Neural and mechanical factors associated with exercise-induced muscle damage and the repeated bout effect.

Electronic versions

Documents

  • Malachy P. McHugh

    Research areas

  • Human physiology, Biochemistry

Abstract

Unfamiliar, predominantly eccentric exercise frequently results in muscle damage. Following recovery, a repeated bout of the same exercise results in minimal symptoms of damage. This has been referred to as the "repeated bout effect" and a specific mechanism has not been identified. Possible neural and mechanical factors associated with symptoms of exercise-induced muscle damage and the repeated bout effect were examined. Surface electromyographic (EMG) signals were recorded from the hamstring muscles during two bouts of submaximal isokinetic eccentric (11 men, 9 women) or concentric (6 men, 4 women) contractions separated by two weeks. EMG/torque and median frequency (MF) were analysed. Hamstring muscle stiffiless, estimated from torquelROM curves during passive stretch, was measured prior to both the initial and repeated exercise bouts and on each of the subsequent three days. The initial bout of eccentric exercise resulted in strength loss, pain, muscle tenderness and elevated plasma CK activity while the repeated eccentric bout resulted in a strength gain, minimal pain, no muscle tenderness and minimal plasII}a CK elevation. Minimal symptoms were seen following either bouts of concentric exercise. EMG analyses suggested that a small number of primarily fast-twitch motor units were recruited for eccentric exercise. This recruitment pattern was similar between eccentric bouts despite the fact that the initial bout resulted in symptoms of muscle damage while the repeated bout did not. Symptoms were greater in subjects with stiffer muscles but no change in passive stiffiless occurred between the repeated bouts. Greater symptoms in stiffer muscles are attributed to the inability of the tendon-aponeurosis complex to absorb the strain imposed by 13 eccentric contractions. However, the repeated bout effect could not be explained by an adaptation in passive stiffuess. Future studies on possible mechanisms for the repeated bout effect should address adaptations which might limit sarcomere strain such as increased myofibrillar cross-bridge stiffuess.

Details

Original languageEnglish
Awarding Institution
  • Bangor University
Supervisors/Advisors
    Award dateMar 1999