High-intensity training reduces CD8+ T Cell Redistribution in Response to Exercise.

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High-intensity training reduces CD8+ T Cell Redistribution in Response to Exercise. / Witard, OC; Turner, James; Jackman, Sarah; Tipton, Kevin; Jeukendrup, Asker; Kies, AK; Bosch, JA.

In: Medicine and Science in Sports and Exercise, 19.04.2012.

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@article{a6f247f246be491aa7c9bbd7969e5740,
title = "High-intensity training reduces CD8+ T Cell Redistribution in Response to Exercise.",
abstract = "PURPOSE:: We examined whether exercise-induced lymphocytosis and lymphocytopenia are impaired with high-intensity training. METHODS:: Eight trained cyclists (V˙ O2 max: 64.2 ± 6.5 mL·kg·min) undertook one week of normal-, and a second week of high-intensity training. On day seven of each week, participants performed a cycling task, consisting of 120 min sub-maximal 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 CD8TL sub-populations on the basis of CD45RA and CD27 expression. RESULTS:: High-intensity training (18,577 ± 10,984 cells·μL× ∼165 min) was associated with a smaller exercise-induced mobilization of CD8TLs compared with normal-intensity training (28,473 ± 16,163 cells·μL× ∼165 min, p = 0.09). The response of highly cytotoxic CD8TLs (CD45RACD27-) to exercise was smaller following one week of high- (3,144 ± 924 cells·μL× ∼165 min) compared with normal-intensity training (6,417 ± 2,143 cells·μL× ∼165 min; p <0.05). High-intensity training reduced post-exercise CD8TL lymphocytopenia (-436 ± 234 cells·μL) compared to normal-intensity training (-630 ± 320 cells·μL; p <0.05). This was driven by a reduced egress of na{\"i}ve CD8TLs (CD27CD45RA). High-intensity training was associated with reduced plasma epinephrine (-37%) and cortisol (-15%) responses (p <0.05). CONCLUSIONS:: High-intensity training impaired CD8+TL mobilization and egress in response to exercise. Highly cytotoxic CD8TLs were primarily responsible for the reduced mobilization of CD8TLs, which occurred in parallel with smaller neuro-endocrine responses. The reduced capacity for CD8TLs to leave blood post-exercise with high-intensity training was accounted for primarily by na{\"i}ve, and also, highly cytotoxic CD8TLs. This impaired CD8TL redistribution in athletes undertaking intensified training may imply reduced immune-surveillance.",
author = "OC Witard and James Turner and Sarah Jackman and Kevin Tipton and Asker Jeukendrup and AK Kies and JA Bosch",
year = "2012",
month = apr,
day = "19",
doi = "10.1249/MSS.0b013e318257d2db",
language = "English",
journal = "Medicine and Science in Sports and Exercise",
issn = "0195-9131",
publisher = "American College of Sports Medicine",

}

RIS

TY - JOUR

T1 - High-intensity training reduces CD8+ T Cell Redistribution in Response to Exercise.

AU - Witard, OC

AU - Turner, James

AU - Jackman, Sarah

AU - Tipton, Kevin

AU - Jeukendrup, Asker

AU - Kies, AK

AU - Bosch, JA

PY - 2012/4/19

Y1 - 2012/4/19

N2 - PURPOSE:: We examined whether exercise-induced lymphocytosis and lymphocytopenia are impaired with high-intensity training. METHODS:: Eight trained cyclists (V˙ O2 max: 64.2 ± 6.5 mL·kg·min) undertook one week of normal-, and a second week of high-intensity training. On day seven of each week, participants performed a cycling task, consisting of 120 min sub-maximal 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 CD8TL sub-populations on the basis of CD45RA and CD27 expression. RESULTS:: High-intensity training (18,577 ± 10,984 cells·μL× ∼165 min) was associated with a smaller exercise-induced mobilization of CD8TLs compared with normal-intensity training (28,473 ± 16,163 cells·μL× ∼165 min, p = 0.09). The response of highly cytotoxic CD8TLs (CD45RACD27-) to exercise was smaller following one week of high- (3,144 ± 924 cells·μL× ∼165 min) compared with normal-intensity training (6,417 ± 2,143 cells·μL× ∼165 min; p <0.05). High-intensity training reduced post-exercise CD8TL lymphocytopenia (-436 ± 234 cells·μL) compared to normal-intensity training (-630 ± 320 cells·μL; p <0.05). This was driven by a reduced egress of naïve CD8TLs (CD27CD45RA). High-intensity training was associated with reduced plasma epinephrine (-37%) and cortisol (-15%) responses (p <0.05). CONCLUSIONS:: High-intensity training impaired CD8+TL mobilization and egress in response to exercise. Highly cytotoxic CD8TLs were primarily responsible for the reduced mobilization of CD8TLs, which occurred in parallel with smaller neuro-endocrine responses. The reduced capacity for CD8TLs to leave blood post-exercise with high-intensity training was accounted for primarily by naïve, and also, highly cytotoxic CD8TLs. This impaired CD8TL redistribution in athletes undertaking intensified training may imply reduced immune-surveillance.

AB - PURPOSE:: We examined whether exercise-induced lymphocytosis and lymphocytopenia are impaired with high-intensity training. METHODS:: Eight trained cyclists (V˙ O2 max: 64.2 ± 6.5 mL·kg·min) undertook one week of normal-, and a second week of high-intensity training. On day seven of each week, participants performed a cycling task, consisting of 120 min sub-maximal 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 CD8TL sub-populations on the basis of CD45RA and CD27 expression. RESULTS:: High-intensity training (18,577 ± 10,984 cells·μL× ∼165 min) was associated with a smaller exercise-induced mobilization of CD8TLs compared with normal-intensity training (28,473 ± 16,163 cells·μL× ∼165 min, p = 0.09). The response of highly cytotoxic CD8TLs (CD45RACD27-) to exercise was smaller following one week of high- (3,144 ± 924 cells·μL× ∼165 min) compared with normal-intensity training (6,417 ± 2,143 cells·μL× ∼165 min; p <0.05). High-intensity training reduced post-exercise CD8TL lymphocytopenia (-436 ± 234 cells·μL) compared to normal-intensity training (-630 ± 320 cells·μL; p <0.05). This was driven by a reduced egress of naïve CD8TLs (CD27CD45RA). High-intensity training was associated with reduced plasma epinephrine (-37%) and cortisol (-15%) responses (p <0.05). CONCLUSIONS:: High-intensity training impaired CD8+TL mobilization and egress in response to exercise. Highly cytotoxic CD8TLs were primarily responsible for the reduced mobilization of CD8TLs, which occurred in parallel with smaller neuro-endocrine responses. The reduced capacity for CD8TLs to leave blood post-exercise with high-intensity training was accounted for primarily by naïve, and also, highly cytotoxic CD8TLs. This impaired CD8TL redistribution in athletes undertaking intensified training may imply reduced immune-surveillance.

U2 - 10.1249/MSS.0b013e318257d2db

DO - 10.1249/MSS.0b013e318257d2db

M3 - Article

C2 - 22525761

JO - Medicine and Science in Sports and Exercise

JF - Medicine and Science in Sports and Exercise

SN - 0195-9131

ER -