Abstract

Intermittent exposure to hypoxia (IHE) increases the production of reactive oxygen and nitrogen species as well as erythropoietin (EPO), which stimulates the adaptation to intense physical activity. However, several studies suggest a protective effect of moderate hypoxia in cardiovascular disease (CVD) events. The effects of intense physical activity with IHE on oxi-inflammatory mediators and their interaction with conventional CVD risk factors were investigated. Blood samples were collected from elite athletes (control n = 6, IHE n = 6) during a 6-day IHE cycle using hypoxicator GO2 altitude. IHE was held once a day, at least 2 hours after training. In serum, hydrogen peroxide (H2O2), nitric oxide (NO), 3-nitrotyrosine (3-Nitro), proinflammatory cytokines (IL-1β and TNFα), high sensitivity C-reactive protein (hsCRP), and heat shock protein 27 (HSP27) were determined by the commercial immunoenzyme (ELISA kits) or colorimetric methods. Serum erythropoietin (EPO) level was measured by ELISA kit every day of hypoxia. IHE was found to significantly increase H2O2, NO, and HSP27 but to decrease 3NT concentrations. The changes in 3NT and HSP27 following hypoxia proved to enhance NO bioavailability and endothelial function. In the present study, the oxi-inflammatory mediators IL-1β and hsCRP increased in IHE group but they did not exceed the reference values. The serum EPO level increased on the 3rd day of IHE, then decreased on 5th day of IHE, and correlated with NO/H2O2 ratio (rs = 0.640, P < 0.05). There were no changes in haematological markers contrary to lipoproteins such as low-density lipoprotein (LDL) and non-high-density lipoprotein (non-HDL) which showed a decreasing trend in response to hypoxic exposure. The study demonstrated that IHE combined with sports activity reduced a risk of endothelial dysfunction and atherogenesis in athletes even though the oxi-inflammatory processes were enhanced. Therefore, 6-day IHE seems to be a potential therapeutic and nonpharmacological method to reduce CVD risk, especially in elite athletes participating in strenuous training.

Highlights

  • Systemic exposure to hypoxia increases the production of reactive oxygen and nitrogen species as well as erythropoietin (EPO), which stimulates the adaptation to intense exercise [1]

  • The concentrations of tumour necrosis factor α (TNFα), interleukin 1β (IL-1β), hydrogen peroxide (H2O2), nitric oxide (NO), and heat shock protein 27 (HSP27) did not change in control group, except for 3-nitrotyrosine which increased by approximately 20%

  • 3NT moderately correlated with conventional cardiovascular disease (CVD) risk factors, such as Total cholesterol (TC), and non-high-density lipoproteins (HDL)

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Summary

Introduction

Systemic exposure to hypoxia increases the production of reactive oxygen and nitrogen species as well as erythropoietin (EPO), which stimulates the adaptation to intense exercise [1]. The narrative review by Ploszczyca et al [2] reported that blood EPO level increased within several hours and reached its peak after 1-3 days of acute hypoxic exposure. The high EPO level is known to result in improved erythropoiesis and exercise capacity. Hypoxic exposure is one of the methods which have been used for decades by professional athletes to increase endurance, strength, and speed, to avoid fatigue and to improve recovery [5,6,7]. A few epidemiologic and physiologic observations have demonstrated positive effects of hypoxia conditions on cardiovascular health [8,9,10].

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