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Examine how exercise could alter pain

This is an excerpt from Exercise Psychology 2nd Edition eBook by Janet Buckworth,Rod K. Dishman,Patrick J. O'Connor & Phillip D. Tomporowski.

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Nociceptors and Sensory Afferents

This section addresses the neurology underlying muscle pain because exercise requires the activation of skeletal muscles, and exercise training most consistently improves medical conditions that involve skeletal muscle pain. Mechanical pressure and algesic biochemicals are the primary causes of skeletal muscle pain.

Nociceptors are a subset of sensory receptors in muscle that respond to noxious stimuli. They usually are small-diameter unmyelinated (known as either type IV or C fibers) or lightly meylinated (type III or A-?) fibers. The majority of muscle nociceptors are type IV. High-intensity mechanical pressure, such as a 250-pound (113.4 kg) American football linebacker running at full speed into the thigh of a running back, activates type III and IV high-threshold mechanosensitive (HTM) receptors. About 60% of high-threshold mechanosensitive receptors respond to noxious pressure. Some of these nociceptors appear to be activated by high-intensity exercise, which creates high intramuscular pressure (Cook et al. 1997).

Chemicals sensitize and activate type IV polymodal nociceptors. Polymodal nociceptors respond to painfully hot and cold temperatures as well as a host of chemical stimuli that activate the nociceptive afferents. These chemical stimuli include adenosine, adenosine triphosphate (ATP), bradykinin, capsaicin, glutamate, histamine, hydrogen ions (H+), interleukins, leukotrienes, nerve growth factor, nitric oxide, prostaglandins, serotonin, and substance P (Mense 2009). These algesic (pain-producing) chemicals usually act on receptors on the surface of nerve cells. This can cause ion channels to open, allowing negative cations, such as sodium (Na+) and potassium (K+), to move into the cell and increase the activity of the nociceptive afferent. Muscle damage and inflammation and ischemia of either cardiac or skeletal muscle during moderate- to high-intensity exercise cause these substances to increase in concentration within the muscle. Based on experimental manipulations of individual algesics, the most important chemical stimulants of skeletal and cardiac muscle pain appear to be the increase in H+, bradykinin, and the actions of ATP or one of its by-products, adenosine (Birdsong et al. 2010; Mense 2009).

In the real world, these chemical stimulants act together. Exceptions can occur for those with genetic abnormalities. For example, people with McArdle’s syndrome have a gene mutation that causes a deficiency in a muscle enzyme called myophosphorylase, which prevents them from using muscle glycogen during exercise. One consequence of the mutation is that these people have no increase in lactate during exercise. If lactate were a cause of muscle pain during exercise, then these patients should have less pain. These patients, however, are characterized by intense muscle pain that can last for several hours after exercise (Paterson et al. 1990). Clearly, and in contrast to popular belief, lactate is not a cause of muscle pain during

Other chemicals inhibit type IV nociceptors. Endogenous opioids and cannabinoids, for example, bind to nociceptive afferents and inhibit their activity. Endogenous opioids (endorphins, enkephalins, dynorphins, and endomorphins) are peptides that have biochemical properties similar to those of exogenous opiates such as heroin and morphine. Endocannabinoids (anandamide, 2-arachidonoylglycerol) are lipids that bind to the same receptors as the active ingredient in marijuana. Moderate- to high-intensity exercise clearly increases endogenous opioid and cannabinoid levels in the periphery, where they can act to inhibit nociceptive afferent activity (Dishman and O’Connor 2009; Sparling et al. 2003).

Spinal Processing

Nociceptive afferents synapse primarily in the dorsal horn of the spinal cord. Nociceptive information is conveyed to the brain by projection neurons that make up several major tracts including the spinothalamic, spinoreticular, and spinomesencephalic tracts. The spinothalamic tract conveys information to numerous brain areas including the reticular formation, periaqueductal gray, hypothalamus, amygdala, and ventral and lateral thalamus—synapsing on cells whose axons project to numerous higher brain regions including the insular and somatosensory cortexes. The spinoreticular tract neurons project to the reticular formation at the levels of the medulla and pons before synapsing in the medial thalamus. Ultimately, neurons in this pathways synapse on key brain areas that are involved in responding to an injury including the locus coeruleus. The spinomesencephalic tract projects to numerous brain areas, and of special note are inputs to the periaqueductal gray. Cell bodies in the periaqueductal gray have axons that project to several limbic system structures including the amygdala and anterior cingulate cortex. Perhaps the key point is that because nociceptive information is critically important, it is conveyed by multiple parallel ascending pathways to a host of subcortical and cortical brain areas that coordinate an effective behavioral response (Price 2000).

Central Nervous System Processing

Within the brain, pain is processed in a widespread network of neurons. This network has many interconnections with diverse brain areas. These brain areas allow for a coordinated response to the threat presented by the noxious stimuli. For example, information is conveyed to brain areas involved in processes such as the following:

  • Orientation, arousal, fear, and vigilance (examples of brain regions known to be involved in these processes include the reticular formation, locus coeruleus, periaqueductal gray, hypothalamus, and amygdala).
  • Coding the intensity of the pain (e.g., primary and secondary somatosensory cortexes [SI, SII]; activity in these regions measured by fMRI is highly correlated to pain intensity ratings (Coghill et al.
  • Attending to the pain (e.g., anterior cingulate cortex, orbitofrontal cortex; Bantick et al. 2002).
  • The cognitive evaluation of the pain (e.g., prefrontal, parietal, and insular cortexes; Kong et al. 2006).
  • Establishing a memory of the pain (e.g., hippocampus; Khanna and Sinclair 1989).
  • Generating useful affective and behavioral responses to the pain (e.g., anterior cingulate, hypothalamus, amygdala, and insula; Price 2000). For example, the facial expression of pain unpleasantness can motivate helping behavior from

Pain Modulation

Pain can be modulated by nerve activity within the spinal cord. The activity of the projection neurons carrying nociceptive information from the spinal cord to the brain can be increased or decreased by neurons that synapse on the projection neurons.

Sensory afferents from the dermatome that is carrying non-nociceptive information converge on the dorsal horn, synapse on the projection neurons or small interneurons that synapse on projection neurons, and can modulate the activity of projection neurons. These non-nociceptive afferents are larger and faster than nociceptive afferents and carry information about light pressure, vibration, warmth, coldness, muscle stretch, and muscle force. This neuroanatomy forms the basis for treatments that reduce pain by increasing the activity of non-nociceptive afferents such as the use of transcutaneous electrical nerve stimulation to treat chronic musculoskeletal pain (Johnson and Martinson 2007).

During exercise, the increased activation of sensory afferent receptors detecting non-noxious pressure, muscle stretch, and muscle force could modify muscle pain intensity. For example, generating 250 watts of power while cycling at 100 rpm would produce a greater activation of muscle stretch receptors than producing the same power output while cycling at 60 rpm. Consequently, this might allow the exercise to be perceived as less painful. Why do professional cyclists ride at a cadence between 90 and 110 rpm while most recreational cyclists ride at a much slower cadence?

The activity of the projection neurons also can be modified by other neural activity within the spinal cord. Thousands of interneurons within the spinal cord synapse on projection neurons and, depending on the neurotransmitter being released, can stimulate (e.g., glutamate, substance P, nitric oxide, calcitonin gene-related peptide) or inhibit (GABA, enkephalin, endorphin, serotonin, norepinephrine) the projection neurons.

Neurons from the brain descend into the spinal cord and can reduce pain by reducing the activity of ascending nociceptive transmission. The activation of the periaqueductal gray (PAG) is a key component of the descending pain modulation system. As illustrated in figure 11.4, the PAG receives afferent inputs not only from ascending projection neurons but from the amygdala and hypothalamus and the prefrontal, frontal, insular, and somatosensory cortexes. Activation of the PAG suppresses ascending nociception through its projections to the rostral ventromedial medulla (RVM) and dorsolateral pontine tegmental (DLPT) areas. Cell bodies in the RVM and DLPT areas project their axons to the dorsal horn of the spinal cord where they inhibit ascending nociceptive transmission directly or indirectly by activating inhibitory interneurons.

The descending pain modulation system is thought to account for numerous types of analgesia, including widespread cases of athletes and soldiers who report little or no pain for several hours after a traumatic injury (Beecher 1956). Acute and chronic exercise plausibly could reduce acute and chronic pain by influencing one or more aspect of the descending pain control system. Currently there is little direct evidence that this does or does not occur.

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