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Kinesiology and Community Health :: University of Illinois at Urbana-Champaign

The Department of Kinesiology and Community Health
College of Applied Health Sciences

Research Article

Regional Brain Activation as a Biological Marker of Affective Responsivity to Acute Exercise: Influence of Fitness

E.E. Hall, P. Ekkekakis, & S.J. Petruzzello, University of Illinois, Urbana, IL 61801

Asymmetrical regional brain activation has been shown to be a biological marker of the predisposition to respond affectively to aerobic exercise. Unknown is the extent to which fitness may influence this relationship. Regional brain activation (via EEG: F3, F4, P3, P4; referenced to linked-ears) was assessed before treadmill running (30 min@75% VO2max) in 67 subjects (37 males, 30 females; 21.4 ± 2.9 yrs). Aerobic fitness was determined from a graded treadmill exercise test. Affect was assessed before and 0, 10, 20, and 30 min post-exercise via Spielberger's 10-item State Anxiety Inventory (SA; Form Y-1) and Thayer's ADACL, which yields measures of Energetic Arousal (EA) and Tense Arousal (TA). Hierarchical regression analyses revealed that, after partialling out pre-exercise EA, resting frontal asymmetry accounted for 7% unique variance in EA (Beta =.26, P=0.0066) at 10-min, 11% (Beta =.34, P=0.0006) at 20-min, and 7% (Beta =.26, P=0.0037) at 30-min post-exercise. In the high fit group (n = 33), frontal asymmetry accounted for 17% unique variance in EA (Beta =.41, P=0.0006) at 10-min, 23% (Beta =.48, P=0.0002) at 20-min, and 16% (Beta =.40, P=0.0007) at 30-min post-exercise. In the low fit group (n = 34), frontal asymmetry did not account for any unique variance in EA. Neither frontal nor parietal EEG accounted for any unique variance in SA or TA for either group. Thus, relatively greater left frontal activation predicted post-exercise increases in EA and this relationship was influenced by level of aerobic fitness. These findings replicate previous exercise-EEG research and support the idea that affective responses to exercise are mediated, in part, by differential levels of activation in the anterior portions of the brain.

Supported by NIMH RO3 MH55513-01.


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