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Dear Editor: We have read with great interest the article by Kong et al. [1] about a new strategy to combat obesity and accompanying adverse features, in which normobaric hypoxia training induced more weight loss than normoxia training after 4 weeks in overweight young adults. Such findings complete the view that a modest intermittent hypoxia influences circulating measures of inflammation in healthy humans as reported in a previous issue of Sleep and Breathing [2]. Indeed, obesity is a growing public health burden affecting affluent societies as well as transition countries [2] with prevalence rates higher than 30 % in many regions. An energy intake higher than the energy expended for basal metabolic rate, physical activity, or thermogenic functions is claimed as the explanation for an excessive fat accumulation, where genetics, obesogenic environmental conditions, and other factors such as inflammation and oxidative stress could also be involved [3]. Current therapies for obesity treatment and different approaches for body weight management involve dietary interventions based on energy restriction and/or shifts on macronutrient distribution, physical activity programs, pharmacological prescription, or surgical procedures. Unfortunately, none of these therapies, either alone or combined, have been able to be fully satisfactory. Therefore, the search for alternative therapies such as the administration of thermogenic agents, satiating compounds, homeorhetic molecules, etc., is underway, including the possibility to use oxygen-based strategies [3]. In this context, abnormal adiposity has been associated not only with self-esteem and image-related psychological problems, but also with insulin resistance, hypertension, osteoarticular problems, cancer, fatty liver disease, etc., where the link between some of these diseases appears to be the mild and chronic inflammation occurring in obesogenic conditions. Thus, one of the mechanisms triggering inflammation has been associated with adipose tissue hypoxia [4] or increased oxygen tension [5], which affects a number of genes such as HIF-1α, MCP-1, IL-6, GLUT-1, ANGPTL-4, and PPAR-γ [6] that could be involved as a cause of or as a consequence reaction to pathologically low or high oxygen conditions. Interestingly, as we hypothesized previously [3] and Kong et al. have nicely demonstrated in their article [1], hypoxia is not only an ethological factor or a manifestation of disease, but also a therapeutic tool following different patterns (hypoxic exposure, hypoxic training, intermittent hypoxia under hyperbaric and normobaric conditions), which has been used for pre-acclimation in climbers or to improve athletes’ performance as well as for heart, respiratory, and nervous system diseases or to regulate body weight [7]. Thus, putative compensatory mechanisms and responses to hypoxia have been described for the respiratory system (hyperventilation, improvement in respiratory function, and increase in lung diffusion capacity), cardiovascular system (increase in basal heart rate, peripheral vasodilation, normalization of blood pressure, or cardiovascular protection), cellular and metabolic phenomena (angiogenesis, insulin sensitivity enhancement, enzymatic P. Gonzalez-Muniesa : J. A. Martinez (*) Centre for Nutrition Research/Department of Nutrition, Food Sciences and Physiology, University of Navarra, 31008 Pamplona, Spain e-mail: jalfmtz@unav.es

Hypoxia: a consequence of obesity and also a tool to treat excessive weight loss