The Effects of Anticipatory Stress on Analgesia and Cortisol Concentrations in Competitive Athletes

This study explored the effects that anticipatory stress before athletic competition may have on human pain perception. Soccer and basketball players were tested for pain thresholds, salivary cortisol concentrations, as well as general arousal before games, practices, as well as a non-exercise baseline session. An analgesic response was demonstrated before practices and games as compared to baseline sessions, however no significant difference was found between the practice and game sessions themselves. In soccer players, cortisol was found to be significantly higher before games as compared to either of the other two sessions. It is proposed that analgesic responses to practices and games may still be due to a stress response. Additionally, confounding factors are discussed such as ambient temperature during testing and the success of the team being tested. Recommendations for future research are also made. Overview Pain, while an unpleasant experience, plays a tremendous role in an organism’s survival. The perception of noxious stimuli is the mechanism by which humans and other organisms are able to prevent tissue damage and other harm. Such stimuli are transmitted via the peripheral and central nervous systems in a process known as nociception. Pain is the body’s signal that something is wrong, and that responsive action should be taken. As a result of pain’s important role in survival, researchers have attempted to understand both the mechanisms of noxious signal transmission as well as behaviors associated with the perception of pain. Hundreds of years ago, Descartes postulated that a pain signal was carried via a channel from the noxious stimulus to the brain (Gatchel, 1999). Beliefs regarding both noxious and innocuous stimuli transmission continued Descartes’ initial idea that a signal is carried from the stimulus itself to our brain. Throughout the 20 century, research focused on Von Frey’s specificity theory of pain, in which specific receptors were believed to be specialized for noxious stimuli (Gatchel, 1999). A reductionist view of pain systems was prominent and pain was still understood, not too unlike Descartes’ postulation, as a tangible signal traveling via nerves from the skin to the brain. Only recently has the transition begun to incorporate a biopsychosocial model of pain (Gatchel, 1999). The notion that the outside environment, including external stressors, can affect nociception has begun to be studied intensely within the past 30 years. This biopsychosocial model acknowledges that while the neurological pathways involved in nociception can be modified by the external environment, pain itself is still a perceptual experience constructed from this nociceptive signal. Accordingly, treatment of pain has also begun to follow this same model (Gatchel, 1999). However, the study of pain and the environmental influences on the sensation is not complete. This study expected to explore how stress, as an environmental stimulus, can affect human pain sensation. Specifically, the current study examined the phenomenon of stress-induced analgesia in competitive athletes immediately before athletic competition. The phenomenon of stress-induced analgesia has been studied extensively in both animals and humans. This topic will be discussed in depth throughout the paper. The current study also measured a cortisol response to confirm that participants were experiencing anticipatory stress before competition. The relationships between stress hormone pathways and analgesia will also be discussed. However, in order to understand fully the phenomena under study, information on the pain pathways themselves must be supplied. In order to do so, the paper will describe the neural pain pathways in both the peripheral and central nervous system. Subsequently, the suspected mechanisms for the modulation of nociception will also be described. Finally, the progression of research that led to the current study will be outlined preceding the description of the current study itself. Background While noxious stimuli can arise from within the body due to injury or illness, the current study focused on noxious stimuli applied to the skin. Innervated by an array of sensory neurons, the skin surface provides a logical starting point for the discussion of pathways involved in nociception. Stimuli to the skin is conveyed to the appropriate brain locations via the peripheral nervous system, which transmits information to the spinal cord. In order to understand fully the process by which nociception information is conveyed, the systems by which it travels must be explained. Comprising the peripheral nociceptive system are three principle fiber types. Together, these fibers make up the nerves that travel throughout the body, providing sensation from the skin surface. The three types of fiber are the Aβ-fiber, the Aδ-fiber, and the C-fiber. Between the three of them, the Aβ-fiber is a larger diameter, myelinated neuron fiber. The Aδ-fiber, while still myelinated, is much thinner in diameter. Finally, the C-fibers are both thin as well as unmyelinated. Due to the differences in diameter and thickness, the conduction speeds along these fibers vary greatly. The myelination and large diameter of the Aβ-fiber allows it to conduct the most rapidly of the three. The other two fiber types conduct much slower because of their thinner diameters. Aδ-fibers conduct at a rate between 5-30m/s while the unmyelinated C-fibers transmit at less than 1m/s (Basbaum & Jessell, 2000). Differentiating the three fibers is their respective roles in nociception. Due to their high firing rate, Aβ-fibers are suitable for fine touch sensation in which minor changes in the texture of a stimulus can be detected as it moves over the skin. For this reason, Aβ-fibers are primarily non-nociceptive and do not respond differentially to noxious stimuli (Fields, 1987). Conversely, in studies which measure potentials along the axons of afferent sensory fibers, both Aδand C-fibers are shown to respond maximally to noxious stimuli (Fields, 1987). Such fibers that respond to noxious stimuli are called “nociceptors. ” Noxious stimuli fall into three distinct categories. Mechanical stimuli are those in which pressure is applied to the innervated tissue itself. Additionally, thermal stimuli involve a change in temperature around the fiber. Finally, chemical stimuli are chemicals (endogenous and exogenous) that are able to initiate an action potential in the peripheral nervous system fibers. All three types of stimuli can be either noxious or innocuous. Concerning thermal stimuli, which are used to assess pain in the current study, nociceptors begin to respond once the temperature around the fibers exceeds a certain threshold. For nociceptors, this temperature is usually around 45°-47° C (Fields, 1987) or below 5°C (Basbaum & Jessell, 2000). While it is important to remember that pain is a conscious perceptual experience and nociception is the stimulation of nociceptive fibers, a positive relationship has been demonstrated between the firing of Aδ-fibers and a reported sensation of pain in human subjects (Fields, 1987). Therefore, pain behaviors in response to noxious stimuli can be used to study the activity in these nociceptive fibers. Signaling in each of the two types of nociceptors is suspected to elicit differing sensations of pain in humans. Studies have approached this phenomenon by selectively blocking transmission in either Aδ-fibers or C-fibers when a noxious stimulus is applied. Aδ-fiber transmission can be disrupted with sufficient compression to the fiber itself (Fields, 1987). Meanwhile, C-fibers are particularly sensitive to the action of local anesthetics (Fields, 1987). Being able to block individual fibers selectively allows researchers to examine the pain sensation associated with transmission along each fiber. First, after using compression to block signaling in Aδ-fibers, researchers can apply a noxious thermal stimulus. Reports of the subject’s sensation are then acquired. Subject reports indicate the initial sharp pain associated with intense thermal stimulus is gone, but remaining is the duller, burning sensation that follows the initial burst of pain (Price et al., 1977). Conversely, when C-fibers are selectively blocked by small amounts of local anesthetic, the dull burning pain is eliminated, but remaining is the initial spike in pain sensation (Campbell & LaMotte, 1983). These results correspond nicely with what has been established about the transmission rates of the two nociceptors. Due to their myelination, Aδ-fibers have a faster rate of transmission than the unmyelinated C-fibers. This difference in speed allows the Aδ-fibers to transmit the first sensations of pain, while the C-fibers’ slower rate contributes to the longer, duller sensation of pain that is stretched over time (Fields, 1987). It is important to remember that noxious stimuli are usually accompanied by nonnociceptive sensations from Aβ-fibers as well. A painfully hot element applied to the skin is also accompanied by an innocuous pressure sensation. In studies that test responses to these stimuli, experimenters must remember that nociceptors are not activated explicitly. Often, noxious stimuli impinge upon the peripheral fibers of the nervous system repeatedly within a short amount of time. Additionally, studies which examine pain behavior often apply multiple stimuli in order to obtain averages over time. A process referred to as sensitization is the nervous system response to multiple noxious stimuli within a short amount of time. Sensitization refers to nociceptors becoming more sensitive to a noxious stimulus after repeated exposure (Fields, 1987). This is observed in both the myelinated and unmyelinated nociceptors. For example, after repeated exposure to a noxious thermal stimulus, nociceptors fire more vigorously with additional exposures. Furthermore, less extreme temperatur