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Inflammatory cytokine, adrenal and a...

Scheett, Timothy Paul.

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Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen./
Author:	Scheett, Timothy Paul.
Description:	226 p.
Notes:	Adviser: Lawrence Armstrong.
Contained By:	Dissertation Abstracts International63-08B.
Subject:	Biophysics, General. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3062097
ISBN:	0493780564

Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen.
Scheett, Timothy Paul.

Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen. - 226 p.

Adviser: Lawrence Armstrong.

Thesis (Ph.D.)--The University of Connecticut, 2002.

These studies examined the relationship between the circulating levels of the inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-1ra) and the endogenous anti-inflammatory hormones (ACTH, cortisol, EPI and NE) during and immediately following a bout of eccentric exercise-induced muscle damage (EE), as well as during a subsequent 5-d period during which the subjects received either ibuprofen (IBU, n = 12), 200 mg qid, hydrocodone bitartrate with ibuprofen (HBI, n = 12), 7.5 mg + 200 mg qid, or placebo (PLA, n = 12). Healthy college males performed 10 sets of 10 single, dominant leg eccentric knee extension repetitions at 120% of their previously tested concentric 1RM with 2 min rest between sets to induced muscle damage. Control (C) subjects (n = 12) followed the same protocol without EE. Serial blood samples were obtained via an indwelling catheter at Pre, Mid, IP, 0.25, 0.5, 1, 2, 4, 6 hours and 1, 2, 3, 4 and 5 days following EE. Significant (p < 0.05) increases in EPI and NE indicate that these variables initiated their anti-inflammatory action in response to the stress of EE. A lack of a significant increase in IL-1β and TNF-α following EE lends support to a theory that eccentric exercise does not stimulate the same inflammatory cytokine cascade associated with aerobic exercise and that stimulation of IL-1β is not required to stimulate the SAM axis. An initial significant decrease (Mid and IP) followed by a subsequent significant increase in IL-6 along with the ensuing significant increase in IL-1ra, following EE, demonstrates that IL-6 exhibits dual pro- and anti-inflammatory functions. The significant (p < 0.05) increases in soreness scores and CK concentrations indicate that EE induced delayed-nset muscle soreness (DOMS). Administration of IBU and HBI significantly reduced DOMS within 24-h and 48-h respectively and resulted in non-significant differences in soreness by day 4 and 5 respectively. Neither IBU nor HBI administration resulted in a significant suppression of CK, following EE. Administration of HBI stimulated an increase in TNF-α, IL-6 and IL-1ra causing the HBI group to respond similar to PLA. Neither IBU nor HBI, provided a physiological benefit over placebo administration following eccentric exercise-induced muscle damage.

ISBN: 0493780564Subjects--Topical Terms:

1019105
Biophysics, General.

Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen.
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245 1 0 $a Inflammatory cytokine, adrenal and autonomic hormonal responses to eccentric exercise-induced muscle damage: Influence of ibuprofen and hydrocodone bitartrate with ibuprofen.
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500 $a Source: Dissertation Abstracts International, Volume: 63-08, Section: B, page: 3618.
502 $a Thesis (Ph.D.)--The University of Connecticut, 2002.
520 $a These studies examined the relationship between the circulating levels of the inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-1ra) and the endogenous anti-inflammatory hormones (ACTH, cortisol, EPI and NE) during and immediately following a bout of eccentric exercise-induced muscle damage (EE), as well as during a subsequent 5-d period during which the subjects received either ibuprofen (IBU, n = 12), 200 mg qid, hydrocodone bitartrate with ibuprofen (HBI, n = 12), 7.5 mg + 200 mg qid, or placebo (PLA, n = 12). Healthy college males performed 10 sets of 10 single, dominant leg eccentric knee extension repetitions at 120% of their previously tested concentric 1RM with 2 min rest between sets to induced muscle damage. Control (C) subjects (n = 12) followed the same protocol without EE. Serial blood samples were obtained via an indwelling catheter at Pre, Mid, IP, 0.25, 0.5, 1, 2, 4, 6 hours and 1, 2, 3, 4 and 5 days following EE. Significant (p < 0.05) increases in EPI and NE indicate that these variables initiated their anti-inflammatory action in response to the stress of EE. A lack of a significant increase in IL-1β and TNF-α following EE lends support to a theory that eccentric exercise does not stimulate the same inflammatory cytokine cascade associated with aerobic exercise and that stimulation of IL-1β is not required to stimulate the SAM axis. An initial significant decrease (Mid and IP) followed by a subsequent significant increase in IL-6 along with the ensuing significant increase in IL-1ra, following EE, demonstrates that IL-6 exhibits dual pro- and anti-inflammatory functions. The significant (p < 0.05) increases in soreness scores and CK concentrations indicate that EE induced delayed-nset muscle soreness (DOMS). Administration of IBU and HBI significantly reduced DOMS within 24-h and 48-h respectively and resulted in non-significant differences in soreness by day 4 and 5 respectively. Neither IBU nor HBI administration resulted in a significant suppression of CK, following EE. Administration of HBI stimulated an increase in TNF-α, IL-6 and IL-1ra causing the HBI group to respond similar to PLA. Neither IBU nor HBI, provided a physiological benefit over placebo administration following eccentric exercise-induced muscle damage.
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