Why the study?
Does hard normobaric hypoxia exposure alter left ventricular end diastolic pressure fluctuations, specific peripheral vascular resistance, and cardiointervals in healthy young men?
Does hard normobaric hypoxia exposure alter left ventricular end diastolic pressure fluctuations, specific peripheral vascular resistance, and cardiointervals in healthy young men?
Absolute Event Rate: 1.99% vs 1.19%
p-value: p=<0.05
Hard normobaric hypoxia exposure alters the phase relationship between left ventricular end diastolic pressure fluctuations, peripheral vascular resistance, and cardiointervals, likely triggered by increased oxyhemoglobin saturation affecting baroreflex realization.
May enhance hypoxic baroreflex timing in healthy volunteers; leaves open relevance for patients or practice.
The study wThe left ventricular end diastolic pressure (EDP) fluctuations, specific peripheral vascular resistance (SPR) and cardiointervals (RR) on the respiration frequency under hard normobaric hypoxia (FIO2 = 0.1) were studied. 7 young men (volunteers) were subject to series of hard hypoxic exposures (6 weeks, every other day, intermittently by 6 × 5 min – FIO2 = 0.1). The hypoxic tests (HT1 and HT2) – FIO2 = 0.1, 15 min continuously) were performed before and after each series. SаO2 at the last 3 m of the tests on average was 82.5 % and 92.0 % respectively (Р < 0.05). During HT1 and HT2 (in comparison with inactivity) were increased: angle of max QRS vector (VQRS) in the frontal plain (68.5° ± 16.68 and 72.94° ± 15.32; 69.62° ± 22.4 and 74.45° ± 17.98 respectively), minutes blood flow (MBF) (6.41 ± 1.98 l/min and 6.87 ± 1.27 l/min; 5,27 ± 1,02 l/min and 5.67 ± 1.19 l/min respectively) (Р < 0.05). SPR was decreased too (27.39 ± 5.45 s.u. and 25.62 ± 4.96 s.u.; 30.59 ± 6.34 s.u. and 27.93 ± 5.77 s.u. respectively) (Р < 0.05). By means of transfer function analysis was shown that EDP fluctuations at HT2 significantly outpace by time (phase) the SPR and RR fluctuations on the respiration frequency (1.19 s ± 0.64 and 1.99 s ± 0.63 or 94.39° ± 43.3 and 125.4° ± 7.54; 1.65 s ± 1.28 and 2.22 s ± 0.87 or 101.4° ± 59.6 and 152.7° ± 21.26 respectively) (Р < 0.05). The increased oxyhemoglobin saturation is a trigger of artery wall smooth muscle relaxation mechanisms and this one is changes the background for beat to beat baroreflex realization on the respiration frequency.
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Radchenko et al. (2013) studied Healthy (n=7). Hard normobaric hypoxia exposure vs. Pre-adaptation baseline was evaluated on Time lead of left ventricular end-diastolic pressure (EDP) fluctuations over specific peripheral vascular resistance (SPR) fluctuations on respiration frequency (seconds) (p=<0.05).
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