Journal of Depression and Anxiety
Open Access

A Short Note on Exercise Induced Hypoalgesia (EIH)

Huang Li^{* *}Correspondence: Huang Li, Department of Nursing, University of Saskatchewan, Saskatoon, Canada, Tel: 2487236892, Email:

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Introduction

In animal models and chronic pain patients it is proven that exercise produces analgesic effects (Exercise-Induced Hypoalgesia (EIH)). But the mechanisms of EIH especially the emotional aspects of pain is still not fully understood. The mesocorticolimbic system of the brain initiates the EIH effects through two dopaminergic pathways. The amygdala is a key component of the limbic system which regulates emotions closely associated with chronic pain like fear and anxiety. Some recent studies examined the association between the Amyg and EIH effects with the help of Neuropathic Pain (NPP) model mice. Voluntary Exercise (VE) activated Glutamate (Glu) neurons in the average basal Amyg projecting to the Nucleus Accumbens (NAc) sidelong shell, while it totally stifled NPPincited enactment of GABA neurons in the focal nucleus of the Amyg (CeA). Voluntary Exercise inhibited activation of pyramidal neurons in the ventral hippocampus-CA1 region to contextual, conditioning and the retrieval of fear memory. Anxiety and fear are the main psychological factors related to pain, these factors have an important role in establishing chronic pain. Anxiety and fear of pain in the ventral hippocampus form a habit of memory which catastrophizing is common in chronic pain patients. Therefore, when the consideration of patients is confined exclusively to their aggravation, they stay away from any ways of behaving that foresee enlistment of torment, prompting an emotional decrease in active work and foundation of dormancy. Actual dormancy can bring about a several disorders, for example, degradation of skeletal muscle capacity, depression, and social withdrawal, and can deliver an endless loop that is supported by relentless torment. Chronic pain is established through a vicious cycle consisting of anxiety, fear which lead to worsening of chronic lower back pain this is the fear-avoidance of chronic pain.` All these findings make sure that effective therapies and a well-defined method help to reduces behaviors caused by pain-related fear and anxiety to reduce and relieve chronic pain. This is possible through exercise therapy. Exercise therapy helps to relive chronic pain through Exercise-Induced Hypoalgesia (EIH) in mesolimbic reward system via later dorsal tegmental nucleus and hypothalamus of brain.

Description

Defective functioning of mesocorticolimbic system in chronic pain state

Studies of human brain imaging have indicated that chronic pain is produced through plastic changes in brain ventral hippocampus regions, closely associated with the emotional aspects of pain, such as anxiety and fear. The meso cortico limbic system of the brain which consist of the Medial Prefrontal Cortex (mPFC), Amygdala (Amyg), Nucleus Accumbens (NAc), Hippocampus (HIP), and Ventral Tegmental Area (VTA), these parts play essential role in the chronification of pain on the grounds that these locales are firmly connected with mental and passionate parts of pain [1].

The mammalian mPFC is divided into the Pre-limbic cortex (PL) and the Infra Limbic cortex (IL). The mPFC is unequivocally innervated by the Amygdala and hippocampus and goes about as a hub for mental capacities, for example, working recollections and direction, notwithstanding its job as a hierarchical regulator of torment through hearty projections to the NAc, Amyg, and Periaqueductal Gray (PAG).

Noxious information that was modified by past painful experiences and mood states via the central nervous system is received into the CeA via the BLA (BLA–CeA pathway) [3].

The HIP (hippocampus) is separated into the dorsal and Ventral HIP (vHIP), which assumes significant, parts in a few mental and enthusiastic capacities, including spatial memory, learning, fear, and nervousness. The vHIP is firmly innervated by the mPFC and the BLA and sends projections to the mPFC, the BLA, and the CeA that add to the expression of fear memories and tension. Neurogenesis in the hippocampal Dentate Gyrus (DG) is known to be hindered in mouse models of NPP, an observing that might clarify the lessening in HIP volume saw in ongoing torment patients [2].

Brain contraption of EIH

Meta-analysis and experimental animal studies have exhibited that activities like running or swimming, can advance pain relieving impacts and that the capacity of activity to further develop constant torment (pain) is grounded in people and animals. It has been suggested that EIH might be the consequence of a few plastic changes in the peripheral nerves, spinal cord, and cerebrum stem following various sorts of activities. These perceptions propose that activity is a substantial intercession that is prescribed preceding pharmacological treatment to work on improving chronic pain, on the grounds that contrasted and pharmacological treatment, exercise therapy can be performed with practically no secondary effects. Also, chances to increase the degrees of individual actual work are generally introduced in day to day existence, like driving, cleaning, shopping, and family tasks. In this manner, the straightforwardness and comfort of activity treatment gives it an incredible benefit over different intercessions. This large number of occasions might be important to upgrade the actuation of the mesocorticolimbic framework and may bring about expanded inspiration to perform further VE [4].

Impedance of fear memories contributing to EIH effects

Chronic pain patients show anxiety, depression, and learning and memory shortfalls, which might be somewhat actuated by means of decay and brokenness of the HIP. Complex Regional Pain Syndrome (CRPS) patients and chronic lower back pain patients showed critical abatements in HIP volume. It has been shown that the capacity to douse context oriented contextual fear memories is altogether debilitated in NPP model mice, and that neurogenesis in the hippocampal dentate gyrus is additionally hindered in NPP model mice[3,4].

Conclusion

Therefore, appropriate exercise in chronic pain conditions can initiate the mesocorticolimbic system to set off relief from discomfort and a decrease in physical inactivity brought about by dread (fear) and tension of development prompted torment (pain). These mechanisms might alleviate chronic pain patients of "fear avoidance belief" and work with EIH impacts. The appropriate type, power, and span of exercise expected to upgrade EIH impacts have not yet been completely inspected in animal and human investigations. Moreover, the most importantly hub that is actuated by VE feeling has not yet been determined in animals and people. Accordingly, further endeavors to investigate these issues might be basic to additionally comprehend the mind components fundamental EIH impacts.

References

1. Meints SM, Edwards RR. Evaluating psychosocial contributions to chronic pain outcomes. Prog Neuropsychopharmacol Biol Psychiatry. 2018;87:168–182.

   [Cross Ref] [GoogleScholar][Indexed]

2. Lethem J, Slade PD, Troup JD, Bentley G. Outline of a Fear-Avoidance Model of exaggerated pain perception-I. Behav Res. 1983;21:401–408.

   [CrossRef][Google Scholar][Indexed]

3. Zhang Z, Gadotti VM, Chen L, Souza IA, Stemkowski PL, Zamponi GW. Role of Prelimbic GABAergic Circuits in Sensory and Emotional Aspects of Neuropathic Pain. Cell Rep. 2015;12:752–759.

   [CrossRef] [GoogleScholar][Indexed]

4. Cai YQ, Wang W, Paulucci HA, PanZZ. Brain Circuits Mediating Opposing Effects on Emotion and Pain. J Neurosci. 2018;38: 6340–6349.

   [CrossRef][GoogleScholar] [Indexed]