Exertional rhabdomyolysis: physiological response or manifestation of an underlying myopathy?

Abstract

Exertional rhabdomyolysis is characterised by muscle breakdown associated with strenuous exercise or normal exercise under extreme circumstances. Key features are severe muscle pain and sudden transient elevation of serum creatine kinase (CK) levels with or without associated myoglobinuria. Mild cases may remain unnoticed or undiagnosed. Exertional rhabdomyolysis is well described among athletes and military personnel, but may occur in anybody exposed to unaccustomed exercise. In contrast, exertional rhabdomyolysis may be the first manifestation of a genetic muscle disease that lowers the exercise threshold for developing muscle breakdown. Repeated episodes of exertional rhabdomyolysis should raise the suspicion of such an underlying disorder, in particular in individuals in whom the severity of the rhabdomyolysis episodes exceeds the expected response to the exercise performed. The present review aims to provide a practical guideline for the acute management and postepisode counselling of patients with exertional rhabdomyolysis, with a particular emphasis on when to suspect an underlying genetic disorder. The pathophysiology and its clinical features are reviewed, emphasising four main stepwise approaches: (1) the clinical significance of an acute episode, (2) risks of renal impairment, (3) clinical indicators of an underlying genetic disorders and (4) when and how to recommence sport activity following an acute episode of rhabdomyolysis. Genetic backgrounds that appear to be associated with both enhanced athletic performance and increased rhabdomyolysis risk are briefly reviewed.

Keywords: Exercise; Muscle damage/injuries; Neuromuscular; Training.

Figure 1

Pathophysiology of rhabdomyolysis. The pathophysiological events in rhabdomyolysis follow a common pathway, irrespective of its cause. CK, creatine kinase; SR, sarcoplasmic reticulum.

Figure 2

Rise and fall of myoglobin and creatine kinase (CK) during the course of rhabdomyolysis. Myoglobin is the first enzyme that increases, but returns to normal levels within the first 24 hours after onset of symptoms. CK increases a few hours later, reaches its peak value within the first 24 hours, and remains at these levels for 3 days. Even though the presence of myoglobin in serum is the key feature of rhabdomyolysis, CK is considered to be a more useful marker for the diagnosis and assessment of the severity of muscular injury due to its delayed clearance from the plasma and the wide availability for diagnostic testing. (Reprinted from Giannoglou et al Copyright 2007, with permission from Elsevier).