The term “breathing dysfunction” is referred to quite often in physical therapy discussion groups/threads as having an influence on musculoskeletal disorders. However it’s often described in a rather nebulous and vague manner with questionable explanations for what is being observed clinically. Similarly, the mechanisms for addressing “breathing dysfunction” are also vague with questionable veracity. As someone with a particular interest in this area, I would appreciate thoughts and opinions on this topic.
Deep slow breathing (DSB) and mindfulness has been shown to improve symptoms of pain, both chronic and acute. Though autonomic responses such as increased heart rate variability and reduced skin conductance (markers of increased parasympathetic tone) have been observed following DSB, their influence on pain rating has been questionable. More recent evidence suggests that the effects of DSB are likely more due to achieving a relaxed state or distraction from the noxious stimuli. Therefore these changes in autonomic activity in following DSB are more likely a reflection of supraspinal activity due to achieving a relaxed or non-threatened state than the cause.
It has also been demonstrated that patients with LBP have demonstrated altered diaphragm position and function, increased diaphragmatic fatigue, impaired maximal inspiratory pressure (MIP or PiMax) and reductions in spinal proprioception. Acute fatigue directed at the inspiratory muscles (primarily the diaphragm) have been shown to alter postural control. Similarly, inspiratory muscle training (IMT), which primarily loads the diaphragm, has been shown to improve postural control and pain ratings in patients with LBP. IMT also has been shown to improve exercise performance; especially in patients with cardiopulmonary disease(s) or disorders. Therefore “breathing and inspiratory muscle function” ARE important and clinically relevant changes can be observed by addressing it appropriately. However, it is important that the mechanisms attributed to clinical observations and treatment effects are based on scientific evidence that accurately reflects what is most likely occurring. It is also critical that these mechanisms are fully understood by clinicians and disseminated accurately to patients.
In summary, clinicians should continue to utilize these techniques as there is decent support for their implementation clinically. However, ascribing these observed effects to inaccurate and unsubstantiated mechanisms is not recommended and neither is disseminating them to patients. A clinician’s accurate understanding of the physiological responses to a treatment is critical to providing accurate and effective education to patients. With patient education being one of the most important components of clinical practice.