Effect of physical training on the capacity to secrete epinephrine

1988 ◽  
Vol 64 (1) ◽  
pp. 11-16 ◽  
Author(s):  
M. Kjaer ◽  
H. Galbo
Keyword(s):  
Hypobaric Hypoxia ◽  
Plasma Norepinephrine ◽  
Plasma Epinephrine ◽  
O2 Uptake ◽  
Acute Hypobaric Hypoxia ◽  
Arterial Pco2 ◽  
Norepinephrine Concentration ◽  
Arterial Po2 ◽  
Secretory Capacity ◽  
Epinephrine Concentration

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.

The human sympathochromaffin system

1984 ◽  
Vol 247 (3) ◽  
pp. E380-E384 ◽  
Author(s):  
S. D. Shah ◽  
T. F. Tse ◽  
W. E. Clutter ◽  
P. E. Cryer
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Norepinephrine ◽  
Plasma Epinephrine ◽  
Norepinephrine Release ◽  
Norepinephrine Concentration ◽  
Sympathetic Nervous ◽  
Biological Actions ◽  
Chromaffin Tissue ◽  
Epinephrine Concentration

Hypoglycemia stimulates adrenomedullary epinephrine secretion; standing stimulates sympathetic neural norepinephrine release. In five bilaterally adrenalectomized persons plasma epinephrine, measured with a sensitive single-isotope derivative assay, rose from 15 +/- 2 to 35 +/- 7 pg/ml (P less than 0.02) during hypoglycemia but did not increase during standing. In contrast, plasma norepinephrine rose during standing but not during hypoglycemia. Thus, in humans 1) extra-adrenal epinephrine secretion is regulated and derived from innervated cells other than sympathetic postganglionic neurons; 2) because the plasma levels of epinephrine in adrenalectomized individuals even in response to the potent stimulus of hypoglycemia are below physiological thresholds, any biological actions of extra-adrenal epinephrine in adults must be paracrine rather than endocrine in nature; 3) hypoglycemia does not appear to stimulate the sympathetic nervous system. In view of these findings, we propose that extra-CNS catecholamine-producing tissues be termed the sympathochromaffin system consisting of two components: 1) the sympathetic nervous system that releases the neurotransmitter norepinephrine from its postganglionic neurons, and 2) the chromaffin tissues, including the adrenal medullae, that contain cells that secrete epinephrine, norepinephrine, or dopamine. The plasma epinephrine concentration is a valid measure of its chromaffin tissue (predominantly adrenomedullary) secretion, whereas the plasma norepinephrine concentration is an index of sympathetic neuronal activity under some but not all conditions.

Reduced epinephrine clearance and glycemic sensitivity to epinephrine in older individuals

1998 ◽  
Vol 275 (5) ◽  
pp. E770-E776 ◽  
Author(s):  
James C. Marker ◽  
William E. Clutter ◽  
Philip E. Cryer
Keyword(s):  
Sedentary Lifestyle ◽  
Plasma Norepinephrine ◽  
Older Individuals ◽  
Plasma Epinephrine ◽  
Response Curves ◽  
Older Subjects ◽  
Young Subjects ◽  
Cellular Responsiveness ◽  
The Impact ◽  
Epinephrine Concentration

To test the hypothesis that glycemic sensitivity to epinephrine is reduced in older individuals and to assess the impact of a sedentary lifestyle on responses to the hormone, we performed 30-min sequential intravenous infusions of epinephrine (0, 41, 82, 164, 246, and 328 pmol ⋅ kg−1⋅ min−1) in young ( n = 10) and older ( n = 23) healthy subjects. We performed these again after 12 mo of physical training, which raised peak O2consumption from 24.4 ± 1.0 to 30.4 ± 1.4 ml ⋅ kg−1⋅ min−1( P < 0.01) in most of the older subjects ( n = 21). During epinephrine infusions, plasma epinephrine concentrations were higher ( P = 0.0001) in older than in young subjects (e.g., final values of 7,280 ± 500 vs. 4,560 ± 380 pmol/l, respectively), indicating that the clearance of epinephrine from the circulation was reduced in the older individuals. Plasma epinephrine concentration-response curves disclosed reduced glycemic sensitivity to the hormone in the older subjects ( P = 0.0001), a finding plausibly attributed to increased sympathetic neural activity, as evidenced here by higher plasma norepinephrine concentrations ( P = 0.0001) in the older subjects and consequent desensitization of cellular responsiveness to catecholamines. Training did not correct reduced epinephrine clearance, reduced glycemic sensitivity to epinephrine, or raised norepinephrine levels. We conclude that aging is associated with reduced clearance of epinephrine from the circulation and reduced glycemic sensitivity to epinephrine, the latter plausibly attributed to an age-associated increase in sympathetic neural norepinephrine release. These age-associated changes are not the result of a sedentary lifestyle.

Effect of exercise on epinephrine turnover in trained and untrained male subjects

1985 ◽  
Vol 59 (4) ◽  
pp. 1061-1067 ◽  
Author(s):  
M. Kjaer ◽  
N. J. Christensen ◽  
B. Sonne ◽  
E. A. Richter ◽  
H. Galbo
Keyword(s):  
Work Load ◽  
Hot Water ◽  
Plasma Epinephrine ◽  
Work Intensity ◽  
O2 Uptake ◽  
Vo2 Max ◽  
Work Time ◽  
Arterial Blood ◽  
Male Subjects ◽  
Secretory Capacity

The kinetics underlying plasma epinephrine concentrations were studied. Six athletes (T) and six sedentary males (C) were given intravenous infusions of 3H-labeled epinephrine, after which arterial blood was drawn. They rested sitting and bicycled continuously to exhaustion (60 min at 125 W, 60 min at 160 W, 40 min at 200 W, and 240 W to the end). Work time was 154 +/- 13 (SE) (T) and 75 +/- 6 (C) min. At rest, epinephrine clearance was identical [28.4 +/- 1.3 (T) vs. 29.2 +/- 1.8 (C) ml . kg-1 . min-1], but plasma concentration [1.42 +/- 0.27 (T) vs. 0.71 +/- 0.16 (C) nmol . l-1] and, accordingly, secretion [2.9 +/- 0.7 vs. 1.5 +/- 0.4 nmol . min-1] were higher (P less than 0.05) in T than C subjects. Epinephrine clearance was closely related to relative work load, decreasing from 15% above the basal level at 30% of maximal O2 uptake (VO2 max) to 22% below at 76% of VO2 max. Epinephrine concentrations increased much more with work intensity than could be accounted for by changes in clearance and were, at exhaustion, higher (P less than 0.05) in T (7.2 +/- 1.6) than in C (2.5 +/- 0.7 nmol . l-1) subjects despite similar glucose, heart rate, and hematocrit values. At a given load, epinephrine clearance rapidly became constant, whereas concentration increased continuously. Forearm extraction of epinephrine invalidated use of blood from a cubital vein or a hand vein arterialized by hot water in turnover measurements. During exercise, changes in epinephrine concentrations reflect changes in secretion rather than in clearance. Training may increase adrenal medullary secretory capacity.

Circulatory response to arterial hyperoxia

1979 ◽  
Vol 46 (5) ◽  
pp. 973-977 ◽  
Author(s):  
Y. Cassuto ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
The Other ◽  
O2 Uptake ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Circulatory Response ◽  
Systemic Artery ◽  
The Right ◽  
Arterial Po2

We have studied the circulatory response to 100% O2 at 1 and 3 atm, using unanesthetized rabbits in which a systemic artery and the right heart had been cannulated previously. One group of animals served as controls; the other was infused with a flurocarbon emulsion that boosted blood O2 solubility to approximately 5 ml.100 ml-1.atm-1. Exposure to hyperoxia caused an identical sustained rise in arterial PO2 in both groups. O2 uptake was measured during normobaric exposure to 100% O2 and was found to be the same as in control conditions. There was an immediate rise in right heart PO2, more marked in infused animals, but this increase was only temporary, and PO2 dropped, while the right heart-arterial PCO2 difference rose, indicating a gradual fall in cardiac output. This readjustment occurred at a faster rate in the infused animals, a difference that led us to conclude that the peripheral response to hyperoxia is influenced by factors other than arterial PO2. The pronounced decrease in cardiac output seen in infused rabbits was accompanied by lactic acidosis, implying that some of the animals' tissues were becoming hypoxic in the presence of arterial hyperoxia.

Hypotension during vasopressin receptor blockade: role of V2 receptors and sympathetic nervous system

1991 ◽  
Vol 260 (6) ◽  
pp. H1878-H1887
Author(s):  
V. L. Brooks ◽  
D. C. Hatton
Keyword(s):  
Peripheral Resistance ◽  
Sympathetic Tone ◽  
Plasma Norepinephrine ◽  
Norepinephrine Concentration ◽  
Sympathetic Nervous ◽  
V2 Antagonist ◽  
Dose Dependent ◽  
Nitroprusside Infusion ◽  
Epinephrine Concentration

This study investigated possible mechanisms for the hypotension produced by nitroprusside infusion in conscious dogs pretreated with a V1 vasopressin antagonist. The hypothesis that an action of vasopressin at V2-like receptors contributes to the hypotension was tested by comparing the effects of a V1 antagonist to the effects of a combined V1/V2 antagonist. Nitroprusside infusion produced dose-dependent decreases in arterial and atrial pressures. Larger decreases in pressures were produced in animals pretreated with either antagonist; however, the decreases in V1/V2-blocked dogs were not less than the decreases in V1-blocked dogs. These data suggest that V2-like actions of vasopressin do not contribute to the hypotensive effects of V1 blockade. A second hypothesis was that the greater hypotension was due to activation of a cardiac reflex to cause withdrawal of sympathetic tone, a decrease in peripheral resistance, and adrenal activation. Measurement of cardiac output revealed that the larger decreases in arterial pressure were due to larger decreases in total peripheral resistance. The hypotension was also associated with decreases in heart rate, unchanging plasma norepinephrine concentration, and increases in epinephrine concentration. These data are consistent with the hypothesis that the fall in pressure observed in dogs pretreated with a V1 antagonist is secondary to a decrease in peripheral resistance that is due at least in part to withdrawal of sympathetic tone.

Acute Hypobaric Hypoxia (5486 m) Induces Greater Pulmonary HIF-1 Activation in Hilltop Compared to Madison Rats

2007 ◽  
Vol 8 (4) ◽  
pp. 312-321 ◽  
Author(s):  
Barbara J. Engebretsen ◽  
David Irwin ◽  
Maria E. Valdez ◽  
Mary K. O'Donovan ◽  
Alan Tucker ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Acute Hypobaric Hypoxia

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

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