Exercise stress, intestinal permeability and gastric ulceration in racing Alaskan sled dogs


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Abstract

Sustained strenuous exercise has been shown to produce gastrointestinal disease in athletic species, but the causative factors remain unknown. Since exercise results in oxidative stress and hypercortisolaemia, we tested the hypothesis that oxidative and physiological stress cause gastrointestinal disease in racing Alaskan sled dogs. Dogs from three racing teams were examined before (pre) and immediately after (post) completing a 1770-km sled dog race in approximately 11 days. Serum cortisol and isoprostane concentrations were compared with markers of gastrointestinal barrier integrity and endoscopic evidence of gastric ulceration. Gastric barrier integrity was assessed by measuring the urinary recovery of sucrose and intestinal barrier integrity was assessed using the urinary recovery ratio of lactulose to rhamnose (L/R), administered together by orogastric gavage. Exercise produced a significant increase in median serum cortisol (pre: 1040, 717 – 2946 pg ml−1 (range); post: 8072, 2228 – 29 571 pg ml−1; P < 0.0001) and L/R recovery ratio (pre: 0.110, 0.060 – 0.270; post: 0.165, 0.080 – 0.240; P = 0.009) but not isoprostane (pre: 1007, 656 – 2305 pg ml−1; post: 1164, 23 – 4710 pg ml−1; P = 0.194) concentration. The increased serum cortisol concentration was not correlated with a change in L/R recovery ratio or urine sucrose concentration. Dogs with abnormal gastric endoscopy results (61% of finishers) had higher serum cortisol concentrations than dogs with normal endoscopy results (P = 0.0007). We have demonstrated concurrent hypercortisolaemia and gastrointestinal barrier dysfunction with no correlation of the two. Thus, our data do not provide support for the hypothesis that increased serum cortisol concentration causes exercise-induced gastrointestinal disease.

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