Journal
JOURNAL OF EXPERIMENTAL BIOLOGY
Volume 226, Issue 20, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jeb.246507
Keywords
Achilles tendon; M. triceps surae; Imbalance; Mechanical loading; Biomarkers
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This study investigated the adaptive responses of the human triceps surae muscle-tendon unit to repetitive high tendon strain cyclic loading. The results showed that frequent high strain loading can lead to increased maximal tendon strain and altered collagen turnover.
In response to a mechanical stimulus, tendons have a slower tissue renewal rate compared with muscles. This could, over time, lead to a higher mechanical demand (experienced strain) for the tendon, especially when a high strain magnitude exercise is repeated without sufficient recovery. The current study investigated the adaptive responses of the human triceps surae (TS) muscle-tendon unit (MTU) and extracellular matrix turnover-related biomarkers to repetitive high tendon strain cyclic loading. Eleven young adult males performed a progressive resistance exercise over 12 consecutive days, consisting of high Achilles tendon (AT) strain cyclic loading (90% MVC) with one leg once a day (Leg(T1)) and the alternate leg three times a day (Leg(T3)). Exercise-related changes in TS MTU mechanical properties and serum concentrations of extracellular matrix turnover-related biomarkers were analysed over the intervention period. Both legs demonstrated similar increases in maximal AT force (similar to 10%) over the 12 day period of exercise. A similar to 20% increase in maximal AT strain was found for Leg(T3) (P<0.05) after 8 consecutive exercise days, along with a corresponding decrease in AT stiffness. These effects were maintained even after a 48 h rest period. The AT mechanical properties for Leg(T1) were unaltered. Biomarker analysis revealed no sign of inflammation but there was altered collagen turnover and a delay in collagen type I synthesis. Accordingly, we suggest that tendon is vulnerable to frequent high magnitude cyclic mechanical loading as accumulation of micro-damage can potentially exceed the rate of biological repair, leading to increased maximal tendon strain.
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