The objective of the present study was to investigate whether creatine (Cr) could attenuate the deleterious effects of high doses of dexamethasone (Dexa) on body mass, exercise performance, and respiratory variables of rodents. Forty-four Wistar rats performed incremental maximal exercise tests. They were then assigned to four groups: G1: subcutaneous (s.c.) and intraperitoneal (i.p.) saline; G2: s.c. saline and i.p. Cr (250 mg x kg(-1) x day(-1)); G3: s.c. Dexa (7.5 mg x kg(-1) x day(-1)) and i.p. saline; G4: s.c. Dexa and i.p. Cr. New exercise tests and analysis of the respiratory pattern under resting conditions and after stimulation with doxapram (2 mg/kg i.p.) were performed after 18 days. Post- minus pretreatment differences were compared between groups. G3 and G4 showed a significant impairment in body mass gain compared with G1 and G2 (P < 0.05) (G1: 65.3 +/- 26.1, G2: 93.1 +/- 27.4, G3: -18.4 +/- 20.1, G4: 9.8 +/- 23.1 kg x 10(-3)). Similar results were observed for maximal oxygen consumption (G1: 9.5 +/- 8.5, G2: 25.8 +/- 14.5, G3: -25.5 +/- 6.0, G4: -4.8 +/- 9.5 ml x kg(-1) x min(-1)) and test duration (G1: 43.0 +/- 45.0, G2: 72.0 +/- 59.5, G3: -165.0 +/- 60.6, G4: -48.0 +/- 48.5 s). Simultaneous use of Cr significantly attenuated the Dexa-induced impairment of the last two variables. Cr attenuated Dexa-induced gastrocnemius and diaphragm muscle weight losses and the atrophy of gastrocnemius type IIb fibers. Cr supplementation had only small effects on Dexa-induced respiratory changes. These results suggest that Cr may play a role in the prophylaxis or treatment of steroid-induced myopathy.

Myopathy is a well-known side effect of corticosteroid therapy. Creatine monohydrate (Cr) supplementation has been shown to increase fat-free mass and muscular function. This study aimed to investigate if Cr administration could offset the deleterious functional effects of high doses of steroids. Fifty-six male Syrian golden hamsters were randomized among 4 groups: GI (n = 10), subcutaneous (s.c.) and intraperitoneal (i.p.) saline; GII (n = 10), s.c. saline and i.p. Cr (600 mg.kg(-1).d(-1)); GIII (n = 18), s.c. dexamethasone (7.5 mg.kg(-1).d(-1)) and i.p. saline; and GIV (n = 18), s.c. dexamethasone and i.p. Cr. Daily voluntary running was measured using activity wheels for 18 d. At the end of the study, statistically significant differences in running were observed between all groups, except for GI versus GII (GI, 8878 +/- 2737 m; GII, 9145 +/- 2000 m; GIII, 4289 +/- 2623 m; GIV, 6339 +/- 2345 m). Dexamethasone led to a significant decrease in cross-sectional area of type II fibers of the medial gastrocnemius. The cross-sectional area of type I fibers was significantly larger in GIV than in GIII. In conclusion, Cr administration attenuated the impairment of daily spontaneous running of hamsters receiving a high dose of corticosteroids. Additional research is needed to clarify the clinical implications of this finding.

OBJECTIVE: To investigate the acute effects of intravenous administration of cigarette smoke extract (CSE) on histological, inflammatory, and respiratory function parameters in rats, as well as to compare this potential acute lung injury (ALI) model with that with the use of oleic acid (OA). METHODS: We studied 72 Wistar rats, divided into four groups: control (those injected intravenously with saline); CSE (those injected intravenously with CSE and saline); OA (those injected intravenously with saline and OA); and CSE/OA (those injected intravenously with CSE and OA). RESULTS: Mean lung compliance was significantly lower in the OA and CSE/OA groups (2.12 ± 1.13 mL/cmH2O and 1.82 ± 0.77 mL/cmH2O, respectively)than in the control group (3.67 ± 1.38 mL/cmH2O). In bronchoalveolar lavage fluid, the proportion of neutrophils was significantly higher in the OA and CSE/OA groups than in the control group, as was the activity of metalloproteinases 2 and 9. Pulmonary involvement, as assessed by morphometry, was significantly more severe in the OA and CSE/OA groups (72.9 ± 13.8% and 77.6 ± 18.0%, respectively) than in the control and CSE groups (8.7 ± 4.1% and 32.7 ± 13.1%, respectively), and that involvement was significantly more severe in the CSE group than in the control group. CONCLUSIONS: The intravenous administration of CSE, at the doses and timing employed in this study, was associated with minimal ALI. The use of CSE did not potentiate OA-induced ALI. Additional studies are needed in order to clarify the potential role of this model as a method for studying the mechanisms of smoking-induced lung injury.