Endurance run increases circulating IL-6 and IL-1ra but downregulates ex vivo TNF-alpha and IL-1 beta production

1995 ◽  
Vol 79 (5) ◽  
pp. 1497-1503 ◽  
Author(s):  
J. P. Drenth ◽  
S. H. Van Uum ◽  
M. Van Deuren ◽  
G. J. Pesman ◽  
J. Van der Ven-Jongekrijg ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Ex Vivo ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Trained Subjects ◽  
Norepinephrine Concentration ◽  
Fluid Losses ◽  
Cutaneous Vascular Resistance

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise

1995 ◽  
Vol 79 (5) ◽  
pp. 1487-1496 ◽  
Author(s):  
J. Gonzalez-Alonso ◽  
R. Mora-Rodriguez ◽  
P. R. Below ◽  
E. F. Coyle
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Trained Subjects ◽  
Norepinephrine Concentration ◽  
Fluid Losses ◽  
Cutaneous Vascular Resistance

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Exercise plasma catecholamines in dogs: role of adrenals and cardiac nerve endings

1981 ◽  
Vol 241 (2) ◽  
pp. H243-H247 ◽  
Author(s):  
F. Peronnet ◽  
R. A. Nadeau ◽  
J. de Champlain ◽  
P. Magrassi ◽  
C. Chatrand
Keyword(s):  
Adrenal Medulla ◽  
Species Difference ◽  
Plasma Catecholamines ◽  
Vena Cava ◽  
Moderate Intensity ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Moderate Exercise ◽  
Norepinephrine Concentration ◽  
Severe Exercise

The plasma norepinephrine concentration (NE, ng . ml-1) in the pulmonary artery of dogs increased above resting values (0.22 +/- 0.04) for moderate (0.53 +/- 0.06) and severe exercise (1.45 +/- 0.23) and during prolonged exercise of moderate intensity (2.06 +/- 0.14). The plasma epinephrine concentration (E) increased above resting values (0.14 +/- 0.04) for severe exercise only (0.76 +/- 0.10) or when moderate exercise was prolonged (1.81 +/- 0.24). The E response, which appeared greater than that found in humans, is probably related to the species difference in the vasomotor response to exercise between humans and dogs, the latter not being subjected to compensatory vasoconstriction in nonworking areas. The activity of the adrenal medulla is confirmed by the plasma catecholamine (CA) gradient between proximal and distal posterior vena cava at rest (0.20 +/- 0.09) and during short- (0.35 +/- 0.08) and long-duration exercise (1.37 +/- 0.23). On the contrary, the heart is not a source of plasma CA in dogs: coronary sinus CA did not exceed aortic CA at rest and for moderate exercise and was lower than aortic CA for severe exercise (4.80 +/- 0.25 vs. 6.55 +/- 0.76 ng . ml-1).. The sources of plasma NE remain unclear in exercising dogs. Significant amounts of NE may be released by the adrenal medulla.

Plasma and platelet catecholamine and catecholamine sulfate response to various exercise tests

1994 ◽  
Vol 267 (4) ◽  
pp. E537-E543
Author(s):  
G. Strobel ◽  
B. Friedmann ◽  
J. Jost ◽  
P. Bartsch
Keyword(s):  
Average Power ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
O2 Consumption ◽  
Exercise Tests ◽  
Trained Subjects ◽  
Low Intensity ◽  
Average Power Output ◽  
Response To Exercise ◽  
Sympathoadrenergic Activity

We tested the hypothesis that platelet and plasma catecholamine sulfates (CA-S) and platelet catecholamines (CA) reflect the overall sympathoadrenergic activation by exercise of 1 h duration. Ten well-trained subjects performed a low-intensity [62% maximum O2 consumption (VO2max); LI] and a high-intensity exercise test (77% VO2max; HI) and two tests at a similar average power output that consisted of 20 min at 77% VO2max and 40 min at 62% VO2max (HI/LI) and vice versa (LI/HI). Plasma norepinephrine sulfate (NE-S) increased to higher levels after HI than after LI exercise (15.5 +/- 2.1 vs. 8.9 +/- 0.7 nmol/l). Immediately after HI/LI and LI/HI plasma NE-S was similarly increased (9.59 +/- 1.1 vs. 9.96 +/- 1.3 nmol/l), whereas norepinephrine was higher after LI/HI than after HI/LI (23.0 +/- 3.2 vs. 15.7 +/- 2.3 nmol/l). Platelet CA and CA-S were increased only after HI. In conclusion, the plasma NE-S response to exercise parallels the overall sympathetic activation. These results support the hypothesis that plasma NE-S measured immediately after exercise reflects the overall sympathoadrenergic activity over prolonged periods of exercise. Platelet CA and CA-S poorly reflect sympathoadrenergic activation.

Influence of caffeine on metabolic responses of men at rest in 28 and 5 degrees C

1990 ◽  
Vol 68 (5) ◽  
pp. 1889-1895 ◽  
Author(s):  
K. W. MacNaughton ◽  
P. Sathasivam ◽  
A. L. Vallerand ◽  
T. E. Graham
Keyword(s):  
Cold Stress ◽  
Respiratory Exchange Ratio ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
O2 Consumption ◽  
Plasma Epinephrine ◽  
Double Blind ◽  
Caffeine Ingestion ◽  
Adult Men ◽  
Norepinephrine Metabolism

Cold stress and caffeine ingestion are each reported to increase plasma catecholamines, free fatty acid (FFA) concentrations, and energy metabolism. This study examined the possible interaction of these two metabolic challenges in four double-blind counterbalanced trials. Young adult men (n = 6) ingested caffeine (5 mg/kg) or placebo (dextrose, 5 mg/kg) and rested for 2 h in 28 or 5 degrees C air. Cold stress alone elevated (P less than 0.05) plasma norepinephrine, metabolism (O2 consumption, VO2), and respiratory exchange ratio (RER). Caffeine alone increased (P less than 0.05) plasma epinephrine and FFA but not RER. When the two challenges were combined (caffeine plus 5 degrees C for 2 h) norepinephrine and epinephrine were increased (P less than 0.05) as was FFA. However, VO2, RER, and skin and rectal temperatures were not different from the responses observed at 5 degrees C after placebo ingestion. The data suggest that caffeine selectively increases plasma epinephrine, whereas cold air increases norepinephrine. During the cold exposure, increasing epinephrine and FFA above normal levels did not appear to influence the metabolic or thermal responses to the cold stress. In fact the increase in RER suggested a greater carbohydrate oxidation.

Hemodynamics of orthostatic intolerance: implications for gender differences

2004 ◽  
Vol 286 (1) ◽  
pp. H449-H457 ◽  
Author(s):  
Qi Fu ◽  
Armin Arbab-Zadeh ◽  
Merja A. Perhonen ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Cardiac Mechanics ◽  
Plasma Norepinephrine ◽  
Stroke Index ◽  
Orthostatic Tolerance ◽  
Norepinephrine Concentration ◽  
Pulmonary Capillary ◽  
Cardiac Filling

Women have a greater incidence of orthostatic intolerance than men. We hypothesized that this difference is related to hemodynamic effects on regulation of cardiac filling rather than to reduced responsiveness of vascular resistance during orthostatic stress. We constructed Frank-Starling curves from pulmonary capillary wedge pressure (PCWP), stroke volume (SV), and stroke index (SI) during lower body negative pressure (LBNP) and saline infusion in 10 healthy young women and 13 men. Orthostatic tolerance was determined by progressive LBNP to presyncope. LBNP tolerance was significantly lower in women than in men (626.8 ± 55.0 vs. 927.7 ± 53.0 mmHg × min, P < 0.01). Women had steeper maximal slopes of Starling curves than men whether expressed as SV (12.5 ± 2.0 vs. 7.1 ± 1.5 ml/mmHg, P < 0.05) or normalized as SI (6.31 ± 0.8 vs. 4.29 ± 0.6 ml·m–2·mmHg–1, P < 0.05). During progressive LBNP, PCWP dropped quickly at low levels, and reached a plateau at high levels of LBNP near presyncope in all subjects. SV was 35% and SI was 29% lower in women at presyncope (both P < 0.05). Coincident with the smaller SV, women had higher heart rates but similar mean arterial pressures compared with men at presyncope. Vascular resistance and plasma norepinephrine concentration were similar between genders. We conclude that lower orthostatic tolerance in women is associated with decreased cardiac filling rather than reduced responsiveness of vascular resistance during orthostatic challenges. Thus cardiac mechanics and Frank-Starling relationship may be important mechanisms underlying the gender difference in orthostatic tolerance.

Catecholamine-fuel interrelationships during exercise in fasting men

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres
Keyword(s):  
Maximal Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Adrenergic Response ◽  
Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

Influnce of the beta-adrenergic agonist clenbuterol on plasma catecholamines and lymphocyte beta-receptors

1986 ◽  
Vol 1 (3) ◽  
pp. 234-236
Author(s):  
B. Bondy ◽  
M. Ackenheil ◽  
G. Laakmann ◽  
H.T. Munz
Keyword(s):  
Specific Binding ◽  
Plasma Catecholamines ◽  
Adrenergic System ◽  
Plasma Norepinephrine ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Receptors ◽  
Β Receptor ◽  
Beta Adrenergic Agonist ◽  
The Brain

SummaryThe influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-adrenergic agonists exercise a similar effect on the peripheral adrenergic system and on the adrenergic system in the brain.

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.

Altered plasma catecholamines and numbers of α- and β-adrenergic receptors in platelets and leucocytes in hyperthyroid patients normalized under antithyroid treatment

1985 ◽  
Vol 110 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Dieter Ratge ◽  
Sabine Hansel-Bessey ◽  
Hermann Wisser
Keyword(s):  
Dissociation Constants ◽  
Plasma Catecholamines ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Plasma Norepinephrine ◽  
Thyroid State ◽  
Antithyroid Treatment ◽  
Equilibrium Dissociation Constants ◽  
Equilibrium Dissociation ◽  
Hyperthyroid Patients

Abstract. We measured plasma catecholamines, α- and β-adrenoreceptor numbers and the accumulation of cyclic adenosine monophosphate (cAMP) in the unstimulated state and in response to 10 μmol/l (-) isoproterenol in blood cells from 29 euthyroid controls and from 18 patients with spontaneous hyperthyroidism. In the thyrotoxic patients plasma norepinephrine (1.14 ± 0.5 nmol/l) and epinephrine (0.3 ±0.14 nmol/l) were significantly decreased compared with plasma norepinephrine (1.87 ± 0.7 nmol) and epinephrine (0.41 ± 0.19 nmol/l) in the controls (P < 0.01 and P < 0.05, respectively) and the values obtained in subjects rendered euthyroid by antithyroid treatment (P < 0.001, respectively). α-adrenoceptor density in platelet membranes obtained from patients in the hyperthyroid state (114 ± 38 sites per cell) was significantly decreased when compared with controls (159 ± 48 sites per cell, P < 0.01) and the values from patients under effective antithyroid treatment (136 ± 35 sites per cell, P < 0.01). On the contrary, a significant increase in β-adrenoceptor density in mononuclear leucocyte (MNL) membranes was found in hyperthyroid patients (1751 ± 237 sites/cell) when compared with controls (1510 ± 351 sites/cell, P < 0.05) and the same patients following antithyroid treatment (1455 ± 260 sites/cell, P < 0.001). The equilibrium dissociation constants (KD) did not change in hyperthyroidism. Basal cAMP concentrations in MNL were higher in untreated thyrotoxicosis (45 ± 18 pmol/106 cells/10 min) than in patients in the euthyroid state (35 ± 9 pmol/106 cells/10 min, P < 0.05). Our data support the hypothesis that the balance of α- and β-adrenoceptors depends on the thyroid state. However, before the reputed catecholamine supersensitivity in hyperthyroid man can be accepted, the relationship between alterations in adrenoceptors and the biological responsiveness to catecholamines has to be demonstrated in different human tissues.

Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1340-1350 ◽  
Author(s):  
S. J. Montain ◽  
E. F. Coyle
Keyword(s):  
Blood Flow ◽  
Prolonged Exercise ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Sodium Concentration ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Warm Environment ◽  
Cardiovascular Drift ◽  
Highly Correlated

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20–22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.

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