Resting electroencephalograph (EEG) asymmetry is a biological marker of the propensity to respond affectively to, and a measure of change in affect associated with, acute aerobic exercise. This study examined the EEG-affect-exercise relationship. Twenty participants performed each of three randomly assigned 30-min conditions: (a) a nonexercise control, (b) a cycling exercise at 55% VO2max, and (c) a cycling exercise at 70% VO2max. EEG and affect were assessed pre- and 0, 5, 10, 20, and 30 min postcondition. No significant results were seen in the control or 55% conditions. In the 70% exercise condition, greater relative left frontal activation preexercise predicted increased positive affect and reduced state anxiety postexercise. Participants (n = 7) with extreme relative left frontal activation postexercise reported concomitant decreases in anxiety, whereas participants (n = 7) with extreme relative right frontal activation postexercise reported increases in anxiety. These findings (a) replicate prior work, (b) suggest a dose-response intensity effect, and (c) support the idea that exercise is an emotion-eliciting event. Affective responses seem to be mediated in part by differential resting levels of activation in the anterior brain regions. Ongoing anterior brain activation reflected concurrent postexercise affect.

Although proposed as an explanation for increases in positive and decreases in negative affect, little evidence supports the notion of a stronger efficacy‐affect relationship as acute aerobic exercise intensity increases. Relationships between self‐efficacy (SE), positive affect (PA), and negative affect (NA) were examined with respect to 3 randomly assigned conditions: (a) no exercise (control), (b) cycling at 55% VO2max, and (c) cycling at 70% VO2max. Twenty subjects (age = 22.6 years; M VO2max= 47.8 ml · kg−1· min−1) participated in each. Preexercise SE predicted in‐task NA and postexercise PA in the 55% condition and postexercise PA in the 70% condition (ps < .05). Although SE significantly increased from pre‐ to postexercise, in‐task affect failed to predict these increases in SE. These data suggest that in a fit college‐aged population, a stronger reciprocal relationship between preexercise SE, in‐task affect, and postexercise SE does not exist with increasing levels of exercise intensity. Contrary to self‐efficacy theory, no evidence was found for a reciprocal relationship. However, the relationship between efficacy and affect was such that when collapsed across conditions and time, subjects with higher SE scores reported lower NA (p < .05).

Until new forms of drug combinations are made available, the use of dual-therapy containing a LABA and ICS remain as the most logical and appropriate approach for the treatment of patients suffering from severe and very severe COPD with repeated exacerbations.

To reveal contributions of different subdivisions of the lateral geniculate nucleus (LGN) to visuomotor behavior, segments of either layer A or the C layers were inactivated with microinjections of gamma-aminobutyric acid while cats made saccades to retinally stabilized spots of light placed either in affected regions of visual space or mirror-symmetric locations in the opposite hemifield. Inactivating layer A reduced the success rate for saccades to targets presented in affected locations from 82.4 to 26.8% while having no effect on saccades to the control hemifield. Saccades to affected sites had reduced accuracy and longer initiation latency and tended to be hypometric. In contrast, inactivating C layers did not affect performance. Data from all conditions fell along the same saccade velocity/amplitude function ("main sequence"), suggesting that LGN inactivations cause localization deficits, but do not interfere with saccade dynamics. Cerebral cortex is the only target of the A layers, so behavioral decrements caused by inactivating layer A must be related to changes in cortical activity. Inactivating layer A substantially reduces the activity of large subsets of corticotectal cells in areas 17 and 18, whereas few corticotectal cells depend on C layers for visually driven activity. The parallels between these behavioral and electrophysiological data along with the central role of the superior colliculus in saccadic eye movements suggests that the corticotectal pathway is involved in both deficits and remaining capacities resulting from blockade of layer A.

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