Muscle fiber conduction slowing and decreased levels of circulating muscle proteins after short-term dexamethasone administration in healthy subjects
Fabio Lanfranco1, Marco Alessandro Minetto1,2, Alberto Botter2, Matteo Domenico Baldi1, Giovanna Motta1, Ezio Ghigo1 & Emanuela Arvat1
Context: Glucocorticoids are known to decrease protein synthesis and impair membrane excitability of muscle fibres. However, their short-term effects on muscle structure and function of healthy subjects remain poorly understood.
Objective: To investigate whether steroid administration could decrease the circulating levels of muscle proteins and modify myoelectric indexes of sarcolemmal excitability and fatigability.
Design: Single-blind, placebo controlled study in twenty men randomized to receive dexamethasone (8 mg once daily per os) or placebo for 1 week. Blood sampling, force measurements for knee extensors and elbow flexors, and electrophysiological tests for biceps brachii, vastus lateralis and medialis, tibialis anterior muscles were performed before and after the intervention.
Results: Dexamethasone administration improved force by 6.0±6.0% (P=0.01) for elbow flexors and by 8.5±5.5% (P<0.01) for knee extensors, decreased levels of creatine kinase by 50.5±30.0% (P<0.01) and myoglobin by 41.8±17.5% (P<0.01), and impaired sarcolemmal excitability, as shown by the decline of muscle fiber conduction velocity for the four muscles (range from −6 to −10.5%, P<0.05). Moreover, significant reductions of the myoelectric manifestations of fatigue were observed for the four muscles: the decrease in the rate of change of the mean frequency of the EMG power spectrum ranged from −22.6 to −43.9% (P<0.05). In contrast, no significant changes were observed in muscle excitability and fatigability in subjects who received the placebo.
Conclusions: The demonstration that glucocorticoid-induced muscle impairments can be unravelled by means of blood sampling and non-invasive electrophysiological tests has clinical implications for the early identification of subclinical or preclinical forms of myopathy in treated patients.