Biomedical subjects

H Galbo

Publications and source records attributed to H Galbo.

At least 127 records · Page 7Linked to original sources

PubMed1989

Mobilization of glucoregulatory hormones and glucose by hypothalamic locomotor centers.

Recent studies suggest that, in addition to classical humoral metabolic feedback mechanisms, the mobilization of glucoregulatory hormones and glucose in exercise may be regulated by motor centers in the brain. We, therefore, studied the effect of electrically stimulating the posterior hypothalamic locomotor region (PHLR) for 10 min in decorticated (n = 6) and alpha-chloralose-anesthetized (n = 8) cats. Blood pressure and heart rate were measured, and blood samples were drawn for analysis of hormones and metabolites before, during, and after 10 min of PHLR stimulation. Feedback from contracting muscles was prevented by neuromuscular blockade in decorticated cats and by the anesthesia in anesthetized cats. In decorticated cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 54 +/- 16 mumol.min-1.kg-1), plasma glucose (delta 2.2 +/- 0.7 mmol/l), epinephrine (delta 4.9 +/- 1.8 pmol/l), norepinephrine (delta 2.2 +/- 0.9 pmol/l), glucagon (delta 16 +/- 5 pmol/l), decreases (2 P less than 0.05) in plasma insulin (delta 27 +/- 7 pmol/l), and increases (2 P less than 0.05) in blood pressure (delta 48 +/- 9 mmHg) and heart rate (delta 26 +/- 7 beats/min). In anesthetized cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 12 +/- 4 mumol.min-1.kg-1), plasma glucose (delta 0.4 +/- 0.1 mmol/l), blood pressure (delta 39 +/- 7 mmHg), and heart rate (delta 28 +/- 7 beats/min), whereas changes in catecholamine and insulin concentrations did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Ventromedial hypothalamic regulation of hormonal and metabolic responses to exercise.

Recent studies have indicated a neural regulation of hormonal and metabolic responses to exercise. Studies on the ventromedial hypothalamus (VMH) suggest that the VMH might be involved in neural control of exercise metabolism. We therefore studied 25 rats with or without Marcain-anesthetized VMH (Marcain and control rats, respectively) at rest or during treadmill running (26 m/min). The rats had cannulas aimed bilaterally at the VMH and chronic catheters in the left jugular vein and right carotid artery. At rest, glucose turnover and plasma concentrations of glucose, lactate, glycerol, epinephrine, norepinephrine, insulin, and corticosterone remained stable in control rats, whereas in Marcain rats these parameters, except for unchanged insulin and glucose utilization, increased after Marcain administration along with increases in hepatic and muscular glycogenolysis. During exercise, glucose turnover, hepatic and muscular glycogenolysis, and plasma concentrations of glucose, lactate, glycerol, catecholamines, and corticosterone increased, and insulin decreased in both Marcain and control rats. However, during exercise, initial hepatic glucose production, plasma catecholamines, and subsequent plasma glucose concentrations and overall hepatic glycogenolysis were lower in Marcain compared with control rats. In conclusion, glucose mobilization is enhanced by the VMH during exercise. The results suggest that decreased and increased activity in sympathetic inhibitory and facilitating VMH areas, respectively, are involved in the VMH's response to exercise.

Animals↗

PubMed1989

Effect of liver glycogen content on glucose production in running rats.

The influence of supranormal compared with normal hepatic glycogen levels on hepatic glucose production (Ra) during exercise was investigated in chronically catheterized rats. Supranormal hepatic glycogen levels were obtained by a 24-h fast-24-h refeeding regimen. During treadmill running for 35 min at a speed of 21 m/min, Ra and plasma glucose increased more (P less than 0.05) and liver glucogen breakdown was larger in fasted-refed compared with control rats, although the stimuli for Ra were higher in control rats, the plasma concentrations of insulin and glucose being lower (P less than 0.05) in control compared with fasted-refed rats. Also, plasma concentrations of glucagon and both catecholamines tended to be higher and muscle glycogenolysis lower in control compared with fasted-refed rats. Lipid metabolism was similar in the two groups. The results indicate that hepatic glycogenolysis during exercise is directly related to hepatic glycogen content. The smaller endocrine glycogenolytic signal in face of higher plasma glucose concentrations in fasted-refed compared with control rats is indicative of metabolic feedback control of glucose mobilization during exercise. However, the higher exercise-induced increase in Ra, plasma glucose, and liver glycogen breakdown in fasted-refed compared with control rats indicates that metabolic feedback mechanisms are not able to accurately match Ra to the metabolic needs of working muscles.

Animals↗

PubMed1989

Effect of training on the dose-response relationship for insulin action in men.

Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] were subjected to three sequential hyperinsulinemic euglycemic clamps 15 h after having performed their last training session (T). Results were compared with findings in seven untrained subjects (VO2max 44 +/- 2 ml.min-1.kg-1) studied both at rest (UT) and after 60 min of bicycle exercise at 150 W (UT-ex). In T and UT-ex compared with UT, sensitivity for insulin-mediated whole-body glucose uptake was higher [insulin concentrations eliciting half-maximal glucose uptake being 44 +/- 2 (T) and 43 +/- 4 (UT-ex) vs. 52 +/- 3 microU/ml (UT), P less than 0.05] and responsiveness was higher [13.4 +/- 1.2 (T) and 10.9 +/- 0.7 (UT-ex) vs. 9.5 +/- 0.7 mg.min-1.kg-1 (UT), P less than 0.05]. Furthermore, responsiveness was higher (P less than 0.05) in T than in UT-ex. Insulin-stimulated O2 uptake and maximal glucose oxidation rate were higher in T than in UT and UT-ex. Insulin-stimulated conversion or glucose to glycogen and muscle glycogen synthase was higher in T than in UT and UT-ex. However, glycogen storage in vastus lateralis muscle was found only in UT-ex. No change in any glucoregulatory hormone or metabolite could explain the increased insulin action in trained subjects. It is concluded that physical training induces an adaptive increase in insulin responsiveness of whole-body glucose uptake, which does not reflect increased glycogen deposition in muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effects of acute exercise and detraining on insulin action in trained men.

Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] underwent sequential hyperinsulinemic euglycemic clamps on three occasions: 1) in the "habitual state" 15 h after the last training bout (C), 2) after 60 min of bicycle exercise at 72 +/- 3% of VO2max performed in the habitual state (E), and 3) 5 days after the last ordinary training session (detrained, DT). Sensitivity for insulin-mediated whole-body glucose uptake was not affected by acute exercise [insulin concentrations eliciting 50% of maximal insulin-mediated glucose uptake being 44 +/- 2 (C) vs. 46 +/- 3 (E) microU/ml] but was decreased after detraining (54 +/- 2 microU/ml, P less than 0.05) to levels comparable to those found in untrained subjects [Am. J. Physiol. 254 (Endocrinol. Metab. 17): E248-E259, 1988]. Near-maximal insulin-mediated glucose uptake (responsiveness) was higher than in untrained subjects and not influenced by acute exercise or detraining [13.4 +/- 1.2 (C), 12.2 +/- 0.9 (E), and 12.2 +/- 0.3 (DT) mg.min-1.kg-1]. Calculated by indirect calorimetry, the glucose-to-glycogen conversion was not influenced by E but was reduced during detraining (P less than 0.05) yet remained higher than previously found in untrained subjects (P less than 0.05). However, only on E days did muscle glycogen increase during insulin infusion. Glycogen synthase activity was increased on E and decreased on DT compared with C days.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗

PubMed1989

Effect of exercise on insulin action in human skeletal muscle.

The effect of 1 h of dynamic one-legged exercise on insulin action in human muscle was studied in 6 healthy young men. Four hours after one-legged knee extensions, a three-step sequential euglycemic hyperinsulinemic clamp combined with arterial and bilateral femoral vein catheterization was performed. Increased insulin action on glucose uptake was found in the exercised compared with the rested thigh at mean plasma insulin concentrations of 23, 40, and 410 microU/ml. Furthermore, prior contractions directed glucose uptake toward glycogen synthesis and increased insulin effects on thigh O2 consumption and at some insulin concentrations on potassium exchange. In contrast, no change in insulin effects on limb exchange of free fatty acids, glycerol, alanine or tyrosine were found after exercise. Glycogen concentration in rested vastus lateralis muscle did not increase measurably during the clamp even though indirect estimates indicated net glycogen synthesis. In contrast, in exercised muscle estimated and biopsy-verified increases in muscle glycogen concentration agreed. Local contraction-induced increases in insulin sensitivity and responsiveness play an important role in postexercise recovery of human skeletal muscle.

Adult↗

PubMed1989

Fatigue and cardiac and endocrine metabolic response to exercise after abdominal surgery.

Subjective feeling of fatigue was quantified before and 20 days after elective uncomplicated abdominal surgery in 16 otherwise-healthy patients and compared with changes in heart rate and various hormonal and substrate responses to a 10-minute bicycle exercise (65% of preoperative maximal work capacity) preoperatively and postoperatively. Postoperatively, fatigue increased (p less than 0.001) from 3.0 +/- 0.5 to 5.3 +/- 0.5 arbitrary units (mean +/- SEM). Heart rate, plasma catecholamines, and serum growth hormone, lactate, alanine, and glycerol values always increased, whereas serum insulin values decreased in response to exercise (p less than 0.01). During exercise, only heart rate (p less than 0.01) and lactate (p less than 0.05) values were higher postoperatively compared with preoperatively. Increase in fatigue postoperatively correlated significantly to increase in heart rate (p less than 0.01) and correlated positively, but not significantly, to increase in plasma levels of noradrenaline (p = 0.08), growth hormone (p = 0.09), and alanine (p = 0.08) during exercise, but not to increase in serum lactate values (p greater than 0.8). Thus, after uncomplicated surgery, there was increased fatigue and amplified metabolic and cardiovascular response to a given absolute work load. These findings are similar to those observed during detraining and suggest a therapeutic role of exercise in the treatment of postoperative fatigue.

Abdomen↗

PubMed1988

Modulation of natural killer cell activity in peripheral blood by physical exercise.

The present study was designed to examine the effect of physical exercise on human natural killer (NK) cells. Six healthy volunteers underwent two different acute physical exercise tests with an interval of at least 1 week: (1) 60 min bicycle exercise at 80% of maximal oxygen uptake (VO2max) and (2) 60 min back-muscle training at up to 29% of VO2max; blood samples were collected before and during the last few minutes of exercise, as well as 2 h and 24 h afterwards. The NK cell activity (lysis/fixed number of mononuclear cells) increased during bicycle exercise, dropped to a minimum 2 h later and returned to pre-exercise levels within 24 h. Back-muscle exercise did not significantly influence NK cell activity. Plasma levels of adrenaline, noradrenaline, and cortisol were elevated during bicycling, but not during back-muscle exercise, indicating that exercise intensity is a determinant of NK cell activity. During bicycle exercise the NK cell subset (CD16- cells) of mononuclear cells increased significantly. Furthermore an improved interleukin 2 (IL-2) boosting of the NK cell activity was found during work as compared to IFN-alpha and indomethacin-enhanced NK cell activity. These results indicate that NK cells with a high IL-2 response capacity are recruited to the peripheral blood during exercise. The decreased NK cell activity demonstrated 2 h after work was probably not due to fluctuations in size of the NK cell pool, since the proportion of CD16+ cells was normal. The finding that indomethacin fully restored the suppressed NK cell activity in vitro and the demonstration of a twofold increase in monocyte (CD20+ cells) proportions 2 h after work, strongly indicate that prostaglandins released by monocytes during the heavy physical exercise are responsible for the down-regulation of the NK cells.

Adult↗

PubMed1988

Arterial blood pressure at the onset of dynamic exercise in partially curarized man.

In six young men, heart rate and arterial mean blood pressure responses to the onset of light dynamic exercise 99 W (range 59-138) on a stationary bicycle were followed during partial neuromuscular blockade with tubocurarine. Tubocurarine was used in order to accentuate the central nervous (central command) influence on the cardiovascular variables and reduced hand-grip strength to 42% (36-47) of control. At the onset of exercise heart rate increased immediately and similarly with and without neuromuscular blockade. Mean arterial blood pressure remained constant during the first 6 s of control exercise and then increased. With tubocurarine a decrease of 9 mmHg (3-12) was seen during the first 6 s (P less than 0.01) before blood pressure increased. The similar heart rate responses seen with and without neuromuscular blockade indicate that central command has little influence on this variable at the onset of dynamic exercise. The constant blood pressure at the onset of control exercise suggests that the immediate changes in cardiac output and peripheral vascular resistance, respectively, are accurately matched. The decrease in blood pressure at the onset of exercise with tubocurarine suggests that central command stimulates vasodilatating nerves to arterioles in the working muscles.

Adult↗

PubMed1988

Effect of physical exercise on sensitivity and responsiveness to insulin in humans.

The effect of acute physical exercise on insulin sensitivity and responsiveness of glucose uptake and hepatic glucose production was studied. Seven untrained men were subjected to four sequential euglycemic hyperinsulinemic clamps after rest (R), immediately after exercise (E), as well as 48 h after 60 min of 150 W ergometer exercise (ER). Insulin-mediated glucose uptake was higher on E and ER days compared with R days. Apparent Km decreased after exercise (52 +/- 3 R vs. 43 +/- 4 E and 40 +/- 3 ER microU/ml, means +/- SE) and Vmax increased (9.5 +/- 0.8 R vs. 10.9 +/- 0.7 E and 10.7 +/- 0.8 ER mg.min-1.kg-1). Glucose oxidation increased with the increasing insulin infusion rate, and maximal glucose oxidation rate was lower on E days compared with R days. The maximal conversion rate of glucose to glycogen was higher on E and ER days (8.0 +/- 0.3 and 7.2 +/- 0.2, respectively) than on R days (5.7 +/- 0.6 mg.min-1 kg-1). Muscle glycogen synthase I activity was higher immediately after exercise and remained higher for the next 48 h. No change in any glucoregulatory hormone or metabolite could explain the increased insulin action seen after exercise. In additional experiments (n = 3), no remaining effect existed 5 days after exercise. Both insulin and exercise suppressed the pancreatic secretion of insulin and proinsulin. The conclusions drawn are that prolonged moderate exercise increases insulin action on glucose uptake in humans by reducing apparent Km and increasing Vmax. This effect lasts 48 h but not 5 days. The increased insulin action may be related to an exercise-induced increase in glycogen synthase activity.

Adult↗

PubMed1988

Effect of prior immobilization on muscular glucose clearance in resting and running rats.

In vitro studies have shown that prior disuse impairs the glucose clearance of red skeletal muscle because of a developed insensitivity to insulin. We studied whether an impaired glucose clearance is present in vivo in 42-h immobilized muscles of resting rats and, furthermore, whether the exercise-induced increase in glucose clearance of red muscles is affected by prior immobilization. The 2-[3H]deoxy-D-glucose (2DG) bolus injection method was used to determine glucose clearance of individual muscles. At rest, glucose clearance was markedly impaired in rats with previously immobilized red muscles compared with nonimmobilized control rats (red gastrocnemius 0.46 +/- 0.02 vs. 0.99 +/- 0.08 and soleus 1.10 +/- 0.30 vs. 3.97 +/- 0.54 ml.min-1.100 g-1, P less than 0.005). During running (18 m/min), glucose clearance did not differ between muscles in previously immobilized and control rats. Insulin levels were always similar in the two groups and decreased during exercise. Intracellular nonphosphorylated 2DG was present in tissues with high glucose clearances. In conclusions, 42 h of immobilization markedly impairs glucose clearance of resting red muscle fibers in vivo. Apparently, physical inactivity in particular affects steps involved in insulin-mediated action that are not part of contraction-induced glucose uptake and metabolism. Presence of intracellular 2DG shows that separate determination of phosphorylated 2DG is necessary for accurate estimates of glucose metabolism and that accumulation of phosphorylated 2DG does not accurately reflect glucose transport.

Animals↗

PubMed1988

Hormonal response to exercise in humans: influence of hypoxia and physical training.

Hypoxia and physical training alter the responses of glucoregulatory hormones to absolute work loads in opposite directions. These effects have tentatively been ascribed to changes in maximal O2 consumption (VO2 max) and ensuing changes in relative work loads. However, hypoxia as well as training may more specifically influence the hormonal response. We therefore differentiated the influence of hypoxia, training, and VO2 max, respectively, on the hormonal response to bicycle exercise. Responses to hypoxia in a low-pressure chamber (PB = 465 vs. 730 Torr) were studied at given absolute and relative (85% VO2 max) work loads in seven endurance-trained athletes (T) and 7 age and weight-matched sedentary subjects (C). Concentrations in plasma of norepinephrine, growth hormone, adrenocorticotropic hormone, and cortisol were always closely related to the relative work load. However, the epinephrine response in T, but not in C, was at the same relative work load higher during hypoxia (5.84 +/- 0.83 nmol/l) than during normoxia (4.26 +/- 0.44, P less than 0.05). These results indicate that the hormonal response is influenced by hypoxia and physical training, mainly via changes in the relative work load. However, in trained subjects both at rest and during exercise, an enhancing effect of hypoxia per se on the epinephrine response is seen, probably due to an increased adrenal medullary secretory responsiveness in long-term endurance-trained subjects.

Adrenocorticotropic Hormone↗

PubMed1988

Role of metabolic feedback regulation in glucose production of running rats.

Hepatic glucose production (Ra) was studied in phlorizin (P)- and saline (C)-infused rats running for 35 min at 21 m/min in the postabsorptive state (series I) or 18 m/min in the fed state (series II). Phlorizin-induced increase in glucose clearance would increase or not affect Ra, depending on whether metabolic feedback mechanisms or central command from central nervous system (CNS), respectively, regulate Ra during exercise. Initial exercise-induced increases in Ra were similar in P and C rats of both series, although glucose clearance was higher and plasma glucose lower, however not hypoglycemic, in P rats. After 5 min of exercise, Ra remained similar in P and C rats in series I, whereas in series II, Ra increased almost twice as much in P compared with C rats. In both series muscle glycogenolysis and lipolysis were higher in P than in C rats. The results suggest a central command regulation of Ra from CNS motor centers and that this primary setting may be modulated by metabolic feedback mechanisms. Hypoglycemia is not needed to activate metabolic feedback. A variety of substrates rather than glucose specifically is mobilized by metabolic feedback mechanisms associated with decreased glucose availability.

3-Hydroxybutyric Acid↗

PubMed1988

Effect of physical training on the capacity to secrete epinephrine.

Epinephrine responses to hypoglycemia and to identical relative work loads have been shown to be higher in endurance-trained athletes than in untrained subjects. To test the hypothesis that training increases the adrenal medullary secretory capacity, we studied the effects of glucagon (1 mg/70 kg iv), acute hypercapnia (inspired O2 fraction = 7%), and acute hypobaric hypoxia (inspired Po2 = 87 Torr), respectively, on the epinephrine concentration in arterialized hand vein blood in eight endurance-trained athletes [T, O2 uptake = 66 (62-70) ml.min-1.kg-1] and seven sedentary males [C, O2 uptake = 46 (41-50)]. In response to identical increments in glucagon concentrations, plasma epinephrine increased more in T than in C subjects [0.87 +/- 0.11 vs. 0.38 +/- 0.14 (SE) nmol/l, P less than 0.05]. In response to hypercapnia [arterial PCO2 = 56 +/- 0.7 Torr (T) and 55 +/- 0.4 (C), P greater than 0.05], the increment in epinephrine was significant in T (0.38 +/- 0.11 nmol/l) but not (P less than 0.1) in C subjects (0.22 +/- 0.11). Hypoxia [arterial PO2 = 42 +/- 2 Torr (T) and 41 +/- 2 (C), P greater than 0.05] increased epinephrine in T (0.22 +/- 0.10 nmol/l, P less than 0.05) but not in C subjects (0.01 +/- 0.07). The plasma norepinephrine concentration never changed, whereas heart rate always increased, the increase being higher (P less than 0.05) in T than in C subjects only during hypercapnia. The results indicate that training increases the capacity to secrete epinephrine.

Adrenal Medulla↗

PubMed1988

Postexercise dose-response relationship between plasma glucose and insulin secretion.

To investigate whether exertion changes beta-cell reactivity to glucose stimulation and to characterize the beta-cell response to glucose in humans, we performed four sequential 90-min hyperglycemic clamps (7, 11, 20, and 35 mM). Concentrations of hormones and metabolites involved in glucoregulation were measured. Metabolic rate and substrate utilization were studied by indirect calorimetry. Studies were performed without prior exercise, as well as 2 and 48 h after 60 min of bicycle exercise at 150 W. We found 1) a progressive increase in insulin concentrations reaching 1,092 +/- 135 microU/ml with increasing glucose levels, 2) linear relationships between glucose concentrations and concentrations of C-peptide (r = 0.931 +/- 0.008) and proinsulin (r = 0.952 +/- 0.009),3) increased glucose oxidation with increasing glucose uptake, 4) increased plasma norepinephrine, O2 uptake, and beta-hydroxybutyrate at greater than or equal to 20 mM glucose, and 5) no change in beta-cell response or glucose-induced thermogenesis after one bout of exercise despite no compensating changes in plasma concentrations of hormones or metabolites. We conclude that the beta-cell has a very large secretory potential. Secretion of the beta-cell increases linearly with prolonged, graded hyperglycemia. The processing of proinsulin is unchanged during prolonged beta-cell stimulation. In addition, hyperglycemia and sympathetic nervous activity induced by hyperinsulinemia enhance metabolic rate and ketone body production. Finally, a single bout of exercise does not influence either the beta-cell response to intravenous glucose or glucose-induced thermogenesis.

3-Hydroxybutyric Acid↗

PubMed1988

Stimulatory role for endogenous opioid peptides on postexercise insulin secretion in rats.

Endogenous opioid peptides (EOP) and prior exercise may modulate the stimulatory effect of glucose on insulin secretion. To gain insights into these relationships, we studied male Wistar rats (187-245 g) during sustained hyperglycemia by use of the glucose clamp technique. Four groups of sedentary fed rats (n = 8/group) either ran (Ex) at 24 m/min, 0% grade, or rested (R) for 40 min. Thirty minutes after Ex or R, arterial blood glucose was elevated to and maintained at 11 mM for 2 h by a variable glucose infusion. At the start of Ex or R rats had saline (Sal) or naloxone (Nal, an opioid antagonist) intravenous infusions for 160 min (40 min Ex + 30 min R + 90 min of a 120-min glucose clamp). Steady-state glucose infusion rates (SSGIR) were approximately 55 mg.kg-1.min-1 at the start of the clamp and declined significantly over the 2nd h to approximately 45 mg.kg-1.min-1. No significant differences existed in SSGIR between groups. R-Sal and Ex-Sal groups did not differ in their insulin response to hyperglycemia. In contrast, when all groups were compared at the end of the Nal or Sal infusion, Ex-Nal had the lowest insulin concentration (749 +/- 174 pmol/l), whereas the R-Nal group had the highest (1,581 +/- 216 pmol/l, P less than 0.05). These data suggest a stimulatory role for EOP on insulin secretion that is expressed after a prior stress (Ex). Thus one function of exercise-induced activation of EOP may be to regulate insulin secretion in the immediate postexercise period.

Animals↗

PubMed1988

Regulation of hepatic glucose production in running rats studied by glucose infusion.

The importance of metabolic feedback regulation vs. feedforward regulation of hepatic glucose production (HGP) during exercise was investigated in rats by infusing glucose intravenously from the onset of running. Glucose infusion equaled the average exercise-induced increase from basal to steady state in HGP found in saline-infused control rats. Rats were studied at two work loads, running at 21 (series I) or 18 m/min (series II) for 35 min. Glucose turnover was measured by means of an intravenous [3H]glucose infusion. HGP was suppressed by glucose infusion corresponding to the infused amount of glucose in both series, except for late in exercise in series I, where HGP plus infused glucose tended to exceed HGP in saline-infused rats (P less than 0.10). Muscle glycogenolysis and fat metabolism were similar in both groups in the two series. Plasma glucose was never elevated, whereas insulin was, in glucose- vs. saline-infused rats of both series. Plasma catecholamines were lower in glucose- compared with saline-infused rats in series II. In conclusion, HGP is very sensitive to metabolic feedback inhibition at low exercise intensities. Feedforward control of HGP may play a role at higher work loads (series I). Exogenously supplied glucose, in moderate amounts, may replace HGP specifically without concomitant changes in mobilization of other substrates.

3-Hydroxybutyric Acid↗

PubMed1987

Metabolic and cardiovascular responses to epinephrine in diabetic autonomic neuropathy.

Norepinephrine-induced vasoconstriction, which is mediated by alpha-adrenergic receptors, is accentuated in patients with autonomic neuropathy. In contrast, responses mediated by beta-adrenergic receptors, including vasodilatation and metabolic changes, have not been evaluated in these patients. To study these responses, we administered epinephrine in a graded intravenous infusion (0.5 to 5 micrograms per minute) to seven diabetic patients without neuropathy, seven diabetic patients with autonomic neuropathy, and seven normal subjects. Mean arterial pressure decreased significantly in the patients with autonomic neuropathy (P less than 0.01) but was unchanged in the other groups. Since cardiac output increased to a similar extent in the three groups, the decrease in blood pressure was due to a significantly larger decrease (P less than 0.01) in total peripheral vascular resistance in the patients with autonomic neuropathy. The heart rate increased significantly more during the infusions in the patients with neuropathy than in those without neuropathy. Epinephrine produced a greater increase in blood glucose, the glucose-appearance rate, lactate, glycerol, and free fatty acids in the patients with autonomic neuropathy than in the other groups (P less than 0.05). These findings indicate that several beta-receptor-mediated responses to epinephrine are enhanced in patients with diabetic autonomic neuropathy. The underlying mechanism remains to be elucidated.

Adult↗