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Micah Zuhl

Researcher at RMIT University

Publications -  54
Citations -  1039

Micah Zuhl is an academic researcher from RMIT University. The author has contributed to research in topics: Medicine & Aerobic exercise. The author has an hindex of 11, co-authored 44 publications receiving 707 citations. Previous affiliations of Micah Zuhl include Central Michigan University & University of New Mexico.

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Intestinal epithelial barrier function and tight junction proteins with heat and exercise.

TL;DR: The effects of exertional or nonexertional (passive hyperthermia) heat stress on tight junction barrier function in in vitro and in vivo models and changes in tight junction proteins in response to exercise or hyperthermic conditions are reviewed.
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Regulatory Coordination between Two Major Intracellular Homeostatic Systems HEAT SHOCK RESPONSE AND AUTOPHAGY

TL;DR: It is found for the first time that heat shock response controls autophagy thus connecting and coordinating the two extreme ends of the homeostatic systems in the eukaryotic cell.
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Exercise regulation of intestinal tight junction proteins

TL;DR: The function and physiology of tight junction regulation is explained, the effects of prolonged and high-intensity exercise on tight junction permeability leading to gastrointestinal distress are discussed and agents that may increase or decrease tight junction integrity during exercise are reviewed.
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Effects of oral glutamine supplementation on exercise-induced gastrointestinal permeability and tight junction protein expression.

TL;DR: GLN supplementation prevented exercise-induced permeability, possibly through HSF-1 activation and prevented the proinflammatory response, and occludin expression were measured.
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The effects of acute oral glutamine supplementation on exercise-induced gastrointestinal permeability and heat shock protein expression in peripheral blood mononuclear cells

TL;DR: An acute dose of oral glutamine prior to exercise reduces intestinal permeability along with activation of the heat shock response leading to inhibition of pro-inflammatory markers and suppresses NF-κB activation in peripheral blood mononuclear cells.