Metabolic and contractile responses of fast- and slow-twitch rat skeletal muscles to ischemia

Abstract

Complete occlusion of blood flow to rat hind limb by tourniquet was used to study the effects of total ischemia for 1, 2, and 3 h on contractile function and metabolic behaviour of two muscles composed predominantly of either fast-twitch (extensor digitorum longus, EDL) or slow-twitch (soleus, SOL) fibres. Percent loss in twitch force (Pt) was greater (p < 0.05) in SOL than EDL during the first 45 min of ischemia. Following 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 dry weight). Thereafter, the decline in ATP was greater, with approximately 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 levels 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 weight, and a large increase in lactate, from 25.0 +/- 3.0 to 114 +/- 10 mmol/kg dry weight. As ischemia was prolonged, only lactate was increased (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% in SOL, respectively. These results support the hypothesis that both high energy phosphate transfer and anerobic glycolysis are of major importance in defending ATP hemostasis, particularly during the 1st h of ischemia, and that the resulting metabolic disturbances are responsible for the large fatigability observed. The mechanisms underlying the greater resistance to fatigue observed for the SOL compared with the EDL during the earlier period of ischemia remain uncertain.

Exercise training exacerbates tourniquet ischemia-induced decreases in GLUT4 expression and muscle atrophy in rats

“…This result is different from previous studies in that 1-h of tourniquet ischemia significantly reduced glycogen levels (Carvalho et al, 1996;Fraser et al, 1998). It could be due to the treatment protocol utilized, allowing a 30-min recovery following ischemia, which elicited a rapid hypoxia-induced increase in glucose transport.…”

“…This is demonstrated by the fact that ischemia significantly decreases muscle glycogen levels (Purshottam et al, 1977;Fraser et al, 1998;Carvalho et al, 1996;Katz, 1988); and treatments that enhances carbohydrate metabolism protects muscles from severe ischemic damage (Lopaschuk, 2000;Keller et al, 1998). GLUT4 protein, the main glucose transporter expressed in skeletal muscle (Olson and Pessin, 1996), is found to play a key role in the regulation of muscle glycogen storage (Ren et al, 1993;Hansen et al, 1995;Tsao et al, 1996).…”

Muscle fibre activation and fatigue with low‐load blood flow restricted resistance exercise—An integrative physiology review

“…In contrast, Dietz suggested that high threshold motor units rather than low threshold units are inhibited during acute ischemia. Nevertheless, studies on rat muscles have shown a greater decline in twitch force in slow muscle than in fast muscle during the first 45 minutes of ischemia, particularly during the first 15‐30 minutes . Likewise, Gossen et al reported markedly greater declines in twitch force in slow contracting motor units than in fast units during very low‐force (~5%‐10% of MVC) voluntary ischemic contractions in human subjects.…”

Neurobiology of Chronic Tension-Type Headache

“…The free radical NO is a messenger molecule involved in various biological functions (10–12). NO is synthesized by a complex family of nitric oxide synthase (NOS) enzymes (13).…”