Is Maximal Heart Rate Decrease Similar Between Normobaric Versus Hypobaric Hypoxia in Trained and Untrained Subjects?

2019 ◽  
Vol 20 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Laurent Mourot ◽  
Grégoire P. Millet
1984 ◽  
Vol 59 (1) ◽  
pp. 203-211 ◽  
Author(s):  
Vilfredo De Pascalis ◽  
Maria L. Alberti ◽  
Raffaele Pandolfo

8 women and 8 men took Cattell's IPAT-anxiety questionnaire and later McFarland's test of ability to perceive heart activity. The second test involved subjects' tracking their own heart rates, then they enrolled in an EKG biofeedback session to evaluate ability to increase and decrease heart rate from subjects' resting baselines. At the end of the session each subject completed Blanchard, et al.'s questionnaire to specify the cognitive strategies used for heart-rate control. Heart rate, abdominal respiration rate, respiration amplitude, EEG percent power in theta, alpha, and beta bands were evaluated. Success of heart-rate decrease seemed to depend mainly on activity levels: the subjects who achieved high scores on the activity test decreased heart rate significantly better than did low scorers. The relationship between scores for perception of heart and increases in heart rate was nonsignificant: increased heart-rate seemed to depend on differences in respiration between the rest and periods of increase. The significant, negative correlation between trait anxiety and perceptions of heart activity suggested that anxiety affected subjects' ability to perceive heart rate. The theta EEG power of the right hemisphere was significantly higher in subjects scoring high than for those low in perception of heart activity. During heart-rate increase tasks subjects mainly reported use of ‘arousal responses,’ similarly during heart-rate decrease tasks they reported use of relaxation responses.


2011 ◽  
Vol 29 ◽  
pp. e1
Author(s):  
S. Meani ◽  
C. Cuspidi ◽  
F. Negri ◽  
C. Valerio ◽  
C. Sala ◽  
...  

2019 ◽  
Vol 24 (6) ◽  
pp. 674-683
Author(s):  
Ya. I. Poleshchenko ◽  
D. A. Oleynikov ◽  
V. Yu. Lukichev ◽  
D. A. Khromikhin ◽  
M. A. Krylova ◽  
...  

Background.Vagus nerve stimulation has been proposed for the treatment of a number of diseases. The positive effects of vagus nerve stimulation on ischemic and reperfusion myocardial injury has been tested in experimental models. However, the escape effect of vagus activation on heart rate and the methodology to overcome this effect have not been reported properly.Objective. The purpose of the study is to evaluate parameters of prolonged stimulation that decrease heart rate and allow overcoming the escape effect of vagus nerve activation.Design and methods. We used Wistar rats (n = 9). Cervical section was performed under general anesthesia. Left vagus nerve isolated from adjacent tissue was contacted with custom stimulation electrodes and a custom pulse generator. Blood pressure was measured in the right common carotid artery. Limb electrocardiogram was continuously recorded. First, stimulation parameters repeatedly evoking vagal reaction (decrease in heart rate) without nerve damage were evaluated. Second, parameters of intermittent stimulation that allowed repeat and consistent heart rate decrease were assessed.Results. During experiments, in 5 animals the following parameters leading to sustained 30 ± 20 % heart rate reduction were found: rectangular pulse, 30 Hz, 0,5 ms, 1–2 V (0,6– 0,8 mA). Stimulation with 50 Hz frequency led to nerve damage in 1 case. Stimulation with 20 Hz frequency led to heart rate over-suppression of heart rate and blood pressure. Intermittent nerve stimulation was tested in 4 animals and led to repeated heart rate decrease by 38 ± 15 %. The parameters which helped to avoid escape effect on heart rate change were the following: the length of stimulation episode of 45 s and interruption of stimulation for 15 s.Conclusion. Intermittent electrical stimulation evokes vagal reactions on heart rate and allows overcoming the escape effect of vagal activation. 


Author(s):  
Olivia C. Coiado ◽  
Elaine B. Buiochi ◽  
William D. O'brien

2011 ◽  
Vol 151 (1) ◽  
pp. e19-e21
Author(s):  
Emanuel C. Furtado ◽  
João Felipe C. Franca ◽  
Claudio Gil S. Araújo

Cancer ◽  
2013 ◽  
Vol 119 (11) ◽  
pp. 1969-1975 ◽  
Author(s):  
Sai-Hong Ignatius Ou ◽  
Wilson P. Tong ◽  
Michele Azada ◽  
Christina Siwak-Tapp ◽  
Joni Dy ◽  
...  

1998 ◽  
Vol 84 (1) ◽  
pp. 164-168 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
Richard L. Clancy ◽  
Yoshihiro Moue ◽  
Jean-Paul Richalet

Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue, and Jean-Paul Richalet. Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude. J. Appl. Physiol. 84(1): 164–168, 1998.—Maximal exercise heart rate (HRmax) is reduced after acclimatization to hypobaric hypoxia. The low HRmax contributes to reduce maximal cardiac output (Q˙max) and may limit maximal O2 uptake (V˙o 2 max). The objective of these experiments was to test the hypothesis that the reduction inQ˙max after acclimatization to hypoxia, due, in part, to the low HRmax, limitsV˙o 2 max. If this hypothesis is correct, an increase inQ˙max would result in a proportionate increase inV˙o 2 max. Rats acclimatized to hypobaric hypoxia [inspired[Formula: see text]([Formula: see text]) = 69.8 ± 3 Torr for 3 wk] exercised on a treadmill in hypoxic ([Formula: see text] = 71.7 ± 1.1 Torr) or normoxic conditions ([Formula: see text] = 142.1 ± 1.1 Torr). Each rat ran twice: in one bout the rat was allowed to reach its spontaneous HRmax, which was 505 ± 7 and 501 ± 5 beats/min in hypoxic and normoxic exercise, respectively; in the other exercise bout, HRmax was increased by 20% to the preacclimatization value of 600 beats/min by atrial pacing. This resulted in an ∼10% increase inQ˙max, since the increase in HRmax was offset by a 10% decrease in stroke volume, probably due to shortening of diastolic filling time. The increase inQ˙max was accompanied by a proportionate increase in maximal rate of convective O2 delivery (Q˙max × arterial O2 content), maximal work rate, and V˙o 2 max in hypoxic and normoxic exercise. The data show that increasing HRmax to preacclimatization levels increasesV˙o 2 max, supporting the hypothesis that the low HRmax tends to limitV˙o 2 maxafter acclimatization to hypoxia.


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