([Ca 2ϩ ]i) homeostasis is impaired following muscle contractions. It is unclear to what degree this behavior is contingent upon fiber type and muscle oxygenation conditions. We tested the hypotheses that: 1) the rise in resting [Ca 2ϩ ]i evident in diabetic rat slow-twitch (type I) muscle would be exacerbated in fast-twitch (type II) muscle following contraction; and 2) these elevated [Ca 2ϩ ]i levels would relate to derangement of microvascular partial pressure of oxygen (PmvO 2 ) rather than sarcoplasmic reticulum dysfunction per se. Adult male Wistar rats were divided randomly into diabetic (DIA: streptozotocin ip) and healthy (CONT) groups. Four weeks later extensor digitorum longus (EDL, predominately type II fibers) and soleus (SOL, predominately type I fibers) muscle contractions were elicited by continuous electrical stimulation (120 s, 100 Hz). Ca 2ϩ imaging was achieved using fura 2-AM in vivo (i.e., circulation intact). DIA increased fatigability in EDL (P Ͻ 0.05) but not SOL. In recovery, SOL [Ca 2ϩ ]i either returned to its resting baseline within 150 s (CONT 1.00 Ϯ 0.02 at 600 s) or was not elevated in recovery at all (DIA 1.03 Ϯ 0.02 at 600 s, P Ͼ 0.05). In recovery, EDL CONT [Ca 2ϩ ]i also decreased to values not different from baseline (1.06 Ϯ 0.01, P Ͼ 0.05) at 600 s. In marked contrast, EDL DIA [Ca 2ϩ ]i remained elevated for the entire recovery period (i.e., 1.23 Ϯ 0.03 at 600 s, P Ͻ 0.05). The inability of [Ca 2ϩ ]i to return to baseline in EDL DIA was not associated with any reduction of SR Ca 2ϩ -ATPase (SERCA) 1 or SERCA2 protein levels (both increased 30 -40%, P Ͻ 0.05). However, Pmv O 2 recovery kinetics were markedly slowed in EDL such that mean Pmv O 2 was substantially depressed (CONT 27.9 Ϯ 2.0 vs. DIA 18.4 Ϯ 2.0 Torr, P Ͻ 0.05), and this behavior was associated with the elevated [ ] i following contraction in Type 1 diabetes, which remain to be resolved.The greater physiological fragility of fast-twitch fibers under atrophic conditions such as diabetes may relate, in part, to impaired microvascular structure (47) and hemodynamics (26). These effects impact the fine balance of O 2 delivery-to-O 2 utilization, at least within the spinotrapezius muscle, such that very low Pmv O 2 values are evident at rest and both during and following contractions (6,37,38). It is conceivable that the ϳ60% fast-twitch fibers that comprise the spinotrapezius (13) are driving these aberrant Pmv O 2 profiles.Predicated on the evidence presented above that SERCA activity is preserved/increased in isolated intact (or skinned) single muscle fibers in diabetes, we rationalized that impaired [Ca 2ϩ ] i homeostasis may relate to impaired microcirculatory hemodynamics (i.e., oxygenation, Pmv O 2 ) during/following contractions.