The aim of this study was to investigate whether or not the human immune system can be activated by a noninfectious stimulus, thereby improving the physiological status of the individual. The effect of a single cold water immersion (14 degrees C for 1 h) on the immune system of athletic young men, monitored immediately after immersion, was minimal. With the continuation of the cold water immersions (three times a week for a duration of 6 weeks) a small, but significant, increase in the proportions of monocytes, lymphocytes with expressed IL2 receptors (CD25) and in plasma tumour necrosis factor alpha content was induced. An increase in the plasma concentrations of some acute phase proteins, such as haptoglobin and haemopexin, was also observed. After 6 weeks of repeated immersions a trend towards an increase in the plasma concentrations of IL6 and the amount of total T lymphocytes (CD3), T helper cells (CD4), T suppressor cells (CD8), activated T and B lymphocytes (HLA-DR) and a decrease in the plasma concentration of alpha 1-antitrypsin was observed. Concentrations of IL1 beta, neopterin, C-reactive protein, orosomucoid, ceruloplasmin, macroglobulin, immunoglobulins (IgG, IgM, IgA) and C3, C4 components of the complement, as well as the total number of erythrocytes, leucocytes, granulocytes and neutrophils showed no significant changes after the repeated cold water immersions. It was concluded that the stress-inducing noninfectious stimuli, such as repeated cold water immersions, which increased metabolic rate due to shivering the elevated blood concentrations of catecholamines, activated the immune system to a slight extent. The biological significance of the changes observed remains to be elucidated.

To differentiate between the effect of cold and hydrostatic pressure on hormone and cardiovascular functions of man, a group of young men was examined during 1-h head-out immersions in water of different temperatures (32 degrees C, 20 degrees C and 14 degrees C). Immersion in water at 32 degrees C did not change rectal temperature and metabolic rate, but lowered heart rate (by 15%) and systolic and diastolic blood pressures (by 11 %, or 12%, respectively), compared to controls at ambient air temperature. Plasma renin activity, plasma cortisol and aldosterone concentrations were also lowered (by 46%, 34%, and 17%, respectively), while diuresis was increased by 107%. Immersion at 20 degrees C induced a similar decrease in plasma renin activity, heart rate and systolic and diastolic blood pressures as immersion at thermoneutrality, in spite of lowered rectal temperature and an increased metabolic rate by 93%. Plasma cortisol concentrations tended to decrease, while plasma aldosterone concentration was unchanged. Diuresis was increased by 89%. No significant differences in changes in diuresis, plasma renin activity and aldosterone concentration compared to subjects immersed to 32 degrees C were observed. Cold water immersion (14 degrees C) lowered rectal temperature and increased metabolic rate (by 350%), heart rate and systolic and diastolic blood pressure (by 5%, 7%, and 8%, respectively). Plasma noradrenaline and dopamine concentrations were increased by 530% and by 250% respectively, while diuresis increased by 163% (more than at 32 degrees C). Plasma aldosterone concentrations increased by 23%. Plasma renin activity was reduced as during immersion in water at the highest temperature. Cortisol concentrations tended to decrease. Plasma adrenaline concentrations remained unchanged. Changes in plasma renin activity were not related to changes in aldosterone concentrations. Immersion in water of different temperatures did not increase blood concentrations of cortisol. There was no correlation between changes in rectal temperature and changes in hormone production. Our data supported the hypothesis that physiological changes induced by water immersion are mediated by humoral control mechanisms, while responses induced by cold are mainly due to increased activity of the sympathetic nervous system.

The purpose of this study was to monitor changes in body and skin temperatures, heat production, subjective shivering, cold sensation and body fat content in humans after intermittent cold water immersion. Repeated exposures of young sportsmen to cold water (head out, 14 degrees C, 1 h, 3 times per week for 4-6 weeks) induced changes in regulation of thermal homeostasis. "Cold acclimated" subjects exhibited an hypothermic type of adaptation. Central and peripheral body temperatures at rest and during cold immersion were lowered. The metabolic response to cold was delayed and subjective shivering was attenuated. The observed hypothermia was due to the shift of the threshold for induction of cold thermogenesis to lower body temperatures. "Cold acclimated" subjects also showed a lowered cold sensation. Because of the observed physiological changes, about 20% of the total heat production was saved during one cold water immersion of "cold acclimated" subjects. Maximal aerobic and anaerobic performances were not altered. No change in the thermosensitivity of the body temperature controller, as assessed from the unchanged slope of the relation between the deep body temperature and total heat production, was observed. Changes in cold sensation and regulation of cold thermogenesis were noticed first after four cold water immersions and persisted for at least 2 weeks after termination of the adaptation procedure. A trend towards a small increase in the body fat content was also observed. This finding, as well as the increased vasoconstriction, evidenced by the lowered skin temperature, indicate that slight changes in body insulation may also occur after "cold acclimation" in humans.

The purpose of this study was to determine whether or not repeated short-term cold water immersions can induce a change in the activity of the sympathetic nervous system and, consequently, in cardiovascular functions in healthy young athletes. Changes in some plasma hormone concentrations were also followed. A single cold water immersion (head-out, at 14 degrees C, for 1 h) increased sympathetic nervous system activity, as evidenced by a four-fold increase (P < 0.05) in plasma noradrenaline concentration. Plasma adrenaline and dopamine concentrations were not increased significantly. Plasma renin-angiotensin activity was reduced by half (P < 0.05) during immersion but plasma aldosterone concentration was unchanged. Stimulation of the sympathetic nervous system during immersion did not induce significant changes in heart rate, but induced peripheral vasoconstriction (as judged from a decrease in skin temperature) and a small increase (by 10%) in systolic and diastolic blood pressures. No clear change in reactivity of the sympathetic nervous system was observed due to repeated cold water immersions (three times a week, for 6 weeks). Neither the plasma renin-angiotensin activity, aldosterone concentration nor cardiovascular parameters were significantly influenced by repeated cold water immersions. A lowered diastolic pressure and an increase in peripheral vasoconstriction were observed after cold acclimation, however. Evidently, the repeated cold stimuli were not sufficient to induce significant adaptational changes in sympathetic activity and hormone production.

Background: The aim of the study was to determine pregnancy-associated plasma protein-A (PAPP-A), which was recently described as a new marker of cardiovascular events, in patients with chronic renal insufficiency/failure and to find out its relationship to renal function and to prominent markers of oxidative stress (advanced oxidation protein products – AOPP) and inflammation (C-reactive protein – CRP). Methods: The studied group consisted of 36 chronic hemodialysis patients (HD), 10 patients treated with continuous ambulatory peritoneal dialysis (CAPD) and 38 patients with chronic renal insufficiency (CHRI) not yet dialyzed. PAPP-A was measured by Time Resolved Amplified Cryptate Emission technology. Determination of AOPP is based on a spectrophotometric method. Results: PAPP-A levels are statistically significantly elevated in the both groups of dialyzed patients in comparison with healthy subjects (27.0 ± 16.5 mIU/l in HD and 14.07 ± 6.73 mIU/l in CAPD vs. 8.22 ± 2.7 mIU/l in the control group, p < 0.0001 and p < 0.001, respectively, p < 0.05 HD vs. CAPD). The mean serum PAPP-A levels in the CHRI patients not yet dialyzed were not significantly higher in comparison with the control group (9.72 ±4.44 vs. 8.22 ± 2.7 mIU/l, n.s.). In the CHRI not dialyzed patients, we found a significant positive correlation between serum creatinine and PAPP-A levels (r = 0.68, p < 0.05). In comparison with controls, AOPP and CRP levels were significantly higher in HD patients [AOPP 155.0 ± 37.9 µmol/l, p < 0.0001 vs. controls, CRP 10.0 (4.6– 26.9) mg/l (median, interquartile range), p < 0.0001 vs. controls], CAPD patients [AOPP 118.5 ± 25.8 µmol/l, p < 0.0001 vs. controls, CRP 7.7 (2.0–18.8) mg/l, p < 0.01 vs. controls] and AOPP levels in chronic renal failure patients not yet dialyzed (98.5 ± 43.24 µmol/l, p < 0.01 vs. controls). The correlations between PAPP-A and AOPP (r = 0.49, p < 0.05) and PAPP-A and CRP (r = 0.48, p < 0.05) serum concentration were statistically significant in HD patients. In CAPD patients, neither a correlation between PAPP-A and AOPP nor a correlation between PAPP-A and CRP were found. Conclusion: We can conclude that serum PAPP-A levels sensitively reflect the changes in renal function, depend on dialysis modality, and may represent a novel marker associated with inflammation and oxidative stress in chronic renal failure patients.

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