Effects of Muscle Damage on Stretch-Shortening Cycle Function and Muscle Stiffness Control

2004 ◽  
Vol 18 (4) ◽  
pp. 771 ◽  
Author(s):  
Andrew J. Harrison ◽  
Simon D. Gaffney
1999 ◽  
Vol 82 (3) ◽  
pp. 1622-1626 ◽  
Author(s):  
Pietro G. Morasso ◽  
Marco Schieppati

A stiffness control model for the stabilization of sway has been proposed recently. This paper discusses two inadequacies of the model: modeling and empiric consistency. First, we show that the in-phase relation between the trajectories of the center of pressure and the center of mass is determined by physics, not by control patterns. Second, we show that physiological values of stiffness of the ankle muscles are insufficient to stabilize the body “inverted pendulum.” The evidence of active mechanisms of sway stabilization is reviewed, pointing out the potentially crucial role of foot skin and muscle receptors.


1999 ◽  
Vol 24 (3) ◽  
pp. 234-248 ◽  
Author(s):  
Priscilla M. Clarkson ◽  
Stephen P. Sayers

Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis. the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise. Key words: eccentric exercise, inflammation, stress proteins, muscle function


1998 ◽  
Vol 30 (3) ◽  
pp. 415-420 ◽  
Author(s):  
HEIKKI KYR??L??INEN ◽  
TIMO E. S. TAKALA ◽  
PAAVO V. KOMI

1999 ◽  
Vol 86 (4) ◽  
pp. 1292-1300 ◽  
Author(s):  
Janne Avela ◽  
Heikki Kyröläinen ◽  
Paavo V. Komi ◽  
Daniel Rama

The mechanisms related to the acute and delayed secondary impairment of the stretch reflex function were investigated after long-lasting stretch-shortening cycle exercise. The results demonstrated a clear deterioration in muscle function immediately after fatigue, which was accompanied by a clear reduction in active and passive reflex sensitivity. For active and passive stretch reflexes, this reduction was biphasic ( P < 0.05 to P < 0.001). However, for the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential, only one significant reduction was seen immediately after fatigue (71.2%, P < 0.01). A similar significant ( P < 0.01) decrease in the stretch-resisting force of the muscle was also detected. Clear increases were found in the indirect markers of muscle damage (serum creatine kinese activity and skeletal troponin I), which could imply the occurrence of ultrastructural muscle damage. It is suggested that the acute reduction in reflex sensitivity is of reflex origin and due to two active mechanisms, disfacilitation and presynaptic inhibition. However, the delayed second decline in the sensitivity of some reflex parameters may be attributable to the secondary injury, because of some inflammatory response to the muscle damage. This might emphasize the role of presynaptic inhibition via group III and IV muscle afferents.


2018 ◽  
Vol 1 (108) ◽  
pp. 25-29
Author(s):  
Albertas Skurvydas ◽  
Gediminas Mamkus ◽  
Dalia Mickevičienė ◽  
Diana Karanauskienė ◽  
Dovilė Valančienė ◽  
...  

Background. The aim of this study was to follow symptoms of exercise induced muscle damage in response to 50, 100 and 200 drop jumps with maximal intensity. Methods. Three groups of young healthy men (n = 10 in each group) performed a bout of mechanically demanding stretch shortening cycle exercise consisting of 50, 100 and 200 drop jumps. Voluntary and electrically induced knee extension torque, creatine kinase, muscle soreness were measured before and 24 h after exercise. Results. Indirect symptoms of exercise induced damage were dependent on DJs volume: the higher the numbers of jumps, the more symptoms were observed. Only after 200 DJs compared to 50-100 DJ there was decrease of CAR and H of DJ, and 24 h after 200 DJs CK was greater than after 50-100 DJs. Conclusion. In response to acute severe muscle-damaging exercise (after 200 DJs), indirect symptoms of exercise-induced muscle damage occurred.


Sign in / Sign up

Export Citation Format

Share Document