By Micheal A. Clark, Aaron Nelson, Tyler Wallace &
Micheal A. Clark, MS, PT, NASM-PES, CSCS, is President and Physical Therapist and Tyler Wallace, NASM-PES, is Performance Enhancement Specialist at the National Academy of Sports Medicine. Aaron Nelson, ATC, NASM-PES, CSCS, is Head Athletic Trainer and Casey Smith, MS, ATC, NASM-PES, is Assistant Athletic Trainer and Head Performance Enhancement Specialist for the Phoenix Suns.
Training & Conditioning, 13.8, November 2003, http://www.momentummedia.com/articles/tc/tc1308/nbaknee.htm
Sometimes it seems that basketball and knee injuries go together like high-flying dunks and the NBA. From recreational players to world-class all-stars, the jumping and twisting in the sport often wreaks havoc on the vulnerable knee. The good news for basketball players is that, with proper treatment, most ought to be able to return to their pre-injury levels.
Some injuries, however, are so deeply rooted in larger neuro-physio-anatomical problems that traditional rehab protocols only touch the surface. Athletes with these injuries return to their sport but don’t recover fully. They require a more in-depth assessment and whole-body rehabilitation.
Early this summer, an 11-year NBA veteran came to our performance academy with just that problem. (We will refer to him as LK, left knee, to protect his privacy.) LK had suffered a contact injury to the posterior-lateral compartment of his left knee in 1997. The injury resulted in damage to the lateral meniscus, and he underwent a subsequent lateral menisectomy. He then underwent a micro-fracture procedure on the same knee in 2000 and a lateral compartment debridement in 2001.
The athlete was able to return to the court and perform at a high level, but continued to complain of posterior knee pain, and decreased range of motion (ROM) (primarily flexion), strength, and power. These led to decreased performance and playing time. He said he had posterior-lateral knee pain for approximately five years.
LK had undergone a traditional sports medicine rehabilitation following damage to his lateral meniscus, but did not return to his previous level of functional ability. Therefore, when he came to us, we knew we wanted to look at more than just his left knee.
We took the approach that LK may have had a complex dysfunction resulting from an imbalance in a kinetic-chain component. A tight muscle stuck in a shortened state may have altered joint position, setting off a proprioceptive chain reaction that worsened the imbalance and left him functionally weak. Therefore, we began by looking at the entire kinetic chain.
A Whole-Body Approach
The kinetic chain is made up of the muscular, skeletal, and nervous systems, which work together to allow optimum function. If any component of the system is out of balance, it leads to a complex dysfunction.
Muscles work most efficiently in specific positions. They have an ideal length-tension point or position from which they can produce the most force. If a muscle is “stuck” in a lengthened or shortened position, then force production decreases.
Likewise, joints also function in an ideal position. During movement, two joint surfaces roll, glide, or spin on one another. The path of instantaneous center of rotation is the path that one joint takes on another during motion—think of the head of the humerus moving on the glenoid fossa of the scapula as you lift your arm over your head.
Muscles and joints have sensory receptors that are constantly sending proprioceptive feedback to the central nervous system. When the muscles are the right length and the joints are moving correctly, the central nervous system receives the correct information to allow optimum performance.
However, if muscles are too short or too long, they change the position of the joints to which they attach. Both muscle length and altered joint position change proprioception to the central nervous system. This altered kinesthetic awareness leads to synergistic dominance, reciprocal inhibition, athrokinetic inhibition, and decreased flexibility.
Muscles work in synergy to produce force, reduce force, and dynamically stabilize the kinetic chain during function. If one muscle is too long (underactive) or too short (overactive), then other muscles in the chain become over-dominant. This is called synergistic dominance. An example might be the hamstrings becoming synergistically dominant during hip extension if the gluteus maximus is underactive or weak.
In assessing LK, we used a team that included a physical therapist, athletic trainer, and performance enhancement specialist. We conducted several static, transitional, and dynamic tests to gauge underlying muscle imbalances, joint dysfunctions, and neuromuscular inefficiencies that could be leading to the lack of progress and persistent pain.
The first test we conducted was a Squat Print™ (developed by the National Academy of Sports Medicine and Biotonix), which allows assessment of integrated kinetic chain movements. For the test, LK performed overhead squats and we examined his movements by following a kinetic chain checkpoint list. This involves systematically looking at each functional segment of the movement to determine efficiency.
If the athlete has proper flexibility, balance, core strength, functional segment strength, and neuromuscular efficiency, then he or she should be able to squat to parallel or below without compensating at the foot/ankle, knee, lumbar spine, or upper extremity. However, if he or she has altered length-tension relationships (muscle tightness), altered force-couple relationships (weakness of a primary muscle with compensation from a secondary synergist), or joint hypomobility, then you will see abnormal movements. These are easily picked up during the movement pattern.
From there, we did more testing. To test range of motion, we used goniometric assessment using AAOS criteria. We conducted manual muscle testing and positional kinematics. We also asked the athlete to do two performance tests: a vertical jump test and shark skill test, which assesses single-leg balance, eccentric deceleration, and stabilization.
Overview of Imbalances
The results of this athlete’s assessment revealed several movement dysfunctions. During the overhead squat test we noted bilateral external rotation of the feet and eversion of the left foot. This demonstrates tightness in the lateral gastrocnemius, soleus, peroneals, and short of the biceps femoris, which was confirmed with the goniometric assessment. We also found weakness in the anterior tibialis, posterior tibialis, medial gastrocnemius, popliteus, and gracilis, which was confirmed with muscle testing.
Another problem we uncovered during the overhead squat was that the athlete’s left knee adducted and internally rotated. This suggested a tightness in the adductor complex, which was confirmed in the goniometric testing. It also points to a weakness in the gluteus medius, and we confirmed this with muscle testing. Weakness in the gluteus medius leads to dominance of the adductor complex, tensor fascia latae (TFL), and piriformis. Overactivity in the piriformis causes the sacrum to rotate into extension. This was confirmed in LK with positional kinematic testing.
Functionally, these combined deficits cause several problems. Lack of dorsiflexion (tight lateral gastrocnemius, soleus, and peroneals, with decreased posterior glide of the talus) during running, cutting, jumping, and landing causes the foot to externally rotate and evert. This causes the femur to adduct and internally rotate over a fixed tibia, creating tremendous compressive forces on the lateral tibio-femoral joint. When the femur adducts and internally rotates, the gluteus medius and maximus are not as efficient in controlling deceleration of femoral adduction and internal rotation. This also leads to increased compressive forces at the knee.
Weakness and underactivity of the gluteus medius also causes synergistic dominance of the TFL. The TFL attaches to the IT band, which attaches to the distal tibia and the lateral patella (fascial slips). Tightness in the IT band forces the tibia to externally rotate. During closed-chain movements, if the tibia is restricted from internally rotating during knee flexion, then the femur is forced to internally rotate and adduct over the fixed tibia. This again causes excessive compressive forces at the tibio-femoral joint.
Clearly, the above biomechanical and neuromuscular deficits were causing repetitive stress to the entire kinetic chain, with the greatest damage to the lateral tibio-femoral joint. Therefore, it is very probable that LK’s chronic knee pain had been caused from decreased ROM and strength in the ankle and the hip.
Focusing solely on the knee would lead to only partial recovery. Fully alleviating this athlete’s complex kinetic chain imbalances required an integrated approach. Our integrated approach included manual therapy to correct joint and muscle imbalances, exercises to correct flexibility and strength deficits, and an integrated strength and conditioning program.
The manual therapy we used with LK included positional release therapy, soft tissue release therapy, active release therapy, and joint mobilization.
The goal of the positional release therapy was to decrease hypertonicity in overactive muscles. Positional release techniques were used on all muscles held in a lengthened position. Muscles treated included: bilateral medial gastrocnemius, bilateral anterior tibialis, bilateral posterior tibialis, left distal gracilis, and left gluteus medius.
To increase soft tissue extensibility, we initiated soft tissue release therapy on muscles that were in a shortened position. The muscles we treated were the bilateral soleus, lateral gastrocnemius, peroneals, short head of biceps femoris, vastus lateralis, adductor magnus, left adductor complex, tensor fascia latae, piriformis, and biceps femoris.
Active release therapy was used to increase soft tissue extensibility and antagonist activation. We treated the same muscles as we did during soft tissue release.
The one addition to our active release therapy was using the athlete’s voluntary contraction of the antagonist to stretch tight muscles. For example, we had the athlete contract the anterior tibialis while performing active release on the lateral gastrocnemius and soleus. This allowed us to develop improved neuromuscular control in the antagonist muscles.
To improve joint mobility in segments with limited mobility, we used joint mobilization techniques. These included: bilateral talus posterior mobilization, left tibio-femoral joint internal rotation, left iliofemoral joint inferior glide, right iliosacral joint posterior rotation, left iliosacral joint anterior rotation, and left sacroiliac joint flexion/rotation.
LK was also given a comprehensive corrective flexibility exercise program. He started by using self-myofascial release (with foam roll) on the following areas: bilateral soleus, lateral gastrocnemius, peroneals, left adductor complex, left IT band/tensor fascia latae, left piriformis, and bilateral shoulder posterior rotator cuff and capsule.
Static stretching was then done on the following: bilateral soleus, lateral gastrocnemius, left peroneals, left adductor complex, right psoas, left rectus femoris, left biceps femoris, left piriformis, and bilateral pectorals, latissimus dorsi, and posterior rotator cuff.
Neuromuscular stretching was accomplished on the same areas with the assistance of the physical therapist or athletic trainer.
Immediately after the manual therapy and flexibility exercises, we had LK do isolated corrective strengthening, consisting of multi-planar isometrics and controlled isotonics. This sequence helps improve neuromuscular efficiency by focusing on intra-muscular coordination. Specific contraction of each muscle in the synergy helps prevent synergistic dominance from a stronger muscle in the synergy. This also serves as a form of active isolated flexibility and preparation for the integrated strength exercises that will follow.
Isolated strengthening exercises were each performed in two sets of 20 repetitions. For the bilateral anterior tibialis, posterior tibialis, and medial gastrocnemius we used an ankle isolator to make sure that we were able to focus the force specifically to each muscle. We also worked on the left popliteus, left gracilis and pectineus, and left gluteus medius.
Next up was integrated corrective strengthening. We started with two sets of an iso-abdominal series made up of the following 30-second holds: prone with isometric, prone with hip extension, and prone with hip abduction. Second were two sets of 15 reps of a stability-ball core series consisting of bridges, crunches, and prone cobra.
Neuromuscular stabilization exercises were third. We did these as positional isometrics in a closed-chain position to facilitate total kinetic stability prior to transitional and dynamic movements. We started with single-leg stability (3x30), then did single-leg stability with multi-planar reaching (3x10 each plane of motion). This was followed by single-leg stability with upper-extremity activity. We accomplished this through a cable/tubing series—chest press, row, rotation, chops, lifts —at 2x10 and a medicine ball series of throw and catch (2x10).
The above exercises were performed on progressively less stable surfaces (foam roll, Airex pad, Reebok core board, and pivot plate) to facilitate increased proprioceptive activity. These exercises themselves are not functional but they do prepare the athlete for transitional and dynamic movements.
The fourth part of our integrated corrective strengthening consisted of a tube walking series. To conduct these exercises, we placed tubing around the ankles, and had the athlete twice walk 10 steps. We did side-to-side walking in an athletic stance using perfect form and front-to-back walking both straight and diagonally.
LK eventually progressed to an integrated strength and conditioning program. We use what we call Optimum Performance Training™ (OPT), which incorporates flexibility, core training, balance training, reactive training, speed/agility/quickness training, integrated strength training, metabolic conditioning, and skill training. The program has seven phases, each with specific acute variables that are modified in an innovative periodization strategy to develop optimum performance. The phases of training work through stability, strength, and power and include the following:
1. Corrective exercise training to correct muscle and joint imbalances
2. Integrated stabilization training for neuromuscular efficiency
3. Stabilization equivalent training for stability and strength
4. Muscular development training
5. Maximum strength training
6. Elastic equivalent training
7. Maximum power training
A Better Athlete
LK progressed very well using the individualized OPT program. He reports 90 percent functional capacity compared to 60 percent functional capacity prior to training. He played six weeks in a summer league without any complaints of knee pain or decreased function, and his performance levels have improved to pre-injury levels.
This athlete will continue to follow the OPT program during the competitive season. During the next off-season, LK will be able to train at a significantly higher level because we took the time to identify and correct the imbalances that were causing him pain and hindering his performance for almost five years.
This case study illustrates a problem that is all too common. Many athletes “recover” from surgery, showing the classic signs of decreased pain, swelling, and restored ROM. Many of these athletes, however, are left with poor neuromuscular control, muscle and joint imbalances, and poor movement patterns that may have predisposed them to an injury in the first place. By performing a comprehensive kinetic chain assessment, we can pin-point exactly what to do with each athlete to ensure he or she returns to optimum performance.
Movement deficiencies can have a wide range of causes depending on where they are located. This chart explains some common causes of typical deficiencies.
Muscles: tightness in the peroneals and lateral gastrocnemius; weakness in the posterior tibialis, anterior tibialis, and medial gastrocnemius
Joints: decreased mobility of the talus
Muscles: tightness in the soleus and lateral gastrocnemius; weakness in the medial gastrocnemius, medial hamstring complex, gracilis, and sartorius
Joints: decreased mobility of the talus and proximal tibio-femoral joint
Muscles: tightness in piriformis, gluteus medius, and biceps femoris; weakness in the adductor complex and medial hamstring complex
Joints: decreased mobility in the hip joint (iliofemoral joint)
Muscles: tightness in the adductor complex, medial hamstring complex, gluteus minimus, and the tensor fascia latae; weakness in the gluteus medius and maximus
Joints: decreased mobility in the hip joint (iliofemoral joint)
Muscles: tightness in the erector spinae, latissimus dorsi, and psoas; weakness in the rectus abdominus, external oblique, and intrinsic spinal stabilizers
Joints: decreased mobility in the lumbar facet joints
Muscles: tightness in the rectus abdominus, external obliques, hamstrings, and gluteus maximus; weakness in the erector spinae, psoas, latissimus dorsi, and intrinsic spinal stabilizers
Joints: decreased mobility in the SI joint and illiofemoral joint