Heart Rate Variability in Rats Acclimatized to High Altitude

Abstract

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.

Normobaric hypoxia conditioning reduces blood pressure and normalizes nitric oxide synthesis in patients with arterial hypertension

“…The results of multiple studies on protective effects of intermittent hypoxia suggest other mechanisms, including improved O 2 delivery and utilization in tissues [38], IHC-induced increases in sodium and water excretion [7], increased parasympathetic [39] and decreased sympathetic nervous activity [40][41][42], reduction of peripheral vascular resistance [43], potentiation of antioxidant defense due to increased activity of antioxidant enzymes [44], and prevention of vessel rarefaction, especially in brain and skeletal muscles [45,46], due to increased expression of vascular endothelial growth factor [47]. As any long-term, effective antihypertensive treatment can improve endothelial function, including enhancement of eNOS activity [48,49], the reduction of BP induced by these antihypertensive mechanisms may by itself serve to normalize nitric oxide metabolism.…”

Paradoxical effects of endurance training and chronic hypoxia on myofibrillar ATPase activity

“…Hypobaric hypoxia was obtained in steel chambers [fitted with a clear plastic glass door to illuminate and observe the animals] by using a specific vacuum pump (Becker Mot63, Rambouillet, France) as previously described by Melin et al (28). In each chamber, barometric pressure (MPX2100AP, Conrad, Lille, France), humidity (GSH 14; Conrad), and temperature (PT100/ DINB; Conrad) conditions were continuously monitored by using electronic sensors and analyzed with Direct View software (5500MF; ADAC, Atlanta, GA).…”

“…The running skills of the N and H group were maintained by performing two sessions a week of 10 min at 40% of MAV. This training program was chosen, as it has been used in our laboratory for several years and is effective to induce changes in MAV, muscular, and cardiovascular parameters (16,28,31).…”

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

“…A relationship between changes in VO 2 max and HRV alterations during acute hypobaric hypoxia has also been observed, with a decrease in the power of the high (HF) and low frequency (LF) bands and an increase in the LF/HF ratio. 15,16 Moreover, recent studies on acute mountain sickness (AMS) showed that the predomination of sympathetic activity during high altitude exposure may reflect varying capacity of acute hypobaric hypoxia adaptation 17,18 and that parameters like HRV could enhance the predictability of AMS susceptibility. 18 A similar behaviour for cardiorespiratory parameters has also been described for acute simulated altitude exposure.…”