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Effects of Interval and Continuous Exercise Regimens on Aquaporin‐1‐mediated Osmotic Fragility of Erythrocyte under Hypoxic Stress
Author(s) -
Huang YuChieh,
Wang JongShyan
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1240.6
Subject(s) - erythrocyte fragility , tonicity , medicine , endocrinology , chemistry , red blood cell , erythrocyte deformability , aquaporin 1 , hemolysis , water channel , mechanical engineering , engineering , inlet
Physical exercise or hypoxic exposure influences erythrocyte susceptibility to osmotic stress. Aquaporin‐1 (AQP1) channel facilitates water transport in erythrocytes. This study investigated how aerobic interval training (AIT) and moderate continuous training (MCT) affect osmotic stress‐mediated rheological function and AQP1 activity of erythrocytes under hypoxic stress. Thirty healthy sedentary males were randomized to engage either AIT (3‐minute intervals at 40% and 80% VO 2max , n=15) or MCT (sustained 60% VO 2max , n=15) for 30 minutes/day, 5 days/week for 6 weeks. Erythrocyte rheological responses to HE (100W under 12%O 2 for 30 minutes) were determined before and after various regimens. The results showed that acute HE increased osmotic fragility and decreased deformability of erythrocytes, as well as, depressed erythrocyte AQP1 activity indicated by increased HgCl 2 ‐induced instability of erythrocyte membrane under hypotonic conditions. Following 6 weeks of the intervention, the AIT group exhibited higher maximal work‐rate and VO 2max than the MCT group. Moreover, both AIT and MCT diminished the extents of enhanced osmotic fragility, reduced deformability, and AQP1 activity of erythrocytes caused by HE. Hence, we conclude that AIT is superior to MCT for enhancing aerobic capacity. Moreover, either AIT or MCT effectively alleviates the impairments of erythrocyte rheological characteristics and AQP1 function evoked by HE.