Heart rate and blood pressure relative to jump. Heart rate and MAP relative to jump are shown. Both values changed significantly during the study, indicating that bungee jumping affected blood pressure and heart rate (P < 0.05). Heart rate response in time differed significantly between both groups (P < 0.05). Asterisks at the end of each curve indicate a significant (P < 0.05) change of the parameter during the experiment. P values indicate curve comparison. # Significant posttests between groups at the 

Heart rate and blood pressure relative to jump. Heart rate and MAP relative to jump are shown. Both values changed significantly during the study, indicating that bungee jumping affected blood pressure and heart rate (P < 0.05). Heart rate response in time differed significantly between both groups (P < 0.05). Asterisks at the end of each curve indicate a significant (P < 0.05) change of the parameter during the experiment. P values indicate curve comparison. # Significant posttests between groups at the 

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Article
Although a relation between diminished human immunity and stress is well recognized both within the general public and the scientific literature, the molecular mechanisms by which stress alters immunity remain poorly understood. We explored a novel model for acute human stress involving volunteers performing a first-time bungee jump from an altitud...

Contexts in source publication

Context 1
... is well recognized that cognitive per- ception of the environment is a major de- terminant of immune function, and conditions loosely grouped under the common denominator of stress are per- ceived as a significant risk factor for infection and autoimmunity (1–3). The activation of the stress response system influences the close relationship between the hypothalamic-pituitary-adrenal axis, the sympathetic nervous system and the immune system (4). Therefore, stress pre- sumably interacts with immunity owing to the release of stress hormones such as catecholamines and cortisol. Epinephrine, norepinephrine and cortisol in general may result in antiinflammatory effects. These antiinflammatory properties have been reproduced experimentally in humans using the model of intravenous in- jection of lipopolysaccharide (LPS) (5–8). We postulated that acute stress- induced release of stress hormones causes an immune suppressive phenotype and aimed to investigate this by using a novel human model of acute stress. For investigating the molecular basis of stress- dependent changes in immunity, use of human models seems inevitable. Practical and ethical considerations hamper investigations on the effects of severe stress on human immunity, and there is a need for an ethically acceptable human model that produces severe stress with moderate in- traindividual variation. High-altitude jumping seems to be almost universally associated with substantial induction of flight/fright responses. A recent study showed that during height exposure in all participants, fear, dizziness and body sway were increased, indicating that exposure to substantial heights induces a universal stress response (9). We decided to examine the usefulness of this phe- nomenon for investigating the effect of human stress on immune physiology. To this end, healthy male volunteers naive to bungee jumping were exposed to a jump from an altitude of 60 m. To study the role of catecholamines in the responses observed, half of the volunteers were pretreated with the β -receptor antagonist propranolol. A prospective clinical trial was con- ducted in a single center. Twenty healthy male volunteers, naive to bungee jumping or skydiving and aged between 18 and 35 years, were included in the study. Mean age was 27 years (range 18–35, n = 10) in the control group and 31 years (range 23–35, n = 10) in the propranolol group. Subjects were randomized between the use of propranolol, 40 mg 3 × a day for 3 d, or no pretreatment (control). The study was reviewed and approved by the local medical ethics committee. Written informed consent was obtained from all subjects. The study site was located at the hospital grounds, where a crane was placed. Bungee jumps took place from an altitude of 60 m, under supervision and guidance from an experienced commercial bungee jump crew. On the morning of the study day, an intravenous access catheter was placed in the cubital vein. Exactly 2 h before the jump, the first blood sample was drawn (in total 20 mL blood). Subsequent samples (20 mL) were drawn directly before the jump (while elevated at jump level), immediately after the jump and 2 h after jumping. Blood was drawn in Va- cutainer tubes (Becton-Dickinson, Breda, the Netherlands) containing EDTA-K3, for leukocyte and differential counts; in sodium citrate–containing tubes for measurement of coagulation and en- dothelial cell activation markers; in sodium heparin–containing tubes for ex vivo stimulations, phagocytosis and cortisol measurements; or in tubes containing reduced glutathione-EGTA buffer for measurement of epinephrine and norepinephrine. Plasma was separated and stored at –80°C until assays were performed. Measurements of blood pressure and heart rate were performed 30 min before, directly before, directly after and 2 h after the bungee jump using an automated device (Omron HEM-705CP, Omron Healthcare, Kyoto, Japan) (10). Plasma epinephrine and norepinephrine were assayed, as described previously, by reversed phase high- performance liquid chromatography (RP-HPLC) with fluorimetric detection after solvent extraction and derivatiza- tion with 1,2-diphenylethylenediamine (11). Cortisol was measured using a lu- minescence enzyme immunoassay (Im- mulite, Siemens Healthcare Diagnostics, Deerfield, IL, USA). Leukocyte counts, differentials, and CD4/CD8 numbers were assessed by using standard methods at the institutional clinical laboratory. Levels of tumor necrosis factor (TNF)- α , interleukin (IL)-1 β , IL-8 and IL-10 were determined by cytometric bead array (CBA; BD Biosciences, Breda, the Netherlands). Factor VIII levels were measured using an automated coagulation analyzer (Behring Coagulation System) with reagents and protocols from the manu- facturer (Dade Behring, Marburg, Ger- many). Measurements of prothrombin fragment F1 + 2 (Dade Behring), thrombin-antithrombin (TAT) complexes (Dade Behring), tissue-type plasminogen activator (tPA; Innotest, Innogenetics, Gent, Belgium) and von Willebrand factor antigen (antibodies from Dako, Glostrup, Denmark) were performed by enzyme-linked immunosorbent assay. Whole blood was mixed with an equal volume of plain RPMI 1640 (Invitrogen, Breda, the Netherlands) or with RPMI 1640 containing LPS (from Escherichia coli 0111:B4, ultra pure; InVivoGen, San Diego, CA, USA; 100 ng/mL). Blood was incubated at 37°C in 5% CO 2 for 24 h for cytokine measurement. Kinome array analysis was done as described earlier (12,13). In short, the peptide arrays (Pepscan Presto, Lelystad, the Netherlands) were incubated with cell lysates, containing 33 P- γ -ATP or 33 P- α -ATP (Perkin Elmer, Waltham, MA, USA) for 2 h at 37°C. Subsequently, the arrays were washed, dried and exposed to a phospho-imag- ing screen for 72 h and scanned on a phospho-imager (Storm 860, Molecular Dynamics, Stanford, CA, USA). For each peptide, the average and standard deviation of phosphorylation were determined and plotted in an amplitude- based hierarchical fashion. Peptides of which the average phosphorylation minus 1.96 times the standard deviation was higher than the value expected from describing the background distribution were considered to represent true phosphorylation events. Phospho-Fyn deter- minations were performed in blood taken 2 h before the jump and directly after jumping in four volunteers from the control group, as described earlier (14,15). In short, blood was lysed and the remaining leukocyte fraction was solubilized and subsequently subjected to immunoprecipitation using a Fyn antibody and blotted with a pan phospho- Src family antibody (Cell Signaling Tech- nology, Bioké, Leiden, the Netherlands). Phagocytosis of E . coli by blood granulocytes and monocytes was determined as described (16). Briefly, 100 μ L blood was added to 20 μ L fluorescein isothiocyanate–labeled opsonized E . coli and incubated at 37°C for 10 min. Cells were quenched and washed. Thereafter, erythrocytes were lyzed and DNA stain- ing solution was added. Cells were analyzed within 1 h on a FACScan flow cytometer. All values are means ± SEM. Changes related to time to jump were analyzed by one-way analysis of variance (repeated measures). Differences between groups were analyzed by two-way analysis of variance. A P value <0.05 was considered statistically significant. With regard to kinome profiles, statistical significance was tested by determining individual-term binomial distribution probability on paired samples from the same volunteer before and after jumping. Mean arterial blood pressure (MAP) increased directly before the bungee jump relative to 2 h earlier in both groups (both P < 0.05, Figure 1). Directly after the jump, mean arterial blood pressure had decreased again, which was followed by a further decrease until the end of the ob- servation period. Heart rate increased in a similar fashion in volunteers not pretreated with propranolol, but this change was absent in volunteers who were pretreated with propranolol (see Figure 1). Bungee jumping resulted in a time- dependent increase in the plasma concentrations of both epinephrine and norepinephrine directly before the jump in both groups ( P < 0.05 for both catecholamines for both groups, Figure 2A). A sharp decrease in epinephrine levels was observed directly after the bungee jump, whereas norepinephrine concentrations remained elevated longer. Cortisol levels remained unaltered before the jump but increased significantly during the jump (Figure 2B). Propranolol did not influence the release of catecholamines or ...
Context 2
... is well recognized that cognitive per- ception of the environment is a major de- terminant of immune function, and conditions loosely grouped under the common denominator of stress are per- ceived as a significant risk factor for infection and autoimmunity (1–3). The activation of the stress response system influences the close relationship between the hypothalamic-pituitary-adrenal axis, the sympathetic nervous system and the immune system (4). Therefore, stress pre- sumably interacts with immunity owing to the release of stress hormones such as catecholamines and cortisol. Epinephrine, norepinephrine and cortisol in general may result in antiinflammatory effects. These antiinflammatory properties have been reproduced experimentally in humans using the model of intravenous in- jection of lipopolysaccharide (LPS) (5–8). We postulated that acute stress- induced release of stress hormones causes an immune suppressive phenotype and aimed to investigate this by using a novel human model of acute stress. For investigating the molecular basis of stress- dependent changes in immunity, use of human models seems inevitable. Practical and ethical considerations hamper investigations on the effects of severe stress on human immunity, and there is a need for an ethically acceptable human model that produces severe stress with moderate in- traindividual variation. High-altitude jumping seems to be almost universally associated with substantial induction of flight/fright responses. A recent study showed that during height exposure in all participants, fear, dizziness and body sway were increased, indicating that exposure to substantial heights induces a universal stress response (9). We decided to examine the usefulness of this phe- nomenon for investigating the effect of human stress on immune physiology. To this end, healthy male volunteers naive to bungee jumping were exposed to a jump from an altitude of 60 m. To study the role of catecholamines in the responses observed, half of the volunteers were pretreated with the β -receptor antagonist propranolol. A prospective clinical trial was con- ducted in a single center. Twenty healthy male volunteers, naive to bungee jumping or skydiving and aged between 18 and 35 years, were included in the study. Mean age was 27 years (range 18–35, n = 10) in the control group and 31 years (range 23–35, n = 10) in the propranolol group. Subjects were randomized between the use of propranolol, 40 mg 3 × a day for 3 d, or no pretreatment (control). The study was reviewed and approved by the local medical ethics committee. Written informed consent was obtained from all subjects. The study site was located at the hospital grounds, where a crane was placed. Bungee jumps took place from an altitude of 60 m, under supervision and guidance from an experienced commercial bungee jump crew. On the morning of the study day, an intravenous access catheter was placed in the cubital vein. Exactly 2 h before the jump, the first blood sample was drawn (in total 20 mL blood). Subsequent samples (20 mL) were drawn directly before the jump (while elevated at jump level), immediately after the jump and 2 h after jumping. Blood was drawn in Va- cutainer tubes (Becton-Dickinson, Breda, the Netherlands) containing EDTA-K3, for leukocyte and differential counts; in sodium citrate–containing tubes for measurement of coagulation and en- dothelial cell activation markers; in sodium heparin–containing tubes for ex vivo stimulations, phagocytosis and cortisol measurements; or in tubes containing reduced glutathione-EGTA buffer for measurement of epinephrine and norepinephrine. Plasma was separated and stored at –80°C until assays were performed. Measurements of blood pressure and heart rate were performed 30 min before, directly before, directly after and 2 h after the bungee jump using an automated device (Omron HEM-705CP, Omron Healthcare, Kyoto, Japan) (10). Plasma epinephrine and norepinephrine were assayed, as described previously, by reversed phase high- performance liquid chromatography (RP-HPLC) with fluorimetric detection after solvent extraction and derivatiza- tion with 1,2-diphenylethylenediamine (11). Cortisol was measured using a lu- minescence enzyme immunoassay (Im- mulite, Siemens Healthcare Diagnostics, Deerfield, IL, USA). Leukocyte counts, differentials, and CD4/CD8 numbers were assessed by using standard methods at the institutional clinical laboratory. Levels of tumor necrosis factor (TNF)- α , interleukin (IL)-1 β , IL-8 and IL-10 were determined by cytometric bead array (CBA; BD Biosciences, Breda, the Netherlands). Factor VIII levels were measured using an automated coagulation analyzer (Behring Coagulation System) with reagents and protocols from the manu- facturer (Dade Behring, Marburg, Ger- many). Measurements of prothrombin fragment F1 + 2 (Dade Behring), thrombin-antithrombin (TAT) complexes (Dade Behring), tissue-type plasminogen activator (tPA; Innotest, Innogenetics, Gent, Belgium) and von Willebrand factor antigen (antibodies from Dako, Glostrup, Denmark) were performed by enzyme-linked immunosorbent assay. Whole blood was mixed with an equal volume of plain RPMI 1640 (Invitrogen, Breda, the Netherlands) or with RPMI 1640 containing LPS (from Escherichia coli 0111:B4, ultra pure; InVivoGen, San Diego, CA, USA; 100 ng/mL). Blood was incubated at 37°C in 5% CO 2 for 24 h for cytokine measurement. Kinome array analysis was done as described earlier (12,13). In short, the peptide arrays (Pepscan Presto, Lelystad, the Netherlands) were incubated with cell lysates, containing 33 P- γ -ATP or 33 P- α -ATP (Perkin Elmer, Waltham, MA, USA) for 2 h at 37°C. Subsequently, the arrays were washed, dried and exposed to a phospho-imag- ing screen for 72 h and scanned on a phospho-imager (Storm 860, Molecular Dynamics, Stanford, CA, USA). For each peptide, the average and standard deviation of phosphorylation were determined and plotted in an amplitude- based hierarchical fashion. Peptides of which the average phosphorylation minus 1.96 times the standard deviation was higher than the value expected from describing the background distribution were considered to represent true phosphorylation events. Phospho-Fyn deter- minations were performed in blood taken 2 h before the jump and directly after jumping in four volunteers from the control group, as described earlier (14,15). In short, blood was lysed and the remaining leukocyte fraction was solubilized and subsequently subjected to immunoprecipitation using a Fyn antibody and blotted with a pan phospho- Src family antibody (Cell Signaling Tech- nology, Bioké, Leiden, the Netherlands). Phagocytosis of E . coli by blood granulocytes and monocytes was determined as described (16). Briefly, 100 μ L blood was added to 20 μ L fluorescein isothiocyanate–labeled opsonized E . coli and incubated at 37°C for 10 min. Cells were quenched and washed. Thereafter, erythrocytes were lyzed and DNA stain- ing solution was added. Cells were analyzed within 1 h on a FACScan flow cytometer. All values are means ± SEM. Changes related to time to jump were analyzed by one-way analysis of variance (repeated measures). Differences between groups were analyzed by two-way analysis of variance. A P value <0.05 was considered statistically significant. With regard to kinome profiles, statistical significance was tested by determining individual-term binomial distribution probability on paired samples from the same volunteer before and after jumping. Mean arterial blood pressure (MAP) increased directly before the bungee jump relative to 2 h earlier in both groups (both P < 0.05, Figure 1). Directly after the jump, mean arterial blood pressure had decreased again, which was followed by a further decrease until the end of the ob- servation period. Heart rate increased in a similar fashion in volunteers not pretreated with propranolol, but this change was absent in volunteers who were pretreated with propranolol (see Figure 1). Bungee jumping resulted in a time- dependent increase in the plasma concentrations of both epinephrine and norepinephrine directly before the jump in both groups ( P < 0.05 for both catecholamines for both groups, Figure 2A). A sharp decrease in epinephrine levels was observed directly after the bungee jump, whereas norepinephrine concentrations remained elevated longer. Cortisol levels remained unaltered before the jump but increased significantly during the jump (Figure 2B). Propranolol did not influence the release of catecholamines or ...

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People can speak, and this provides opportunities to analyze human emotions using perceived experiences communicated via language, as well as through measurement and imaging techniques that are also applicable to other higher animal species. Here I compare four qualitative methodological approaches to test if, and how, thrill depends on fear. I use eight high-risk, high-skill, real-life outdoor adventure recreation activities to provide the test circumstances. I present data from: >4000 person-days of participant observation; interviews with 40 expert practitioners; retrospective autoethnography of 50 critical incidents over 4 decades; and experimental autoethnography of 60 events. Results from different methods are congruent, but different approaches yield different insights. The principal findings are as follows. Individuals differ in their fear and thrill responses. The same individual may have different responses on different occasions. Fear boosts performance, but panic causes paralysis. Anxiety or apprehension prior to a risky action or event differs from fear experienced during the event itself. The intensity of pre-event fear generally increases with the immediacy of risk to life, and time to contemplate that risk. Fear must be faced, assessed and overcome in order to act. Thrill can occur either during or after a high-risk event. Thrill can occur without fear, and fear without thrill. Below a lower threshold of perceived risk, thrill can occur without fear. Between a lower and upper threshold, thrill increases with fear. Beyond the upper threshold, thrill vanishes but fear remains. This there is a sawtooth relation between fear and thrill. Perceived danger generates intense focus and awareness. Fear and other emotions can disappear during intense concentration and focus. Under high risk, the usual emotional sequence is fear before the action or event, then focus during the action or event, then thrill, relief, or triumph afterward. The emotionless state persists only during the most intense concentration. For events long enough to differentiate time within the events, fear and thrill can arise and fade in different fine-scale sequences.