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Appears in Collections:Faculty of Health Sciences and Sport Journal Articles
Peer Review Status: Refereed
Title: High-Intensity Training Reduces CD8+ T-cell Redistribution in Response to Exercise
Authors: Witard, Oliver
Turner, James E
Jackman, Sarah R
Tipton, Kevin
Jeukendrup, Asker E
Kies, Arie K
Bosch, Jos A
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Issue Date: Sep-2012
Publisher: American College of Sports Medicine
Citation: Witard O, Turner JE, Jackman SR, Tipton K, Jeukendrup AE, Kies AK & Bosch JA (2012) High-Intensity Training Reduces CD8+ T-cell Redistribution in Response to Exercise, Medicine and Science in Sports and Exercise, 44 (9), pp. 1689-1697.
Abstract: Purpose: We examined whether exercise-induced lymphocytosis and lymphocytopenia are impaired with high-intensity training. Methods: Eight trained cyclists (V˙O2max = 64.2 ± 6.5 mL·kg-1·min-1) undertook 1 wk of normal-intensity training and a second week of high-intensity training. On day 7 of each week, participants performed a cycling task, consisting of 120 min of submaximal exercise followed by a 45-min time trial. Blood was collected before, during, and after exercise. CD8+ T lymphocytes (CD8+TLs) were identified, as well as CD8+TL subpopulations on the basis of CD45RA and CD27 expression. Results: High-intensity training (18,577 ± 10,984 cells per microliter × ∼165 min) was associated with a smaller exercise-induced mobilization of CD8+TLs compared with normal-intensity training (28,473 ± 16,163 cells per microliter × ∼165 min, P = 0.09). The response of highly cytotoxic CD8+TLs (CD45RA+CD27-) to exercise was smaller after 1 wk of high-intensity training (3144 ± 924 cells per microliter × ∼165 min) compared with normal-intensity training (6417 ± 2143 cells per microliter × ∼165 min, P < 0.05). High-intensity training reduced postexercise CD8+TL lymphocytopenia (-436 ± 234 cells per microliter) compared with normal-intensity training (-630 ± 320 cells per microliter, P less than 0.05). This was driven by a reduced egress of naive CD8+TLs (CD27+CD45RA+). High-intensity training was associated with reduced plasma epinephrine (-37%) and cortisol (-15%) responses (P less than 0.05). Conclusions: High-intensity training impaired CD8+TL mobilization and egress in response to exercise. Highly cytotoxic CD8+TLs were primarily responsible for the reduced mobilization of CD8+TLs, which occurred in parallel with smaller neuroendocrine responses. The reduced capacity for CD8+TLs to leave blood after exercise with high-intensity training was accounted for primarily by naive, and also, highly cytotoxic CD8+TLs. This impaired CD8+TL redistribution in athletes undertaking intensified training may imply reduced immune surveillance.
Type: Journal Article
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Affiliation: Sport
University of Birmingham
University of Birmingham
University of Birmingham
DSM Food Specialties, Delft, The Netherlands
University of Birmingham

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