Hypercapnic hypoxia as a potential means to extend life expectancy and improve physiological activity in mice.

The application of combined hypoxia and hypercapnia (hypercapnic hypoxia) during respiratory exercises results in a maximum increase in resistance to acute hypoxia and ischemic tolerance of the brain. The results of those researches allow the assumption that hypercapnic hypoxia is a promising method for prophylaxis, treatment, and rehabilitation, as well as a means to increase life expectancy. The study was conducted to verify the hypothesis that it is possible to extend the life span through regular courses of respiratory exercises with hypercapnic hypoxia. In the present experimental research carried out on mice, the geroprotective effect of regular hypercapnic-hypoxic exercises (PO2-90 mm Hg and PCO2-50 mm Hg) was assessed in the context of the average life expectancy and the main criteria of its quality (reproductive function, muscle strength, and behavior). Results suggest that with regular training, life span is extended significantly by 16%. This result was accompanied by improved reproductive and cognitive functions, increased motor and search activities, and physical stamina in old age mices. This important phenomenon is accompanied by improved reproductive and cognitive functions, high motor function and search activity, as well as better physical stamina in old-aged mices. Recurring respiratory training under combined hypoxia and hypercapnia (hypercapnic hypoxia) during the lifetime significantly extended the life span of mice in the experiments.

Combined exposure to hypercapnia and hypoxia provides its maximum neuroprotective effect during focal ischemic injury in the brain.

BACKGROUND: In the present research, we compared the neuroprotective efficiency of combined and isolated exposure to hypoxia and hypercapnia preceding focal cerebral ischemic injury in rats. The study was conducted to verify the hypothesis of a possible increase in normobaric hypoxia (NbH; 90 mm Hg) efficiency when combined with permissive hypercapnia (PH; 50 mm Hg). METHODS: The rats from the test groups were subjected to a 15-fold exposure to NbH (90 mm Hg) and/or PH (50 mm Hg). After the 15th exposure, cerebral ischemic injury was induced by photochemical thrombosis. Seventy-two hours later, neurologic deficit was determined on the Neurological Severity Score scale and by the rotarod test, and the volume of cerebral infarction was measured after focal photochemical thrombosis. RESULTS: The neurologic deficit decreased most efficiently in rats that underwent PH and hypercapnic hypoxia (HH) exposure, whereas NbH had no impact on the neurologic status of the animals. On the contrary, motor coordination disturbances were minimal during exposure to hypoxia and HH. All respiratory interventions reduced the cerebral ischemic infarction volume in rats. The smallest infarction volumes were registered in the area of photochemical thrombosis in rats from the hypercapnic-hypoxic impact group, whereas exposure to NbH or PH did not show any cross difference. CONCLUSIONS: The impact of PH has greater neuroprotective potential compared with NbH. Thus, we can assume that hypercapnia is a predominant factor in providing neuroprotection in combination with hypoxia.