METABOLIC AND CONTRACTILE RESPONSES OF FAST-TWITCH AND SLOW-TWITCH RAT SKELETAL-MUSCLES TO ISCHEMIA

Citation
Aj. Carvalho et al., METABOLIC AND CONTRACTILE RESPONSES OF FAST-TWITCH AND SLOW-TWITCH RAT SKELETAL-MUSCLES TO ISCHEMIA, Canadian journal of physiology and pharmacology, 74(12), 1996, pp. 1333-1341
Citations number
23
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
00084212
Volume
74
Issue
12
Year of publication
1996
Pages
1333 - 1341
Database
ISI
SICI code
0008-4212(1996)74:12<1333:MACROF>2.0.ZU;2-Y
Abstract
Complete occlusion of blood flow to rat hind limb by tourniquet was us ed to study the effects of total ischemia for 1, 2, and 3 h on contrac tile function and metabolic behaviour of two muscles composed predomin antly of either fast-twitch (extensor digitorum longus, EDL) or slow-t witch (soleus, SOL) fibres. Percent loss in twitch force (P-t) was gre ater (p < 0.05) in SOL than EDL during the first 45 min of ischemia. F ollowing 1 h of ischemia, ATP concentration was lower (p < 0.05) than in the contralateral control (20.8 +/- 2.0 vs. 26.4 +/- 1.5 mmol/kg dr y weight). Thereafter, the decline in ATP was greater, with approximat ely 95% depleted by 3 h of ischemia (1.46 +/- 0.46 mmol/kg dry weight) . The effect of ischemia on ATP levels in the SOL was similar to ATP l evels in the EDL. In the EDL, 1 h of ischemia also resulted in a large decrement in PCr, from 50.1 +/- 2.9 to 11.7 +/- 2.4 mmol/kg dry weigh t, and a large increase in lactate, from 25.0 +/- 3.0 to 114 +/- 10 mm ol/kg dry weight. As ischemia was prolonged, only lactate was increase d (p < 0.05) both at 2 h (171 +/- 12 mmol/kg dry weight) and 3 h (208 +/- 5.4 mmol/kg dry weight). Similar trends were found for SOL. By 3 h of ischemia, glycogen was depleted (p < 0.05) by 88% in EDL and 92% i n SOL, respectively. These results support the hypothesis that both hi gh energy phosphate transfer and anerobic glycolysis are of major impo rtance in defending ATP homeostasis, particularly during the Ist h of ischemia, and that the resulting metabolic disturbances are responsibl e for the large fatigability observed. The mechanisms underlying the g reater resistance to fatigue observed for the SOL compared with the ED L during the earlier period of ischemia remain uncertain.