Mechanisms of muscle injury after eccentric contraction

1999 ◽  
Vol 2 (3) ◽  
pp. 253-265 ◽  
Author(s):  
Richard L Lieber ◽  
Jan Fridén
2011 ◽  
Vol 27 (1) ◽  
pp. 55-65 ◽  
Author(s):  
Mandy Gault ◽  
Richard Clements ◽  
Mark Willems

Eccentric contraction-induced muscle injury does not change walking economy in older adultsThe aim of the study was to examine whether self-selected walking speed during downhill treadmill walking by older adults would result in muscle injury and changes in physiological responses during level walking. Twenty-six participants (age: 67 ± 4 yrs; height: 1.69 ± 0.09 m; body mass: 74.9 ± 13.1kg) were assigned to level (n = 11, 30 min, 0%) or downhill walking (n=15, 30 min, -10%) at a self-selected walking speed. Self-selected walking speed and exercise intensity were similar for both groups (level: 4.2±0.4 km·hr-1, 42±6% VO2max; downhill: 4.6±0.6 km·hr-1, 44±15% VO2max). After 48-hours, downhill walking had reduced maximal voluntary isometric force of the m. quadriceps femoris (-15%, P<0.001), indicative of muscle injury, but no changes were observed for walking economy, minute ventilation, heart rate and respiratory exchange ratio during level walking. For older adults, downhill walking at a selfselected walking speed causes muscle injury without any detrimental effect on walking economy. Regular downhill walking at a self-selected walking speed by older adults is an eccentric endurance activity that may have the potential to improve cardiovascular fitness and muscle strength.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mirko Manetti ◽  
Alessia Tani ◽  
Irene Rosa ◽  
Flaminia Chellini ◽  
Roberta Squecco ◽  
...  

Abstract Although telocytes (TCs) have been proposed to play a “nursing” role in resident satellite cell (SC)-mediated skeletal muscle regeneration, currently there is no evidence of TC-SC morpho-functional interaction following tissue injury. Hence, we explored the presence of TCs and their relationship with SCs in an ex vivo model of eccentric contraction (EC)-induced muscle damage. EC-injured muscles showed structural/ultrastructural alterations and changes in electrophysiological sarcolemnic properties. TCs were identified in control and EC-injured muscles by either confocal immunofluorescence (i.e. CD34+CD31− TCs) or transmission electron microscopy (TEM). In EC-injured muscles, an extended interstitial network of CD34+ TCs/telopodes was detected around activated SCs displaying Pax7+ and MyoD+ nuclei. TEM revealed that TCs invaded the SC niche passing with their telopodes through a fragmented basal lamina and contacting the underlying activated SCs. TC-SC interaction after injury was confirmed in vitro by culturing single endomysial sheath-covered myofibers and sprouting TCs and SCs. EC-damaged muscle-derived TCs showed increased expression of the recognized pro-myogenic vascular endothelial growth factor-A, and SCs from the same samples exhibited increased MyoD expression and greater tendency to fuse into myotubes. Here, we provide the essential groundwork for further investigation of TC-SC interactions in the setting of skeletal muscle injury and regenerative medicine.


2018 ◽  
Vol 50 (5S) ◽  
pp. 143
Author(s):  
Kazuki Hotta ◽  
Brad J. Behnke ◽  
Kazuto Masamoto ◽  
Rie Shimotsu ◽  
David C. Poole ◽  
...  

2003 ◽  
Vol 285 (6) ◽  
pp. R1490-R1495 ◽  
Author(s):  
Christopher R. Rathbone ◽  
J. C. Wenke ◽  
Gordon L. Warren ◽  
R. B. Armstrong

The purpose of this study was to determine if the elimination of satellite cell proliferation using γ-irradiation would inhibit normal force recovery after eccentric contraction-induced muscle injury. Adult female ICR mice were implanted with a stimulating nerve cuff on the common peroneal nerve and assigned to one of four groups: 1) irradiation- and eccentric contraction-induced injury, 2) eccentric contraction-induced injury only, 3) irradiation only, and 4) no intervention. Anterior crural muscles were irradiated with a dose of 2,500 rad and injured with 150 in vivo maximal eccentric contractions. Maximal isometric torque was determined weekly through 35 days postinjury. Immediately after injury, maximal isometric torque was reduced by ∼50% and had returned to normal by 28 days postinjury in the nonirradiated injured mice. However, torque production of irradiated injured animals did not recover fully and was 25% less than that of injured nonirradiated mice 35 days postinjury. These data suggest that satellite cell proliferation is required for approximately half of the force recovery after eccentric contraction-induced injury.


2001 ◽  
Vol 26 (4) ◽  
pp. 323-335 ◽  
Author(s):  
Antonios Kyparos ◽  
Chrysoula Matziari ◽  
Maria Albani ◽  
Georgios Arsos ◽  
Sofia Sotiriadou ◽  
...  

The purpose of the present study was to investigate the immediate and 48-hr post-exercise effects of eccentric contraction-biased exercise on the contractile properties of the soleus muscle in situ. Adult male Wistar rats were categorised into sedentary control rats (n = 10), rats studied immediately (n = 10), and rats studied 48 hours after the exercise (n = 10). The exercise protocol consisted of a 90-min intermittent downhill running (-16°, 16 m/min) on a motor-driven treadmill. The contractile properties of the soleus muscle were recorded following i.p. chloral hydrate anaesthesia. Isometric twitch force (Pt), time-to-peak tension (TPT), half-relaxation time (1/2 RT), and tetanic force at stimulation frequencies of 40, 80, and 100 Hz were recorded. A low-frequency muscle fatigue protocol (stimulation at 4 Hz for 5 min) was applied to test for fatigability. The main findings indicated that Pt generation dropped both immediately and 48 hr after the exercise, while tetanic force was partially restored after 48 hr. Exercise-induced E-C coupling failure and contractile machinery disorganisation due to muscle injury are put forward as the main force reduction causes. Key words: eccentric exercise, muscle injury, SR, E-C coupling, tension recording


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Benjamin Corona ◽  
Andrea K Wilson ◽  
Clement Rouviere ◽  
Susan L Hamilton ◽  
Christopher P Ingalls

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