TY - JOUR
T1 - Dynamics of pleasure–displeasure at the limit of exercise tolerance
T2 - Conceptualizing the sense of exertional physical fatigue as an affective response
AU - Hartman, Mark E.
AU - Ekkekakis, Panteleimon
AU - Dicks, Nathan D.
AU - Pettitt, Robert W.
N1 - Publisher Copyright:
© 2019. Published by The Company of Biologists Ltd.
PY - 2019/2
Y1 - 2019/2
N2 - The search for variables involved in the regulation and termination of exercise performance has led to integrative models that attribute a central role to the brain and utilize an array of psychological terms (e.g. sensation, perception, discomfort, tolerance). We propose that theorizing about exercise regulation would benefit from establishing cross-disciplinary bridges to research fields, such as affective psychology and neuroscience, in which changes along the dimension of pleasure–displeasure are considered the main channel via which homeostatic perturbations enter consciousness and dictate corrective action (slowing down or stopping). We hypothesized that ratings of pleasure–displeasure would respond to the severity of homeostatic perturbation and would be related to time to exhaustion during exercise performed at an unsustainable intensity. In a within-subjects experiment (N=15, 13 men and 2 women, age 23.4±2.2 years; maximal oxygen uptake 46.0 ±8.0 ml kg −1 min− 1 ), we compared the slope of ratings of pleasure–displeasure (acquired every 1 min) during cycling exercise at a power output 10% above critical power until volitional termination under glycogen-loaded and glycogen-depleted conditions. As hypothesized, ratings of pleasure–displeasure declined more steeply under glycogen depletion (P=0.009, d=0.70) and correlated closely with time to exhaustion under both glycogen-loaded (r=0.85; P<0.001) and glycogen-depleted conditions (r=0.83; P<0.001). We conclude that in exercise, as in other domains, changes in pleasure–displeasure may be the main channel via which homeostatic perturbations enter consciousness. This proposal may have important implications for conceptualizing and identifying the neurobiological mechanisms of the sense of exertional physical fatigue.
AB - The search for variables involved in the regulation and termination of exercise performance has led to integrative models that attribute a central role to the brain and utilize an array of psychological terms (e.g. sensation, perception, discomfort, tolerance). We propose that theorizing about exercise regulation would benefit from establishing cross-disciplinary bridges to research fields, such as affective psychology and neuroscience, in which changes along the dimension of pleasure–displeasure are considered the main channel via which homeostatic perturbations enter consciousness and dictate corrective action (slowing down or stopping). We hypothesized that ratings of pleasure–displeasure would respond to the severity of homeostatic perturbation and would be related to time to exhaustion during exercise performed at an unsustainable intensity. In a within-subjects experiment (N=15, 13 men and 2 women, age 23.4±2.2 years; maximal oxygen uptake 46.0 ±8.0 ml kg −1 min− 1 ), we compared the slope of ratings of pleasure–displeasure (acquired every 1 min) during cycling exercise at a power output 10% above critical power until volitional termination under glycogen-loaded and glycogen-depleted conditions. As hypothesized, ratings of pleasure–displeasure declined more steeply under glycogen depletion (P=0.009, d=0.70) and correlated closely with time to exhaustion under both glycogen-loaded (r=0.85; P<0.001) and glycogen-depleted conditions (r=0.83; P<0.001). We conclude that in exercise, as in other domains, changes in pleasure–displeasure may be the main channel via which homeostatic perturbations enter consciousness. This proposal may have important implications for conceptualizing and identifying the neurobiological mechanisms of the sense of exertional physical fatigue.
KW - Homeostasis
KW - Oxygen uptake kinetics
KW - Perceived exertion
KW - Slow component
UR - http://www.scopus.com/inward/record.url?scp=85061032578&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85061032578&partnerID=8YFLogxK
U2 - 10.1242/jeb.186585
DO - 10.1242/jeb.186585
M3 - Article
C2 - 30559299
AN - SCOPUS:85061032578
SN - 0022-0949
VL - 222
JO - Journal of Experimental Biology
JF - Journal of Experimental Biology
IS - 3
M1 - jeb186585
ER -