Individualized intermittent hypoxia training: Principles and practices

Abstract

Individual variation of homeostatic response to hypoxia has been recognized by investigators from the former Soviet Union as well as Western countries. The proven influence of both hereditary and environmental parameters on physiological responses must drive the selection of individual regimes for athletic training, disease treatment, and outcome prognostication. Our longitudinal examinations of identical twins both at sea level and altitudes have shown that the ventilatory response to hypoxic stimulus is a rigid, genetically determined, physiological characteristic reflecting an organism's overall nonspecific reactivity. On the basis of our twin investigations, we have designed a nomogram to estimate individual nonspecific reactivity and functional reserves for prognosis of subject adaptation to hypoxia. Various strategies of adaptation were identified for persons with differing hypoxic ventilatory sensitivity. Intermittent hypoxic training (IHT) regimes can be customized to match this known individual reactivity. Mechanisms that mediate interindividual variation of adaptation to hypoxia were primarily determined by making measurements in animals with high (HR) and low (LR) resistance to acute hypoxia. Although there are several possible causes for such variation, much of the interest in Russian/Ukraine has focused on mitochondria. The researchers found that, when compared to LR rats, HR rats had: (1) greater mitochondrial enzyme complex I activity, (2) increased nitric oxide inhibition of Ca2+-ATPase activity with concomitant decreased intracellular Ca2+, (3) enhanced antioxidant activity, and (4) increased gene expression. Differential selective oxidation of two Krebs cycle substrates, alpha-ketoglutarate versus succinate, acts more intensively in HR animals, thereby enhancing cholinergic status. Our investigations have shown that l-arginine injections as well as IHT increase mitochondrial calcium capacity in LR rats to the same level as HR rats. Mitochondrial ATP-dependent potassium channel openers affected mitochondrial respiration differently in HR and LR rats. These differences were similar to the IHT effects. Nevertheless, there is a continued search for potential universal marker(s) for individual prognosis of adaptation to hypoxia. Future investigations will shed light on this very important question. Collectively, we can envisage a bright future for individualized IHT, which may play a significant role in the fast-developing field of personalized preventive medicine against various human diseases.