Gastrointestinal Regulatory Peptide Responses in Long-Distance Runners

Sullivan, Stephen N.; Champion, M C; Christofides, Nicos; Adrian, TE; Bloom, Steve

doi:10.1080/00913847.1984.11701902

Cited by 35 publications

(25 citation statements)

References 42 publications

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“…Previous studies have reported that circulating plasma GIP levels do not change during 3 h of cycling exercise at 40% V O 2 max (22), during cycling at 75% V O 2 max until exhaustion (2), or during a 30-km run (41). The findings of the present study are in agreement.…”

Section: Discussionsupporting

confidence: 83%

The gastroenteroinsular response to glucose ingestion during postexercise recovery

O’Connor¹,

Pola

Ward

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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-This study examined gastrointestinal hormone and peptide responses when glucose was ingested after prolonged exercise. Six endurance-trained male athletes ran on a treadmill for 2 h at 60% V O2 max. Immediately after the run, the athletes consumed 75 g of glucose in 250 ml of water (ExGLU) or flavored water as a placebo control (ExPL). On a separate visit, the athletes rested for 2 h and then consumed glucose (Con-GLU). During the first 60 min of recovery from exercise alone (ExPL), plasma vasoactive intestinal peptide (VIP), gastrin, and glucagon-like peptide-1 (GLP-1) all increased significantly, whereas glucose, insulin, and gastric inhibitory polypeptide (GIP) were unchanged from the immediate postexercise value. When glucose was ingested after exercise (ExGLU), glucose, insulin, VIP, gastrin, GLP-1, and GIP were all increased (P Ͻ 0.01). However, when glucose was ingested after resting for 2 h (ConGLU), VIP levels were unaffected, although glucose, insulin, gastrin, GLP-1, and GIP levels increased (P Ͻ 0.05). The plasma glucose response was greater (P Ͻ 0.03) and the plasma insulin response lower (P Ͻ 0.004) during ExGLU compared with ConGLU. There was a significantly higher (P Ͻ 0.01) VIP response during the initial period of recovery in ExGLU than there was with both ExPL and ConGLU. Plasma VIP showed a modest negative correlation with circulating glucose (r ϭ Ϫ0.35, P Ͻ 0.03) and insulin (r ϭ Ϫ0.37, P Ͻ 0.03) during the ExGLU recovery period. In summary, when glucose is ingested after prolonged exercise, there is mild insulin resistance and a corresponding rapid transitory increase in plasma VIP. These data suggest that VIP may play an important glucoregulatory role when glucose is ingested during the immediate postexercise recovery period. insulin resistance; gut peptides; exercise performance; carbohydrate THE IMMEDIATE POSTEXERCISE PERIOD appears to be associated with mild reversible insulin resistance, which is characterized by an attenuated insulin response and an increased glucose response to oral glucose (10,21,25,27,33,37,39,43). The physiological basis for the increased glucose response has been shown to be partly a function of greater release of glucose from the splanchnic tissues (20,30,39). Gut peptides and hormones of the enteroinsular axis may also play an important functional role in fuel homeostasis and contribute to maintaining a balance between energy utilization and mobilization. The metabolic role of peptides from the enteroinsular axis, including vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP; also called glucose-dependent insulinotropic polypeptide), and glucagon-like peptide-1 (GLP-1), are known. However, the response of these peptides during recovery from exercise and the role they may play after glucose ingestion in the immediate postexercise period is less clear.VIP is secreted by the central (CNS) and peripheral (including enteric) nervous systems in response to duodenal acidification, gastric distention, and meal consumption (6, 40). Its actions incl...

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Section: Discussionsupporting

confidence: 83%

The gastroenteroinsular response to glucose ingestion during postexercise recovery

O’Connor¹,

Pola

Ward

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…Zsinka and Frenkl (1983) have reported that swimming training increased meal-stimulated pancreatic secretion, but that the same increase did not appear after vagotomy. Since exercise training has been known to increase parasympathetic autonomic tone at rest (Smith et al 1989), the vagus nervous system may play an important role in the It has been reported that several gastrointestinal hormone concentrations in the blood increase during acute exercise (Hilsted et al 1980;Sullivan et al 1984). Increased hormone concentrations probably do not last long and may not aect pancreatic function in otherwise resting animals.…”

Section: Discussionmentioning

confidence: 98%

Effect of endurance training on pancreatic enzyme activity in rats

Minato

1997

European Journal of Applied Physiology

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The effect of chronic exercise on pancreatic enzyme activity and basal pancreatic secretion was investigated in rats. Male Wistar rats were divided into three groups of ten rats each. In a trained (T) group, the animals were exercised on a treadmill at 35 m x min(-1) for 60 min, 5 days x week(-1). A free-fed control (C) group and a pair-fed control (PFC) group were kept sedentary. Food intake in the PFC group was restricted to the T group levels. After 6 weeks, pancreas wet mass per unit of body mass was significantly larger in the T group in comparison to the C and PFC groups. Protein content, and amylase and lipase activities of the pancreas were significantly higher in the T group in comparison to the C and PFC groups. Basal amylase but not bile-pancreatic juice volume was higher in the T group than in the other two groups. There were no significant differences between groups C and PFC in any of the above parameters. These results would suggest that pancreatic enzyme synthesis and basal secretion are accelerated with physical endurance training. This adjustment would be a beneficial adaptation to chronic endurance exercise, which requires a large energy supply from food.

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“…One tempting explanation is a reduction of biliary stasis, brought about by an increase of gallbladder motility [38,82,83], mediated through increased neural stimulation, cholecystokinin secretion [84,85] and/or an increase of gastrointestinal transit rates [82]; however, as yet the empirical data supporting such a decrease in biliary stasis is quite limited.…”

Section: Possible Mechanisms Of Benefitmentioning

confidence: 98%