Pyruvate accumulation may contribute to acceleration-induced impairment of physical and cognitive abilities: an experimental study.

BACKGROUND: Fatigue can be induced after acceleration exposure, however its mechanism is still unclear. The aim of the present study was to examine whether metabolites' changes can decrease cognitive and physical function after acceleration. METHODS: Graybiel scale and Fatigue Self-rating scale were used to assess the seasickness and fatigue degrees of 87 male seafarers respectively after sailing. To test the effect of pyruvate on cognitive and physical functions, five different doses of pyruvate were administrated into rats. Insulin can reduce the accumulation of pyruvate. To observe the insulin effect on pyruvate, cognitive and physical functions after acceleration, insulin administration or treatment of promoting insulin secretion was used. Physical and cognitive functions were assessed using open field test (OFT), morris water maze (MWM) and loaded swimming test (LST) in animals. RESULTS: Physical and cognitive abilities were decreased obviously, and serum pyruvate increased mostly in human and rats after acceleration. Compared with vehicle group, physical and cognitive abilities were significantly decreased after pyruvate administration. Besides, we found a significant decline in adenosine triphosphate (ATP) concentration and pyruvate dehydrogenase (PDH) activity in the hippocampus, prefrontal cortex, liver, and muscle of rats treated with acceleration or pyruvate injection, while insulin administration or treatment of promoting insulin secretion markedly alleviated this decline and the impairment of physical and cognitive abilities, compared with the control group. CONCLUSION: Our results indicate that pyruvate has a negative effect on physical and cognitive abilities after acceleration. Insulin can inhibit pyruvate accumulation and cognitive and physical function after acceleration exposure.

Impact of oral vitamin C on histamine levels and seasickness.

BACKGROUND: Seasickness is a risk aboard a ship. Histamine is postulated as a causative agent, inversely related to the intake of vitamin C. Persons with mastocytosis experienced improvement of nausea after the intake of vitamin C. OBJECTIVE: To determine whether vitamin C suppresses nausea in 70 volunteers who spent 20 minutes in a life raft, exposed to one-meter-high waves in an indoor pool. METHOD: Double-blind placebo-controlled crossover study. Two grams of vitamin C or placebo was taken one hour before exposure. Blood samples were taken one hour before and after exposure to determine histamine, diamine oxidase, tryptase, and vitamin C levels. Symptom scores were noted on a visual analog scale. On the second day the test persons were asked which day they had felt better. RESULTS: Seven persons without symptoms were excluded from the analysis. Test persons had less severe symptoms after the intake of vitamin C (p < 0.01). Scores on the visual analog scale were in favor of vitamin C, but the difference was not significant. Twenty-three of 63 persons wished to leave the raft earlier: 17 after the intake of placebo and 6 after the intake of vitamin C (p < 0.03). Women (p < 0.02) and men below 27 years of age (p < 0.02) had less pronounced symptoms after the intake of vitamin C. Histamine (p < 0.01) and DAO levels were increased after the intake of vitamin C (p < 0.001) and after placebo (n.s.). The fact that the second test day was rated less stressful by most volunteers is indicative of habituation. CONCLUSIONS: Some of the data show that vitamin C is effective in suppressing symptoms of seasickness, particularly in women and men younger than 27 years of age, and is devoid of side effects. Histamine levels were initially increased after the test persons had been exposed to waves.

Serum levels of immunoglobulins (IgG, IgA, IgM) in Antarctic summer expeditioners and their relationship with seasickness.

The Antarctic continent is full of environmental extremes like isolation, cold, UV exposure, and blizzards etc. The present study was conducted to analyze the effect of ship borne journey and the impact of Antarctic harsh environment on serum immunoglobulin (IgG, IgM, IgA) levels and their relationship with seasickness in Indian expeditioners. It was observed that one month onboard ship journey induced an increase in serum IgA levels and decrease in IgG levels while after being one month off board at the Indian research station Maitri, decreased levels of IgG and increased levels of IgA were found. IgM levels were not altered in comparison to the base line control. Moreover, serum IgG level showed a positive correlation while IgA level showed a negative correlation with seasickness. The stimulation of human peripheral blood mononuclear cells (PBMCs) with serum of expeditioner at different places showed that IgA at lower dose induces the release of pro-inflammatory IL-1ß, and IL-6 cytokines from PBMCs while higher dose of IgA decreases proinflammatory cytokine production. The release of anti-inflammatory cytokines TGF-ß1 and IL-10 was not significantly altered. Thus, the present study concluded that ship borne journey and Antarctic environment lead to increased serum IgA levels while decreased IgG levels. It also suggests that serum IgA level could be a possible biomarker for environmental stress.

[Image and quantity analysis of prostaglandin in rats' blood plasma and Na(+)-K(+)-ATPase in their cerebellum during the prevention of motion sickness by cinnarizine].

To study the mechanism of cinnarizine in preventing motion sickness, TXB2, 6-Keto-PGF1 alpha in rats' blood plasma and Na(+)-K(+)-ATPase activity in the endothelial cells of their cerebellar capillary were measured and analysed by a radioactive immunity analyser and a computer image system. The results showed that TXB2 and 6-Keto-PGF1 alpha in rats' blood plasma in the cinnarizine preventing group (CPG) decreased remarkably, compared with those in the motion sickness group(MSG) (p < 0.05). The activity of Na(+)-K(+)-ATPase in the endothelial cells of rats' cerebellar capillary in CPG was higher than that in MSG (p < 0.01). The authors suggest that the lower concentration of TXB2 and 6-Keto-PGF1 alpha in rats' blood plasma in CPG is closely related to cinnarizine which prevents Ca2+ from entering into the platelets and into the endothelial cells of blood vessels. The higher activity of Na(+)-K(+)-ATPase in the cerebellum may be caused by cinnarizene which dilates the blood vessels in the brain, increases the blood flow therein, and hinders Ca2+ from getting into the cerebellum cells. These change are believed to be the important mechanism of how cinnarizine prevents motion sickness.

Hormonal changes after parabolic flight: implications on the development of motion sickness.

Twenty-two different humoral parameters including stress-, gastrointestinal- and volume-regulating hormones were measured before and within 45 min after parabolic flight maneuvers of twenty healthy adult subjects. We compared hormonal data of motion sickness-affected participants with those unaffected. Changes in cortisol and vasoactive intestinal peptide plasma levels were significantly different (p less than 0.002 and p less than 0.004) between the two groups with increasing plasma levels of both hormones during motion sickness but decreasing levels within the control group. Growth hormone and prolactin plasma levels increased by 400% and 115% within the motion sickness-affected group and to a smaller degree (120% and 40% increases, respectively) within the control group, while ACTH levels were almost unchanged within both groups. Pancreatic polypeptide and gastrin plasma levels as well as plasma levels of insulin and C-peptide were significantly decreased within both groups after the parabolic flight. Plasma renin, aldosterone, atrial natriuretic peptide and cyclic GMP levels were unchanged within the control group. Within the motion sickness-affected group, plasma renin and aldosterone levels were decreased and atrial natriuretic peptide levels increased after the flight. Humoral parameters of the thyroid gland were neither changed within the groups nor different between the groups. The present data confirm previous results that increases in plasma levels of certain stress hormones participate in motion sickness. Furthermore, increases in vasoactive intestinal peptide levels participate in motion sickness. These increases could explain some of the gastrointestinal symptoms in motion sickness and might serve as markers for a discrimination between regular stress and motion sickness.

Serum levels of eleven steroid hormones following motion sickness.

In order to grade motion sickness objectively, the following 11 adrenal hormones were investigated in subjects with different motion sickness susceptibility: Aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-OH-progesterone, 11-deoxycortisol, cortisol, cortisone, testosterone, androstendione, dehydroepiandrosterone sulfate. Motion sickness was induced by the coriolis effect on a rotary chair. Both severe kinetosis after short rotation time and mild motion sickness after 30 min of rotation occurred together with small hormonal changes. Androstendione and 11-deoxycortisol appear to be sensitive indicators of motion sickness if the rotation time is taken into consideration. A significant increase of all hormones except progesterone, cortisone, testosterone, and dehydroepiandrosterone sulfate was observed when pronounced malaise had come after a long rotation stress (24.6 min). The changes in plasma aldosterone concentration appeared to correlate with time only. The present study demonstrates that hormonal analysis can be helpful in estimating the degree of motion sickness.