Chronic exercise and the pro-inflammatory response to endotoxin in the serum and heart

Criswell, David S.; Henry, Kathryn; DiMarco, Nancy M.; Grossie, V. Bruce

doi:10.1016/j.imlet.2004.07.012

Cited by 16 publications

(15 citation statements)

References 39 publications

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“…[31] showed that after a single exercise session combined with a LPS injection, trained rats were observed to have lower TNF-α levels compared to those of sedentary ones. Conversely, 12-week exercise training has been shown to cause increased plasma TNF-α levels in response to LPS injection [32]. These findings are in disagreement with the present study since we found an attenuated effect of LPS on TNF-α by chronic physical exercise (Fig 4C).…”

Section: Discussioncontrasting

confidence: 99%

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Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production

et al. 2017

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We tested the hypothesis that the neuromodulator hydrogen sulfide (H2S) in the preoptic area (POA) of the hypothalamus modulates the febrigenic signaling differently in sedentary and trained rats. Besides H2S production rate and protein expressions of H2S-related synthases cystathionine β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MPST) and cystathionine γ-lyase (CSE) in the POA, we also measured deep body temperature (Tb), circulating plasma levels of cytokines and corticosterone in an animal model of systemic inflammation. Rats run on a treadmill before receiving an intraperitoneal injection of lipopolysaccharide (LPS, 100 μg/kg) or saline. The magnitude of changes of Tb during the LPS-induced fever was found to be similar between sedentary and trained rats. In sedentary rats, H2S production was not affected by LPS. Conversely, in trained rats LPS caused a sharp increase in H2S production rate that was accompanied by an increased CBS expression profile, whereas 3-MPST and CSE expressions were kept relatively constant. Sedentary rats showed a significant LPS-induced release of cytokines (IL-1β, IL-6, and TNF-α) which was virtually abolished in the trained animals. Correlation between POA H2S and IL-6 as well as TNF-α was observed. Corticosterone levels were augmented after LPS injection in both groups. We found correlations between H2S and corticosterone, and corticosterone and IL-1β. These data are consistent with the notion that the responses to systemic inflammation are tightly regulated through adjustments in POA H2S production which may play an anti-inflammatory role downmodulating plasma cytokines levels and upregulating corticosterone release.

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Section: Discussioncontrasting

confidence: 99%

“…These findings are in disagreement with the present study since we found an attenuated effect of LPS on TNF-α by chronic physical exercise (Fig 4C). This discrepancy may be related to the different experimental designs used in the studies since both previous reports [31, 32] injected LPS at higher doses than that one of the present study.…”

Section: Discussioncontrasting

confidence: 58%

Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production

et al. 2017

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“…In vivo administration of lipopolysaccharide to healthy, young, trained or untrained men revealed tissue‐specific induced inflammatory responses: Compared with their untrained counterparts, trained subjects had an enhanced lipopolysaccharide‐induced TNF‐α and IL‐6 mRNA expression in skeletal muscle and slightly reduced responses systemically and in adipose tissue 37. Some animal studies also report increases in ex vivo lipopolysaccharide‐stimulation models, with exercise training leading to increases in TNF‐α but not IL‐6 in rats38, 39 in interleukin‐1ß, interleukin‐12, TNF‐α, and interferon‐γ in mice,40, 41, 42, 43 and in TNF‐α and interferon‐ß in horses 44…”

Section: Discussionmentioning

confidence: 99%

Aerobic Exercise Training and Inducible Inflammation: Results of a Randomized Controlled Trial in Healthy, Young Adults

Sloan

Shapiro

McKinley

et al. 2018

JAHA

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BackgroundConsensus 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 anti‐inflammatory effects of aerobic training elusive.Methods and ResultsWe 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‐α) 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.ConclusionsThe 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.

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“…While the study by Akita and colleagues is important because it is the first to investigate exercise-induced late cardioprotection in mice, almost all of the other studies investigating exercise-induced cardioprotection were carried out using rats. It is very unlikely that iNOS plays a significant role in exercise-induced late preconditioning in this species because the enzyme is not elevated in the rat heart by chronic exercise programs (7,14) or 24 h following 2 and 5 consecutive days of treadmill exercise for 60 min/day (24,36). Furthermore, Taylor et al (36) found that exerciseinduced cardioprotection against I-R injury in rats is not abolished by inhibition of NOS.…”

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confidence: 99%

Reactive oxygen species are not a required trigger for exercise-induced late preconditioning in the rat heart

Taylor

Starnes

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Reactive oxygen species (ROS) have been reported to play a primary role in triggering the cardioprotective adaptations by some preconditioning procedures, but whether they are required for exercise-induced preconditioning is unclear. Thus in this study we used the free radical scavenger N-(2-mercaptopropionyl)glycine (MPG) to test the hypothesis that ROS is the trigger for exercise-induced preconditioning of the heart against ischemia-reperfusion injury. Male F344 rats were assigned to four groups: sedentary (SED, n = 7), SED/MPG (100 mg/kg ip daily for 2 days, n = 12), exercised on a treadmill for 2 days at 20 m/min, 6° grade, for 60 min (RUN, n = 7), and RUN/MPG with 100 mg/kg MPG injected 15 min before exercise (n = 10). Preliminary experiments verified that MPG administration maintained myocardial redox status during the exercise bout. Twenty-four hours postexercise or MPG treatment isolated perfused working hearts were subjected to global ischemia for 22.5 min followed by reperfusion for 30 min. Recovery of myocardial external work (percentage of preischemic systolic pressure times cardiac output) for SED (50.4 ± 4.5) and SED/RUN (54.7 ± 6.6) was similar and improved in both exercise groups (P < 0.05) to 77.9 ± 3.0 in RUN and 76.7 ± 4.5 in RUN/MPG. A 2 × 2 ANOVA also revealed that exercise decreased lactate dehydrogenase release from the heart during reperfusion (marker of cell damage) without MPG effects or interactions. Expression of the cytoprotective protein inducible heat shock protein 70 increased by similar amounts in the left ventricles of RUN and RUN/MPG compared with sedentary groups (P < 0.05). We conclude that ROS are not a necessary trigger for exercise-induced preconditioning in rats.

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Chronic exercise and the pro-inflammatory response to endotoxin in the serum and heart

Cited by 16 publications

References 39 publications

Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production

Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production

Aerobic Exercise Training and Inducible Inflammation: Results of a Randomized Controlled Trial in Healthy, Young Adults

Reactive oxygen species are not a required trigger for exercise-induced late preconditioning in the rat heart

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