Background: Hypoxia is the reduction of oxygen availability due to external or internal causes. There is large individual variability of response to hypoxia.
Objective: The aim of this study was to define individual and typological features in susceptibility to hypoxia, its interrelation with hypoxic and hypercapnic ventilatory responses (HVR and HCVR, respectively) and their changes after cold acclimation.
Design: Twenty-four healthy men were tested. HVR and HCVR were measured by the rebreathing method during hypoxic and hypercapnic tests, respectively. These tests were carried out in thermoneutral conditions before and after cold exposures (nude, at 13°C, 2 h daily, for 10 days). Susceptibility to hypoxia (sSaO2) was determined as haemoglobin saturation slope during hypoxic test.
Results: It was found that HVR and HCVR significantly increased and susceptibility to hypoxia (sSaO2) tended to decrease after cold acclimation. According to sSaO2 results before cold exposures, the group was divided into 3: Group 1--with high susceptibility to hypoxia, Group 2--medium and Group 3--low susceptibility. Analysis of variances (MANOVA) shows the key role of susceptibility to hypoxia and cold exposures and their interrelation. Posterior analysis (Fisher LSD) showed significant difference in susceptibility to hypoxia between the groups prior to cold acclimation, while HVR and HCVR did not differ between the groups. After cold acclimation, susceptibility to hypoxia was not significantly different between the groups, while HCVR significantly increased in Groups 1 and 3, HVR significantly increased in Group 3 and HCVR, HVR did not change in Group 2.
Conclusions: Short-term cold exposures caused an increase in functional reserves and improved oxygen supply of tissues in Group 1. Cold exposure hypoxia has caused energy loss in Group 3. Group 2 showed the most appropriate energy conservation reaction mode to cold exposures. No relation was found between the thermoregulation and the susceptibility to hypoxia.
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http://dx.doi.org/10.3402/ijch.v72i0.21574 | DOI Listing |
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Department of Hydrobiology, Ichthyology and Biotechnology of Reproduction, West Pomeranian University of Technology in Szczecin, Kazimierza Królewicza 4, 71-550 Szczecin, Poland.
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School of Biological Sciences, National Institute of Science Education and Research (NISER) Bhubaneswar, P.O. Bhimpur-Padanpur, Jatni, Khurda, Odisha 752050, India; Homi Bhabha National Institute (HBNI), Training School Complex, Anushaktinagar, Mumbai 400094, India. Electronic address:
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Jiangsu Province Engineering Research Center for Aquatic Animals Breeding and Green Efficient Aquacultural Technology, Jiangsu Key Laboratory of Ocean-Land Environmental Change and Ecological Construction, School of Marine Science and Engineering, Nanjing Normal University, Nanjing 210023, Jiangsu, China; Co-Innovation Center for Marine Bio-Industry Technology of Jiangsu Province, Lianyungang 222005, China. Electronic address:
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Type 1 diabetes (T1D) is caused by the immune-mediated loss of pancreatic β-cells. Hypoxia-inducible factor 1α (HIF-1α) is a transcription factor which is crucial for cellular responses to low oxygen. Here, we investigate the role of β-cell HIF-1α in β-cell death and diabetes after exposure to multiple low-dose streptozotocin (MLDS).
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