Home > Injury Prevention, Movement Dysfunction > Decreased Gluteus Maximus Activation Following Hip Joint Effusion – Presence of Arthrogenic Muscle Inhibition?

Decreased Gluteus Maximus Activation Following Hip Joint Effusion – Presence of Arthrogenic Muscle Inhibition?


Freeman S, Mascia A, McGill S.  Arthrogenic neuromusculature inhibition: A foundational investigation of existence in the hip joint.  Clinical Biomechanics 2012 Dec 20. pii: S0268-0033(12)00271-9. doi: 10.1016/j.clinbiomech.2012.11.014. [Epub ahead of print]


What issue was addressed in the study, and why?

Arthrogenic muscle inhibition (AMI) is a reflexive inhibition of musculature surrounding a joint due to pain and/or joint effusion.  AMI results in reduced voluntary muscle activation and ultimately decreases in muscle force output.  AMI has been repeatedly shown to occur in the quadriceps muscles following knee joint injury or effusion.  It is possible that other joints and muscles may also experience AMI, similar to the knee joint and quadriceps muscles.

The gluteus maximus is theorized to be weakened and inhibited in those with lower extremity injury.   However, the neurophysiologic mechanism for this is not yet understood.  It is possible that the gluteus maximus may experience AMI in the presence of hip joint injury or effusion; however, this has not been previously investigated.  Therefore, the purpose of this study was to examine the effects of simulated hip joint effusion on voluntary gluteus maximus muscle activation.  It was theorized that the presence of hip joint effusion would cause facilitate AMI of the gluteus maximus, thereby result in decreased voluntary gluteus maximus muscle activation.

Who were the participants in the study?

A control (9 healthy participants) and intervention (12 participants who complained of hip pain and dysfunction and demonstrated findings of hip labral pathology during physical examination) group of participants were utilized in the study.

What did the researchers do for this study?

Surface EMG electrodes were attached to the gluteus maximus muscle of all subjects to measure the activation amplitude during 4 different exercises: 1) supine pelvic bridge, 2) prone hip extension, 3) active straight leg raise, 4) active hip abduction.

Both intervention and control groups were tested pre-intervention and post-intervention.  The intervention group subjects had a sterile saline solution injected into their pathologic hip joint until the point of near full capsular distension.  The control group subjects rested between test sessions and did not receive an injection.

What new information was learned from this study?

The intervention group demonstrated significantly decreased gluteus maximus activation during the supine pelvic bridge and prone hip extension exercises.  There were no such changes during the active straight leg raise and active hip abduction exercises for the intervention group.  No changes were observed in the control group between pre- and post-intervention measures of gluteus maximus activation.

Decreases in gluteus maximus activation of intervention group subjects was isolated to the side of the injection/joint effusion as there were no changes in contralateral gluteus maximus activation.  Thus, these findings indicate that voluntary activation of the gluteus maximus muscle is decreased following hip joint effusion.

What are the clinical applications of this study?

These findings extend previous research demonstrating the presence of AMI in the quadriceps muscle group following knee joint effusion and suggest a similar phenomenon occurs at the hip joint.  Decreased gluteus maximus activation following hip joint effusion may result reduced force output/strength, which may alter normal lower extremity biomechanics.  Interventions aimed to reduce AMI of the gluteus maximus following hip joint injury/effusion may be required to fully restore normal gluteal muscle function.  Research has not investigated specific interventions to combat AMI of the gluteus maximus; however, research investigating quadriceps AMI suggests that the following are important components and may be considered for treatment of gluteus maximus AMI:

  • Pain and effusion control (cryotherapy)
  • TENS (transcutaneous electrical stimulation) to stimulate spinal reflexive pathways
  • NMES (neuromuscular electrical stimulation) to stimulate inhibited muscles
  • TMS (transcranial magetic stimulation) to increase cortical motor excitability

What are the limitations of the study, and what areas should be considered for future research?

Only voluntary activation of the gluteus maximus was quantified.   Previous research investigating AMI of the quadriceps utilized electrical stimulation to examine the H-reflex, which is analogous to the spinal stretch reflex.  Thus, while AMI of the gluteus maximus appears to occur following hip joint effusion, the specific neural pathways by which AMI results cannot be determined through this study.  Future research examining the specific neural pathways and mechanisms for gluteus maximus AMI post joint effusion is needed to better establish effective therapeutic interventions.

Research is needed to identify targeted interventions to combat gluteus maximus AMI.  In addition, it is important that these interventions be part of an integrated rehabilitation strategy to restore neuromuscular control and movement efficiency once gluteus maximus activation deficits have been restored.

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