent fibers of different origins in evoking a prolonged facilitation of the flexor reflex in the rat. J Neurosci 6: 1433-1442, 1986
Experimental Knee Pain Reduces Muscle Strength Marius Henriksen,* Sara Rosager,* Jens Aaboe,* Thomas Graven-Nielsen,y and Henning Bliddal*,y * Clinical Motor Function Laboratory, The Parker Institute, Frederiksberg Hospital, Frederiksberg, Denmark. y Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.
Abstract: Pain is the principal symptom in knee pathologies and reduced muscle strength is a common observation among knee patients. However, the relationship between knee joint pain and muscle strength remains to be clarified. This study aimed at investigating the changes in knee muscle strength following experimental knee pain in healthy volunteers, and if these changes were associated with the pain intensities. In a crossover study, 18 healthy subjects were tested on 2 different days. Using an isokinetic dynamometer, maximal muscle strength in knee extension and flexion was measured at angular velocities 0, 60, 120, and 180 degrees/second, before, during, and after experimental pain induced by injections of hypertonic saline into the infrapatellar fat pad. On a separate day, isotonic saline injections were used as control condition. The pain intensity was assessed on a 0- to 100-mm visual analogue scale. Knee pain reduced the muscle strength by 5 to 15% compared to the control conditions (P < .001) in both knee extension and flexion at all angular velocities. The reduction in muscle strength was positively correlated to the pain intensity. Experimental knee pain significantly reduced knee extension and flexion muscle strength indicating a generalized muscle inhibition augmented by higher pain intensities. Perspective: This study showed that knee joint pain has a significant impact on muscle function. The findings provide evidence of a direct inhibition of muscle function by joint pain, implying that rehabilitative strengthening exercises may be antagonized by joint pain. ª 2011 by the American Pain Society Key words: Knee pain, muscle strength, physical function, exercise.
K
nee pain is the cardinal symptom in knee osteoarthritis (OA), and reduced knee muscle strength is common among these patients.3,21 Pain reduction and restoration of muscle function are thus primary goals in the treatment of knee OA and in fact there is ample evidence that muscle strengthening exercises result in improvements in pain.3 Structurally knee OA is characterized by cartilage loss, joint contractures, deformities, and laxity, yet the pathogenesis of knee OA is generally unknown. Impaired muscle function is suspected to play a pathogenetic role in the structural degeneration of the knee joint,32 Received May 5, 2010; Revised September 8, 2010; Accepted September 26, 2010. Supported by grants from The Oak Foundation and The Association of Danish Physiotherapists Research Foundation, and The Association of Danish Physiotherapists Practice Foundation. The authors have no conflicts of interest regarding this article. Address reprint requests to Marius Henriksen, PT, PhD, Clinical Motor Function Laboratory, The Parker Institute, Frederiksberg Hospital, Ndr. Fasanvej 57, DK-2000 Frederiksberg C, Denmark. E-mail: marius. [email protected] 1526-5900/$36.00 ª 2011 by the American Pain Society doi:10.1016/j.jpain.2010.10.004
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and exercise may be beneficial for articular cartilage.30 Many of the structural changes are progressive with disease severity.22 While pain traditionally is weakly correlated to radiographical knee OA severity,5,8 a recent large cohort study has shown the opposite,27 and other structural changes, such as quantification of synovitis by means of magnetic resonance imaging techniques, show better correlations to pain.1,19 Knee pain has been shown to alter many aspects of motor function, including the dynamics of walking16 and muscle coordination,20,41 and reduced muscle function is suggested to be involved in structural disease progression.32 Thus, adaptations in muscle function due to pain could be a possible source for development of the structural changes. However, the isolated effects of knee pain on muscle strength are unknown. The multiple changes associated with knee OA may introduce unwanted variability in muscle function assessments. By consequence, it is difficult to assess the isolated effects of pain on muscle function in a patient population. Experimental techniques to induce pain in healthy subjects are thus advantageous in this respect. A harmless technique inducing reversible, localized
Henriksen et al pain in the infrapatellar fat pad of the knee has been used in experimental studies2,16,20,41 allowing assessments of pain adaptations in the muscle function. The infrapatellar fat pad is a source of pain in knee osteoarthritis,1,19 and injections of hypertonic saline into the fat pad with a medial approach produce antero-medial knee pain with similar qualities as clinical pain in the anterior knee.2 Strategies for physical therapy treatment and prevention of knee OA pain are mainly empirical, and a better understanding of underlying sensory-motor mechanisms would be 1 step forward towards optimizing therapy. The purpose of this study was to assess the effects of experimental infrapatellar fat pad pain on maximal isometric and isokinetic knee extensor and flexor muscle strength in healthy subjects. We hypothesized that experimental infrapatellar fat pad pain reduced knee extensor and flexor muscle strength and that reductions in muscle strength would be associated with the pain intensity.
Methods Subjects Healthy subjects (9 females and 9 males) with no history of musculoskeletal problems gave voluntary written informed consent to participate in the study. Their mean age was 26.5 years (SD 6.8), mean height was 1.75 m (SD .13) and mean body mass was 62.0 kg (SD 4.2). The study was approved by the ethics committee for the Capitol Region of Denmark (j. no. H-C-2007-0053).
Protocol The study was designed as a crossover study with each subject tested on 2 days separated by at least 1 week. During a test day, 3 series of muscle-strength tests were performed. Series 1 and 2 were separated by a 5-minute break, during which the subjects rested. Immediately before the second series, an intra-articular saline injection was given in the infrapatellar fat pad. The saline solution was either hypertonic or isotonic for the painful and control conditions, respectively. On a single test day only 1 type of saline solution was injected according to the randomization process: The order of the saline solution injections was allocated using an envelope based randomization technique allowing equal numbers of subjects starting with isotonic and hypertonic saline, respectively. After the second muscle-strength assessment series, a 20-minute break was held to ensure that any pain had vanished before the third series of musclestrength assessments. The person performing the muscle-strength measurement (SR) was blinded to the randomization. All subjects were informed about the study design and that they would receive 1 painful injection and one nonpainful control injection, but the subjects were blinded to the order of injections.
Muscle-Strength Measurements Before the muscle-strength measurements, the subjects warmed up by 15 minutes of submaximal cycling
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on a bicycle ergometer. The subjects’ right knees were determined to be the test knee. The maximal muscle strength was measured using an isokinetic dynamometer (Biodex System 3, pro set; Biodex Medical Systems Inc, Shirley, NY). The subjects were seated comfortably in the dynamometer, and strapped to the chair with nonelastic shoulder straps and a body belt. The dynamometer axis of rotation was aligned with the axis of knee flexion and extension that was assumed to pass through the medial and lateral femoral epicondyles. The distal part of the subject’s right leg was held against the dynamometer with a cuff around the ankle. The patients were asked to extend and flex their knee in a 0 to 90 degrees range of motion with maximal effort and force, and loud verbal encouragement was given during the tests, as well as visual feedback from the dynamometer computer monitor. Muscle-strength measurements were done isometrically at 60-degrees knee flexion and isokinetically at 60, 120, and 180 degrees/second in both knee extension and flexion. Three repetitions in each direction at each angular velocity were performed with short breaks between each angular velocity in which the dynamometer settings were changed and the subjects scored their pain intensities. The order of angular velocities was fixed with the isometric measurement first followed by measurements at 60, 120, and 180 degrees/ second. From each muscle-strength test series, 3 peak torque values from each direction (knee extension and flexion) and each angular velocity (isometric, 60, 120, and 180 degrees/second) were extracted, yielding a total of 24 peak torque values per test series (Pre, During, Recovery). All values were used in the statistical analysis, ie, no averaging was done.
Experimental Knee Pain Pain was induced by injections of sterile hypertonic saline (5.8% solution) into the infrapatellar fat pad of the subjects’ right knees. Sterile isotonic saline (.9% solution) injections were given as nonpainful control. The saline injections were bolus injections of 1 mL, and were given ultrasound-guided to ensure correct placement of the bolus in the middle of the fat pad, directly behind the patellar tendon. Injections were directed at 45 with a medial approach in a posterior-lateral direction using a .4 mm needle (27G) mounted on a 1-mL syringe. The subjects rated the pain intensities after every muscle-strength testing at each angular velocity using a 100-mm visual analogue scale (VAS) with extremes being 0 mm (‘‘no pain’’) and 100 mm (‘‘worst imaginable pain’’).
Statistics Data are presented as mean 6 standard error of the mean (SE). For the analysis of the effects of experimental pain on muscle strength, a mixed linear model was applied using the SAS software (SAS Institute, Cary, NC). All observations were used and each direction (knee flexion and extension) was analyzed separately. The analyses focused on the fixed effects analyses analyzing whether there was an interaction between time (3 levels:
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Pre, During, and Recovery), saline (2 levels: Hypertonic and isotonic), and angular velocity (4 levels: 0, 60, 120, and 180 degrees/second), including each factor as main effects and their corresponding double interactions in the model with gender as a covariate and a random effect for subject. Any statistically significant interactions were broken down post hoc by exploring the pairwise differences comparing hypertonic to isotonic saline injections at times = Pre, During and Recovery measurements, respectively. To analyze the association between pain intensities and reductions in muscle strength, the relative changes in peak torque from the average Pre measurement (expressed as %) to the measurements during pain (hypertonic saline injections) were calculated for each subject, with positive values reflecting muscle-strength reductions. A mixed linear model was applied analyzing the main effects of pain intensity and angular velocity, including the interaction, on the relative change in muscle strength. For each angular velocity, the mixed model produced a best-fit linear regression equation, from which the slopes (beta coefficients) were extracted. To assess if the slopes were significantly different from 0, a T score (beta coefficient divided by standard error) was computed and a Student’s two-tailed t-test was applied. Statistical significance was accepted at P < .05.
Results One female subject was excluded during the data acquisition because of an error in the saline allocation resulting in two hypertonic saline injections given to the subject.
Pain Intensity Hypertonic saline injections effectively induced knee pain compared to isotonic saline injections (P < .0001 [time saline interaction]; post hoc: P < .0001 [hypertonic versus isotonic at time = During]). The VAS scores were similar across angular velocities as seen by a nonsignificant triple time saline angular velocity interaction (P = .41). Average pain intensities following hypertonic saline injection (ie, During pain) pooled across directions (extension and flexion) are shown in Fig 1. The average pain intensity following hypertonic saline injections, pooled across angular velocities and directions, was 32.0 mm (95% confidence interval 29.2 to 34.9 mm). At Baseline and Recovery measurements and During the control condition (ie, following isotonic saline injections) no subjects reported any pain (ie, 0 6 0 mm).
Knee Pain and Muscle Strength
Figure 1. Average (6SE) pain intensity data recorded on a 100-mm visual analogue scale during the muscle-strength tests before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). Muscle strength was measured isometrically, and isokinetically at 60 degrees/second, 120 degrees/second, and 180 degrees/second. There were no significant differences in pain intensity scores across angular velocities. Please note that the pain recordings at baseline (pre) and recovery all were 0 mm (SE 0).
P < .0001; 60 degrees/second: –15.1% 6 1.7%, P < .0001; 120 degrees/second: –14.1% 6 1.8%, P < .0001; 180 degrees/second: –9.8% 6 1.9%, P < .0001; Fig 2). At the pain Recovery measurements, the knee extension peak torques returned to Pre measurement levels, except the isometric and 60 degrees/second peak torques that were reduced by –5.8% 6 1.8% (post hoc: P = .001) and –6.3% 6 1.6% (post hoc: P = .0001), respectively, compared to the control Recovery measurement (Fig 2). In knee flexion, there was a significant effect of pain (hypertonic saline) on muscle strength (P < .0001 [time saline interaction]), and the effect was different across angular velocities (P = .035 [time saline angular velocity interaction]; Fig 3). During pain, the isometric peak torques and the 60 and 120 degrees/second isokinetic peak torques were reduced compared to the
Muscle Strength In knee extension, there was a significant effect of pain (hypertonic saline) on muscle strength (P < .0001 [time saline interaction]), and the effect of pain on muscle strength was independent of the angular velocity (P = .37 [time saline angular velocity interaction]; Fig 2). During pain, the peak torque was reduced at all angular velocities compared to during the nonpainful control condition (post hoc: isometric: –15.0% 6 1.8%,
Figure 2. Average (6SE) knee extension maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second, before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). *P < .001.
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Linear Relationships Between Pain Intensity and Reductions in Muscle Strength at Different Angular Velocities in Knee Extension and Flexion and Pooled Across All Velocities
Table 1.
PAIN
Figure 3. Average (6SE) knee flexion maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second, before, during, and after experimental pain by injections of painful hypertonic saline (open bars) into the infrapatellar fat pad or a control injection of nonpainful isotonic saline (grey bars). *P < .0001. control condition (post hoc: isometric: –7.5% 6 1.7%, P < .0001; 60 degrees/second: –11.4% 6 2.0% P < .0001; 120 degrees/second: –5.3% 6 1.8% P = .0004; Fig 3). The difference in peak torques at 180 degrees/second isokinetic did not reach statistical significance (post hoc hypertonic versus isotonic at time = During: P = .08). At the pain Recovery measurements, the peak torques returned to Pre measurement levels, except the isometric knee flexion peak torque that was reduced by –7.9% 6 1.5% compared to the control Recovery measurement (post hoc: P < .0001; Fig 3).
Relative Reductions in Muscle Strength Associated With the Pain Intensity In both knee extension and flexion, the relative change in muscle strength due to pain was the same across angular velocities (extension: P = .57 and flexion: P = .90 [pain angular velocity interactions]). There was a significant association between pain intensities and relative change in muscle strength in both directions (extension: P = .0004 [pain intensity main effect] and flexion: P = .0041 [pain intensity main effect]). The relative muscle-strength change was not associated with angular velocities (extension: P =.73 [angular velocity main effect] and flexion: P = .57 [angular velocity main effect]). The estimated slopes from the mixed linear regression equations showed that at all angular velocities in both knee extension and flexion, the pain intensity was positively related to reductions in muscle strength, ie, higher pain intensity led to larger muscle-strength reduction (Table 1). The relationships between pain intensity and relative reductions in muscle strength are illustrated in Figs 4 and 5.
Discussion This is the first study to investigate the isolated effects of experimentally induced knee joint pain on muscle strength assessed across different angular velocities.
MUSCLE STRENGTH VARIABLES
P FOR INTERACTION
Knee extension Isometric 60 degrees/second 120 degrees/second 180 degrees/second Pooled Knee flexion Isometric 60 degrees/second 120 degrees/second 180 degrees/second Pooled
.2703
SLOPE (SE)
P FOR SLOPE
R2
.51 (.15) .53 (.13) .40 (.13) .31 (.11) .39 (.09)
.0007 <.0001 .0024 .0039 .0001
.09 .15 .09 .08 .24
.52 (.15) .41 (.13) –.42 (.13) .32 (.11) .38 (.10)
.0010 .0027 .0025 .0053 .0004
.08 .09 .09 .07 .21
.5715
Abbreviation: SE, standard error. NOTE. The linear relationships are presented as best linear fit regression slopes (beta-coefficients). P for interaction values represent the pain angular velocity interactions indicating if the relationships (slopes) are different across angular velocities. P for slope values represent beta-coefficients tested against 0, indicating if the relationship is significantly negative or positive. A positive slope value indicates that with higher pain intensities the reduction in muscle strength caused by knee pain increases. R2 values indicate the amount of variation in muscle strength reduction that can be explained by pain intensities.
The reduction comprised both knee extension and flexion muscle strength and the reductions were correlated positively with pain intensity. These effects were similar across angular velocities. Muscle weakness is a well-accepted impairment in knee osteoarthritis, with patients being reported 20 to 40% weaker than healthy controls.3 The source of weakness is important to consider because it will determine how muscle strength is restored. In the present study, experimental knee joint pain reduced the muscle strength by 5 to 15%, which indicates that pain is a significant source of muscle weakness in knee osteoarthritis patients. Joint pain may be elicited from a number of structures, including the infrapatellar fat pad, which has nociceptive innervation4 and is a source of clinical pain.19 Saline-induced pain in the infrapatellar fat pad has been shown to cause changes in knee joint dynamics during level walking and quadriceps muscle coordination during stair walking consistent with clinical observations,16,20 which suggests that knee pain affects central nervous mechanisms, as previously demonstrated using experimental muscle pain.12 The nociceptive-motor interaction occurs at numerous levels in the nervous system, yet little is known about the reflexive pathways between joint nociceptors and the motor neurons. Motor neurons receive input from joint nociceptors31 and reflex discharges can be elicited by stimulation of articular nerves or joint receptors.38 Accordingly, quadriceps coordination and motor neuron recruitment have been shown to be altered by experimental pain in the
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Knee Pain and Muscle Strength
Figure 4. Scatter plots of pain intensities versus relative reductions in knee extension maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second during pain together with the best fit linear regression lines (solid) with 95% confidence interval (dashed lines). Pain intensities are scored on a 100-mm visual analog scale (VAS) with 0 representing no pain and 100 worst imaginable pain. Positive values on the y-axis represent MVC reductions in % from baseline measurements. Please note that each subject is represented by 3 data points.
infrapatellar fat pad.20,41 The present study challenges physiological concepts based on reflex recordings in animal studies, generally describing excitatory influences of joint afferents on motor neuron activity.10,24,43 In contrast, the motor neuron reflexes have been shown to be inhibited during experimental joint inflammation in cats,15 although this change needed time to develop. To the best of our knowledge, there are no studies investigating the reflex patterns during experimental knee pain in humans, but the present study indicates an inhibitory effect of knee joint pain on muscle activation. The sustained muscle inhibition postpain during isometric and slow angular velocities indicates that the immediate adaptive response to knee joint pain in muscle strength is not unadapted when the nociceptive input has vanished, but is maintained for at least 20 minutes postpain. This is in accordance with previous observations showing that pain inhibition of muscle function still occurs when the pain is no longer present.9,17,18,33,35 A postpain inhibition can be of either peripheral or central origin, but the underlying mechanisms are unknown. While the muscle inhibition during conscious pain perception can be considered as an appropriate protective response, the sustained inhibition beyond conscious pain perception may represent an inappropriate adaptation. This might contribute to a development of chronic disability.
Our results show that stronger pain intensities led to stronger muscle-strength inhibition. However, despite significant slopes, the relatively low R2 values indicate that the majority of variability in muscle-strength reductions is not explained by pain intensity. This may be due to the subjective nature of pain and the mismatch between conscious pain sensation and neural activity caused by nociceptive stimuli.25 Nevertheless, the pooled slopes indicate that with each mm increase in pain intensity, the muscle strength is reduced by approximately .4 % compared to the baseline measurements. This may have profound consequences in that pain intensities of 30 mm and above are not unusual in knee OA patients. Such pain intensity corresponds to a reduction in muscle strength of approximately 12%. These findings corroborate the negative correlation between pain and quadriceps muscle strength observed cross-sectionally among knee OA patients.34 Knee extension torque is solely produced by the quadriceps muscle, and knee flexion torque is predominantly attributed to the hamstrings, although the gastrocnemius muscle also functions as a knee flexor.23 While we have no data to evaluate the individual muscle inhibitions, it is possible that both hamstring and gastrocnemius muscles are inhibited by knee pain, indicating a generalized muscle inhibition augmented by higher pain intensities. The inhibition of muscle strength was not caused by mechanical stimulation of the fat pad
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Figure 5. Scatter plots of pain intensities versus relative reductions in knee flexion maximal voluntary contraction (MVC) peak torque data recorded isometrically, and isokinetically, at 60 degrees/second, 120 degrees/second, and 180 degrees/second during pain together with the best fit linear regression lines (solid) with 95% confidence interval (dashed lines). Pain intensities are scored on a 100-mm visual analog scale (VAS) with 0 representing no pain and 100 worst imaginable pain. Positive values on the y-axis represent MVC reductions in % from baseline measurements. Please note that each subject is represented by 3 data points.
because no effects were observed during the isotonic saline injections of the same saline volume. Also, the volumes injected were small (1 mL), and it has previously been shown that quadriceps inhibition only occurs at increased intraarticular pressure induced by experimental joint effusion of more than 20 mL.39 A limitation to this study is that experimental pain is acute and transient, and does not necessarily reproduce clinical or chronic knee pain, and the association between experimental pain and changes in muscle strength cannot directly be transferred to clinical conditions. However, for obvious reasons, it is not possible to induce chronic pain experimentally in human experiments. Nevertheless, patients with knee pathologies have reduced muscle strength,6,7,11,21,26 and knee pain is negatively correlated to quadriceps muscle strength in knee osteoarthritis patients.34 It has been suggested that reduced quadriceps muscle strength precedes development of symptomatic (ie, painful) as well as radiographic knee osteoarthritis.36,37 Indeed, the present study indicates that reduced muscle strength in knee OA, and other painful knee joint conditions, is not exclusively due to inactivity or disuse, but that the pain intensity itself reduces the muscle strength. If reduced muscle strength plays a role in knee OA progression, as indicated by Segal et al,32 then knee pain in the early disease stages may accelerate the degenerative processes via muscular inhibition.
The clinical importance of this is that patients with painful knee joint conditions may be caught in a vicious circle of pain, decreased level of activity, and increasing muscle weakness as a pain-avoidance strategy.14 Other patients may adopt a pain-endurance strategy and maintain their level of activity in spite of pain.13 Pain endurance will not necessarily be associated with muscle-strength preservation because many activities of daily living can be performed with significant muscle inhibition. An example is sustained walking ability in spite of considerable quadriceps inhibition.40 Thus, pain endurers may also be caught in a vicious circle, yet with increased risks of overload/overuse and accelerated disease progression. Likewise, pain avoiders may also be at risk of accelerated progression as inactivity is related to both muscle weakness29 and joint degeneration.42 Accordingly, patients should be encouraged to exercise within a therapeutic window to maintain or increase muscle strength despite pain, although the beneficial range of exercise—even with pain—is not established. While there is ample evidence of clinical effects of strengthening exercises on strength, pain, function, and quality of life,28 there is a risk of overuse to be considered in the individual exercise prescription. The dose-response relationship between exercise and pain remains to be clarified together with the risk-benefit relationship of pain relief (eg, nonpharmacological techniques or medication) used in this context.
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The magnitude of strength gain achieved with exercises varies considerably from 5 to 71% with numerous factors, including training intensity, specificity, and patient compliance as suggested sources of variation.3 However, this study suggests that a gain in muscle strength may be antagonized by knee pain due to the reduced maximal contraction capacity, leading to smaller stimuli of the neuromuscular system during exercise. On the other hand, therapeutic exercises for knee osteoarthritis are performed at submaximal contraction levels (usually 60 to 80% of the 1-repetition maximum), and the inhibitory role of joint pain on submaximal muscle contractions is not known. Although increased muscle strength by itself may have positive effects on clinical
knee pain, even light pain relief during the course of an exercise regime might enhance the gain in muscle strength and thus speed up the rehabilitation, and amplify the long-term clinical effects of exercise on knee osteoarthritis pain. In conclusion, experimental knee pain significantly reduced knee extension and flexion muscle strength, both isometrically and isokinetically in healthy subjects. The reduction in muscle strength was positively correlated to the pain intensity. This suggests that knee joint pain induces a widespread muscle strength inhibition across muscles and angular velocities that can be modulated by pain intensity. These mechanisms may have strong impact on efficiency of rehabilitation of symptomatic knee OA patients.
References
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