Neural factors account for strength decrements observed after short-term muscle unloading

Abstract

Strength decrements observed after extended (4-6 wk) periods of muscle unloading are associated with significant atrophy. Because early (up to 2 wk) strength gains from resistance exercise are related to improved neural recruitment, we hypothesized that the loss of strength resulting from 2 wk of muscle unloading [unilateral lower limb suspension (ULLS)] was due to impaired neural activation of the affected muscle. Blood samples, muscle biopsy specimens, muscle function data, and electromyography (EMG) recordings were analyzed before and after 14 days of muscle unloading. Pre- to postunloading data showed significant (P < or = 0.05) decrements in peak torque and total work performed by knee extensors and flexors. This was coupled with decreased EMG activity, but no change in neuromuscular efficiency (total torque/EMG). Resistance to muscle fatigue was enhanced after ULLS. The 14-day intervention failed to alter the size or fiber type distribution of muscle samples. However, resting plasma cortisol levels were significantly increased after muscle unloading, suggesting an endocrine environment favorable to muscle atrophy. Our data confirm that the diminution in muscle function displayed after 2 wk of unloading is mainly due to neural, rather than contractile, disturbances.

Prehabilitation: The Void in the Management of Anterior Cruciate Ligament Injuries—A Clinical Review

“…Berg et al reported similar results and interestingly found that these changes were completely reversed after 7 weeks of recovery [73]. A reduction of strength power likely caused by altered neural function may precede atrophy in periods of decreased activity [65]. Failure of voluntary activation from the central nervous system to the quadriceps muscle as a result of disruption of the ACL has been implicated [74].…”

“…Decreased levels of physical activity [54][55][56], weightbearing status [56][57][58], and immobilization [59][60][61] can lead to progressive atrophy. Several factors including decreased protein synthesis [62][63][64], increased levels of plasma cortisol [65], arthrogenic inhibition [66,67], and altered afferent inflow [66] may be responsible for atrophy after trauma or in periods of prolonged muscular disuse. Though evidence is lacking, this notion alone supports the possible benefits of prehabilitation in preoperative ACL-deficient patients.…”

Adaptações neuromusculares de flexores dorsais e plantares a duas semanas de imobilização após entorse de tornozelo

“…redução na atividade elétrica do TA seja consequência da inibição muscular, que é a incapacidade de ativar ao máximo todas as unidades motoras de um músculo durante o esforço voluntário. Os mecanismos que impedem a ativação completa dos músculos após uma lesão ainda não são bem compreendidos, mas a presença da lesão, o edema, a dor ou até mesmo a apreensão do sujeito (medo de sentir dor ao realizar a contração) pode inibir o limiar de disparo das unidades motoras (28) . Tendo em vista que músculos uniarticulares, com função antigravitacional e composição predominante de fibras lentas aparentemente são os mais afetados pelo desuso (10) , era esperada a redução de ativação EMG do SO.…”

Activation of respiratory muscles does not occur during cold-submergence in bullfrogs,Lithobates catesbeianus

“…Overwintering submergence presents a springtime challenge because disuse of neuromotor processes typically leads to loss-offunction through muscle atrophy and neuroplastic motor defects, especially in humans and laboratory rodents (Bonaldo and Sandri, 2013;Clark et al, 2006;Cormery et al, 2005;Deschenes et al, 2002;Seki et al, 2007). Hibernating, overwintering and estivating vertebrates provide interesting exceptions to this rule as they use integrative mechanisms to curtail muscle atrophy and motor decline during extended inactivity (Hudson and Franklin, 2002).…”