Exercise regulates breast cancer cell viability: systemic training adaptations versus acute exercise responses

Christine Dethlefsen; Christian Lillelund; Julie Midtgaard; Christina Andersen; Bente Klarlund Pedersen; Jesper Frank Christensen; Pernille Hojman

doi:10.1007/s10549-016-3970-1

Exercise regulates breast cancer cell viability: systemic training adaptations versus acute exercise responses

Christine Dethlefsen, Christian Lillelund, Julie Midtgaard, Christina Andersen, Bente Klarlund Pedersen, Jesper Frank Christensen, Pernille Hojman

37 Citationer (Scopus)

Abstract

Purpose

Exercise decreases breast cancer risk and disease recurrence, but the underlying mechanisms are unknown. Training adaptations in systemic factors have been suggested as mediating causes. We aimed to examine if systemic adaptations to training over time, or acute exercise responses, in breast cancer survivors could regulate breast cancer cell viability in vitro.

Methods

Blood samples were collected from breast cancer survivors, partaking in either a 6-month training intervention or across a 2 h acute exercise session. Changes in training parameters and systemic factors were evaluated and pre/post exercise-conditioned sera from both studies were used to stimulate breast cancer cell lines (MCF-7, MDA-MB-231) in vitro.

Results

Six months of training increased VO_2peak (16.4 %, p < 0.001) and muscle strength, and reduced resting levels of plasma cholesterol (−18.2 %, p = 0.003) and cytokines. Yet, these systemic adaptations had no effect on breast cancer cell viability in vitro. During 2 h of acute exercise, increases in serum lactate (6-fold, p < 0.001), epinephrine (2.9-fold, p = 0.009), norepinephrine (2.2-fold, p < 0.001), and cytokines, including IL-6 (2.1-fold, p < 0.001) were detected. Incubation with serum obtained after exercise reduced viability by −9.2 % in MCF-7 (p = 0.04) and −9.4 % in MDA-MB-231 (p < 0.001) compared to resting serum.

Conclusion

Systemic changes to a 2 h exercise session reduced breast cancer viability, while adaptations to 6 months of training had no impact. Our data question the prevailing dogma that training-dependent baseline reductions in risk factors mediate the protective effect of exercise on breast cancer. Instead, we propose that the cancer protection is driven by accumulative effects of repeated acute exercise responses.

Originalsprog	Engelsk
Tidsskrift	Breast Cancer Research and Treatment
Vol/bind	159
Udgave nummer	3
Sider (fra-til)	469-479
Antal sider	11
ISSN	0167-6806
DOI	https://doi.org/10.1007/s10549-016-3970-1
Status	Udgivet - 1 okt. 2016

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title = "Exercise regulates breast cancer cell viability: systemic training adaptations versus acute exercise responses",

abstract = "PurposeExercise decreases breast cancer risk and disease recurrence, but the underlying mechanisms are unknown. Training adaptations in systemic factors have been suggested as mediating causes. We aimed to examine if systemic adaptations to training over time, or acute exercise responses, in breast cancer survivors could regulate breast cancer cell viability in vitro.MethodsBlood samples were collected from breast cancer survivors, partaking in either a 6-month training intervention or across a 2 h acute exercise session. Changes in training parameters and systemic factors were evaluated and pre/post exercise-conditioned sera from both studies were used to stimulate breast cancer cell lines (MCF-7, MDA-MB-231) in vitro.ResultsSix months of training increased VO2peak (16.4 %, p < 0.001) and muscle strength, and reduced resting levels of plasma cholesterol (−18.2 %, p = 0.003) and cytokines. Yet, these systemic adaptations had no effect on breast cancer cell viability in vitro. During 2 h of acute exercise, increases in serum lactate (6-fold, p < 0.001), epinephrine (2.9-fold, p = 0.009), norepinephrine (2.2-fold, p < 0.001), and cytokines, including IL-6 (2.1-fold, p < 0.001) were detected. Incubation with serum obtained after exercise reduced viability by −9.2 % in MCF-7 (p = 0.04) and −9.4 % in MDA-MB-231 (p < 0.001) compared to resting serum.ConclusionSystemic changes to a 2 h exercise session reduced breast cancer viability, while adaptations to 6 months of training had no impact. Our data question the prevailing dogma that training-dependent baseline reductions in risk factors mediate the protective effect of exercise on breast cancer. Instead, we propose that the cancer protection is driven by accumulative effects of repeated acute exercise responses.",

keywords = "Breast cancer viability, Acute exercise, Long-term training, Endurance exercise, Breast cancer survivors",

author = "Christine Dethlefsen and Christian Lillelund and Julie Midtgaard and Christina Andersen and Pedersen, {Bente Klarlund} and Christensen, {Jesper Frank} and Pernille Hojman",

year = "2016",

month = oct,

day = "1",

doi = "10.1007/s10549-016-3970-1",

language = "English",

volume = "159",

pages = "469--479",

journal = "Breast Cancer Research and Treatment",

issn = "0167-6806",

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number = "3",

}

TY - JOUR

T1 - Exercise regulates breast cancer cell viability

T2 - systemic training adaptations versus acute exercise responses

AU - Dethlefsen, Christine

AU - Lillelund, Christian

AU - Midtgaard, Julie

AU - Andersen, Christina

AU - Pedersen, Bente Klarlund

AU - Christensen, Jesper Frank

AU - Hojman, Pernille

PY - 2016/10/1

Y1 - 2016/10/1

N2 - PurposeExercise decreases breast cancer risk and disease recurrence, but the underlying mechanisms are unknown. Training adaptations in systemic factors have been suggested as mediating causes. We aimed to examine if systemic adaptations to training over time, or acute exercise responses, in breast cancer survivors could regulate breast cancer cell viability in vitro.MethodsBlood samples were collected from breast cancer survivors, partaking in either a 6-month training intervention or across a 2 h acute exercise session. Changes in training parameters and systemic factors were evaluated and pre/post exercise-conditioned sera from both studies were used to stimulate breast cancer cell lines (MCF-7, MDA-MB-231) in vitro.ResultsSix months of training increased VO2peak (16.4 %, p < 0.001) and muscle strength, and reduced resting levels of plasma cholesterol (−18.2 %, p = 0.003) and cytokines. Yet, these systemic adaptations had no effect on breast cancer cell viability in vitro. During 2 h of acute exercise, increases in serum lactate (6-fold, p < 0.001), epinephrine (2.9-fold, p = 0.009), norepinephrine (2.2-fold, p < 0.001), and cytokines, including IL-6 (2.1-fold, p < 0.001) were detected. Incubation with serum obtained after exercise reduced viability by −9.2 % in MCF-7 (p = 0.04) and −9.4 % in MDA-MB-231 (p < 0.001) compared to resting serum.ConclusionSystemic changes to a 2 h exercise session reduced breast cancer viability, while adaptations to 6 months of training had no impact. Our data question the prevailing dogma that training-dependent baseline reductions in risk factors mediate the protective effect of exercise on breast cancer. Instead, we propose that the cancer protection is driven by accumulative effects of repeated acute exercise responses.

AB - PurposeExercise decreases breast cancer risk and disease recurrence, but the underlying mechanisms are unknown. Training adaptations in systemic factors have been suggested as mediating causes. We aimed to examine if systemic adaptations to training over time, or acute exercise responses, in breast cancer survivors could regulate breast cancer cell viability in vitro.MethodsBlood samples were collected from breast cancer survivors, partaking in either a 6-month training intervention or across a 2 h acute exercise session. Changes in training parameters and systemic factors were evaluated and pre/post exercise-conditioned sera from both studies were used to stimulate breast cancer cell lines (MCF-7, MDA-MB-231) in vitro.ResultsSix months of training increased VO2peak (16.4 %, p < 0.001) and muscle strength, and reduced resting levels of plasma cholesterol (−18.2 %, p = 0.003) and cytokines. Yet, these systemic adaptations had no effect on breast cancer cell viability in vitro. During 2 h of acute exercise, increases in serum lactate (6-fold, p < 0.001), epinephrine (2.9-fold, p = 0.009), norepinephrine (2.2-fold, p < 0.001), and cytokines, including IL-6 (2.1-fold, p < 0.001) were detected. Incubation with serum obtained after exercise reduced viability by −9.2 % in MCF-7 (p = 0.04) and −9.4 % in MDA-MB-231 (p < 0.001) compared to resting serum.ConclusionSystemic changes to a 2 h exercise session reduced breast cancer viability, while adaptations to 6 months of training had no impact. Our data question the prevailing dogma that training-dependent baseline reductions in risk factors mediate the protective effect of exercise on breast cancer. Instead, we propose that the cancer protection is driven by accumulative effects of repeated acute exercise responses.

KW - Breast cancer viability

KW - Acute exercise

KW - Long-term training

KW - Endurance exercise

KW - Breast cancer survivors

U2 - 10.1007/s10549-016-3970-1

DO - 10.1007/s10549-016-3970-1

M3 - Journal article

C2 - 27601139

SN - 0167-6806

VL - 159

SP - 469

EP - 479

JO - Breast Cancer Research and Treatment

JF - Breast Cancer Research and Treatment

IS - 3

ER -

Exercise regulates breast cancer cell viability: systemic training adaptations versus acute exercise responses

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