by Angela Spontelli Gisselman PT, DPT, OCS

PhD candidate in Physiotherapy

Centre for Health, Activity, and Rehabilitation Research, School of Physiotherapy
University of Otago

Twitter: @ASGPhysio

Email: Angela.Gisselman@postgrad.otago.ac.nz

Who, what & why?

As an orthopaedic physiotherapist, I am intrigued by the puzzle of musculoskeletal overuse injuries. Unlike an acute injury, which is associated with a defined injury event, the progression of an overuse injury is often unpredictable and challenging to rehabilitate, let alone prevent. As you may have experienced when faced with an overuse injury, pain is not a reliable measure of the degree to which your overused tendon or muscle has healed. And, indeed, studies exploring the root causes of painful versus non-painful tendon overuse injuries have demonstrated that an overuse injury is often well-developed before the onset of pain [1, 2].

Mechanical loading of a muscle, tendon or bone is central to the health of these tissues as it promotes a process of tissue breakdown and repair. When you load your body through aerobic or strength training, a series of inflammatory events occur within the tissue under stress which, under “optimal” conditions and loading, are part of the healthy balance between tissue breakdown and repair. Alternatively, in conditions when the amount of loading is no longer “optimal”, excessive tissue breakdown occurs, setting off an abnormal biological response which can result in degenerative changes of the tissue. We don’t know why this system shifts from one of healthy breakdown and repair to that of unhealthy degeneration but, we are slowly uncovering how the autonomic nervous system (ANS) may contribute to this scene[3, 4].

The ANS is one of the primary systems responsible for maintaining our body’s homeostasis in the presence of stressful stimuli. At the level of our muscle, this system is also involved in processes responsible for tissue breakdown and repair. If we had the ability to understand the status of the ANS in the presence of an accumulating injury, might we be able to establish a more accurate picture as to how our tissue (i.e.: muscle, bone) is responding to loading?  Herein lies the question at the center of my research: can we monitor and interpret changes of the ANS, via HRV, in response to accumulating injury?

What did we do?

After a review of the HRV and overuse injury literature, we noted a number of studies which investigated HRV patterns in response to training load or overtraining, but we found no studies which explored the relationship between HRV monitoring and development of an overuse injury. Therefore, in our article we[5]:

1. Identified the gaps in our current methods of overuse injury prevention
2. Provided an overview of the role of ANS activity in tissue healing
3. Summarized the biological link between ANS activity and HRV
4. Proposed how modulations in HRV may be able to indicate signs of tissue overload prior to the onset of perceived pain
5. Highlighted two overuse injury risk factors and hypothesized how HRV monitoring may allow us to modulate the influence of these factors on injury development

What’s next?

Many unanswered questions remain in our understanding of how and why overuse injuries occur. The purpose of our hypothesis was: to highlight important but as yet unmonitored physiological mechanisms influencing overuse injury development; and, to present a theory as to how we can incorporate these mechanisms into our current injury screening methods. We acknowledge that HRV alone will not fill the gaps in overuse injury prevention research, but we believe it is an area well-worth investigating. We are currently developing our protocol for an upcoming study which will explore the relationship between injury incidence, fatigue, training load and HRV in a cohort of team sport athletes – stay tuned!

When I’ve presented this hypothesis to different audiences, the most common criticism I face points to the nature of HRV in that it can be modulated by a multitude of external factors (i.e.: sleep quality, nutrition, psychological stress) in addition to those changes that may be attributed to injury. Although this is a valid point, I view this specific challenge of HRV as one of its most valuable assets. As illustrated in Simon’s February blog post, HRV has the ability to paint a comprehensive picture of one’s overall health. Because HRV reflects other factors which influence how our body responds to biological and psychological loading, I believe this index has the potential to contribute to our understanding of how ANS homeostasis influence’s one’s risk of developing overuse injury.

In physiotherapy school, we were frequently reminded to, “treat the patient, not the injury”. If we, as clinicians, seek to treat the patient as a whole and not just the site of injury, we need to gain an improved appreciation and understanding of whole body systems, such as the ANS, and their role in the body’s response to physiological loading.

References

1. Littlewood, C., et al., The central nervous system – An additional consideration in ‘rotator cuff tendinopathy’ and a potential basis for understanding response to loaded therapeutic exercise. Manual Therapy, 2013. 18(6): p. 468-472.
2. Rio, E., et al., The Pain of Tendinopathy: Physiological or Pathophysiological? Sports Medicine, 2014. 44(1): p. 9-23.
3. Ackermann, P.W., et al., Neuronal pathways in tendon healing and tendinopathy–update. Front Biosci (Landmark Ed), 2014. 19: p. 1251-78.
4. Dean, B., S. Franklin, and A. Carr, The Peripheral Neuronal Phenotype is Important in the Pathogenesis of Painful Human Tendinopathy: A Systematic Review. Clinical Orthopaedics and Related Research®, 2013. 471(9): p. 3036-3046.
5. Gisselman, A.S., et al., Musculoskeletal overuse injuries and heart rate variability: Is there a link? Medical Hypotheses, 2016. 87: p. 1-7.