Acute endurance exercises induce disorders of the gastro- intestinal integrity in a murine model
Many endurance athletes complain about gastrointestinal (GI) symptoms. GI problems are probably the most common cause of underperformance in endurance events. Up to 90 % of distance runners experience intestinal problems related to exercise. It is assumed that exercise induced shift of perfusion with consecu- tive hypoperfusion of the enteral vascular system leads to an increased GI permeability and tissue damage. Therefore, the aim of the study was to investigate permeability, apoptosis, electrogenic ion transport (Isc), and tissue conductance (Gt) of the small intestine in a murine exercise model. After measuring the aerobic capacity by using a rodent treadmill spirometry (custom made), 8- to 12-week-old male Swiss CD-1 mice (31.1 ± 0.5 g; n = 8 per investigation-group) were subjected to an intensive treadmill exercise (80 % VO2max). Sedentary mice served as controls. The small intestine was removed at several time intervals post-exercise. Apoptotic cells were determined by the TUNEL method, while fluorescein isothiocyanate dextran permeation indicated intestinal permeability. The Gt and Isc measurements were carried out in a modified Ussing chamber. Apoptosis of epithelial cells increased continuously until 24 hr after exercise (0.8 ± 0.4 versus 39.2 ± 26.0 %; p < .05). Compared with the control group the permeability increased 2 hours after exercise (0.47 ± 0.07 versus 0.67 ± 0.14 FU/min; p < .05). Isc measurements of the ileum were augmented after 24 hr (3.33 ± 0.56 versus 5.77 ± 1.16 μEq/h/cm2; p < .05). At this time the Gt increased as well (28.80 ± 3.37 versus 32.5 ± 2.59 mS/cm2; p < .05). In the murine exercise model, there is evidence that after intense endurance exercise repair processes occur in small intestinal epithelial cells, which affect perme- ability, Gt, and Isc. The formation of lamellipodia to close the “leaky” tight junctions caused by apoptosis might be an underlying mechanism.
ฝึกความอดทนเฉียบพลันก่อให้เกิดความผิดปกติของความ gastro - ลำไส้สมบูรณ์ในรุ่น murineMany endurance athletes complain about gastrointestinal (GI) symptoms. GI problems are probably the most common cause of underperformance in endurance events. Up to 90 % of distance runners experience intestinal problems related to exercise. It is assumed that exercise induced shift of perfusion with consecu- tive hypoperfusion of the enteral vascular system leads to an increased GI permeability and tissue damage. Therefore, the aim of the study was to investigate permeability, apoptosis, electrogenic ion transport (Isc), and tissue conductance (Gt) of the small intestine in a murine exercise model. After measuring the aerobic capacity by using a rodent treadmill spirometry (custom made), 8- to 12-week-old male Swiss CD-1 mice (31.1 ± 0.5 g; n = 8 per investigation-group) were subjected to an intensive treadmill exercise (80 % VO2max). Sedentary mice served as controls. The small intestine was removed at several time intervals post-exercise. Apoptotic cells were determined by the TUNEL method, while fluorescein isothiocyanate dextran permeation indicated intestinal permeability. The Gt and Isc measurements were carried out in a modified Ussing chamber. Apoptosis of epithelial cells increased continuously until 24 hr after exercise (0.8 ± 0.4 versus 39.2 ± 26.0 %; p < .05). Compared with the control group the permeability increased 2 hours after exercise (0.47 ± 0.07 versus 0.67 ± 0.14 FU/min; p < .05). Isc measurements of the ileum were augmented after 24 hr (3.33 ± 0.56 versus 5.77 ± 1.16 μEq/h/cm2; p < .05). At this time the Gt increased as well (28.80 ± 3.37 versus 32.5 ± 2.59 mS/cm2; p < .05). In the murine exercise model, there is evidence that after intense endurance exercise repair processes occur in small intestinal epithelial cells, which affect perme- ability, Gt, and Isc. The formation of lamellipodia to close the “leaky” tight junctions caused by apoptosis might be an underlying mechanism.
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