The primary goal of anterior cruciate ligament reconstruction (ACL-R) and postoperative rehabilitation is returning patients to preinjury levels of exercise or sport within a reasonable time frame. Unfortunately, an alarming number of ACL-R patients are unable to reach their preinjury activity levels (2,28). Recent reports suggest that only 70% of high school and collegiate soccer and football athletes are able to return to play after ACL-R (5,32). Those that do return are at a greater risk for acute lower-extremity injuries (18,29) and posttraumatic osteoarthritis (30,35). These patients often experiences joint instability during physical activity (12,34) and persistent muscle weakness (17,39) that may be related to these poor outcomes.
Proprioception encompasses the sensory input from articular, muscular, and cutaneous mechanoreceptors regarding changes in joint kinetics and kinematics. Functional joint stability relies on the sensorimotor system to interpret proprioceptive sensory signals in the central nervous system and initiate feedforward and feedback muscular responses (41). Damage to articular tissues and joint mechanoreceptors due to ACL injury and reconstruction disrupts proprioceptive contributions to the sensorimotor system (21,39), causing impaired joint stability and muscle activation.
Various experimental techniques have been used to assess proprioceptive and sensorimotor function in ACL-R patients. Joint reposition acuity is a task used to assess conscious proprioception. Patients attempt to actively reproduce a previously maintained angle of sagittal joint range of motion and the magnitude of error is used to quantify proprioceptive acuity (1,3,6,27,37,38). Impairments in ACL injured patients have been well documented using this technique (3,37). In ACL-R patients, some evidence suggests that reposition acuity is restored to levels of healthy controls as early as 3 wk postsurgery (1,37), whereas one study has found that ACL-R reposition acuity was still inferior to uninjured controls at 3 yr postsurgery (3). Center of pressure (COP) excursions during static, unipedal stance have been used to evaluate postural control and sensorimotor function (15,16,33). These tasks evaluate the sensorimotor system’s ability to detect subtle joint perturbations and initiate corrective muscular responses to maintain balance. Some evidence has shown that ACL-R patients demonstrate greater COP velocity and sway (33,36) during static, unipedal stance when compared with healthy controls, whereas in contrast, some studies have observed no such difference (31). Unfortunately, current evidence has measured both proprioceptive and sensorimotor function in individuals with a history of ACL-R during a physically rested state, limiting the applicability of the results toward patients returning to physical activity.
Proprioceptive and sensorimotor deficits may be present in ACL-R patients during physical activity. The effects of exercise and fatigue on proprioceptive, sensorimotor, and neuromuscular measures have been widely investigated in healthy individuals. Experimental exercise protocols have been shown to impair knee joint reposition acuity (27,38), to hinder postural control (15,16), to decrease lower-extremity muscle activation (25), and to alter lower extremity biomechanics (4,22). Despite evidence that exercise causes altered sensory and motor function, the vast majority of healthy individuals can successfully participate in exercise and sport without experiencing joint dysfunction. Individuals with ACL-R knees may be experiencing an abnormal proprioceptive and sensorimotor response to exercise that results in joint dysfunction when returning to physical activity. The objective of this study was to assess this theory by comparing the effects of a 36-min exercise protocol on measures of joint reposition acuity and postural control in individuals with a history of ACL-R and healthy controls.
We used a pretest and a posttest controlled laboratory design with independent variables of group (ACL-R, control) and time (baseline, postexercise). The dependent variables were absolute angular error (AAE) and relative angular error (RAE) at 45° (AAE45, RAE45) and 15° (AAE15, RAE15) of knee flexion during a knee joint reposition acuity task, as well as COP medial–lateral (COPML-SD) and anterior–posterior (COPAP-SD) SD, velocity (COPVel), and area (COPArea) during static unipedal stance. The study was approved by the Institutional Review Board for Health Sciences Research of the University of Virginia, and all participants provided written informed consent.
Forty individuals (20 ACL-R and 20 healthy controls) volunteered for participation (Table 1) and were selected using convenience sampling. All participants were recreationally active (13), with no history of lower extremity injury in the previous 6 months, no current knee pain, no significant change in physical activity 48-h prior, and no history of cardiopulmonary disorder. Participants in the ACL-R group (10 men and 10 women) were an average of 5.0 yr postprimary ACL-R and were released for full activity by their physician. Participants in the control group (10 men and 10 women) had no history of lower extremity joint surgery.
Participants reported to the research laboratory for one data collection session. The reconstructed limb in the ACL-R group and a randomly selected limb in the control group were used for all testing. For participants with a history of bilateral ACL-R (n = 3), the most recently reconstructed knee was used for testing. Knee extensor maximum volitional isometric contraction (MVIC) and quadriceps central activation were measured for descriptive purposes using the superimposed burst technique with previously described methods (25). Baseline measures of postural control and joint reposition error were then completed, followed by the standardized exercise protocol. Postexercise measures were performed in the same order and completed with 10 min of exercise.
COP excursions were collected using an Accusway PLUS Force-Plate (Advanced Medical Technology, Inc., Watertown, MA). The static unipedal stance involved participants standing on the test limb, foot centered on the force plate, contralateral hip and knee flexed to 30° and 45°, and arms held across the chest. The average of three, 10-s trials was used for analysis. Failed trials (participants opened their eyes, uncrossed their arms, or touched their contralateral leg to the ground) were discarded.
Joint reposition acuity
The knee range of motion was measured using a twin-axis electric goniometer (Biometrics, Ltd., Ladysmith, VA), calibrated using a Biodex dynamometer (System 3; Biodex Medical Systems, Inc., Shirley, NY), and secured to the lateral aspect of the participant’s knee using adhesive spray and tape. In an effort to reduce visual and cutaneous cues, participants wore leg-blinding goggles (Lifetime®, Clearfield, UT) that blocked the lower aspect of the visual field and were position with a 5-cm space between the posterior knee and the chair. Subjects were seated with the test leg hanging at 90° of knee flexion. The investigator passively extended the subject’s knee to the “target angle” of either 45° or 15° of knee flexion, maintained the position for 5 s, and then returned to the limb to 90°. Subjects then attempted to actively reproduce the target angle (Fig. 1). Subjects verbally notified the investigator when they sensed they had achieved the “reproduced angle.” This procedure was repeated for each trial. Three alternating trials were performed at each target angle, and the average of the three trials was used for analysis.
After baseline testing, participants completed a 36-min exercise protocol. The protocol consisted of six repeating cycles of exercise. Each cycle consisted of 5 min of inclined treadmill walking at a self-selected pace between 3.0 and 3.5 mph followed by 1 min of jumping exercises (squat jumps and lateral jumps). The treadmill incline began at 0.0% and was progressively increased by 1.0% after each minute of walking until reaching a maximum inclination of 15.0%, where it was maintained for the remainder of the protocol. Physiological and subjective effects of the exercise protocol were monitored by measuring HR and Borg’s RPE (42) at baseline, after each bout of walking, and postexercise, and using a visual analog scale (VAS) for perceived fatigue at baseline and postexercise. HR was measured using a chest-strap HR monitor (Sportline, Yonkers, NY) that was wirelessly synched to the treadmill’s display screen.
COPML-SD and COPAP-SD were calculated as the SD of the mean medial–lateral and anterior–posterior amplitudes (cm). COPVel was calculated as the total COP displacement per the 10-s trial (cm·s−1). COPArea was calculated as the area of a 95% confidence interval ellipse (cm2). AAE and RAE at 45° and 15° were calculated using the following equations: AAE = |(reproduced angle) − (target angle)|; RAE = (reproduced angle) − (target angle).
Descriptive measures, including knee extensor MVIC and quadriceps activation, patient reported outcomes, and exercise-related outcomes were compared between groups using independent sample t-tests. All dependent variables were evaluated for skewness and kurtosis. A 2 (group: ACL-R and healthy control) × 2 (time: preexercise and postexercise) ANOVA with repeated measures was used to compare the baseline with the postexercise changes in normally distributed dependent variables (RAE45, RAE15, and COPVel). Data that were not normally distributed (AAE45, AAE15, COPML-SD, COPAP-SD, and COPArea) were compared using planned, nonparametric comparisons. Mann–Whitney U-tests were used to compare between-group differences at baseline and at postexercise. Wilcoxon signed-rank tests were used to assess baseline to postexercise differences within each group. Change scores (Δ = postexercise measure − baseline measure) were calculated for all dependent variables. The effects of exercise on dependent variables were calculated for each group using Cohen’s D effect sizes with pooled SD. Statistical analyses were performed using the Statistical Package for the Social Sciences (version 17.0; SPSS Inc., Chicago, IL). Statistical significance for all tests was set a priori at P ≤ 0.05.
The ACL-R group had significantly greater mass (t 38 = −2.74, P = 0.01) and BMI (t 38 = −2.41, P = 0.02) as well as significantly lower LEFS (t 38 = 3.09, P = 0.01) and IKDC (t 38 = 3.90, P = 0.001) scores compared with the control group (Table 1). There were no significant differences between groups for any of the additional descriptive measures.
There were no significant differences between the ACL-R and the control groups’ measures of HR, RPE, or VAS for fatigue at any time point before, during, or after the exercise protocol (Fig. 2).
Joint reposition acuity
The results for all joint reposition acuity measures are shown in Table 2.
AAE45 was significantly greater at baseline in the ACL-R group compared with controls (Z = −1.99, P = 0.05); however, AAE45 was not different between groups postexercise (Z = 0.05, P = 0.96). AAE45 significantly increased after exercise in the control group (Z = −1.98, P = 0.05) but did not change after exercise in the ACL-R group (Z = 0.62, P = 0.54). Effect sizes and 95% confidence intervals for AAE45 are shown in Figure 3.
There were no significant group main effects on RAE45 (F 1,48 = 1.28, P = 0.27) or RAE15 (F 1,48 = 0.50, P = 0.48). There were significant time main effects on RAE45 (F 1,48 = 18.46, P < 0.001) and RAE15 (F 1,48 = 9.31, P = 0.004), suggesting exercise increased RAE45 and RAE15 in both groups. There were no significant group-by-time interactions on RAE45 (F 1,48 = 1.94, P = 0.71) or RAE15 (F 1,48 = 0.20, P = 0.66).
AAE15 was not different between groups at baseline (Z = −1.26, P = 0.21) and postexercise (Z = 0.37, P = 0.72). AAE15 did not change after exercise in either the control group (Z = −0.08, P = 0.94) or the ACL-R group (Z = −0.50, P = 0.62).
The results for all postural control measures are shown in Table 3.
There was no significant group main effect on COPVel (F 1,48 = 2.67, P = 0.11). There was a significant time main effect on COPVel (F 1,48 = 4.33, P = 0.01), suggesting COPVel significantly increased after exercise in both groups. There were no significant group-by-time interactions on COPVel (F 1,48 = 0.01, P = 0.93).
COPML-SD was not different between groups at baseline (Z = −0.73, P = 0.47) or postexercise (Z = −1.45, P = 0.15). COPML-SD significantly increased after exercise in the control group (Z = −2.06, P = 0.04) but did not change after exercise in the ACL-R group (Z = −0.63, P = 0.53). Effect sizes and 95% confidence intervals for COPML-SD are shown in Figure 3.
COPAP-SD was not different between groups at baseline (Z = −1.04, P = 0.30) and postexercise (Z = −1.29, P = 0.20). COPAP-SD significantly increased after exercise in both the control group (Z = −3.64, P < 0.001) and the ACL-R group (Z = −2.69, P = 0.01).
COPArea was not different between groups at baseline (Z = −0.69, P = 0.49) and postexercise (Z = −1.53, P = 0.13). COPArea significantly increased after exercise in both the control group (Z = −2.46, P = 0.01) and the ACL-R group (Z = −2.28, P = 0.02).
The purpose of this study was to compare the effects of exercise on proprioceptive (joint reposition acuity) and sensorimotor (COP excursions) function in recreationally active patients with a history of ACL-R compared with healthy controls. Our most interesting finding was in the midrange proprioceptive measure (AAE45). The participants with a history of ACL-R did not experience any change in midrange joint acuity after exercise, whereas the controls experienced significant proprioceptive impairment. The effect size of the baseline to postexercise change was moderate to large and of clinical importance in the control but small and of nonclinical importance in the ACL-R group. A similar pattern of preserved muscle function has been observed in ACL-R patients when measuring quadriceps strength after a similar exercise protocol (25), electrically induced muscle fatigue (43), and tendon vibrations (23,24).
Proprioception is highly dependent on afferent contributions from muscular mechanoreceptors, with additional contributions from articular and cutaneous mechanoreceptors at end ranges of motion (41). We included both a midrange (45°) and end range (15°) reposition angles in an attempt to assess all sensory contributions to proprioception. The midrange joint reposition measure is thought to be highly dependent on muscle spindle activity (38). Gamma motoneurons (γ-MN) innervate intrafusal muscle fibers within the spindles that adjust the receptor’s sensitivity to changes in muscle length during joint motion (20,21,24). Afferent information from muscle spindles, articular receptors, and cutaneous receptors can influence γ-MN activation (20,21,24); therefore, damage to articular mechanoreceptors may affect γ-MN activity and muscle spindle sensitivity (20,21,24). This theory might explain the greater error in midrange reposition acuity (AAE45) observed in our ACL-R group at baseline. Following the same theory, the observed impairments in joint repositon acuity after exercise may be explained by evidence suggesting that exercise-related substances (KCl, lactic acid, arachidonic acid, bradykinin, and 5-HT) and hypoxia might attenuate Ia afferents from muscle spindles (9,10,19,26). A change in Ia afferents would also affect γ-MN activity and might impair the sensitivity of muscle spindles to changes in muscle length (19,20,23).
Previous studies have used an outcome measure of quadriceps strength and a patella tendon vibration intervention to assess γ-MN function in ACL-deficient patients (24), patients with a history of ACL-R (23,24), and patients with knee osteoarthritis (40). Similar to exercise, tendon vibration on healthy knees attenuated Ia afferents, impairing γ-MN and muscle spindle functions and decreasing quadriceps strength. In patients with articular injury, vibration had no effect on quadriceps strength. These authors suggest those with injury suffer from a “dysfunctional” γ-MN loop, meaning the usual neurophysiological process by which vibration causes impairment was already compromised by injury. Applying this theory to the current study, exercise had no effect on muscle spindle function and joint reposition acuity in the ACL-R patients because these patients were already experiencing injury-induced γ-MN loop dysfunction. Further research is necessary to better understand the neurophysiological mechanism of γ-MN loop dysfunction and how this dysfunction might contribution to poor outcomes when ACL-R patients return to exercise and sport.
We found significantly impaired proprioception (AAE45) in a group of patients that were an average of 5 yr post-ACL-R, whereas most evidence suggests that proprioception is restored soon after reconstruction (1,6,37). A relationship may exist between proprioceptive acuity and outcomes after ACL injury and ACL-R (14), suggesting the potential clinical importance of these measures. A limitation of these findings was that there was no observed impairment in either of the relative error measures (RAE45 and RAE15) or the end-range absolute measure (AAE15). Considering these findings, it is possible that an important aspect of reposition error in patients with ACL-R is absolute, not relative error. For example, it may not matter the direction of error (more flexed or extended), just that an error in proprioception exists in patients with a history of ACL-R. Further, the observation of greater AAE at 45° and not 15° in the ACL-R group suggests that proprioception in midrange sagittal plan knee motion is influenced by chronic ACL-R. In the healthy control group, both absolute and relative error seemed influenced by exercise. Collectively, participants in the current study tended to move past the target toward a greater degree of extension after they completed the exercise intervention. In theory, poor proprioception during activity might alter movement patterns and joint loading during gait, exposing joint structures to risk of injury. In the ACL-R group, AAE45 was unaffected by exercise, suggesting a mechanism may exist to preserve proprioceptive acuity during prolonged activity. We can only speculate at the mechanism of this observation, and we cannot draw conclusions about whether this observation is detrimental or a characteristic response in persons with a history of chronic ACL-R or existing proprioceptive deficits
COP excursions while balancing represents typical behavior of the sensorimotor system to explore and use solutions to maintain postural equilibrium. However, altered postural control strategies after injury suggest system constraints that limit the normal availability of sensorimotor strategies (8). Davids et al. (7) found that ACL-deficient individuals demonstrated decreased COP velocity during a dynamic balance task compared with controls, suggesting that ACL injury was a limiting constraint on normal exploration of postural control strategies. In the current study, we observed no differences in postural control strategies between the individuals with a history of ACL-R and the controls. It is possible that our static, unipedal stance task did not place enough task constraint on the system to detect a difference between groups.
In the current study, the ACL-R group did not experience the same change in frontal plane postural control variability after exercise compared with controls. Increases in COP excursions during exercise are a normal consequence of exercise and associated fatigue. Increases in COP velocity (15,16) and velocity SD (44) in the medial–lateral plane have been observed during unipedal stance in healthy individuals after exercise. Previously, these changes have been attributed to subjects using a more hip-dominant strategy while balancing (15,16,44). In the current study, we saw a different response in patients with chronic ACL-R, where these patients experienced no change in COPML-SD after exercise whereas healthy controls did. This may indicate that constraints experienced by individuals with ACL-R may result in adaptations during exercise that act to preserve or prolong gait. This similar pattern has been seen in the response of quadriceps strength to exercise in patients with ACL-R (25,43). However, because the effect sizes for the changes in COPML-SD were small (Fig. 3), the clinical importance may be limited.
In the current study, we reported findings from a small, convenience (not random) sample of recreationally active individuals from our university’s surrounding community in a nonlongitudinal design. Larger scale prospective designs are needed to further establish the clinical importance of impaired proprioceptive acuity in the posttraumatic knee. The ACL-R group had significantly higher mass and BMI than our healthy controls, but we did not feel this affected the outcomes of our study because both groups reported similar levels of physical activity on the two questionnaires and both groups had similar HR and RPE scores throughout the exercise protocol. Also, both groups perceived the exercise level as “hard” and fatiguing and experienced increases in HR up to average of 91% of their max ([220 − mean age] / mean postexercise HR). These differences may be a factor of higher BMI being a risk factor for ACL injury (11), or due to fact that all the ACL-R participants would have had period of inactivity after injury and during surgery recovery that could result in weight gain. Overall, this group of ACL-R patients was able to participate in similar levels of physical activity and had similar quadriceps muscle strength and activation as the control group. However, despite normal levels of physical activity and muscle function, the ACL-R group continued to experience poorer knee function.
In addition, our measurement technique involved the placement of the electronic goniometer on unshaven skin. There is a possibility that this could have influenced proprioceptive acuity. There was an equal distribution of men and women in each group, indicating that this potential source of confound was evenly distributed among groups. In addition, the magnitudes of the differences between groups and after exercise were small. Interestingly, previous authors have found that even small differences in trunk reposition error (mean 0.7°–0.9°) significantly increased the odds of knee injury in female athletes (45). Therefore, small changes in knee reposition acuity may have clinical relevance due to the possibility that small deviations in joint arthrokinematics during prolonged and repetitive movements (such as walking and jogging) may have a clinically important influence on long-term joint health.
ACL-R patients exhibited impaired midrange absolute reposition acuity. Exercise significantly impaired knee joint proprioception and postural control. Midrange absolute reposition error did not change after exercise in patients with ACL-R in contrast to the increased error observed in healthy controls.
There was no external financial funding received for this study.
The authors have no conflicts of interest to disclose.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
1. Angoules AG, Mavrogenis AF, Dimitriou R, et al. Knee proprioception
following ACL reconstruction; a prospective trial comparing hamstrings with bone-patellar tendon-bone autograft. Knee. 2011; 18 (2): 76–82.
2. Ardern CL, Taylor NF, Feller JA, Webster KE. Return-to-sport outcomes at 2 to 7 years after anterior cruciate ligament reconstruction surgery. Am J Sports Med. 2012; 40 (1): 41–8.
3. Barrett DS. Proprioception
and function after anterior cruciate reconstruction. J Bone Joint Surg Br. 1991; 73 (5): 833–7.
4. Brazen DM, Todd MK, Ambegaonkar JP, Wunderlich R, Peterson C. The effect of fatigue
on landing biomechanics in single-leg drop landings. Clin J Sport Med. 2010; 20 (4): 286–92.
5. Brophy RH, Schmitz L, Wright RW, et al. Return to play and future ACL injury risk after ACL reconstruction in soccer athletes from the Multicenter Orthopaedic Outcomes Network (MOON) group. Am J Sports Med. 2012; 40 (11): 2517–22.
6. Co FH, Skinner HB, Cannon WD. Effect of reconstruction of the anterior cruciate ligament on proprioception
of the knee and the heel strike transient. J Orthop Res. 1993; 11 (5): 696–704.
7. Davids K, Glazier P, Araujo D, Bartlett R. Movement systems as dynamical systems: the functional role of variability and its implications for sports medicine. Sports Med. 2003; 33 (4): 245–60.
8. Davids K, Kingsbury D, George K, O’Connell M, Stock D. Interacting constraints and the emergence of postural behavior in ACL-deficient subjects. J Mot Behav. 1999; 31 (4): 358–66.
9. Djupsjobacka M, Johansson H, Bergenheim M. Influences on the gamma-muscle-spindle system from muscle afferents stimulated by increased intramuscular concentrations of arachidonic acid. Brain Res. 1994; 663 (2): 293–302.
10. Djupsjobacka M, Johansson H, Bergenheim M, Wenngren BI. Influences on the gamma-muscle spindle system from muscle afferents stimulated by increased intramuscular concentrations of bradykinin and 5-HT. Neurosci Res. 1995; 22 (3): 325–33.
11. Evans KN, Kilcoyne KG, Dickens JF, Rue JP, Giuliani J, Gwinn D, et al. Predisposing risk factors for non-contact ACL injuries in military subjects. Knee Surg Sports Traumatol Arthrosc. 2012; 20 (8): 1554–9.
12. Fernandes TL, Fregni F, Weaver K, Pedrinelli A, Camanho GL, Hernandez AJ. The influence of femoral tunnel position in single-bundle ACL reconstruction on functional outcomes and return to sports. Knee Surg Sports Traumatol Arthrosc. 2012:[Epub ahead of print].
13. Garber CE, Blissmer B, Deschenes MR, et al. American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Med Sci Sports Exerc. 2011; 43 (7): 1334–59.
14. Gokeler A, Benjaminse A, Hewett TE, et al. Proprioceptive deficits after ACL injury: are they clinically relevant? Br J Sports Med. 2012; 46 (3): 180–92.
15. Gribble PA, Hertel J. Effect of hip and ankle muscle fatigue
on unipedal postural control. J Electromyogr Kinesiol. 2004; 14 (6): 641–6.
16. Gribble PA, Hertel J. Effect of lower-extremity muscle fatigue
on postural control. Arch Phys Med Rehabil. 2004; 85 (4): 589–92.
17. Hart JM, Pietrosimone B, Hertel J, Ingersoll CD. Quadriceps activation following knee injuries: a systematic review. J Athl Train. 2010; 45 (1): 87–97.
18. Hui C, Salmon LJ, Kok A, Maeno S, Linklater J, Pinczewski LA. Fifteen-year outcome of endoscopic anterior cruciate ligament reconstruction with patellar tendon autograft for “isolated” anterior cruciate ligament tear. Am J Sports Med. 2011; 39 (1): 89–98.
19. Johansson H, Djupsjobacka M, Sjolander P. Influences on the gamma-muscle spindle system from muscle afferents stimulated by KCl and lactic acid. Neurosci Res. 1993; 16 (1): 49–57.
20. Johansson H, Sjolander P, Sojka P. Activity in receptor afferents from the anterior cruciate ligament evokes reflex effects on fusimotor neurones. Neurosci Res. 1990; 8 (1): 54–9.
21. Johansson H, Sjolander P, Sojka P. A sensory role for the cruciate ligaments. Clin Orthop Relat Res. 1991; (268): 161–78.
22. Kernozek TW, Torry MR, Iwasaki M. Gender differences in lower extremity landing mechanics caused by neuromuscular fatigue
. Am J Sports Med. 2008; 36 (3): 554–65.
23. Konishi Y, Aihara Y, Sakai M, Ogawa G, Fukubayashi T. Gamma loop dysfunction in the quadriceps femoris of patients who underwent anterior cruciate ligament reconstruction remains bilaterally. Scand J Med Sci Sports. 2007; 17 (4): 393–9.
24. Konishi Y, Fukubayashi T, Takeshita D. Possible mechanism of quadriceps femoris weakness in patients with ruptured anterior cruciate ligament. Med Sci Sports Exerc. 2002; 34 (9): 1414–8.
25. Kuenze C, Hertel J, Hart JM. Effects of exercise on lower extremity muscle function after anterior cruciate ligament reconstruction. J Sport Rehabil. 2013; 22 (1): 33–40.
26. Lagier-Tessonnier F, Balzamo E, Jammes Y. Comparative effects of ischemia and acute hypoxemia on muscle afferents from tibialis anterior in cats. Muscle Nerve. 1993; 16 (2): 135–41.
27. Lattanzio PJ, Petrella RJ, Sproule JR, Fowler PJ. Effects of fatigue
on knee proprioception
. Clin J Sport Med. 1997; 7 (1): 22–7.
28. Lentz TA, Zeppieri G, Tillman SM, et al. A cross sectional study of return to pre-injury sports participation following anterior cruciate ligament reconstruction: contributions of demographic, knee impairment, and self-report measures. J Orthop Sports Phys Therapy. 2012; 42: 893–901.
29. Leys T, Salmon L, Waller A, Linklater J, Pinczewski L. Clinical results and risk factors for reinjury 15 years after anterior cruciate ligament reconstruction: a prospective study of hamstring and patellar tendon grafts. Am J Sports Med. 2012; 40 (3): 595–605.
30. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007; 35 (10): 1756–69.
31. Mattacola CG, Perrin DH, Gansneder BM, Gieck JH, Saliba EN, McCue FC 3rd. Strength, functional outcome, and postural stability after anterior cruciate ligament reconstruction. J Athl Train. 2002; 37 (3): 262–8.
32. McCullough KA, Phelps KD, Spindler KP, et al. Return to high school- and college-level football after anterior cruciate ligament reconstruction: a Multicenter Orthopaedic Outcomes Network (MOON) cohort study. Am J Sports Med. 2012; 40 (11): 2523–9.
33. Mohammadi F, Salavati M, Akhbari B, Mazaheri M, Khorrami M, Negahban H. Static and dynamic postural control in competitive athletes after anterior cruciate ligament reconstruction and controls. Knee Surg Sports Traumatol Arthrosc. 2012; 20 (8): 1603–10.
34. Moller E, Weidenhielm L, Werner S. Outcome and knee-related quality of life after anterior cruciate ligament reconstruction: a long-term follow-up. Knee Surg Sports Traumatol Arthrosc. 2009; 17 (7): 786–94.
35. Oiestad BE, Engebretsen L, Storheim K, Risberg MA. Knee osteoarthritis after anterior cruciate ligament injury: a systematic review. Am J Sports Med. 2009; 37 (7): 1434–43.
36. Okuda K, Abe N, Katayama Y, Senda M, Kuroda T, Inoue H. Effect of vision on postural sway in anterior cruciate ligament injured knees. J Orthop Science. 2005; 10 (3): 277–83.
37. Reider B, Arcand MA, Diehl LH, et al. Proprioception
of the knee before and after anterior cruciate ligament reconstruction. Arthroscopy. 2003; 19 (1): 2–12.
38. Ribeiro F, Venancio J, Quintas P, Oliveira J. The effect of fatigue
on knee position sense is not dependent upon the muscle group fatigued. Muscle Nerve. 2011; 44 (2): 217–20.
39. Rice DA, McNair PJ. Quadriceps arthrogenic muscle inhibition: neural mechanisms and treatment perspectives. Semin Arthritis Rheum. 2010; 40 (3): 250–66.
40. Rice DA, McNair PJ, Lewis GN. Mechanisms of quadriceps muscle weakness in knee joint osteoarthritis: the effects of prolonged vibration on torque and muscle activation in osteoarthritic and healthy control subjects. Arthritis Res Ther. 2011; 13 (5): R151.
41. Riemann BL, Lephart SM. The sensorimotor
system, part I: the physiologic basis of functional joint stability. J Athl Train. 2002; 37 (1): 71–9.
42. Scherr J, Wolfarth B, Christle JW, Pressler A, Wagenpfeil S, Halle M. Associations between Borg’s rating of perceived exertion and physiological measures of exercise intensity. Eur J Appl Physiol. 2013; 113 (1): 147–55.
43. Snyder-Mackler L, Binder-Macleod SA, Williams PR. Fatigability of human quadriceps femoris muscle following anterior cruciate ligament reconstruction. Med Sci Sports Exerc. 1993; 25 (7): 783–9.
44. Soleimanifar M, Salavati M, Akhbari B, Moghadam M. The interaction between the location of lower extremity muscle fatigue
and visual condition on unipedal postural stability. Eur J Appl Physiol. 2012; 112 (10): 3495–502.
45. Zazulak BT, Hewett TE, Reeves NP, Goldberg B, Cholewicki J. The effects of core proprioception
on knee injury: a prospective biomechanical-epidemiological study. Am J Sports Med. 2007; 35 (3): 368–73.