Abstract

The purpose of this study was to investigate if exertional rhabdomyolysis induced by an acute bout of plyometric exercise in untrained individuals was associated with histological characteristics of skeletal muscle, creatine kinase (CK) polymorphism or secondary damage. Twenty-six healthy male untrained individuals completed a bout of plyometric exercise (10 sets of 10 maximal squat jumps, with each standardized to achieve at least 95% of individual maximal jump height). Blood samples were taken, and perceived pain was scored immediately before the exercise intervention and 6 h, 1, 2, and 3 days post-intervention. Muscle biopsies were collected 9 or 4 days before (baseline) and 3 days after plyometric jumps. Subjects were divided into two groups, high (n = 10) and low responders (n = 16), based on a cut-off limit for exertional rhabdomyolysis of peak CK activity ≥ 1000 U/L in any post-exercise blood sample. Perceived pain was more severe assessed in squat than standing position. Low responders perceived more pain at 6 h and 1 day, while high responders perceived more pain than low responders on days three and four after exercise; structural (dystrophin staining) and ultra-structural (transmission electron microscopy) analysis of muscle fibers revealed no baseline pathology; damage was evident in all individuals in both groups, with no difference between high and low responders in either damage or fiber type proportion. High responders had significantly higher total white blood cell and neutrophil counts 6 h and significantly higher C-reactive protein (CRP) 6 h and days one and two after exercise compared to low responders. High responders had significantly greater muscle myeloperoxidase (MPO) levels in baseline and 3 day post-exercise biopsies compared to baseline of low responders. MLCK C49T single polymorphism was present in 26% of volunteers, whose CK responses were not higher than those with MLCK CC or CT genotype. In conclusion, perceived pain is more effectively assessed with potentially affected muscle under eccentric strain, even if static. High CK responders also have pronounced CRP responses to unaccustomed plyometric exercise intervention. Exertional rhabdomyolysis after unaccustomed eccentric exercise may be related to underlying inability to resolve intramuscular MPO.

Highlights

  • Elevated circulating creatine kinase (CK) is a hallmark of muscle damage caused by intense and unaccustomed exercise including muscle-group targeted eccentric resistance exercise, downhill running and plyometric jumping (Nosaka et al, 2001; Macaluso et al, 2012b, 2013; van de Vyver and Myburgh, 2012)

  • The aim of this study was to probe in untrained individuals different mechanisms which may predispose to exertional rhabdomyolysis, induced by an acute bout of plyometric exercise that results in varying levels of post-exercise circulating CK

  • Time-dependent group differences were evident: while perceived soreness scores were higher in low responders at 6 h post-plyometric exercise, high responders rated their soreness at days 3 and 4 higher than low responders, but only in the squat position

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Summary

Introduction

Elevated circulating creatine kinase (CK) is a hallmark of muscle damage caused by intense and unaccustomed exercise including muscle-group targeted eccentric resistance exercise, downhill running and plyometric jumping (Nosaka et al, 2001; Macaluso et al, 2012b, 2013; van de Vyver and Myburgh, 2012). Literature reports that certain individuals, despite apparently similar characteristics to other study participants, may experience greater increases in CK activity following unaccustomed eccentric exercise (Clarkson et al, 2005; Devaney et al, 2007; Yamin et al, 2008) This biological phenomenon remains unexplained (Sayers and Clarkson, 2002). The laboratory diagnostic cut-off limit for exertional rhabdomyolysis varies across studies and study populations (Sayers and Clarkson, 2002; Warren et al, 2002; Lauritzen et al, 2009), a lower limit for exertional rhabdomyolysis has been suggested to be CK ≥ 1000 U/L (Lee and Clarkson, 2003; Thoenes, 2010) This phenomenon is well described, including the potential for clinical sequelae (Hill et al, 2017), the potential mechanisms pre-disposing certain individuals remains to be elucidated fully

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