TY - JOUR
T1 - Aerobic exercise training and inducible inflammation
T2 - Results of a randomized controlled trial in healthy, young adults
AU - Sloan, Richard P.
AU - Shapiro, Peter A.
AU - McKinley, Paula S.
AU - Bartels, Matthew
AU - Shimbo, Daichi
AU - Lauriola, Vincenzo
AU - Karmally, Wahida
AU - Pavlicova, Martina
AU - Choi, C. Jean
AU - Choo, Tse Hwei
AU - Scodes, Jennifer M.
AU - Flood, Pamela
AU - Tracey, Kevin J.
N1 - Funding Information:
This study was supported by Grant R01 HL094423 from the National Heart, Lung, and Blood Institute (Sloan), Grant UL1 TR001873 from the NIH Center for Advancing Translational Sciences, and the Nathaniel Wharton Fund.
Publisher Copyright:
© 2018 The Authors.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - Background-Consensus panels regularly recommend aerobic exercise for its health-promoting properties, due in part to presumed anti-inflammatory effects, but many studies show no such effect, possibly related to study differences in participants, interventions, inflammatory markers, and statistical approaches. This variability makes an unequivocal determination of the antiinflammatory effects of aerobic training elusive. Methods and Results-We conducted a randomized controlled trial of 12 weeks of aerobic exercise training or a wait list control condition followed by 4 weeks of sedentary deconditioning on lipopolysaccharide (0, 0.1, and 1.0 ng/mL)-inducible tumor necrosis factor-α (TNF-a) and interleukin-6 (IL-6), and on toll-like receptor 4 in 119 healthy, sedentary young adults. Aerobic capacity by cardiopulmonary exercise testing was measured at study entry (T1) and after training (T2) and deconditioning (T3). Despite a 15% increase in maximal oxygen consumption, there were no changes in inflammatory markers. Additional analyses revealed a differential longitudinal aerobic exercise training effect by lipopolysaccharide level in inducible TNF-α (P=0.08) and IL-6 (P=0.011), showing T1 to T2 increases rather than decreases in inducible (lipopolysaccharide 0.1, 1.0 versus 0.0 ng/mL) TNF-α (51% increase, P=0.041) and IL-6 (42% increase, P=0.11), and significant T2 to T3 decreases in inducible TNF-α (54% decrease, P=0.007) and IL-6 (55% decrease, P<0.001). There were no significant changes in either group at the 0.0 ng/mL lipopolysaccharide level for TNF-α or IL-6. Conclusions-The failure to support the primary hypotheses and the unexpected post hoc findings of an exercise-training–induced proinflammatory response raise questions about whether and under what conditions exercise training has anti-inflammatory effects. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01335737.
AB - Background-Consensus panels regularly recommend aerobic exercise for its health-promoting properties, due in part to presumed anti-inflammatory effects, but many studies show no such effect, possibly related to study differences in participants, interventions, inflammatory markers, and statistical approaches. This variability makes an unequivocal determination of the antiinflammatory effects of aerobic training elusive. Methods and Results-We conducted a randomized controlled trial of 12 weeks of aerobic exercise training or a wait list control condition followed by 4 weeks of sedentary deconditioning on lipopolysaccharide (0, 0.1, and 1.0 ng/mL)-inducible tumor necrosis factor-α (TNF-a) and interleukin-6 (IL-6), and on toll-like receptor 4 in 119 healthy, sedentary young adults. Aerobic capacity by cardiopulmonary exercise testing was measured at study entry (T1) and after training (T2) and deconditioning (T3). Despite a 15% increase in maximal oxygen consumption, there were no changes in inflammatory markers. Additional analyses revealed a differential longitudinal aerobic exercise training effect by lipopolysaccharide level in inducible TNF-α (P=0.08) and IL-6 (P=0.011), showing T1 to T2 increases rather than decreases in inducible (lipopolysaccharide 0.1, 1.0 versus 0.0 ng/mL) TNF-α (51% increase, P=0.041) and IL-6 (42% increase, P=0.11), and significant T2 to T3 decreases in inducible TNF-α (54% decrease, P=0.007) and IL-6 (55% decrease, P<0.001). There were no significant changes in either group at the 0.0 ng/mL lipopolysaccharide level for TNF-α or IL-6. Conclusions-The failure to support the primary hypotheses and the unexpected post hoc findings of an exercise-training–induced proinflammatory response raise questions about whether and under what conditions exercise training has anti-inflammatory effects. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01335737.
KW - Clinical trial
KW - Exercise training
KW - Inflammation
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U2 - 10.1161/JAHA.118.010201
DO - 10.1161/JAHA.118.010201
M3 - Article
C2 - 30371169
AN - SCOPUS:85054500700
SN - 2047-9980
VL - 7
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 17
M1 - e010201
ER -