Muscle enzyme adaptation to training and tapering-off in spinal-cord-injured humans

Abstract

The activity of muscle metabolic enzymes depends on the amount and type of physical training. We examined muscle enzyme adaptation to prolonged training followed by a period of lowered activity in spinal-cord-injured individuals (SCI). Ten SCI [mean age 35 (SEM 2) years, mean body mass 78 (SEM 4) kg, mean time post-injury 12 (SEM 2) years and range of lesion C5-T4] were given 12 months of functional electrical stimulation of an upright cycling motion for 30 min a day, three times a week, followed by 6 months of training once a week. Activities of glycolytic (hexokinase HK, lactate dehydrogenase LDH) and oxidative (citrate synthase CS, 3-hydroxyacyl-CoA dehydrogenase HAD) enzymes were determined in biopsies of the vastus lateralis muscle taken at 0, 3, 6, 12, and 18 months of training. The degree of sympathoadrenergic activity was evaluated from arterial concentrations of catecholamines in response to acute exercise. Training three times a week induced increases (P < 0.05) in HK (150%), LDH (40%), CS (100%), and HAD (70%) activities that reached a plateau after 3 months. Peak oxygen uptake and power output during exercise by electrical stimulation rose continuously over the first 12 months. After reducing the amount of training by two-thirds, HK, LDH and CS activities remained elevated above basal levels (P < 0.05), whereas HAD, power output and maximal oxygen uptake returned to pretraining levels (P > 0.05). It is concluded that most improvements in glycolytic and mitochondrial oxidative enzyme activities induced by long-term training can be maintained in spinal-cord-injured individuals despite a marked reduction in training frequency unrelated to performance or to the degree of sympathoadrenergic impairment.

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

“…Our finding that the oxidative capacity after cSCI is impaired is in concurrence with in-vivo and in vitro models of complete SCI in both humans (Kjaer, Mohr et al 2001) and animal models (Gregory, Vandenborne et al 2003). In-vitro studies show that mixed muscles such as the gastrocnemius and the vastus lateralis have significantly lower mitochondrial enzyme activity following spinalization in both cats and rats (Jiang, Roy et al 1991; Gregory, Vandenborne et al 2003).…”

“…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).…”

Effect of load during electrical stimulation training in spinal cord injury

“…The inability to find increases in citrate synthase activity in the dynamically trained leg was unexpected given a previous study indicating that changes in muscle enzymes are unrelated to exercise performance or the magnitude of sympathoadrenergic drive 20. Earlier studies using dynamic‐based exercise have reported increases in citrate synthase activity in the vastus lateralis muscle of up to 160% after 4, 8, and 10 weeks of electrical stimulation–induced cycling 7, 9, 22.…”

Skeletal muscle mitochondrial health and spinal cord injury

“…Eight weeks of FES cycling resulted in an increase in citrate synthase, a marker of mitochondrial mass[ 61 ]. Similarly, studies found increased citrate synthase as well as increased function of enzymes involved in glycolysis and β-oxidation[ 62 , 63 ]. Finally, SDH was increased after 4 wk of training, suggesting that complex II activity is increased with exercise[ 64 ].…”