Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Philipp Baumert,Barry Drust,Mark J Lake,Robert M Erskine,Claire E Stewart

doi:10.1007/s00421-016-3411-1

Philipp Baumert, Barry Drust + Show 3 more

Open Access

https://doi.org/10.1007/s00421-016-3411-1

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Abstract

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation–contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (−308 G>A, rs1800629), IL6 (−174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage.

Highlights

People who engage in unaccustomed, strenuous physical exercise can experience stiff or sore muscles, a feeling that is usually apparent for 24–72 h after exercise
The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, providing a better understanding of exercise-induced muscle damage
Circulating muscle-specific proteins [e.g., creatine kinase (CK), myoglobin and α-actin] are commonly used to indicate exercise-induced muscle damage (Huerta-Alardín et al 2005; Martinez Amat et al 2007), whereas tenascin-C is thought to be an indicator for disruption of the overlying connective tissue and the extracellular matrix (Flück et al 2003)

Summary

Introduction

People who engage in unaccustomed, strenuous physical exercise can experience stiff or sore muscles, a feeling that is usually apparent for 24–72 h after exercise. Several investigations have revealed that these unaccustomed eccentric actions, during which the muscle is lengthened while it is active, provoke stiffer and more tender muscles compared to concentric or isometric contractions (Armstrong 1984; Armstrong et al 1991) These contractions are strongly associated with damage to skeletal muscle consisting of structural disruption of sarcomeres, disturbed excitation–contraction coupling and calcium signalling, leading to an inflammatory response and the activation of several muscle protein degradation pathways. This process has been referred to as exercise-induced muscle damage (Hyldahl and Hubal 2014; Peake et al 2005) and is normally accompanied by swelling, and a temporary reduction in both maximum strength and range of motion (Baird et al 2012; Brown et al 1999; Clarkson et al 1992). Circulating muscle-specific proteins [e.g., creatine kinase (CK), myoglobin and α-actin] are commonly used to indicate exercise-induced muscle damage (Huerta-Alardín et al 2005; Martinez Amat et al 2007), whereas tenascin-C is thought to be an indicator for disruption of the overlying connective tissue and the extracellular matrix (Flück et al 2003)

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