Chronic intermittent hypoxia modulates eosinophil- and neutrophil-platelet aggregation and inflammatory cytokine secretion caused by strenuous exercise in men.
Although acclimatization to intermittent hypoxia (IH) improves exercise performance by increasing oxygen delivery and utilization, the effects of chronic IH on platelet-leukocyte interaction and inflammation-related cytokine secretion caused by strenuous exercise remain unclear. This investigation elucidates how two intensities of IH influence eosinophil- and neutrophil-platelet aggregation (EPA and NPA) as well as pro- and anti-inflammatory cytokines mediated by strenuous exercise. Twenty healthy sedentary men were randomly divided into severe (SIH) and moderate (MIH) IH groups; groups were exposed to 12% O2 (SIH) and 15% O2 (MIH) for 1 h/day, respectively, for 5 days/wk for 8 wk in a normobaric hypoxia chamber. Before IH intervention, 1) exercise up to maximal oxygen consumption promoted shear stress-, LPS-, and N-formyl-methionyl-leucyl-phenylalanine-induced EPA, increased IL-1beta and malondialdehyde levels, and decreased total antioxidant levels in plasma and 2) exposure to 12% O2, but not to 15% O2 for 1 h, enhanced LPS-induced EPA and reduced plasma total antioxidant levels. After IH for 8 wk, hypoxia- and exercise-promoted EPA, IL-1beta, or malondialdehyde levels were suppressed in both MIH and SIH groups, and plasma IL-6 and IL-10 levels in the SIH group were increased. However, the NPA induced by the shear force and chemical agonists was not changed under the two IH regimens. Therefore, both MIH and SIH regimens ameliorate eosinophil- and platelet-related thrombosis, proinflammatory IL-1beta secretion, and lipid peroxidation enhanced by strenuous exercise. Furthermore, SIH simultaneously increases circulatory anti-inflammatory IL-6 and IL-10 concentrations. These findings can help to develop effective IH regimens that improve aerobic fitness and minimize risk of thromboinflammation.
Wang
Jong-Shyan
JS
Graduate Institute of Rehabilitation Science and Center for Gerontological Research, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan. s5492@mail.cgu.edu.tw
Lin
Hung-Yu
HY
Cheng
Mei-Ling
ML
Wong
May-Kuen
MK
D000064:Acclimatization; D000328:Adult; D000531:Altitude; D000975:Antioxidants / Q000378:metabolism; D002908:Chronic Disease; D016207:Cytokines / Q000097:blood*; D004804:Eosinophils / Q000378:metabolism*; D017079:Exercise Tolerance; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D007249:Inflammation / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009504:Neutrophils / Q000378:metabolism*; D010101:Oxygen Consumption; D010973:Platelet Adhesiveness; D012123:Pulmonary Ventilation; D012720:Severity of Illness Index; D013927:Thrombosis / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors
D000975:Antioxidants; D016207:Cytokines; C508609:IL10 protein, human; C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D016753:Interleukin-10; D008315:Malondialdehyde