Heart Rate Variability in Exposure to High Altitude Hypoxia of Short Duration

Zużewicz, Krystyna; Biernat, B.; Kempa, Grzegorz; Kwarecki, K

doi:10.1080/10803548.1999.11076424

Cited by 19 publications

(27 citation statements)

References 7 publications

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“…The decrease was mainly marked in the low-frequency band. These results obtained in animals are in agreement with those of Zuzewicz et al (1999), who showed that all HRV components decreased in humans exposed to acute hypoxia (4500 m). The high decrease in the low-frequency component of HRV (N rats: 297%; CH rats: 288%), unlinked to acclimatization, confirms that sympathetic activation might be the main determinant of perturbations of the chronotropic responses to acute hypoxic stress.…”

Section: Effect Of Preadaptation To Hypoxia On Hrv During Acute Hypoxsupporting

confidence: 95%

Heart Rate Variability in Rats Acclimatized to High Altitude

Melin

Fauchier

Dubuis³

et al. 2003

High Altitude Medicine & Biology

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The aims of this study were to relate heart morphology and functions changes to heart rate variability (HRV) components after acclimatization to high altitude and to define whether preadaptation to hypoxia could modulate HRV responses to acute hypoxic stress. Doppler-echocardiographic studies of the left ventricle were performed in female Wistar rats before, during, and after a 10-week exposure to moderate hypobaric hypoxia (CH rats, approximately 4000 m simulated) or normoxia (N rats, approximately 55 m). Right ventricular morphology and function and pulmonary artery pressure were evaluated using heart catheterization. Spectral analysis of HRV was studied after exposure in conscious unrestrained rats in normoxia and during acute hypoxic stress. Necropsy right ventricular hypertrophy and intraventricular and pulmonary artery hypertension were found in CH rats compared with N rats. Echocardiographic left ventricular morphology and functions were similar between the groups after exposures. Compared to the control group, CH rats had similar heart rates and HRV components when measured in normoxia. During acute hypoxic stress, HRV decreased in all rats, but less in CH rats. These results support the hypothesis that long-term mild hypoxia may moderate sympathetic activation induced by acute hypoxia and that right ventricular hypertrophy cannot be the direct cause of such a shift in sympathovagal nerve interaction during acute hypoxic stress.

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Section: Effect Of Preadaptation To Hypoxia On Hrv During Acute Hypoxsupporting

confidence: 95%

Heart Rate Variability in Rats Acclimatized to High Altitude

Melin

Fauchier

Dubuis³

et al. 2003

High Altitude Medicine & Biology

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“…Heart rate variability (HRV) reflects sympathetic and parasympathetic cardiac autonomic nervous system regulation. Several studies have shown a transient reduction in parasympathetic and increased sympathetic activity during acute exposure to hypobaric hypoxia (Zuzewicz et al, 1999; Sevre et al, 2001; Saito et al, 2005; Hainsworth et al, 2007) which tended to be reversed with acclimatization (Cornolo et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

Heart rate variability changes at 2400 m altitude predicts acute mountain sickness on further ascent at 3000–4300 m altitudes

Karinen¹,

Uusitalo²,

Vähä‐Ypyä³

et al. 2012

Front. Physio.

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Objective: If the body fails to acclimatize at high altitude, acute mountain sickness (AMS) may result. For the early detection of AMS, changes in cardiac autonomic function measured by heart rate variability (HRV) may be more sensitive than clinical symptoms alone. The purpose of this study was to ascertain if the changes in HRV during ascent are related to AMS. Methods: We followed Lake Louise Score (LLS), arterial oxygen saturation at rest (R-SpO2) and exercise (Ex-SpO2) and HRV parameters daily in 36 different healthy climbers ascending from 2400 m to 6300 m altitudes during five different expeditions. Results: After an ascent to 2400 m, root mean square successive differences, high-frequency power (HF2 min) of HRV were 17–51% and Ex-SpO2 was 3% lower in those climbers who suffered from AMS at 3000 to 4300 m than in those only developing AMS later (≥5000 m) or not at all (all p < 0.01). At the altitude of 2400 m RMSSD2 min ≤ 30 ms and Ex-SpO2 ≤ 91% both had 92% sensitivity for AMS if ascent continued without extra acclimatization days. Conclusions: Changes in supine HRV parameters at 2400 m were related to AMS at 3000–4300 m Thus, analyses of HRV could offer potential markers for identifying the climbers at risk for AMS.

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“…The altitude‐related sympathetic activation has been largely demonstrated by elevated levels of catecholamines in plasma and urine, 22 as well as by direct recording of the sympathoadrenergic activity in peripheral nerves 23 . Moreover, several studies have shown that altitude reduces HRV as indirect sign of sympathetic stimulation and vagal withdrawal 3,4 …”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated an increased adrenergic activation during acute and chronic hypoxia exposure at high altitude that in turn determines an increased cardiac output to compensate the reduced arterial oxygen content 1,2 . In particular, an altitude‐related sympathetic hyperactivity has been proven by the analysis in time and frequency domains of heart rate variability (HRV), a noninvasive tool to assess the autonomic cardiovascular regulation and sympathovagal interaction 3,4 . This enhanced sympathetic neural activity can elicit both atrial and ventricular arrhythmias via several mechanisms, including reentry, abnormal automaticity, and triggered activity 5…”

Section: Introductionmentioning

confidence: 99%