Glucoregulation during and after intense exercise: Effects of α-adrenergic blockade

Sigal, Ronald J.; Fisher, Simon J.; Manzon, Anthony; Morais, José A.; Halter, Jeffrey B.; Vranić, Mladen; Marliss, Errol B.

doi:10.1016/s0026-0495(00)90374-3

Cited by 40 publications

(26 citation statements)

References 21 publications

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“…On the basis of these three studies, we have suggested that during intense exercise both ␣-and ␤-receptor effects of catecholamines can increase GP (35,36,40). Because with blockade of either of the receptors the plasma concentrations of catecholamines rose considerably more, this suggests that one system can compensate for the attenuated activity of the other, i.e., there is redundancy in the receptor mechanisms in this specific situation.…”

Section: Responses (F-f) Greater Hyperglycemia With Propranolol (A) mentioning

confidence: 99%

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Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation

2002

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In intense exercise (>80% VO 2max ), unlike at lesser intensities, glucose is the exclusive muscle fuel. It must be mobilized from muscle and liver glycogen in both the fed and fasted states. Therefore, regulation of glucose production (GP) and glucose utilization (GU) have to be different from exercise at <60% VO 2max , in which it is established that the portal glucagon-to-insulin ratio causes the less than or equal to twofold increase in GP. GU is subject to complex regulation by insulin, plasma glucose, alternate substrates, other humoral factors, and muscle factors. At lower intensities, plasma glucose is constant during postabsorptive exercise and declines during postprandial exercise (and often in persons with diabetes). During such exercise, insulin secretion is inhibited by ␤-cell ␣-adrenergic receptor activation. In contrast, in intense exercise, GP rises seven-to eightfold and GU rises three-to fourfold; therefore, glycemia increases and plasma insulin decreases minimally, if at all. Indeed, even an increase in insulin during ␣-blockade or during a pancreatic clamp does not prevent this response, nor does pre-exercise hyperinsulinemia due to a prior meal or glucose infusion. At exhaustion, GU initially decreases more than GP, which leads to greater hyperglycemia, requiring a substantial rise in insulin for 40 -60 min to restore pre-exercise levels. Absence of this response in type 1 diabetes leads to sustained hyperglycemia, and mimicking it by intravenous infusion restores the normal response. Compelling evidence supports the conclusion that the marked catecholamine responses to intense exercise are responsible for both the GP increment (that occurs even during glucose infusion and postprandially) and the restrained increase of GU. These responses are normal in persons with type 1 diabetes, who often report exercise-induced hyperglycemia, and in whom the clinical challenge is to reproduce the recovery period hyperinsulinemia. Intense exercise in type 2 diabetes requires additional study. Diabetes 51 (Suppl. 1):S271-S283, 2002

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Section: Responses (F-f) Greater Hyperglycemia With Propranolol (A) mentioning

confidence: 99%

“…5) or propranolol (Fig. 6) intravenously, starting 30 min before the bout and ending at 60 min of recovery (35,36). With phentolamine (36), the importance of the usual islet ␣-receptor effect of inhibiting insulin secretion during exercise (2,3) is clearly illustrated by the threefold increase in insulin (Fig.…”

Section: Eb Marliss and M Vranicmentioning

confidence: 99%

Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation

2002

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“…Attempts to directly assess a role for catecholamines in stimulating endogenous glucose production during high-intensity exercise (Ͼ80% maximum O 2 uptake) in humans have also been negative (43,49,59,82,83). This is not to say that other factors such as IL-6 (23) or an as yet undefined regulator do not play some role.…”

Section: Studies On the Control Of Glucose Mobilization From The Livermentioning

confidence: 99%

Four grams of glucose

Wasserman¹

2009

American Journal of Physiology-Endocrinology and Metabolism

338

264

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Four grams of glucose circulates in the blood of a person weighing 70 kg. This glucose is critical for normal function in many cell types. In accordance with the importance of these 4 g of glucose, a sophisticated control system is in place to maintain blood glucose constant. Our focus has been on the mechanisms by which the flux of glucose from liver to blood and from blood to skeletal muscle is regulated. The body has a remarkable capacity to satisfy the nutritional need for glucose, while still maintaining blood glucose homeostasis. The essential role of glucagon and insulin and the importance of distributed control of glucose fluxes are highlighted in this review. With regard to the latter, studies are presented that show how regulation of muscle glucose uptake is regulated by glucose delivery to muscle, glucose transport into muscle, and glucose phosphorylation within muscle.

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“…Afferent neuronal feedback signals from contracting muscles associated with central mechanisms coupled with the degree of motor activity might be responsible for part of the increase in glucose mobilization. In addition, several authors have proposed that, during intense exercise, glucoregulation is primarily mediated through a feedfoward mechanism by catecholamines (Kja¨er et al 1986;Kreisman et al 2000Kreisman et al , 2001Marliss et al 1991Marliss et al , 2000Sigal et al 1994Sigal et al , 1996Sigal et al , 2000.…”

Section: Introductionmentioning

confidence: 99%

Plasma glucose, insulin and catecholamine responses to a Wingate test in physically active women and men

Vincent¹,

Berthon²,

Zouhal

et al. 2004

European Journal of Applied Physiology

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The influence of gender on the glucose response to exercise remains contradictory. Moreover, to our knowledge, the glucoregulatory responses to anaerobic sprint exercise have only been studied in male subjects. Hence, the aim of the present study was to compare glucoregulatory metabolic (glucose and lactate) and hormonal (insulin, catecholamines and estradiol only in women) responses to a 30-s Wingate test, in physically active students. Eight women [19.8 (0.7) years] and eight men [22.0 (0.6) years] participated in a 30-s Wingate test on a bicycle ergometer. Plasma glucose, insulin, and catecholamine concentrations were determined at rest, at the end of both the warm-up and the exercise period and during the recovery (5, 10, 20, and 30 min). Results showed that the plasma glucose increase in response to a 30-s Wingate test was significantly higher in women than in men [0.99 (0.15) versus 0.33 (0.20) mmol l(-1) respectively, P<0.05]. Plasma insulin concentrations peaked at 10 min post-exercise and the increase between this time of recovery and the end of the warm-up was also significantly higher in women than in men [14.7 (2.9) versus 2.3 (1.9) pmol l(-1) respectively, P<0.05]. However, there was no gender difference concerning the catecholamine response. The study indicates a gender-related difference in post-exercise plasma glucose and insulin responses after a supramaximal exercise.

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Glucoregulation during and after intense exercise: Effects of α-adrenergic blockade

Cited by 40 publications

References 21 publications

Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation

Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation

Four grams of glucose

Plasma glucose, insulin and catecholamine responses to a Wingate test in physically active women and men

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