Plasma norepinephrine responses of man in cold water

Johnson, David G.; Hayward, J. S.; Jacobs, Thomas P.; Collis, M. L.; Eckerson, J. D.; Williams, Robert H.

doi:10.1152/jappl.1977.43.2.216

Cited by 108 publications

(57 citation statements)

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“…In general, noradrenaline concentration increases in the cold e n v i ro n m e n t , w i t h a d e c re a s e i n c or e ( r e c t a l ) temperature Therminarias et al, 1989). Johnson et al (1977) reported that the plasma noradrenaline response to cold water changes with skin temperature rather than rectal temperature. In the present study, T --sk during swimming in 23°C water was significantly lower than that in 28°C water, but the Tre was not.…”

Section: Discussionmentioning

confidence: 99%

Thermoregulatory Responses to Low-Intensity Prolonged Swimming in Water at Various Temperatures and Treadmill Walking on Land.

Fujishima

Shimizu

Ogaki

et al. 2001

J. Physiol. Anthropol.

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The purpose of the present study was to examine the effect of water temperature on the human body during low-intensity prolonged swimming. Six male college swimmers participated in this study. The experiments consisted of breast stroke swimming for 120 minutes in 23°C, 28°C and 33°C water at a constant speed of 0.4 m · sec -1 in a swimming flume. The same subjects walked on a treadmill at a rate of approximately 50% of maximal oxygen uptake (V • O 2 max) at the same relative int ensit y as the t hree swimming trials. Re ctal temperature (Tre) in 33°C water was unchanged during swimming for 120 minutes. Tre during treadmill walking increased significantly compared to the three different swimming trials. Tre, mean skin temperature (T --sk) and mean body temperature (T --b) in 23°C and 28°C water decreased significantly more than in both the 33°C water and walking on land. V• O 2 during swimming in 23°C water increased more than during swimming in the 28°C and 33°C trials; however, there were no significant differences in V• O 2 between the 23°C swimming trial and treadmill walking. Heart rate (HR) during treadmill walking on land increased significantly compared with HR during the three swimming trials. Plasma adrenaline concentration at the end of the treadmill walking was higher than that at the end of each of the three swimming trials. Noradrenaline concentrations at the end of swimming in the 23°C water and treadmill walking were higher than those during the other two swimming trials. Blood lactate concentration during swimming in 23°C water was higher than that during the other two swimming trials and walking on land. These results suggest that the balance of heat loss and heat production is maintained in the warm water temperature. Therefore, a relatively warm water temperature may be desirable when prolonged swimming or other water exercise is performed at low intensity.

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Section: Discussionmentioning

confidence: 99%

Thermoregulatory Responses to Low-Intensity Prolonged Swimming in Water at Various Temperatures and Treadmill Walking on Land.

Fujishima

Shimizu

Ogaki

et al. 2001

J. Physiol. Anthropol.

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“…For example, cytokines released from activated peripheral monocytes or activated peripheral monocytes themselves could circulate to the spleen and enhance the expression of proinflammatory cytokines in this tissue. Similarly, indirect activation of splenic immune cells via circulating catecholamines may be involved because cold stress increases plasma levels of catecholamines (18,26,46,52), which, in turn, can activate ␣2-adrenergic receptors and enhance proinflammatory cytokine levels (51). Because of this possibility, the present findings suggest that the upregulation of splenic cytokine gene expression to hypothermia under the conditions of the current experiments is not dependent on the sympathetic innervation to the spleen; however, an effect of the sympathetic nervous system via circulating catecholamines cannot be discounted.…”

Section: Discussionmentioning

confidence: 99%

“…Acute cold stress increases plasma concentrations of norepinephrine and epinephrine (18,26,46,52), changes the pattern of synchronized SND bursts (28), influences the frequency-domain relationships between discharge bursts in regionally selective sympathetic nerves (28), and produces nonuniform changes in the level of sympathetic nerve activity to selected target organs (28). With regard to the latter, hypothermia increases lumbar and decreases renal SND without significantly changing the level of activity in the splanchnic and adrenal nerves in anesthetized rats (28) and activates preganglionic cervical SND in anesthetized rabbits (27).…”

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confidence: 99%

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

Ganta

Helwig²,

Blecha³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system. Am J Physiol Regul Integr Comp Physiol 291: R558 -R565, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00846.2005.-Splenic nerve denervation abrogates enhanced splenic cytokine gene expression responses to acute heating, demonstrating that hyperthermia-induced activation of splenic sympathetic nerve discharge (SND) increases splenic cytokine gene expression. Hypothermia alters SND responses; however, the role of the sympathetic nervous system in mediating splenic cytokine gene expression responses to hypothermia is not known. The purpose of the present study was to determine the effect of hypothermia on the relationship between the sympathetic nervous system and splenic cytokine gene expression in anesthetized F344 rats. Gene expression analysis was performed using a microarray containing 112 genes, representing inflammatory cytokines, chemokines, cytokine/chemokine receptors and housekeeping genes. A subset of differentially expressed genes was verified by real-time RT-PCR analysis. Splenic SND was decreased significantly during cooling (core temperature decreased from 38 to 30°C) in splenicintact rats but remained unchanged in sham-cooled splenic-intact rats (core temperature maintained at 38°C). Hypothermia upregulated the transcripts of several genes, including, chemokine ligands CCL2, CXCL2, CXCL10, and CCL20, and interleukins IL-1␣, IL-1␤, and IL-6. Gene expression responses to hypothermia were similar for the majority of cytokine genes in splenic-intact and splenic-denervated rats. These results suggest that hypothermia-enhanced splenic cytokine gene expression is independent of splenic SND.hypothermia; splenic cytokine gene expression; splenic sympathetic nerve discharge EVIDENCE FROM THE DISCIPLINES of neuroscience and immunology demonstrate bidirectional communication pathways between the sympathetic nervous system and the immune system (2, 3, 13, 38). Sympathetic innervation to the spleen provides a connection between central sympathetic neural circuits and immunocompetent cells in the spleen (1,6,9,16,17). For example, chemical sympathectomy alters splenic T and B cell proliferation and natural killer cell activity (36 -40, 45) and diminishes splenic production of immunoglobulin M (31). Results of our recent studies demonstrate that in rats with intact splenic nerves, whole body hyperthermia (19) and central ANG II infusion (20) increase splenic sympathetic nerve discharge (SND) and the expression of selective splenic cytokine genes. Splenic cytokine gene expression responses to whole body hyperthermia and central ANG II infusion are significantly reduced in splenic nerve-denervated compared with splenic nerve-intact rats (19,20), suggesting that activation of splenic SND can enhance splenic cytokine gene expression.Hypothermia, a common side effect of extreme cold environments, anesthesia, and serious traumatic injuries, alters the sympathetic nervous system and immune system regula...

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“…For example, cytokines released from activated peripheral monocytes or activated peripheral monocytes themselves could circulate to the spleen and enhance the expression of proinflammatory cytokines in this tissue. Similarly, indirect activation of splenic immune cells via circulating catecholamines may be involved because cold-stress increases plasma levels of catecholamines (18,26,46,52), which in turn can activate α2-adrenergic receptors and enhance proinflammatory cytokine levels (51). Because of this possibility, the present findings suggest that the upregulation of splenic cytokine gene expression to hypothermia under the conditions of the current experiments is not dependent on the sympathetic innervation to the spleen; however, an effect of the sympathetic nervous system via circulating catecholamines cannot be discounted.…”

Section: Discussionmentioning

confidence: 99%

“…Hypothermia, a common side effect of extreme cold environments, anesthesia, and serious traumatic injuries, alters the sympathetic nervous system and immune system regulation (8, 13-15, 21, 27-29, 47-50). Acute cold stress increases plasma concentrations of norepinephrine and epinephrine (18,26,46,52), changes the pattern of synchronized SND bursts (28), influences the frequency-domain relationships between discharge bursts in regionally selective sympathetic nerves (28), and produces nonuniform changes in the level of sympathetic nerve activity to selected target organs (28). With regards to the latter, hypothermia increases lumbar and decreases renal SND without significantly changing the level of activity in the splanchnic and adrenal nerves in anesthetized rats (28) and activates preganglionic cervical SND in anesthetized rabbits (27).…”

Section: Introductionmentioning

confidence: 99%

#45 Central activation of sympathetic neural circuits alters splenic cytokine gene expression

Ganta

Lü

Helwig

et al. 2005

Brain, Behavior, and Immunity

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Important bidirectional interactions exist between the central nervous system and the immune system. Neural-immune interactions provide a regulatory system in the body and disturbances in these interactions may lead to disease. Although the sympathetic nervous system is thought to play a key role in mediating neural-immune interactions, central neural mechanisms mediating sympathetic-immune interactions and the effect of centrally-induced alterations in sympathetic nerve discharge on immune function is not known. We tested the hypothesis that central activation of sympathetic neural circuits alters splenic cytokine gene expression. In a separate study, we tested the hypothesis that hypothermia-induced changes in visceral sympathetic nerve discharge (SND) would be attenuated in middle-aged and aged compared with young rats. Previous studies have demonstrated that skin sympathoexcitatory responses to skin cooling are attenuated in aged compared with young subjects, suggesting that advancing age influences sympathetic nerve responsiveness to cooling. The effect of age on sympathetic nerves innervating other targets organs during acute cooling remains unknown. Central activation of splenic SND was produced using three different experimental interventions: increased core body temperature produced by acute heating, intracerebroventricular injection of angiotensin II (ANG II), and decreased core body temperature produced by acute cooling. Changes in gene expression profiles were analyzed using inflammatory cytokine-specific gene-array and further validated using real-time RT-PCR analysis. The following observations were made. 1) Splenic SND increased in response to each experimental intervention except in acute cooled young rats where there was a decrease in splenic SND. 2) Splenic cytokine gene expression of pro-inflammatory cytokines (e.g., IL-1β, IL-6, IL-2) and chemokines (GRO1, CXCL2, CCCL2 and, CXCL10) was increased in response to each experimental intervention. 3) Expression of splenic cytokine genes was reduced after splenic-denervation except in acute cooled rats. 4) Progressive hypothermia reduced splenic, renal, and adrenal SND in rats and was generally attenuated in middle-aged and aged rats. These results demonstrate the functional significance of changes in sympathetic nerve activity on splenic immune cell activation and the effect of age on SND responses to core body ABSTRACTImportant bidirectional interactions exist between the central nervous system and the immune system. Neural-immune interactions provide a regulatory system in the body and disturbances in these interactions may lead to disease. Although the sympathetic nervous system is thought to play a key role in mediating neural-immune interactions, central neural mechanisms mediating sympathetic-immune interactions and the effect of centrally-induced alterations in sympathetic nerve discharge on immune function is not known. We tested the hypothesis that central activation of sympathetic neural circuits alters splenic cytokine gene expr...

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Plasma norepinephrine responses of man in cold water

Cited by 108 publications

References 0 publications

Thermoregulatory Responses to Low-Intensity Prolonged Swimming in Water at Various Temperatures and Treadmill Walking on Land.

Thermoregulatory Responses to Low-Intensity Prolonged Swimming in Water at Various Temperatures and Treadmill Walking on Land.

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

#45 Central activation of sympathetic neural circuits alters splenic cytokine gene expression

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