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In clinical practice we often focus on the immediate and obvious direct cause and effect relationships to derive treatment solutions. In the case of ACL injuries, this means the local consequences of the joint injury (pain, swelling, range of motion) are well attended to in standards of care management. However, when the effects are delayed or explained by sources seemingly disparate from the local joint, the right solutions can be less straightforward.
In clinical practice we often focus on the immediate and obvious direct cause and effect relationships to derive treatment solutions. In the case of ACL injuries, this means the local consequences of the joint injury (pain, swelling, range of motion) are well attended to in standards of care management. However, when the effects are delayed or explained by sources seemingly disparate from the local joint, the right solutions can be less straightforward.
ACL injuries are known to have a systemic effect on the neuromuscular system however, these effects are not as immediately obvious as the joint injury itself. Attending to the primary problem (joint injury itself), without intervening or planning ahead for the secondary problems (systemic neuromuscular consequences), can lead to clinical impairments that present when the athlete attempts to return to sport.
ACL injuries are known to have a systemic effect on the neuromuscular system however, these effects are not as immediately obvious as the joint injury itself. Attending to the primary problem (joint injury itself), without intervening or planning ahead for the secondary problems (systemic neuromuscular consequences), can lead to clinical impairments that present when the athlete attempts to return to sport.
A great example of an unintended consequence is the avoidance of high-load eccentric knee extension exercises after ACL reconstruction and the resultant effect this has on strength recovery. The prevailing argument is that open-chain exercises create an unopposed shear force on the knee that places significant strain on the new ACL. Thus, to solve the primary problem, clinical practice guidelines delay or recommend the avoidance of high-load exercises that put tension on the graft altogether. Despite basic evidence to the contrary that directly refutes this argument, demonstrating that high-load open chain exercise is insufficient to harm the graft, the avoidance of these exercises creates a scenario in which strength recovery is delayed or never achieved as interventions that can directly target the weakened muscle are avoided.
A great example of an unintended consequence is the avoidance of high-load eccentric knee extension exercises after ACL reconstruction and the resultant effect this has on strength recovery. The prevailing argument is that open-chain exercises create an unopposed shear force on the knee that places significant strain on the new ACL. Thus, to solve the primary problem, clinical practice guidelines delay or recommend the avoidance of high-load exercises that put tension on the graft altogether. Despite basic evidence to the contrary that directly refutes this argument, demonstrating that high-load open chain exercise is insufficient to harm the graft, the avoidance of these exercises creates a scenario in which strength recovery is delayed or never achieved as interventions that can directly target the weakened muscle are avoided.
For more on the safety of open chain exercise see:
Who's Afraid of the Big Bad Wolf_ Open-Chain Exercises After Anterior Cruciate Ligament Reconstruction.pdfUnlike disuse muscle atrophy, where the benefits of re-engaging in just about any exercise regime is obvious, those with ACL injuries often suffer from persistent muscle weakness even after a full bout of rehabilitation with good compliance. We and others have shown that this is likely due to the broad range of atrophy inducing factors after ACL injury that make muscle recovery difficult (neural inhibition, abundant pro-inflammatory cytokines, reduced satellite cells, increased catabolic pathways). Muscle recovery can only occur if interventions that directly treat the muscle are employed. Changing how we approach muscle loading exercises after ACL injury may be key to optimizing recovery.
For more on the broad range of atrophy inducing factors after ACL injury see:
Muscle Atrophy After ACL Injury_ Implications for Clinical Practice.pdfA primary advantage of muscle is that it is a plastic material, meaning it is constantly adapting to the needs of the system. When a muscle is placed under different loads, it will remodel. The challenge of primarily using only one mode of exercise prescription after injury is that to treat muscle atrophy interventions need to be designed to target the cellular signaling pathways that promote recovery. Unlike concentric exercise, progressive overloading achieved via high-load eccentric exercise provides the muscle with the necessary mechanical stimuli that are needed to promote muscle hypertrophy and improve neural activity (two critical components of muscle function that are negatively altered after injury).
For more on the direct benefits of eccentric muscle contractions see:
Shifting the Current Clinical Perspective_ Isolated Eccentric Exercise as an Effective Intervention to Promote the Recovery of Muscle After Injury.pdfThe Role and Implementation of Eccentric Training in Athletic Rehab.pdfEccentric Exercise to Enhance Neuromuscular Control.pdfOn the basis of the accumulating evidence, we encourage clinicians to re-evaluate their approach to high-load knee extension exercises, recognizing that the solution to the primary problem (avoidance of open chain exercises and eccentrics due to injury) may lead to unintended muscular consequences. The clinical integration of this re-evaluation of high-load exercise is simply to begin prescribing higher load exercises when the patient is clinically ready based on other exam features (full range of motion, absence of joint effusion or pain). Many clinicians still hold patient progress back to “protect the graft” when our best available data simply does not support such a strategy. Of course, clinicians must still manage the full clinical picture for progression, considering pain, effusion, range of motion, inhibition, capacity and so on, but graft protection does not have to be elevated to the same level to dictate progression.
Another unintended consequence of early treatment is the instruction to have patients focus intensely on the injured knee joint musculature to produce repeated contractions. While this approach is certainly vital initially after injury and during early-stage recovery to overcome the initial quadriceps inhibition, the encouragement to engage visual attention to the joint and musculature tends to be common across all stages of therapy. Such a strategy has little downside when returning to normal daily life, where attention can be directed to maintain joint stability, however when returning to sport, this focused attention can lead to secondary problems, as reliance on higher-brain centers (specifically cognitive and visual attention) become the norm to sustain motor control. Such a neural strategy of requiring directed attention to ensure sufficient stability or activation can fail when attention is required to navigate the complex sports environment, reducing the ability to engage in the neural compensation and potentially putting joint stability at risk. Thus, late-stage functional capacity in the visual and attentionally demanding sport environment is limited due to allowed neural compensations inadvertently trained in our rehabilitation. Slight changes to how exercise is prescribed can ensure attainment of the immediate primary consequence (strength restoration) but set the patient up to not depend on direct attention for knee stability and hopefully improve return to sport outcomes.
For more on this rehabilitation approach see:
Principles of Motor Learning to Support Neuroplasticity After ACL Injury_ Implications for Optimizing Performance and Reducing Risk of Second ACL Injury.pdfOptimization of the Anterior Cruciate Ligament Injury Prevention Paradigm_Novel Feedback Techniques to Enhance Motor Learning and Reduce Injury Risk.pdfA clinicians guide to understanding neuroplasticity for ACL rehab.pdfThe correct course of action is sometimes hard to know when an outcome isn't obviously or immediately linked to our care or, in the case of ACL rehab, the unintended consequences of our treatments aren't realized until months later. Understanding the late-stage consequences is the first step to re-thinking our exercise prescription in subtle ways that when applied throughout a long rehabilitation window can have a meaningful impact on patient outcome.
What does the Clinician do? Take home message is that changes in how you prescribe exercises and give feedback and more considerable changing to load management and intensity during rehabilitation can have a big impact down the road! There is no need to compromise late-stage function for early-stage muscle recovery.
What does the Clinician do? Take home message is that changes in how you prescribe exercises and give feedback and more considerable changing to load management and intensity during rehabilitation can have a big impact down the road! There is no need to compromise late-stage function for early-stage muscle recovery.
Our advice is to:
Still address the primary consequences but planning for the eventual end goal of the athlete in subtle exercise prescription changes can ensure both primary and secondary consequences are addressed.
Don’t fear load\stimulus-avoiding exercises that put tension on the muscle (or graft) is harmful to recovery - your body needs this stimulus and it is safe.
Modify attention - does the patient have to attend\stare at their joint\muscle for this exercise?
Example feedback suggestions from cited articles above – attempt to progress your feedback from internal\explicit to external\implicit
Lindsey Lepley
Dr. Lepley is an assistant professor of Athletic Training at the University of Michigan School of Kinesiology. She earned a master's in Education from the University of Virginia and a PhD in Kinesiology from the University of Michigan. Dr. Lepley’s research program focuses on the identification of neuromuscular mechanisms and rehabilitation strategies to treat dysfunction after common orthopedic injury. Much of her previous and current research has identified adaptions in neuromuscular mechanisms that contribute to injury and disease with a particular emphasis on anterior cruciate ligament rupture.
Dustin Grooms
Dr. Grooms is a Professor in the Division of Physical Therapy at Ohio University. His doctorate is in health and rehabilitation sciences from the Ohio State University. He has clinical experience as an athletic trainer and strength coach and has degrees in athletic training, kinesiology, biomechanics and neuroscience. Currently his main research interest is how the brain and movement mechanics change after musculoskeletal injury and therapy.
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