Difference between revisions of "Wallace 2018 FASEB J"
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|abstract=Exercise has been shown to stimulate histamine release, which mediates vasodilation in exercising tissue and is sustained post-exercise. Blockade of H<sub>1</sub> and H<sub>2</sub> receptors with antihistamine drugs attenuates this effect in skeletal muscle. Research examining the effects of exercise-related histamine action on cellular level processes is relatively sparse. There also remains limited understanding of the impacts of histamine receptor blockade on non-exercising tissue, such as the brain. To this end, 36 adult male Wistar rats (75–94 days old, 441.2 ± 39.5 g body wt) were randomly assigned to three groups: (1) given H<sub>1</sub> and H<sub>2</sub> receptor antagonists fexofenadine (7.11 mg/kg) and ranitidine (3.95 mg/kg) via oral gavage 1 hr prior to treadmill exercise (1 hr, 20 cm/s); (2) completed the exercise without drug, and (3) control. All groups received body mass-proportional oral gavage volumes (water or antihistamines). One hour post-exercise, mitochondrial function was assessed in saponin-permeabilized prefrontal cortex and dorsal hippocampus brain sub-regions. There was no effect of exercise or drug treatment on mitochondrial substrate-dependent oxygen consumption (''J''O<sub>2</sub>; high-resolution respirometry), or in mitochondrial hydrogen peroxide emission (mH<sub>2</sub>O<sub>2</sub>; fluorometric monitoring of Amplex Red oxidation) in permeabilized prefrontal cortex or the dorsal hippocampus. These results suggest negligible effects of oral H<sub>1</sub>/H<sub>2</sub> antagonists on mitochondrial metabolism in brain following exercise. This supports prior evidence suggesting the effects of H<sub>1</sub>/H<sub>2</sub> inhibition remain localized in exercising muscle. Other studies report systemic increases in histamine levels following exercise, however, which suggests further research may reveal a relationship between histamine receptor blockade and cellular processes in non-exercising tissues. | |abstract=Exercise has been shown to stimulate histamine release, which mediates vasodilation in exercising tissue and is sustained post-exercise. Blockade of H<sub>1</sub> and H<sub>2</sub> receptors with antihistamine drugs attenuates this effect in skeletal muscle. Research examining the effects of exercise-related histamine action on cellular level processes is relatively sparse. There also remains limited understanding of the impacts of histamine receptor blockade on non-exercising tissue, such as the brain. To this end, 36 adult male Wistar rats (75–94 days old, 441.2 ± 39.5 g body wt) were randomly assigned to three groups: (1) given H<sub>1</sub> and H<sub>2</sub> receptor antagonists fexofenadine (7.11 mg/kg) and ranitidine (3.95 mg/kg) via oral gavage 1 hr prior to treadmill exercise (1 hr, 20 cm/s); (2) completed the exercise without drug, and (3) control. All groups received body mass-proportional oral gavage volumes (water or antihistamines). One hour post-exercise, mitochondrial function was assessed in saponin-permeabilized prefrontal cortex and dorsal hippocampus brain sub-regions. There was no effect of exercise or drug treatment on mitochondrial substrate-dependent oxygen consumption (''J''O<sub>2</sub>; high-resolution respirometry), or in mitochondrial hydrogen peroxide emission (mH<sub>2</sub>O<sub>2</sub>; fluorometric monitoring of Amplex Red oxidation) in permeabilized prefrontal cortex or the dorsal hippocampus. These results suggest negligible effects of oral H<sub>1</sub>/H<sub>2</sub> antagonists on mitochondrial metabolism in brain following exercise. This supports prior evidence suggesting the effects of H<sub>1</sub>/H<sub>2</sub> inhibition remain localized in exercising muscle. Other studies report systemic increases in histamine levels following exercise, however, which suggests further research may reveal a relationship between histamine receptor blockade and cellular processes in non-exercising tissues. | ||
|editor=[[Kandolf G]], | |editor=[[Kandolf G]], | ||
|mipnetlab=CA Antigonish Kane DA | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
Latest revision as of 09:34, 9 July 2018
| Effects of H1/H2 histamine receptor blockade on mitochondrial function in rodent brain following prolonged exercise. |
Link: Open Access
Wallace HE, Davidson LR, Bell MCW, Brebner K, Kane DA (2018)
Event: FASEB J
Exercise has been shown to stimulate histamine release, which mediates vasodilation in exercising tissue and is sustained post-exercise. Blockade of H1 and H2 receptors with antihistamine drugs attenuates this effect in skeletal muscle. Research examining the effects of exercise-related histamine action on cellular level processes is relatively sparse. There also remains limited understanding of the impacts of histamine receptor blockade on non-exercising tissue, such as the brain. To this end, 36 adult male Wistar rats (75–94 days old, 441.2 ± 39.5 g body wt) were randomly assigned to three groups: (1) given H1 and H2 receptor antagonists fexofenadine (7.11 mg/kg) and ranitidine (3.95 mg/kg) via oral gavage 1 hr prior to treadmill exercise (1 hr, 20 cm/s); (2) completed the exercise without drug, and (3) control. All groups received body mass-proportional oral gavage volumes (water or antihistamines). One hour post-exercise, mitochondrial function was assessed in saponin-permeabilized prefrontal cortex and dorsal hippocampus brain sub-regions. There was no effect of exercise or drug treatment on mitochondrial substrate-dependent oxygen consumption (JO2; high-resolution respirometry), or in mitochondrial hydrogen peroxide emission (mH2O2; fluorometric monitoring of Amplex Red oxidation) in permeabilized prefrontal cortex or the dorsal hippocampus. These results suggest negligible effects of oral H1/H2 antagonists on mitochondrial metabolism in brain following exercise. This supports prior evidence suggesting the effects of H1/H2 inhibition remain localized in exercising muscle. Other studies report systemic increases in histamine levels following exercise, however, which suggests further research may reveal a relationship between histamine receptor blockade and cellular processes in non-exercising tissues.
• Bioblast editor: Kandolf G
• O2k-Network Lab: CA Antigonish Kane DA
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Rat
Tissue;cell: Nervous system
Preparation: Permeabilized tissue
HRR: Oxygraph-2k
2018-07
