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1. Long-term electrical stimulation was given during 4 or 8 wk to the peroneal nerve of deafferented hindlimbs in hemispinalized adult cats. Four different stimulation patterns were compared: 100-Hz bursts covering 5% of daily time (F1), 10-Hz bursts covering 5% of daily time (S1), pattern S1 plus added 100-Hz bursts during 0.5% of daily time (S1F2), and, finally, only the latter 100-Hz bursts (F2), again during 0.5% of daily time. 2. During the course of chronic stimulation, frequent noninvasive measurements were made of the twitch of the ankle dorsiflexors. In a terminal acute experiment under general anesthesia, performed after 4 or 8 wk of treatment, measurements were made of isometric contractile properties (speed, force) for one of the stimulated peroneal muscles, m. peroneus longus (PerL). Thereafter, the PerL muscle was removed for further histochemical/histological analysis. 3. Findings from chronically stimulated PerL muscles were compared with three kinds of control PerL muscles: 1) those from the contralateral (control) hindlimb of chronically treated animals, 2) those from the operated side of animals that had been deafferented and hemispinalized but not subjected to chronic stimulation, 3) those from normal animals that had not been subjected to chronic treatment. With respect to the presently studied parameters, the three kinds of control muscles rendered very similar results. 4. All the presently used patterns of chronic stimulation made the PerL muscles slower with respect to twitch contraction time, half-relaxation time, and tension-frequency relation. Patterns covering 5-5.5% of daily time (F1, S1, S1F2) also caused an increase in the percentage of fibers classified as 'slow' (type I) on basis of their staining for myosin adenosine triphosphatase (ATPase). 5. Among patterns covering 5% of daily time, the change in ATPase histochemistry and the degree of physiological slowing was at least as pronounced after chronic stimulation at 100 Hz (F1) as after treatment at 10 Hz (S1). The slowing produced by pattern S1 was not more pronounced than that caused by this pattern (10 Hz) plus an equal number of pulses at 100 Hz (S1F2). 6. The slowing produced by the presently used patterns of chronic stimulation took place within the initial 2-3 wk. 7. Patterns F1 and S1 caused a decrease in maximum tetanic force as well as in mean fiber diameter.(ABSTRACT TRUNCATED AT 400 WORDS)

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Mitochondrially bound hexokinase II (mtHKII) has long been known to confer cancer cells with their resilience against cell death. More recently, mtHKII has emerged as a powerful protector against cardiac cell death. mtHKII protects against ischaemia‐reperfusion (IR) injury in skeletal muscle and heart, attenuates cardiac hypertrophy and remodelling, and is one of the major end‐effectors through which ischaemic preconditioning protects against myocardial IR injury. Mechanisms of mtHKII cardioprotection against reperfusion injury entail the maintenance of regulated outer mitochondrial membrane (OMM) permeability during ischaemia and reperfusion resulting in stabilization of mitochondrial membrane potential, the prevention of OMM breakage and cytochrome C release, and reduced reactive oxygen species production. Increasing mtHK may also have important metabolic consequences, such as improvement of glucose‐induced insulin release, prevention of acidosis through enhanced coupling of glycolysis and glucose oxidation, and inhibition of fatty acid oxidation. Deficiencies in expression and distorted cellular signalling of HKII may contribute to the altered sensitivity of diabetes to cardiac ischaemic diseases. The interaction of HKII with the mitochondrion constitutes a powerful endogenous molecular mechanism to protect against cell death in almost all cell types examined (neurons, tumours, kidney, lung, skeletal muscle, heart). The challenge now is to harness mtHKII in the treatment of infarction, stroke, elective surgery and transplantation. Remote ischaemic preconditioning, metformin administration and miR‐155/miR‐144 manipulations are potential means of doing just that. Linked Articles This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue-8