Food-related inhibitory control, the ability to withhold a dominant response towards highly palatable foods, influences dietary decisions. Food-related inhibitory control abilities may increase following a bout of aerobic exercise; however, the impact of exercise intensity on both food-related inhibitory control and broader cognitive control processes is currently unclear. We used a high-powered, within-subjects, crossover design to test how relative intensity of aerobic exercise influenced behavioral (response time, accuracy) and neural (N2 and P3 components of the scalp-recorded event-related potential [ERP]) measures of food-related inhibitory and cognitive control. Two hundred and thirteen participants completed three separate conditions separated by approximately one week in randomized order: two exercise conditions (35% [moderate] or 70% [vigorous] of VO2max) and seated rest. Directly following exercise or rest, participants completed a food-based go/no-go task and a flanker task while electroencephalogram data were recorded. Linear mixed models showed generally faster response times (RT) and improved accuracy following vigorous exercise compared to rest, but not moderate-intensity exercise; RTs and accuracy did not differ between moderate intensity exercise and rest conditions. N2 and P3 amplitudes were larger following vigorous exercise for the food-based go/no-go task compared to rest and moderate intensity exercise. There were no differences between exercise conditions for N2 amplitude during the flanker task; however, P3 amplitude was more positive following vigorous compared to rest, but not moderate exercise. Gender did not moderate exercise outcomes. Results suggest improved and more efficient food- related recruitment of later inhibitory control and cognitive control processes following vigorous exercise.
Objective:
Extremity compartment syndrome (ECS) is a morbid condition resulting in permanent myoneural damage. Currently, the diagnosis of compartment syndrome relies on clinical symptoms and/or intracompartment pressure measurements, both of which are poor predictors of ECS. Animal models have been used to better define cellular mechanisms, diagnosis, and treatment of ECS. However, no standardized model exists. The purpose of this study was to identify existing animal research on extremity compartment syndrome to summarize the current state of the literature and to identify weaknesses that could be improved with additional research.
Methods:
A MEDLINE database search and reverse inclusion protocol were utilized. We included all animal models of ECS.
Results:
Forty-one studies were included. Dogs were the most commonly used model species, followed by pigs and rats. Most studies sought to better define the pathophysiology of compartment syndrome. Other studies evaluated experimental diagnostic modalities or potential treatments. The most common compartment syndrome model was intracompartment infusion, followed by tourniquet and intracompartment balloon models. Few models incorporated additional soft tissue or osseous injury. Only 65.9% of the reviewed studies confirmed that their model created myoneural injury similar to extremity compartment syndrome.
Conclusions:
Study purpose, methodology, and outcome measures varied widely across included studies. A standardized definition for animal compartment syndrome would direct more consistent research in this field. Few animal models have investigated the pathophysiologic relationship between traumatic injury and the development of compartment syndrome. A validated, clinically relevant animal model of extremity compartment syndrome would spur improvement in diagnosis and therapeutic interventions.
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