Hormonal and metabolic response to three types of exercise of equal duration and external work output

Five normal men, aged 20-30 years, participated in three types of exercise (I, II, III) of equal duration (20 min) and total external work output (120-180 kJ) separated by ten days of rest. Exercises consisted of seven sets of squats with barbells on the shoulders (I; Maximal Power Output Wmax = 600-900 W), continuous cycling at 50 rev X min-1 (II; Wmax = 100-150 W) and seven bouts of intermittent cycling at 70 rev X min-1 (III; Wmax = 300-450 W). Plasma cortisol, glucagon and lactate increased significantly (P less than 0.05) during the exercise and recovery periods of the anaerobic, intermittent exercise (I and III) but not in the continuous, aerobic exercise (II). No consistent significant changes were found in plasma glucose. Plasma insulin levels decreased only during exercise II. The highest increase in cortisol and glucagon was not associated with the highest VE, VO2, Wmax or HR; however it was associated with the anaerobic component of exercise (lactic acid). It is suggested that in exercises of equal duration and total external work output, the continuous, aerobic exercise (II) led to lowest levels of glucogenic hormones.     

Metabolic and circulatory responses to the ingestion of glucose polymer and glucose/electrolyte solutions during exercise in man

Six men exercised on a cycle ergometer for 60 min on two occasions one week apart, at 68 +/- 3% of VO2max. On one occasion, a dilute glucose/electrolyte solution (E: osmolality 310 mosmol X kg-1, glucose content 200 mmol X l-1) was given orally at a rate of 100 ml every 10 min, beginning immediately prior to exercise. On the other occasion, a glucose polymer solution (P: osmolality 630 mosmol X kg-1, glucose content equivalent to 916 mmol X l-1) was given at the same rate. Blood samples were obtained from a superficial forearm vein immediately prior to exercise and at 15-min intervals during exercise; further samples were obtained at 15-min intervals for 60 min at rest following exercise. Heart rate and rectal temperature were measured at 5-min intervals during exercise. Blood glucose concentration was not different between the two tests during exercise, but rose to a peak of 8.7 +/- 1.2 mmol X l-1 (mean +/- SD) at 30-min post-exercise when P was drunk. Blood glucose remained unchanged during and after exercise when E was drunk. Plasma insulin levels were unchanged during exercise and were the same on both trials, but again a sharp rise in plasma insulin concentration was seen after exercise when P was drunk. The rate of carbohydrate oxidation during exercise, as calculated from VO2 and the respiratory exchange ratio, was not different between the two tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Indomethacin does not affect endogenous glucose production in type 2 diabetes mellitus.

In healthy subjects, basal endogenous glucose production is partly regulated by paracrine intrahepatic factors. It is currently unknown whether paracrine intrahepatic factors also influence the increased basal endogenous glucose production in patients with type 2 diabetes mellitus. Administration of indomethacin to patients with type 2 diabetes mellitus stimulates endogenous glucose production and inhibits insulin secretion. Our aim was to evaluate whether this stimulatory effect on glucose production is solely attributable to inhibition of insulin secretion. In order to do this, we administered indomethacin to 5 patients with type 2 diabetes during continuous infusion of somatostatin to block endogenous insulin and glucagon secretion and infusion of basal concentrations of insulin and glucagon in a placebo-controlled study. Endogenous glucose production was measured 3 hours after the start of the somatostatin, insulin and glucagon infusion, for 4 hours after administration of placebo/indomethacin, by primed, continuous infusion of [6,6-(2)H(2)] glucose. At the time of administration of placebo or indomethacin, there were no significant differences in plasma glucose concentrations and endogenous glucose production rates between the two experiments (16.4 +/- 2.09 mmol/l vs. 16.6 +/- 1.34 mmol/l and 17.7 +/- 1.05 micromol/kg/min and 17.0 +/- 1.06 micromol/kg/min), control vs. indomethacin). Plasma glucose concentration did not change significantly in the four hours after indomethacin or placebo administration. Endogenous glucose production in both experiments was similar after both placebo and indomethacin. Mean plasma C-peptide concentrations were all below the detection limit of the assay, reflecting adequate suppression of endogenous insulin secretion by somatostatin. There were no differences in plasma concentrations of insulin (76 +/- 5 vs. 74 +/- 4 pmol/l) and glucagon (69 +/- 8 vs. 71 +/- 6 ng/l) between the studies with levels remaining unchanged in both experiments. Plasma concentrations of cortisol, epinephrine, and norepinephrine were similar in the two studies and did not change significantly. We conclude that indomethacin stimulates endogenous glucose production in patients with type 2 diabetes mellitus by inhibition of insulin secretion.     

Plasma beta endorphin immunoreactivity: effects of sustained hyperglycemia with and without prior exercise

Seven healthy untrained men were studied to determine if sustained hyperglycemia is a stimulus to enhanced plasma levels of beta endorphin (beta-EP) and if so whether prior exercise affects that enhancement. After an overnight fast hyperglycemic glucose clamps were performed on 3 separate days: after prior rest, 2 h after exercise, and 48 h after exercise. Subjects exercised on a bicycle ergometer for 1 h at 150 W (64% VO2 max). Plasma glucose concentration was elevated in 4 continuous sequential stages to 7, 11, 20 and 35 mM with each stage lasting 90 min. Plasma glucose concentrations did not differ for each subject across the three clamps. beta-EP immunoreactivity was measured in arterialized venous blood samples using a specific and sensitive radioimmunoassay. Resting beta-EP at basal glucose concentrations was 3.8 +/- 0.7 fmol X ml-1 (mean +/- se) and prior exercise either 2h (3.2 +/- 0.5 fmol X ml-1) or 48 h (4.3 +/- 0.7 fmol X ml-1) before a clamp study did not effect these levels, (p greater than 0.05). At no time during the 3 hyperglycemic clamps did plasma levels of beta-EP differ significantly from resting values. At the highest level of hyperglycemia (35 mM) beta-EP was 3.1 +/- 0.2, 4.9 +/- 0.6 and 4.8 +/- 0.7 fmol X ml-1 in the resting, 2h and 48 h post exercise clamp studies respectively. The significance of these data is that this lack of a response is in distinct contrast to elevations of this peptide found during hypoglycemic states. We conclude that sustained hyperglycemia is not a stimulus to enhanced secretion of beta-EP into plasma and this lack of a response is not effected by prior exercise.     

Role of liver nerves and adrenal medulla in glucose turnover of running rats

Sympathetic control of glucose turnover was studied in rats running 35 min at 21 m X min-1 on the level. The rats were surgically liver denervated, adrenodemedullated, or sham operated. Glucose turnover was measured by primed constant infusion of [3-3H]glucose. At rest, the three groups had identical turnover rates and concentrations of glucose in plasma. During running, glucose production always rose rapidly to steady levels. The increase was not influenced by liver denervation but was halved by adrenodemedullation. Similarly, hepatic glycogen depletion was identical in denervated and control rats but reduced after adrenodemedullation. Early in exercise, glucose uptake rose identically in all groups and, in adrenodemedullated rats, matched glucose production. Accordingly, plasma glucose concentration increased in liver-denervated and control rats but was constant in adrenodemedullated rats. Compensatory changes in hormone or substrate levels explaining the lack of effect of liver denervation were not found. In rats with intact adrenals, the plasma epinephrine concentration was increased after 2.5 min of running. It is concluded that, in rats carrying out exercise of moderate intensity and duration, hepatic glycogenolysis and glucose production are not influenced by the autonomic liver nerves but are enhanced by circulating epinephrine.     

Increased glucagon secretion during hyperthermia in a sauna

Plasma glucagon, adrenaline, noradrenaline, insulin and glucose concentrations were measured in 7 healthy young males during hyperthermia in a sauna bath: plasma glucagon levels increased from baseline values of 127.0 +/- 12.9 (SEM) pg X ml-1 to a maximum of 173.6 +/- 16.1 (SEM) pg X ml-1 at the 20th min of exposure. No change in plasma insulin and a slight increase in plasma glucose concentration were seen. Since a concomitant moderate increase in plasma catecholamine levels was also present, the adrenergic stimulus is believed to trigger glucagon release during hyperthermia. Diminished visceral blood flow, known to occur in sauna baths, may cause a decrease in the degradation of plasma glucagon and thus contribute to the elevated plasma glucagon levels.     

Plasma renin activity, aldosterone and catecholamine levels when swimming and running

The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19-25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI X ml-1 X h-1) than after swimming (8.66 ng AngI X ml-1 X h-1). The PAC increase was slightly greater after running (123 pg X ml-1) than swimming (102 pg X ml-1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.     

Influence of prior exercise and liver glycogen content on the sensitivity of the liver to glucagon.

The purpose of the present study was to test the hypothesis that a prior period of exercise is associated with an increase in hepatic glucagon sensitivity. Hepatic glucose production (HGP) was measured in four groups of anesthetized rats infused with glucagon (2 microg. kg(-1). min(-1) iv) over a period of 60 min. Among these groups, two were normally fed and, therefore, had a normal level of liver glycogen (NG). One of these two groups was killed at rest (NG-Re) and the other after a period of exercise (NG-Ex; 60 min of running, 15-26 m/min, 0% grade). The two other groups of rats had a high hepatic glycogen level (HG), which had been increased by a fast-refed diet, and were also killed either at rest (HG-Re) or after exercise (HG-Ex). Plasma glucagon and insulin levels were increased similarly in all four conditions. Glucagon-induced hyperglycemia was higher (P < 0.01) in the HG-Re group than in all other groups. HGP in the HG-Re group was not, however, on the whole more elevated than in the NG-Re group. Exercised rats (NG-Ex and HG-Ex) had higher hyperglycemia, HGP, and glucose utilization than rested rats in the first 10 min of the glucagon infusion. HG-Ex group had the highest HGP throughout the 60-min experiment. It is concluded that hyperglucagonemia-induced HGP is stimulated by a prior period of exercise, suggesting an increased sensitivity of the liver to glucagon during exercise.     

Effects of glucose infusion in exercising rats

To determine whether feedforward control of liver glycogenolysis during exercise is subject to negative feedback by elevated blood glucose, glucose was infused into exercising rats at a rate that elevated blood glucose greater than 10 mM. Liver glycogen content decreased 22.4 mg/g in saline-infused rats compared with 13.6 mg/g in glucose-infused rats during the first 40 min of treadmill running (21 m/min, 15% grade). Liver adenosine 3',5'-cyclic monophosphate (cAMP) concentration was significantly lower in the glucose-infused rats during the exercise bout. The concentration of hepatic fructose 2,6-bisphosphate remained elevated throughout the exercise bout in glucose-infused rats but decreased markedly in saline-infused rats. Plasma insulin concentration was higher and plasma glucagon concentration lower in glucose-infused rats than in saline-infused rats during exercise. Early in exercise, liver glycogenolysis proceeds in the glucose-infused rats despite the fact that glucose and insulin concentrations are markedly elevated and liver cAMP is unchanged from resting values. These observations suggest the existence of a cAMP-independent feedforward system for activation of liver glycogenolysis that can override classical negative feedback mechanisms during exercise.     

Plasma volume change during heavy-resistance weight lifting

Blood samples were obtained from six young men before, and over a 60-min period following a bout of heavy-resistance weight lifting to determine changes in plasma volume. Weight lifting consisted of three sets of four exercises (arm curl, bench press, bent-arm row, and squat) performed using 70% of one-repetition maximum for as many repetitions as possible. Plasma volume change was determined from haematocrit and haemoglobin concentration. During weight lifting, mean oxygen uptake and heart rate were 1.96 L X min-1 and 158 bt X min-1, respectively. Plasma volume was decreased -14.3% (p less than 0.05) immediately following exercise and -7.0% (p less than 0.05) at 15 min into recovery, but had returned to the resting level within 30 min. It was concluded that heavy-resistance weight lifting elicits a significant decrease in plasma volume, which is similar in magnitude to that observed during running and cycling at 80-95% of maximal oxygen uptake.     

Metabolic and physiological response of the rabbit to continuous and intermittent treadmill exercise

Our knowledge of the effects of exercise on the heart is limited by the predominant use of rats as an animal model. The rabbit has many advantages over the rat as an animal model to study. However, little work has characterized its capacity to exercise. The purposes of the present study were to determine if the rabbit could (i) learn to run on a motor-driven treadmill at relatively high speeds using different exercise protocols, and (ii) characterize the various physiological and metabolic responses of the rabbit to acute bouts of exercise. We found that female New Zealand white rabbits had the capacity to run continuously on the treadmill for up to 21 min at 20 m/min until exhausted. Continuous, endurance-type exercise resulted in significant elevations in body temperature, heart rate, and plasma lactate levels. Plasma triglyceride concentration decreased as a function of this type of running whereas plasma glucose levels were unchanged. Twenty-four hours after a bout of running, plasma creatine phosphokinase activity was significantly elevated. The rabbits also had the capacity to learn to run using an intermittent, higher speed protocol. These physically untrained animals could achieve speeds of up to 70 m/min for 10 bouts of 15 s run/30 s rest. Their metabolic and physiological responses to this protocol were similar to those of continuous running with the following exceptions. The decrease in plasma triglyceride was less marked and the increase in plasma lactate was greater after intermittent exercise. Glycogen content of the rabbit vastus lateralis muscle was also significantly depleted after exhaustive, intermittent exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucose turnover and hormonal changes during insulin-induced hypoglycemia in trained humans

Eight athletes (T), studied the third morning after the last exercise session, and seven sedentary males (C) (maximal O2 consumption 65 +/- 4 vs. 49 +/- 4 (SE) ml X kg-1 X min-1, for T and C men, respectively) had insulin infused until plasma glucose, at an insulin level of 1,600 pmol X l-1, was 1.9 mmol X l-1. Glucose turnover was determined by primed constant rate infusion of 3-[3H]glucose. Basal C-peptide (0.46 +/- 0.04 vs. 0.73 +/- 0.06 pmol X ml-1) and glucagon (4 +/- 0.4 vs. 10 +/- 2 pmol X l-1) were lower (P less than 0.05) and epinephrine higher (0.30 +/- 0.06 vs. 0.09 +/- 0.03 nmol X l-1) in T than in C subjects. During and after insulin infusion production, disappearance and clearance of glucose changed identically in T and C subjects. However, in spite of identical plasma glucose concentrations, epinephrine (7.88 +/- 0.99 vs. 3.97 +/- 0.40 nmol X l-1), growth hormone (97 +/- 17 vs. 64 +/- 6 mU X l-1), and pancreatic polypeptide (361 +/- 84 vs. 180 +/- 29 pmol X l-1) reached higher levels (P less than 0.05) and glucagon (28 +/- 3 vs. 47 +/- 10 pmol X l-1) lower levels in T than in C subjects. Blood pressures changed earlier in athletes during insulin infusion, and early recovery of heart rate, free fatty acid, and glycerol was faster. Responses of norepinephrine, cortisol, C-peptide, and lactate were similar in the two groups. Training radically changes hormonal responses but not glucose kinetics in insulin hypoglycemia.     

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22-60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.     

Effect of exercise on plasma cyclic AMP

The purpose of this study was to confirm the relationship between cyclic AMP(cAMP) level in plasma and changes of hormones concentrations in blood, during and after physical exercise. The results were as follows: At rest, plasma cAMP were 23.1 p mole/ml on the average and decreased after glucose loading. The level in plasma increased in proportion to the intensity of exercises. Under the 50% condition of the maximal intensity, cAMP level in plasma was about 40 p mole/ml and the contents of both thyroxine and growth hormone in serum clearly increased. And, under the 70% of the maximal, the contents of both adrenaline and noradrenaline in serum as well as that of cAMP in plasma increased. Plasma cAMP level also increased by prolongation of exercise (ca 45 p mole/ml). And when exercise lasted over 1.5 hrs, plasma glucagon level began to rise. The effect of carbohydrate load to lower the levels of plasma cAMP were also found during physical exercise. These results suggested that the cAMP level in plasma was affected, not only by the some regulating factors of glycolytic activities such as adrenaline and glucagon, but also by the production of thyroxine and growth hormone at the onset of exercise.     

Increased epinephrine response and inaccurate glucoregulation in exercising athletes

Epinephrine responses to insulin-induced hypoglycemia have indicated that athletes have a higher adrenal medullary secretory capacity than untrained subjects. This view was tested by an exercise protocol aiming at identical stimulation of the adrenal medulla in the two groups. Eight athletes (T) and eight controls (C) ran 7 min at 60% maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. Plasma epinephrine both at rest and at identical relative work loads [110% VO2max: 8.73 +/- 1.51 (T) vs. 3.60 +/- 1.09 mmol X l-1 (C)] was higher [P less than 0.05) in T than in C. Norepinephrine, as well as heart rate, increased identically in the two groups, indicating identical sympathetic nervous activity. Lactate and glycerol were higher in T than in C after running. Glucose production peaked immediately after exercise and was higher in T than in C. Glucose disappearance increased less than glucose production and was identical in T and C. Accordingly plasma glucose increased, more in T than in C (P less than 0.01). In T glucose levels approached the renal threshold greater than 20 min postexercise. Glucose clearance increased less in T than in C during exercise and decreased postexercise to or below (T, P less than 0.05) basal levels, despite increased insulin levels. Long-term endurance training increases responsiveness of the adrenal medulla to exercise, indicating increased secretory capacity. During maximal exercise this may contribute to higher glucose production, lower clearance, more inaccurate glucoregulation, and higher lypolysis in T compared with C.     

Increased liver glycogen levels enhance exercise capacity in mice

Muscle glycogen depletion has been proposed as one of the main causes of fatigue during exercise. However, few studies have addressed the contribution of liver glycogen to exercise performance. Using a low-intensity running protocol, here, we analyzed exercise capacity in mice overexpressing protein targeting to glycogen (PTG) specifically in the liver (PTG^OE mice), which show a high concentration of glycogen in this organ. PTG^OE mice showed improved exercise capacity, as determined by the distance covered and time ran in an extenuating endurance exercise, compared with control mice. Moreover, fasting decreased exercise capacity in control mice but not in PTG^OE mice. After exercise, liver glycogen stores were totally depleted in control mice, but PTG^OE mice maintained significant glycogen levels even in fasting conditions. In addition, PTG^OE mice displayed an increased hepatic energy state after exercise compared with control mice. Exercise caused a reduction in the blood glucose concentration in control mice that was less pronounced in PTG^OE mice. No changes were found in the levels of blood lactate, plasma free fatty acids, or β-hydroxybutyrate. Plasma glucagon was elevated after exercise in control mice, but not in PTG^OE mice. Exercise-induced changes in skeletal muscle were similar in both genotypes. These results identify hepatic glycogen as a key regulator of endurance capacity in mice, an effect that may be exerted through the maintenance of blood glucose levels.     

Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Effect of sex on counterregulatory responses to exercise after antecedent hypoglycemia in type 1 diabetes

A marked sexual dimorphism exists in healthy individuals in the pattern of blunted neuroendocrine and metabolic responses following antecedent stress. It is unknown whether significant sex-related counterregulatory differences occur during prolonged moderate exercise after antecedent hypoglycemia in type 1 diabetes mellitus (T1DM). Fourteen patients with T1DM (7 women and 7 men) were studied during 90 min of euglycemic exercise at 50% maximal O(2) consumption after two 2-h episodes of previous-day euglycemia (5.0 mmol/l) or hypoglycemia of 2.9 mmol/l. Men and women were matched for age, glycemic control, duration of diabetes, and exercise fitness and had no history or evidence of autonomic neuropathy. Exercise was performed during constant "basal" intravenous infusion of regular insulin (1 U/h) and a 20% dextrose infusion, as needed to maintain euglycemia. Plasma glucose and insulin levels were equivalent in men and women during all exercise and glucose clamp studies. Antecedent hypoglycemia produced a relatively greater (P < 0.05) reduction of glucagon, epinephrine, norepinephrine, growth hormone, and metabolic (glucose kinetics) responses in men compared with women during next-day exercise. After antecedent hypoglycemia, endogenous glucose production (EGP) was significantly reduced in men only, paralleling a reduction in the glucagon-to-insulin ratio and catecholamine responses. In conclusion, a marked sexual dimorphism exists in a wide spectrum of blunted counterregulatory responses to exercise in T1DM after prior hypoglycemia. Key neuroendocrine (glucagon, catecholamines) and metabolic (EGP) homeostatic responses were better preserved during exercise in T1DM women after antecedent hypoglycemia. Preserved counterregulatory responses during exercise in T1DM women may confer greater protection against hypoglycemia than in men with T1DM.     

Diminished hormonal responses to exercise in trained rats

Male rats (120 g) either were subjected to a 12-wk physical training program (T rats) or were sedentary controls (C rats). Subsequently the rats were killed at rest or after a 45- or 90-min forced swim. At rest, T rats had higher liver and muscle glycogen concentrations but lower plasma insulin. During exercise, blood glucose increased 60% in T rats but decreased 20% in C rats. Plasma glucagon and insulin concentrations did not change in T rats but plasma glucagon increased and insulin decreased markedly in C rats. Plasma epinephrine (90 min: range, 0.78-2.96 ng-ml-1, (T) vs. 4.42-15.67 (C)) and norepinephrine (90 min: 0.70-2.22 (T) vs. 2.50-6.10 (C)) were lower in T than in C rats. Hepatic glycogen decreased substantially and, as with muscle glycogen, the decrease was parallel in T and C rats. The plasma concentrations of free fatty acids were higher but lactate and alanine lower in T than in C rats. In trained rats the hormonal response to exercise is blunted partly due to higher glucose concentrations. In these rats adipose tissue sensitivity to catecholamines is increased, and changes in glucagon and insulin concentrations are not necessary for increased lipolysis and hepatic glycogen depletion during exercise.     

Effect of hematocrit reduction on hormonal and metabolic responses to exercise

We wished to determine the effect of a 25% hematocrit reduction on glucoregulatory hormone release and glucose fluxes during exercise. In five anemic dogs, plasma glucose fell by 21 mg/dl and in five controls by 7 mg/dl by the end of the 90-min exercise period. After 50 min of exercise, hepatic glucose production (Ra) and glucose metabolic clearance rate (MCR) began to rise disproportionately in anemics compared with controls. By the end of exercise, the increase in Ra was almost threefold higher (delta 15.1 +/- 3.4 vs. delta 5.2 +/- 1.3 mg X kg-1 X min-1) and MCR nearly fourfold (delta 24.6 +/- 8.8 vs. delta 6.5 +/- 1.3 ml X kg-1 X min-1). Exercise with anemia, in relation to controls resulted in elevated levels of glucagon [immunoreactive glucagon (IRG) delta 1,283 +/- 507 vs delta 514 +/- 99 pg/ml], norepinephrine (delta 1,592 +/- 280 vs. delta 590 +/- 155 pg/ml), epinephrine (delta 2,293 +/- 994 vs. delta 385 +/- 186 pg/ml), cortisol (delta 6.7 +/- 2.2 vs. delta 2.1 +/- 1.0 micrograms/dl) and lactate (delta 12.1 +/- 2.2 vs. delta 4.2 +/- 1.8 mg/dl) after 90 min. Immunoreactive insulin and free fatty acids were similar in both groups. In conclusion, exercise with a 25% hematocrit reduction results in 1) elevated lactate, norepinephrine, epinephrine, cortisol, and IRG levels, 2) an increased Ra which is likely related to the increased counterregulatory response, and 3) we speculate that a near fourfold increase in MCR is related to metabolic changes due to hypoxia in working muscle.(ABSTRACT TRUNCATED AT 250 WORDS)