After a lower-limb injury or operation, some patients still have difficulty climbing stairs, trouble rising from a low chair, or episodes of the knee giving way once pain has eased, the wound has healed, or immobilization has ended. When rehabilitation stalls, the recovery of the primary injury and quadriceps function should both be examined to determine whether muscle atrophy, deficient voluntary activation, or strength loss is present.
Walking on level ground, similar thigh circumference on both sides, or a similar appearance of the two thighs is not sufficient evidence that strength has recovered. Assessment should include active knee extension, objective dynamometry, and functional tests, and training loads should be set according to the state of tissue healing.
Within the range of motion and loading permitted by healing of the primary tissue, active activation exercises, progressive resistance, and movement-control training should start early and overlap. Neuromuscular electrical stimulation and low-load blood flow restriction training, after screening for contraindications, can serve as early bridging adjuncts. If pain, effusion, or catching keeps worsening during training, the primary injury and the surgical site must be reassessed promptly. Not every complaint should be attributed to muscle atrophy, and the patient should not simply be blamed for "not training enough."
1. Distinguishing Strength Loss, Deficient Voluntary Activation, and Muscle Atrophy
Early weakness after lower-limb surgery or acute injury often far exceeds the reduction in muscle size. Mizner et al. [1] studied 20 patients undergoing primary unilateral total knee arthroplasty for osteoarthritis (medial parapatellar approach involving the quadriceps tendon). They made paired measurements of maximal cross-sectional area on MRI and of the central activation ratio (CAR) by superimposed electrical stimulation about 10 days before and 27 days after surgery. At nearly 4 weeks after surgery, maximal isometric knee extension strength had fallen by 62%, while maximal cross-sectional area had decreased by only 10% and CAR by 17%. In multiple regression, the two together explained 85% of the variance in strength loss, and in this sample deficient voluntary activation carried nearly twice the relative weight of muscle atrophy [1]. Preoperative knee pain explained 29% of the variance in preoperative activation, but the perioperative change in pain did not significantly explain the large postoperative decline in activation. This suggests that deficient voluntary activation does not necessarily resolve on its own once pain subsides. Total knee arthroplasty involves considerable surgical trauma, so the 62% decline and the roughly twofold weighting cannot be applied directly to all mild lower-limb injuries [1].
When the muscle and its supplying nerve trunk are intact, restricted voluntary recruitment caused by altered sensory input from joint effusion, inflammation, laxity, or receptor damage is termed arthrogenic muscle inhibition (AMI) [2]. Effusion without severe pain is enough to induce inhibition. Rice et al. [3] recruited 16 healthy participants (1 control withdrew because of a vasovagal reaction during infusion; 15 completed) and infused dextrose saline into the knee joint to 50 mmHg (median 75 mL). Participants reported only mild discomfort and a sensation of tightness or pressure, yet quadriceps isometric peak torque, vastus medialis surface EMG root-mean-square amplitude, and muscle fiber conduction velocity all fell significantly. Beyond acute spinal reflex inhibition, a prolonged course is accompanied by increased intracortical inhibition in the primary motor cortex, increased activity in frontal regions responsible for motor planning and cognition and in compensatory visual areas, and reduced descending corticospinal excitability. These changes can extend to the uninjured side [2,4,5].
The 2024 physiotherapy systematic review by Paço et al. [6] misreports a cited source: in the introduction on PDF page 2, citing Lepley et al. [4], it describes the central changes after anterior cruciate ligament injury as "decreased intracortical inhibition and reduced frontal cortex activity." The cited original (PDF pages 4-5) reports the opposite: increased intracortical inhibition and increased activity in frontal areas for motor planning and cognition. That mechanistic explanation is not used here; the review's synthesis of intervention trials is consistent with other evidence and remains usable.
In a 2026 commentary, Maffiuletti [7] drew a further distinction. Clinical observation, surface EMG, and superimposed electrical stimulation all measure the clinical phenomenon of "quadriceps activation failure (QAF)," which mixes AMI with pain, disuse, fatigue, and anxiety or fear of reinjury. There is currently no gold standard for diagnosing pure AMI on its own.
Deficient voluntary activation combined with external immobilization and non-weight-bearing initiates disuse atrophy and a blunted anabolic response within days. Wall et al. [8] allocated 24 healthy young men in parallel to single-leg cast immobilization for 5 days or 14 days (12 per group; separate groups, not the same individuals measured consecutively). In the 5-day group, quadriceps cross-sectional area on CT decreased by 3.5% and single-leg 1-RM by 9.0%. The sample size and means are identical to those of the 5-day control group in the same team's electrical stimulation trial by Dirks et al. [9], so the two are not treated as independent confirmations. In the 14-day group, the decreases were 8.4% and 22.9%, respectively. Atrophy was marked in the monoarticular vasti, whereas the rectus femoris showed no significant change.
After 5 days of single-leg immobilization in young men, myofibrillar protein synthesis rates in the immobilized quadriceps were 41% lower than in the contralateral leg in the fasted state and 53% lower after ingestion of 25 g whey protein, indicating "anabolic resistance" [10].
Kortebein et al. [11] reported that in healthy older adults (mean age 67 years), 10 days of bed rest (protein 0.8 g/[kg·d]) reduced 24-hour muscle protein synthesis by 30.0%, lower-extremity lean mass by 0.95 kg (-6.3%), and isokinetic knee extension strength at 60°/s by 15.6% in relative terms. Unit error in the original table: the table on PDF page 2 (journal page 1773) misprints the unit of isokinetic knee extension strength as "Nm per s" (torque should be in N·m). Absolute torque values are therefore not cited; only the relative change and the lean mass results are retained [11].
Severe joint trauma such as anterior cruciate ligament rupture also triggers intramuscular remodeling. Two reports from the same University of Kentucky biopsy cohort [12,13] showed that about 6 months after surgery, the injured-side vastus lateralis still had reduced volume (308.7 cm³ vs 503.6 cm³ on the uninjured side before surgery) and low isometric strength (1.7 N/kg vs 2.8 N/kg), together with fewer satellite cells, upregulated myostatin, and collagen deposition.
| Target of assessment | Clinical meaning | Why routine observation often misses it | Practical clinic and rehabilitation tests | Corresponding intervention focus |
|---|---|---|---|---|
| Muscle atrophy | Reduction in muscle fiber cross-sectional area or muscle volume | Subcutaneous fat and postoperative edema mask changes in contour; tape-measured thigh circumference depends heavily on measurement site | Side-to-side comparison of vastus medialis contour; quantification of cross-sectional area by ultrasound or MRI where available | Restore muscle contraction tension and progressive resistance loading as early as protection requirements allow |
| Deficient voluntary activation | Restricted voluntary recruitment of motor units (clinically presenting as activation failure) | Marked suppression of recruitment can persist even when the incision has healed, there is no pain at rest, or the patient can walk on level ground | Observation of supine active terminal knee extension and extension lag; superimposed electrical stimulation or surface EMG in the laboratory | Reduce swelling and pain; local cryotherapy before exercise; hamstring relaxation combined with terminal knee extension recruitment; neuromuscular electrical stimulation |
| Quadriceps strength loss | Combined result of atrophy, deficient voluntary activation, and changes in intramuscular quality | Manual muscle testing has a ceiling effect above antigravity grade; deterioration of the uninjured side inflates the limb ratio | Isokinetic dynamometer or belt-stabilized handheld dynamometer; single-leg repeated sit-to-stand test as a supplement when equipment is unavailable | Progress open- and closed-chain resistance and movement-control training against the preoperative baseline or population norms; resume high-risk sports only after criteria are met |
2. Muscle Function Recovery Requires Separate Assessment
Recovery after surgery cannot be judged solely by the expected number of weeks. Roos et al. [14] followed middle-aged patients (mean age 45 years) undergoing arthroscopic partial meniscectomy. In a survey of 17 orthopaedic surgeons, 9 expected full recovery within 2-4 weeks after surgery (median expected time across all respondents, 3.8 weeks). Yet at follow-up a mean of 14.4 weeks after surgery, 19/63 (30%) participated in recreational or competitive sport. This was an improvement over the 15/71 (21%) after injury but before surgery, but remained far from the preinjury level of 47/74. The proportion who were sedentary rose from 9% before injury to 38%, and Knee injury and Osteoarthritis Outcome Score (KOOS) results were also worse than those of controls (Minor discrepancies in the original report: preinjury sport participation of 47/74 is given as 63% in the abstract on PDF page 1 and as 64% in Table 4 on page 4 [journal page 622], and the postoperative 19/63 is not a paired proportion of the same 63 people. The result shows that activity had not returned to preinjury levels more than 3 months after surgery, not that surgery made previously normal patients worse).
Quantitative dynamometry studies suggest marked variation in recovery between patients. Glatthorn et al. [15] tested 14 patients 6±1 months after unilateral partial medial meniscectomy. Isometric and concentric quadriceps peak torque on the operated side remained 11.6% and 14.5% lower, respectively, than on the uninjured side, and surface EMG of the vastus lateralis and vastus medialis during maximal effort was significantly reduced. Vastus lateralis thickness, pennation angle, and fascicle length measured by ultrasound showed no significant side-to-side differences.
By contrast, Casartelli et al. [16] cross-sectionally assessed 30 patients 6±1 months after surgery (15 after isolated arthroscopic meniscal surgery and 15 after meniscal surgery combined with anterior cruciate ligament reconstruction). In the isolated meniscal group, the mean side-to-side difference in quadriceps maximal voluntary contraction torque was about 5% (not significant), and the side-to-side difference in vastus lateralis ultrasound thickness was 0%. Both were significantly smaller than the 15% torque difference and 6% thickness difference in the group with ligament reconstruction. However, within the isolated meniscal group, patients with greater asymmetry of voluntary activation had lower KOOS quality-of-life scores.
Ericsson et al. [17] re-examined 45 middle-aged patients who had undergone partial meniscectomy for degenerative tears, a mean of 4 years after surgery. Isokinetic knee extension torque on the operated side remained on average 9% lower, patients performed fewer consecutive single-leg rises (11.5 vs 15), and weaker patients had worse symptoms and quality of life.
Strength and activation recover differently among patients who have undergone the same procedure. The need for further rehabilitation should be decided on the basis of the individual's dynamometry results and functional performance.
Two frequently cited studies on the distribution of atrophy across individual muscle heads after meniscal surgery and on the causes of anterior knee pain have methodological or data flaws that affect their conclusions. Akima and Furukawa [18] used MRI to compare thigh muscle group volumes in patients with meniscal injury and after arthroscopic partial meniscectomy, but the statistical methods in the original are flawed: the participant and statistics sections on page 2 of the scanned original (journal page 633) state that 32 patients were enrolled in total. However, 2 or 3 longitudinal measurements taken at least 2 months apart in 10 of these patients were counted directly as different participants, and the data were then analyzed with paired t tests, one-way analysis of variance, and correlation analysis without accounting for the correlation among repeated observations of the same individuals. Because this violates the assumption of independent samples, the study's significance tests cannot be used to determine whether any muscle head atrophies preferentially. Only the smaller quadriceps volume on the operated side compared with the uninjured side can be taken as a descriptive clue [18].
Amestoy et al. [19] in 2021 examined patellofemoral pain and changes in thigh MRI area 6 weeks after arthroscopic partial meniscectomy. Contradictions in the original report: Table 1 on PDF page 4 lists, for the follow-up sample (20 in the pain group, 64 in the pain-free group), preoperative and 6-week postoperative means alongside mean paired differences. In several rows, the listed difference departs from the preoperative minus postoperative means by more than rounding allows. For example, for the vastus lateralis at 15 cm in the pain group, 21.09 minus 15.88 is 5.21 cm², but the table lists 5.11±2.01 cm²; for the vastus medialis at 3.75 cm in the pain group, 17.66 minus 9.67 is 7.99 cm², but the table lists 7.80±2.15 cm². In the same table, the vastus lateralis/vastus medialis ratio rose from 1.35 to 1.76 (change 0.41) in one group and from 1.32 to 1.63 (change 0.31) in the other, yet the difference row is printed as 0.77±0.09 and 0.98±0.13, with no explanation in the methods. Throughout the text, MRI cross-sectional area (cm²) is also misnamed "muscle thickness," and Table 3 on page 5 reports isokinetic strength in "kg" with an unclear meaning. In addition, strength testing at 6 weeks coincided with anterior knee pain, and pain at the time of testing can itself inhibit force output, so these data cannot establish that muscle atrophy caused patellofemoral pain. The observations that remain usable are these: among 84 patients without preoperative patellofemoral pain, 20 (23.8%) developed anterior knee pain 6 weeks after surgery, accompanied by lower muscle function and Lysholm scores [19].
The effects of immobilization and reduced weight bearing also need to be included in the assessment of muscle function. Yamauchi et al. [20] followed 10 middle-aged patients with foot or ankle fractures (mean age 59.0 years) through a mean 28.1-day period of non-weight-bearing in an ankle cast, during which at least 30 hip and knee flexion-extension and abduction exercises were still performed daily. Changes were assessed as the summed MRI cross-sectional areas of multiple slices at the 40% mid-femoral level (not whole-muscle volume). The summed areas of the vastus lateralis, vastus intermedius, and vastus medialis decreased by 10.9%, 8.4%, and 11.2%, respectively, while the rectus femoris showed no significant change. Values had largely recovered after a mean of 56.9 days of outpatient rehabilitation.
Yoshiko et al. [21], from a closely related institution, analyzed mid-thigh composition in 8 patients with foot or ankle fractures before and after a mean of 26 days of non-weight-bearing cast immobilization (whether the samples of the two papers overlap has not been confirmed, so patient numbers are not combined). Contradictory reporting of study participants in the original: the abstract on PDF page 1 and the participants paragraph on page 2 both state that 8 patients with "fifth metatarsal or fibular fractures" were enrolled, but Table 1 on page 2 records patient 6 as having a calcaneal plus navicular fracture and patient 8 a medial cuneiform plus first metatarsal fracture. Following Table 1, the sample should be described as foot and ankle fractures and cannot be equated with a minor ankle sprain. This discrepancy in diagnosis does not affect the area measurements: the cross-sectional area of pure skeletal muscle tissue at mid-thigh (not quadriceps volume) decreased from 85.8±7.6 cm² to 77.1±7.3 cm², with no significant change in intramuscular or intermuscular fat [21].
The monoarticular vasti depend on antigravity loading in standing, and their tension drops sharply during non-weight-bearing, whereas the rectus femoris continues to contract as the hip flexes to swing the leg during crutch walking [8,20]. Grosset et al. [22] reported a 29-year-old woman with a fifth metatarsal fracture whose quadriceps volume, after 28 days in an ankle cast, was 24.1% below the preinjury baseline (-25.3% to -29.5% in the three vasti, -6.2% in the rectus femoris) and remained 5.2% lower 2 months after cast removal. These results come from strict immobilization after fracture; studies of patients with chronic ankle instability have not found the same quadriceps activation inhibition [23].
3. Clinical Reassessment of Persistent Weakness and Symptoms, Long-Term Associations, and Objective Testing
If, several weeks after surgery or removal of external immobilization, a patient still has persistent giving way, weak knee extension, or stalled rehabilitation, the first step is to reassess the primary injury and the surgical site. The problem should not be attributed to muscle atrophy, nor should the patient be blamed for insufficient effort, without examination. Clinically, worsening rest or night pain, recurrent marked joint effusion, local redness, swelling, increased skin temperature or fever, locking or catching, abnormal laxity, calf swelling and tenderness, or persistent tenderness at the fracture site should first prompt a specialist to rule out unhealed primary pathology, failure of a repaired structure, and complications such as infection or thrombosis.
Once structural healing has been confirmed as safe, prolonged reluctance to exert force in some patients is also related to pain-related fear-avoidance. The fear-avoidance model of chronic musculoskeletal pain describes the relationship between pain-related worry and activity avoidance [25]. For patients whose examination findings permit training but who remain afraid to bear load, clinicians should explain what load can be tolerated and increase activity gradually.
Persistent quadriceps weakness is closely associated with sports reinjury and worsening knee symptoms. In an anterior cruciate ligament reconstruction cohort, Grindem et al. [26] followed 100 patients (74 of whom returned to Level I sports involving sudden stops and changes of direction). Patients who returned to sport less than 9 months after surgery had a higher reinjury rate than those who returned after 9 months (39.5% vs 19.4%), and patients whose quadriceps limb symmetry index (LSI) was below 90% before return also had a significantly higher knee reinjury rate (33.3% [15/45] vs 12.5% [3/24]).
For knee osteoarthritis outcomes, worsening symptoms must be distinguished from structural cartilage degeneration. A meta-analysis by Øiestad et al. [27] of 5 cohorts without baseline osteoarthritis (5707 people) showed that knee extensor weakness was associated with an increased risk of incident symptomatic knee osteoarthritis, but the authors also noted that no randomized controlled trial has shown that strengthening can prevent osteoarthritis. Ericsson et al. [28] followed 34 patients after partial meniscectomy to 15 years after surgery and observed that those with higher knee extension strength at 4 years had less joint space narrowing and fewer osteophytes 11 years later. This result is limited by the small observational design and the lack of a preoperative radiographic baseline (Unit error in Table 1 of the original: Table 1 on PDF page 5 misprints the unit of body mass index (BMI) as "years" instead of kg/m²; this typographical error does not affect the correlation analysis between strength and radiographic outcomes).
A meta-analysis by Culvenor et al. [29] of 15 longitudinal studies (more than 8000 people) further showed that low knee extensor strength was significantly associated with worsening WOMAC pain and function, but found no significant increase in the risk of radiographic tibiofemoral joint space narrowing.
Contradictions in the original report: the abstract on PDF page 1 and Figure 2 on page 5 (journal pages 649 and 653) of Culvenor et al. [29] give a pooled OR of 1.15 (95% CI 0.84-1.56) for tibiofemoral joint space narrowing, whereas the text on page 6 (journal page 654) gives OR=1.11 (95% CI 0.81-1.53) for the same analysis without explanation. Neither value should be treated as the definitive figure, but both confidence intervals cross 1, so the negative finding of no significant association with structural progression stands.
The realistic goals of quadriceps strengthening are to reduce pain, improve dynamic stability, and restore movement function; patients should not be promised that it will prevent articular cartilage degeneration [27,29].
In the clinic and during rehabilitation, quadriceps assessment should target activation and absolute strength directly. Visual inspection and tape-measured thigh circumference are easily confounded by edema and subcutaneous fat, and manual muscle testing has a marked ceiling effect above antigravity grade, so it cannot accurately identify moderate strength deficits [30].
For bedside screening, the patient lies supine while active terminal knee extension and vastus medialis contraction are observed. On this basis, Sonnery-Cottet et al. [31] classified clinical presentations as grade 0 (normal contraction), grade 1 (reduced contraction without extension deficit), grade 2 (reduced contraction with reversible extension deficit due to hamstring spasm), and grade 3 (irreversible posterior capsular contracture). In 300 patients with acute anterior cruciate ligament rupture (labeled a cross-sectional study in the title and a case-control study in the abstract, but in fact a consecutive outpatient assessment), they found clinical activation impairment in 56.7% (170 patients). After guided exercises performed on the spot in the clinic, active contraction and knee extension improved immediately in 135 (79%) [32]. Such immediate release indicates only partial relief of acute severe activation failure. It does not mean that strength or muscle volume has recovered, and it cannot by itself confirm a purely arthrogenic mechanism [7,32].
Quantitative strength testing should use an isokinetic dynamometer or a belt-stabilized handheld dynamometer [24,30]. When no dynamometer is available, the number of consecutive single-leg rises from a low chair can serve as a reference for functional endurance [17].
When interpreting limb ratios, clinicians must also guard against patients appearing to meet criteria because the uninjured side has deteriorated at the same time. Wellsandt et al. [33] followed 70 patients after anterior cruciate ligament reconstruction. At 6 months, 57.1% (40/70) met an LSI ≥90% for strength and hop tests calculated against the concurrent uninjured side. When the uninjured side's baseline after injury and before surgery was used instead to calculate the estimated preinjury capacity (EPIC ≥90%), the rate fell to 28.6% (20/70). Of 11 patients with a second anterior cruciate ligament injury, 8 had passed the 6-month LSI criteria, but 6 of these 8 did not meet the EPIC criteria. When setting criteria for return to sport or discharge, clinicians should also compare against preoperative baseline absolute values or norms for age, sex, and activity level [30,33].
4. Rehabilitation Progression and Adjunctive Interventions Under Tissue Protection
Quadriceps rehabilitation must comply with the protection requirements for fracture healing, ligament graft remodeling, or meniscal and cartilage repair. Within the weight bearing and range of motion permitted by the treating physician, clinical guidelines support progression based on objective functional performance combined with minimum biological healing times. Early voluntary activation exercises, progressive resistance, and movement-control training are carried out in overlap, and there is no need to wait for activation to normalize fully before starting strength training. The Aspetar guideline also recommends against routine use of continuous passive motion (CPM) after anterior cruciate ligament reconstruction [30].
In the acute and subacute phases, the priorities are controlling effusion and pain and eliminating active extension lag [5,6,34]. Applying local cryotherapy around the knee for 20-30 minutes before active exercise can reduce inhibition for a short window, so that active recruitment training can follow immediately [5,6]. However, in the experimental effusion trial in healthy people by Rice et al. [3], 20 minutes of icing significantly improved quadriceps torque and muscle fiber conduction velocity, but the between-group difference in vastus medialis surface EMG root-mean-square amplitude was not significant (P=0.13). An experimental model in healthy people also does not establish the same efficacy across all clinical patient groups.
For bedside movement training, patients with an extension deficit due to protective hamstring tension can first perform repeated gentle isometric hamstring contract-relax cycles, prone or with the heel elevated, to relieve flexor spasm. They then immediately practice active terminal knee extension and isometric quadriceps contractions with visual or finger-palpation feedback [31,32]. When knee effusion is marked, pain-free isometric efforts can be performed at 30°-50° of knee flexion, where intra-articular pressure is lower [2].
When early loading of the injured limb is restricted, resistance training of the uninjured side can be added. In the randomized controlled trial by Harput et al. [35] after anterior cruciate ligament reconstruction, adding concentric or eccentric isokinetic training of the uninjured side at 4-12 weeks after surgery helped increase isometric knee extension strength of the injured side at 12 and 24 weeks, but gave no significant advantage in single-leg hop symmetry or IKDC scores at 24 weeks. The Aspetar guideline notes that results of cross-education studies are inconsistent and that this approach cannot replace training of the injured side, but maintaining resistance training on the uninjured side helps prevent a decline in strength of the reference limb [30].
Neuromuscular electrical stimulation (NMES) directly excites intramuscular motor nerve branches and helps patients with restricted early recruitment achieve strong contractions. In a randomized trial of 5-day single-leg cast immobilization in young men, Dirks et al. [9] found that with passive electrical stimulation for 40 minutes twice daily, the decrease in quadriceps cross-sectional area on CT was not significant (about -0.8%, vs a 3.5% decrease in controls). Single-leg 1-RM, however, decreased significantly in both the stimulation and control groups (-6.5% and -9.0%), with no significant between-group difference. This suggests that electrical stimulation alone during immobilization can attenuate short-term atrophy but cannot prevent strength loss or replace active resistance training.
Adding high-intensity, tolerable electrical stimulation to active rehabilitation early after surgery clearly improves strength recovery. Stevens-Lapsley et al. [36] started twice-daily electrical stimulation combined with rehabilitation 48 hours after surgery in 66 patients after total knee arthroplasty. At 3.5 weeks after surgery, the loss of quadriceps torque was significantly smaller (-0.40 vs -0.67 N·m/kg), with concurrent advantages in walking and stair tests. The meta-analysis by Hauger et al. [37] also confirmed that early combined electrical stimulation after anterior cruciate ligament surgery is more beneficial for recovering quadriceps strength than conventional rehabilitation alone.
Li et al. [38] published a similar meta-analysis of electrical stimulation after anterior cruciate ligament surgery in 2025. Its overall direction also supports combined electrical stimulation, but it contains multiple contradictions in the original report:
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Omitted sample count: the abstract on PDF page 1 states that 11 trials included 202 patients, whereas the text on page 3 and Table 1 on page 4 show 202 patients in the intervention groups and 200 in the control groups (402 in total); the abstract omits all control participants;
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Conflicting timing subgroup: the text on page 6 and Figure 4 on page 8 place Delitto (1988), Snyder-Mackler (1991), and Toth (2020) in the "started ≤1 week after surgery" subgroup and claim that starting within 1 week is more effective. This directly conflicts with the start times recorded in Table 1 on page 4: postoperative week 2 or 3, postoperative week 3, and 3 weeks before surgery, respectively;
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Duty cycle calculation errors: in Table 3 on page 6, the duty cycle for the Delitto study (5 s on/50 s off) should be 9.1% but is listed as 25%, and that for the Toth study (10 s on/30 s off) should be 25% but is listed as 33%;
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Inconsistent statistical model and heterogeneity: the abstract on page 1 and the methods on page 3 state that a random-effects model was used, but the text on page 6 and Figure 3 on page 7 actually label a fixed-effects model. The text also gives I²=0% (P=0.49) for pooled strength, whereas Figure 3 shows I²=22% (P=0.24);
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Mismatched groups for functional scores: in extracting 6-week Lysholm scores from the Feil study in Table 4 on page 7 (PS group 87.45, KH group 91.39, control group 88.21), the authors swapped the group assignment of the KH group difference of +3.18 (P<0.01) and the PS group difference of -0.77 (not significant);
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Reversed direction labels on forest plots: in Figures 3-5 on pages 7-8, a positive standardized mean difference indicates higher strength in the experimental group, yet the positive side of the horizontal axis is labeled "Favours [control]".
Accordingly, this paper's subgroup comparison claiming that starting within 1 week after surgery is significantly better than starting later, its unverified precise effect sizes, and the erroneous parameter rows listed above are not used. Support for early combined electrical stimulation after surgery rests on the verified original trials and the Aspetar guideline [30,36,37].
After acute pain and swelling subside, strengthening should progress through closed- and open-chain resistance together with concentric, eccentric, and movement-control training, according to the specific procedure, the healing stage, and the permitted range of motion and loading [24,30]. In anterior cruciate ligament reconstruction, for example, the Aspetar guideline supports early closed-chain exercise and the introduction of open-chain knee extension within a restricted range of 90°-45° of knee flexion from postoperative week 4, with monitoring of the anterior knee pain response. For patients after meniscal repair, cartilage repair, or periarticular or distal fractures, the timing of open-chain exercise and weight bearing must strictly follow the relevant surgical protection protocol. Patients should not increase range or load on their own just because a given movement was pain-free during one session [24,30].
For patients who in the early phase cannot yet tolerate conventional high-load resistance because of pain or loading restrictions, low-load blood flow restriction training with a dedicated pressure-measuring device can serve as a bridge. It requires professional screening for contraindications such as venous thromboembolism and severe vascular disease, and on-site supervision. In musculoskeletal rehabilitation research, its strength gains exceed those of equivalent low-load exercise but remain below those of conventional high-load resistance training; once conditions permit, patients should promptly return to conventional progressive resistance. Patients must never bind the limb themselves with a tourniquet or elastic band [30,39,40].
Nutritional management also needs to take baseline status into account. Dirks et al. [41] found that in healthy older men whose habitual protein intake was already adequate (1.1 g/[kg·d]), taking an additional 20.7 g of whey protein twice daily during 5 days of single-leg cast immobilization did not attenuate the decline in quadriceps cross-sectional area or 1-RM strength. This shows only that additional whey protein alone confers no added benefit during short-term complete immobilization in people with adequate protein intake. It does not imply that protein nutrition is useless during rehabilitation. For people whose habitual diet is inadequate, and for patients who have entered the stage of electrical stimulation and active resistance training, basic energy and protein intake should still be ensured [10,11,41].
Throughout training progression, if knee effusion has increased on waking the next morning, pain at rest worsens, or the active extension angle regresses, that week's training load and volume should be reduced. If new joint locking, marked redness, heat, swelling and pain, or calf swelling and pain appear, training should be stopped and the patient should return to the hospital for review.
References
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