Acute phase response in exercise. II. Associations between vitamin E, cytokines, and muscle proteolysis.

@article{Cannon1991AcutePR,
  title={Acute phase response in exercise. II. Associations between vitamin E, cytokines, and muscle proteolysis.},
  author={Joseph Gerard Cannon and Simin Nikbin Meydani and Roger A Fielding and Maria A. Fiatarone and Mohsen Meydani and Mojtaba Farhangmehr and S. F. Orencole and Jeffrey B. Blumberg and William J Evans},
  journal={The American journal of physiology},
  year={1991},
  volume={260 6 Pt 2},
  pages={
          R1235-40
        }
}
Cytokines such as interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and interleukin 6 (IL-6) mediate a variety of host responses to trauma and infection, including skeletal muscle proteolysis. This investigation assesses the influence of damaging eccentric exercise on in vitro production and plasma concentrations of cytokines and their relationship to muscle protein breakdown. In a double-blind placebo-controlled protocol, 21 male subjects took vitamin E supplements (800 IU/day… 

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The cytokine response to strenuous exercise 1

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Vitamin E supplementation decreases muscular and oxidative damage but not inflammatory response induced by eccentric contraction

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Circulating cytokines and hormones with immunosuppressive but neutrophil-priming potentials rise after endurance exercise in humans

Results suggested that exercise-induced pathogenesis including previously reported immunosuppression and neutrophil hyper-reactivity might be attributed, at least partly, to the systemic dynamics of the above bioactive substances.

A dietary supplement attenuates IL-6 and CRP after eccentric exercise in untrained males.

It is suggested that exercise-induced inflammation, evaluated by changes in IL-6 and CRP, was significantly reduced by the dietary supplement.

Acute phase response in exercise III. Neutrophil and IL-1p accumu lation in skeletal muscle

Data indicate that after eccentric exercise ultrastructural damage to skeletal muscle is associated with neu- trophil infiltration and muscle IL-lp accumulation.

Endurance exercise causes interaction among stress hormones, cytokines, neutrophil dynamics, and muscle damage.

The results indicate that stress-induced systemic release of bioactive substances may determine neutrophil mobilization and functional status, which then may affect local tissue damage of susceptible organs.

Exercise and immune function: effect of ageing and nutrition

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Acute Phase Responses and Cytokine Secretion in Chronic Fatigue Syndrome

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Effect of prolonged, submaximal exercise and carbohydrate ingestion on monocyte intracellular cytokine production in humans

Data suggest that circulating monocytes are not the origin of increased levels of plasma IL‐6 during exercise: prolonged cycling exercise increased the number of monocytes producing cytokines upon stimulation, but these cells produced less cytokines post‐exercise.
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References

SHOWING 1-10 OF 39 REFERENCES

Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release.

The association of enzyme efflux with neutrophil mobilization and function supports the concept that neutrophils are involved in the delayed increase in muscle membrane permeability after damaging exercise.

Infusion of tumor necrosis factor/cachectin promotes muscle catabolism in the rat. A synergistic effect with interleukin 1.

It is concluded that rats exposed systemically to sublethal doses of TNF respond with increasing muscle and decreasing liver proteolysis, similar to that observed in inflammation and in cancer.

Physiological mechanisms contributing to increased interleukin-1 secretion.

Interleukin-1 (IL-1) is a monocyte-derived polypeptide that mediates many host defense adaptations to environmental and infectious stresses and the possibility that IL-1 secretion may be mediated by stress hormones associated with exercise was examined.

The acute splanchnic and peripheral tissue metabolic response to endotoxin in humans.

The in vivo alterations in organ-specific substrate processing and endogenous mediator production induced by endotoxin were investigated in healthy volunteers and the net cachectin efflux from the splanchnic organs demonstrates that these tissues are a major site for production of this cytokine.

Circulating interleukin-1 and tumor necrosis factor in septic shock and experimental endotoxin fever.

The concept that plasma IL-1 beta and TNF-alpha concentrations are regulated independently and are associated with different clinical outcomes is supported.

Interleukin 1 and tumor necrosis factor do not regulate protein balance in skeletal muscle.

It is demonstrated that although interleukin 1 and tumor necrosis factor-alpha induce a PGE2 response by skeletal muscle in vitro, some macrophage product distinct from either interleucin 1 or tumor necrot factor- alpha is responsible for the accelerated skeletal protein degradation seen with partially purified human blood monocyte products.

Administration of endotoxin, tumor necrosis factor, or interleukin 1 to rats activates skeletal muscle branched-chain alpha-keto acid dehydrogenase.

It is concluded that cytokine-mediated activation of muscle BCKAD may contribute to accelerated BCAA oxidation in septicemia.

Transcription, not synthesis, of interleukin-1 and tumor necrosis factor by complement.

It is concluded that transcription of mRNA for IL-1 beta and TNF alpha during HD is primarily caused by complement activation by Cup, but that LPS or other factors are required for translation of IL- 1 beta andTNF alpha mRNA transcribed during HD.

Activation of protein breakdown and prostaglandin E2 production in rat skeletal muscle in fever is signaled by a macrophage product distinct from interleukin 1 or other known monokines.

A still-unidentified product of activated monocytes appears to be responsible for the negative nitrogen balance that accompanies infectious illness.