Epinephrine infusion during moderate intensity  exercise increases glucose production and uptake

Kreisman, Stuart H.; Mew, Nicholas Ah; Arsenault, Mylène; Nessim, Sharon J.; Halter, Jeffrey B.; Vranić, Mladen; Marliss, Errol B.

doi:10.1152/ajpendo.2000.278.5.e949

Cited by 34 publications

(28 citation statements)

References 42 publications

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“…Glucose specific activity (SA) was maintained by increasing the tracer infusion incrementally to a maximum of sixfold the rates at rest during the infusion period in CCI and then returning it to the pre-exercise rate in early recovery. The goal was to introduce labeled glucose into the circulation at a rate proportional to endogenous R a , thereby attenuating changes in [ 3 H]glucose SA to Ͻ25% during the rapid changes in glucose kinetics, as in previous experiments (5,6,9,10,22,23). This step would ensure the validity of glucose turnover calculations, even if there were changes in pool fraction during this time.…”

Section: Methodsmentioning

confidence: 99%

“…Another study (17) with Epi infusion during 40% V O 2max exercise suggested that Epi contributes to, but does not fully account for, the R a increment of IE. Our recent studies of Epi (22) or NE (23) infusions during 50% V O 2max exercise suggest that plasma levels of each could provide a sizable contribution toward the R a increment of IE. Therefore, to test the hypothesis that catecholamines are the primary mediators of the markedly greater R a response to IE than to moderate exercise (ME), we studied the metabolic effects of an incremental combined catecholamine infusion (CCI) designed to approximate the pattern of changes of IE.…”

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confidence: 98%

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Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

et al. 2003

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Intense exercise (IE) (>80% V O 2max ) causes a seven-to eightfold increase in glucose production (R a ) and a fourfold increase in glucose uptake (R d ), resulting in hyperglycemia, whereas moderate exercise (ME) causes both to double. If norepinephrine (NE) plus epinephrine (Epi) infusion during ME produces the plasma levels and R a of IE, this would prove them capable of mediating these responses. G lucoregulation during low-and moderate-intensity exercise is primarily mediated by an increase in the portal venous glucagon-to-insulin ratio (1), which stimulates hepatic glucose output, maintaining euglycemia largely through a feedback mechanism (2-4) that matches the increment to the increased requirements. However, in intense exercise (IE) 80% V O 2max , an up to eightfold increase in glucose production (R a ) and a rise in glycemia occur, but plasma insulin (immunoreactive insulin [IRI]) changes little and glucagon (immunoreactive glucagon [IRG]) increases less than twofold (5). It seems unlikely that such changes, even insofar as they reflect portal vein concentrations, would mediate the R a response in IE. Furthermore, the R a response was unaffected in islet cell clamp studies using somatostatin and exogenous hormone infusions, in which peripheral IRG-to-IRI ratios (representative of portal levels) were kept unchanged or even decreased (6).A "feedforward" control of R a during IE has been proposed (4,7). We (5) and others (7,8) have proposed that the rapid and marked catecholamine response of IE could be such a mechanism. Plasma norepinephrine (NE) and epinephrine (Epi) concentrations both increase 15-fold, and we have demonstrated highly significant correlations of both with R a during IE (5). We recently found that the patterns of responses of plasma catecholamines and R a persist in glucose-infused subjects (9) and in the postprandial state (10). These are situations in which endogenous R a suppression from hyperinsulinemia must be overcome, the latter being the situation under which most IE is performed. In contrast, at lower-intensity exercise, attenuation or prevention of the R a increment occurs with exogenous glucose infusion (2)(3)(4)11,12).Catecholamine infusions stimulate R a in both dogs (13-15) and humans (16 -21). Most of these studies involved only Epi and were done at rest. Although some (16,19) produced Epi levels comparable to those of IE, the 1.5-to 2.5-fold increments in R a were considerably smaller. One study of Epi infusion during exercise was performed on celiac-ganglion-blocked and islet cell-clamped human subjects exercising at 74% V O 2max . Epi was doubled, to concentrations typical of IE, causing a further increment in R a over that of the exercise alone (18). Another study (17) with Epi infusion during 40% V O 2max exercise suggested that Epi contributes to, but does not fully account for, the R a increment of IE. Our recent studies of Epi (22) or NE (23) infusions during 50% V O 2max exercise suggest that plasma levels of each could provide a sizable contribution toward the...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 98%

Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

et al. 2003

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“…Therefore, fit normal subjects were exercised for 40 min at 50% VO 2max , and either the individual catecholamines were infused for the last 10 min or both together were infused during the last 14 min. Figure 8 illustrates the effects of EPI infusion at a constant rate that produced circulating concentrations that peaked in the range found in intense exercise (27). This infusion induced rapid increases in GP from the typical twofold increment over resting rates to over half the peak rate of intense exercise (Fig.…”

Section: Effects Of Epi and Ne Infusion Of During Moderate Exercisementioning

confidence: 97%

“…8B). Once again, given the absence of "appropriate" changes in insulin and glucagon during the infusions (27,28,50), virtually the whole of the glucoregulatory responses can be attributed to the levels of catecholamines achieved. These results clearly indicate the capacity of NE and EPI to explain the huge increase in GP of intense exercise.…”

Section: Effects Of Epi and Ne Infusion Of During Moderate Exercisementioning

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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Exercise Management and Hypoglycaemia in Type 1 Diabetes

Gallen

Lumb

2013

Hypoglycaemia in Clinical Diabetes

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Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

Cited by 34 publications

References 42 publications

Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

Combined Infusion of Epinephrine and Norepinephrine During Moderate Exercise Reproduces the Glucoregulatory Response of Intense Exercise

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

Exercise Management and Hypoglycaemia in Type 1 Diabetes

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