Metabolism of rat skeletal muscle after spinal cord transection

Abstract

We investigated the energy metabolism of the gastrocnemius muscle of the rat after spinal cord transection, using in vivo 31P magnetic resonance spectroscopy (MRS). Spectra were obtained at rest and during exercise and recovery before, and at different time‐points after, spinal cord transection. At rest, the adenosine triphosphate (ATP) level was not altered and the intracellular pH became permanently more alkaline. In electrically stimulated muscle, cord transection caused a greater phosphocreatine depletion than in control animals, and the maximum rate of oxidative ATP synthesis was significantly diminished; at days 30 and 60 after transection, an intracellular acidification was observed at the end of exercise. These effects indicate that, as in humans, spinal cord transection in rats leads to a decrease in mitochondrial oxidative metabolism and probably to an increase in anaerobic metabolism. This experimental model may prove useful for evaluating various approaches to improve muscle function in paraplegia. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1561–1568, 2000

In vivo 31P NMR spectroscopy assessment of skeletal muscle bioenergetics after spinal cord contusion in rats

“…After a cSCI, we do not observe increases in the resting inorganic phosphate content. However, similar to what is seen after a complete spinal cord transection in rats (Durozard, Gabrielle et al 2000), the trend towards an increase in the resting [Pi]/[PCr] ratios after a cSCI is accompanied with concurrent decreases in the [PCr] content. The exact mechanism of declines in [PCr] content at rest remains unknown, but is suggestive of an imbalance in the resting phosphorylation potential such that the energy available for muscle contraction and other cellular work is decreased (Taylor, Kemp et al 1993).…”

“…The exact mechanism of declines in [PCr] content at rest remains unknown, but is suggestive of an imbalance in the resting phosphorylation potential such that the energy available for muscle contraction and other cellular work is decreased (Taylor, Kemp et al 1993). Additionally, similar to spinal transection in rats (Durozard, Gabrielle et al 2000), we observed a slight increase in the baseline pH values; possibly indicating a shift to anaerobic metabolism after paralysis.…”

“…Studies have well established that during recovery from exercise, glycolysis ceases and PCr in the muscle cell is replenished at the expense of ATP produced via mitochondrial oxidative phosphorylation (Durozard, Gabrielle et al 2000). Accordingly, k PCr has been extensively used in both healthy and diseased muscles as estimates of muscle oxidative capacity (Meyer 1988; Paganini, Foley et al 1997; McCully, Mancini et al 1999; Argov and Arnold 2000; Kent-Braun and Ng 2000; Pathare, Vandenborne et al 2007).…”

“…Measurements of Q max during recovery in this way, is independent of end exercise pH and PCr (Kemp, Sanderson et al 1996; Durozard, Gabrielle et al 2000). …”

“…Drastic declines in mitochondrial enzyme activity, capillary density and a shift in fiber type composition to type II glycolytic fibers of the paralyzed skeletal muscles is well documented after complete SCI in humans (Kjaer, Mohr et al 2001) and in spinalized animal models (Jiang, Roy et al 1991; Durozard, Gabrielle et al 2000; Gregory, Vandenborne et al 2003). Skeletal muscle metabolic dysfunction has the potential to decrease oxidative capacity and to negatively impact muscle fatigability (Wang, Hiatt et al 1999; Bhambhani, Tuchak et al 2000; McCully, Mulcahy et al 2011; Erickson, Ryan et al 2013).…”