Whether ischaemia induces angiogenesis in skeletal muscle is controversial, which may be due to a differential response in capillary supply to tonically active (e.g. oxidative soleus, SOL) and phasically active (e.g. glycolytic extensor digitorum longus, EDL) muscles. It may also depend on the time course of ischaemia, with most studies examining chronic responses alone. Finally, a differential response may occur where there are regional differences in fibre cross sectional area (FCSA) and/or fibre type composition. Consequently, the response of SOL and EDL muscles to progressive chronic ischaemia was investigated at 2, 4 and 6 weeks, using coordinate-dependant sampling to identify specific regions (Deveci et al. 2001). Contralateral muscles were used as control. Male Wistar rats (n=5 for each group; body mass ~250g) underwent hindlimb ischaemia by unilateral ligation of the left common iliac artery under aseptic conditions and anaesthesia (combination of xylazine (3-10 mg kg^-1) and ketamine (90 mg kg^-1, i.p.); animals were treated post operatively with antibiotics (0.1 ml s.c. Engemycin, Deva). Wounds were examined daily with topical antiseptic application (Betadine), and observations made to detect any signs of pain or discomfort (such as staring coat, loss of appetite). Animals were killed by anaesthetic overdose. Muscles were rapidly frozen and histochemical sections stained for alkaline phosphatase to depict all capillaries (Deveci et al. 2001). Capillary-to-fibre ratio (C:F) significantly increased only after 6 weeks ischaemia in SOL compared to controlateral control muscles (from 2.46±0.08 to 3.15±0.11, mean±S.E.M., P0.05). In EDL, there were also no significant alterations in FCSA or CD, either as a whole muscle average or within individual sample regions. However, there was significant fibre atrophy in SOL muscle at 4 weeks (7114±274 – 5905±408 μm², P<0.05), and also significantly increased CD at both 4 and 6 weeks (362±15 – 458±22 mm^-2, P<0.01). It is well known that oxidative activity of SOL muscle is higher and FCSA (average 6921±347 μm) larger than glycolytic EDL (average 4328±327 μm²). Therefore, these data show that the muscle with the higher oxidative capacity, larger FCSA and is also tonically active (SOL) was more affected by ischaemia leading to angiogenesis, compared with the muscle which has low oxidative capacity, smaller FCSA and is phasically active (EDL). In conclusion, endogenous angiogenesis in skeletal muscle depends not only on the time course of ischaemia, but also multifactorial aspects of muscle phenotype.