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Mediators of Inflammation
Volume 2013, Article ID 279365, 8 pages
http://dx.doi.org/10.1155/2013/279365
Review Article

Can High Altitude Influence Cytokines and Sleep?

1Departamento de Psicobiologia, Campus São Paulo, UNIFESP, Rua Botucatu 862, Vila Clementino, São Paulo, SP, Brazil
2Centro de Estudos em Psicobiologia e Exercício, (CEPE), São Paulo, SP, Brazil
3Departamento de Biociências, Campus da Baixada Santista, UNIFESP, Avenida Almirante Saldanha da Gama, 89, Ponta da Praia, 11030-400 Santos, SP, Brazil
4Centro de Estudos em Psicobiologia e Exercício, UNIFESP, Rua Professor Francisco de Castro 04020-050, 93, Vila Clementino, São Paulo, SP, Brazil
5Laboratório do Movimento Humano, Universidade São Judas Tadeu, São Paulo, SP, Brazil
6Unidade de Hipertensão, Instituto do Coração (InCor), Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil

Received 16 November 2012; Revised 27 February 2013; Accepted 21 March 2013

Academic Editor: Gustavo Duarte Pimentel

Copyright © 2013 Valdir de Aquino Lemos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The number of persons who relocate to regions of high altitude for work, pleasure, sport, or residence increases every year. It is known that the reduced supply of oxygen (O2) induced by acute or chronic increases in altitude stimulates the body to adapt to new metabolic challenges imposed by hypoxia. Sleep can suffer partial fragmentation because of the exposure to high altitudes, and these changes have been described as one of the responsible factors for the many consequences at high altitudes. We conducted a review of the literature during the period from 1987 to 2012. This work explored the relationships among inflammation, hypoxia and sleep in the period of adaptation and examined a novel mechanism that might explain the harmful effects of altitude on sleep, involving increased Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) production from several tissues and cells, such as leukocytes and cells from skeletal muscle and brain.