scholarly journals Decremental Oscillation Curve Fitting of Heart Rate Response Following Face Immersion into Cold Water.

1997 ◽  
Vol 47 (6) ◽  
pp. 545-551 ◽  
Author(s):  
Youkou TOMINAGA ◽  
Takaaki NAKATSU ◽  
Shozo KUSACHI ◽  
Masahiro MURAKAMI ◽  
Shinji TOYONAGA ◽  
...  
1973 ◽  
Vol 34 (6) ◽  
pp. 770-774 ◽  
Author(s):  
S K Hong ◽  
T O Moore ◽  
D A Lally ◽  
J F Morlock

1983 ◽  
Vol 54 (1) ◽  
pp. 166-171 ◽  
Author(s):  
Y. C. Lin ◽  
K. K. Shida ◽  
S. K. Hong

Five series of breath-hold (BH) experiments were conducted on eight male subjects with the purpose of partitioning the effects of apnea per se, hypercapnia, and hypoxia on the development and maintenance of BH bradycardia. All BH were 90 s in duration and were achieved by face immersion at room temperature. Of the five series of BH, one was a continuous BH and the remaining included rebreathing at 15-s intervals while the face remained immersed. Comparison of heart rate (HR) responses between the continuous BH with air and that interrupted every 15 s by rebreathing without improving the alveolar gas composition yields the attenuating effect of respiratory activity. The hypercapnic effect was calculated from the difference in HR responses between two series of BH with O2, in which hypoxia was not present and rebreathing was common to both; in one rebreathing was through a CO2 scrubber thus creating different alveolar CO2 levels in the two series. The effect of hypoxia was deduced by finding the difference between the total bradycardial response (continuous BH) and the summed effects of hypercapnia and apnea per se. By this procedure, it was found that apnea and hypoxia reduced the HR by 19 and 18%, respectively, from the pre-BH value, and hypercapnia increased HR by 6% from the pre-BH level, thus accounting for the total 31% reduction in HR in a continuous BH.


2002 ◽  
Vol 93 (3) ◽  
pp. 882-886 ◽  
Author(s):  
Johan P. A. Andersson ◽  
Mats H. Linér ◽  
Elisabeth Rünow ◽  
Erika K. A. Schagatay

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10°C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% ( P < 0.001) and the blood pressure increase from 34 to 42% ( P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion ( P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial Po 2 and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.


1983 ◽  
Vol 54 (3) ◽  
pp. 661-665 ◽  
Author(s):  
B. H. Natelson ◽  
C. A. Nary ◽  
G. A. Curtis ◽  
D. Creighton

Thirteen young healthy human volunteers immersed their faces in warm or cold water on one day while breathing through a snorkel and on another day while breath holding. The magnitude of the elicited bradycardia was most prominently due to water temperature, with apnea playing a less important role. Perceived stress could affect the magnitude of the response, but it was less important than the other variables. Thus statistically significant nonparametric correlations were found for the group but not for most individuals between a scoring technique that assessed perceived stress and heart rate. In contrast to animals, these data indicate that bradycardia may be reliably elicited in humans by face immersion in cold water and that stress is neither necessary nor sufficient to produce this phenomenon. Adaptation did not seem to play a role in the development of this physiological response.


1957 ◽  
Author(s):  
Philip J. Bersh ◽  
Joseph M. Notterman ◽  
William N. Schoenfeld

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy


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