Hormonal consequences of different timings of exercise and nutrients
This is an excerpt from Advanced Exercise Endocrinology by Katarina Borer.
Hormonal Consequences of Different Timings of Exercise and Nutrients
Hormonal responses to exercise follow a predictable pattern according to intensity-dependent energy requirements when exercise is performed in the postprandial state. Human desire to improve duration and intensity of exercise has led to attempts to overcome the limited availability of muscle and liver glycogen. Early attempts to spare muscle glycogen involved oral supplementation of sugars shortly before the onset of moderate or intense exercise. This strategy led to elevations of plasma insulin concentration that coincided with increased muscle glucose uptake during exercise. The result was a precipitous decrease in blood glucose during the first 20 min of exercise, caused by the combined hypoglycemic actions of insulin and muscle contractions followed by a partial recovery during the remaining hour (Horowitz & Coyle, 1993). The supplementation strategy did not affect exercise-associated changes in muscle glycogen that are dependent on exercise intensity and are unresponsive to carbohydrate supplementation (Coyle at al., 1986).
The second strategy for enhancing exercise intensity by carbohydrate supplementation during prolonged exercise had somewhat different outcomes depending on exercise intensity and timing of glucose administration. If 90 g of glucose was provided before (Ahlborg & Felig, 1977) or after the first 90 min of low-intensity exercise (Ahlborg & Felig, 1976), increases in plasma glucose concentration led to protracted elevation of plasma insulin and suppression of release of glucagon, other counterregulatory hormones, and FFA during the remaining 2 h of exercise. This hormonal milieu led to increased muscle carbohydrate metabolism, an outcome that countered attempts to spare muscle glycogen. On the other hand, exercise intensity was sustained at 70% of maximal effort and maintained at glucose utilization was about 1.5 to 2 g/min when carbohydrate was ingested at a rate of about 1 g/min during the second and third hours of exercise. At that stage of exercise, both the glycogen-depleted muscle and low plasma glucose could not support this level of exercise intensity without carbohydrate supplementation (Coggan & Coyle, 1989). Although hormones were not measured in this study, it is unlikely that intake of glucose after 2 h of exercise of moderately high intensity would have increased plasma insulin and blocked the release of counterregulatory hormones and the mobilization and utilization of metabolic fuels.
When moderate-intensity exercise is repeated twice in a day in a fasted state, it triggers a greater insulin response to a meal than does exercise in a postprandial state and a lowering of the glucagon glycemic threshold (concentration of glucose that elicits glucagon secretion in response to a subsequent hypoglycemic stimulus; Borer et al., 2009). The difference in hormonal and metabolic response to a change in timing of exercise and meals is likely due to the preferential uptake of glucose by the muscle and to protracted reduction in glucose availability to the liver when two bouts of exercise are performed before the meals. Thus, manipulation of nutrient status by exercise or by specific macronutrient intake can alter hormonal control of metabolism during exercise.
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