Mechanisms for fiber-type specificity of skeletal muscle atrophy

Abstract

Purpose of review There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. Recent findings Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. Summary Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.

Estrogens maintain skeletal muscle and satellite cell functions

“…Indeed, estrogens prevent HIF1α activation, leading to the suppression of osteoclast activity (Miyauchi et al 2013). Nuclear factor-κB (NF-κB), a transcription factor of inflammatory genes, induces muscle atrophy, along with the loss of slow-twitch fibers (Li et al 2008, Wang & Pessin 2013. Estrogens suppress inflammation responses by inhibiting the activation of NF-κB (Stice & Knowlton 2008).…”

In vivo Ca2+ buffering capacity and microvascular oxygen pressures following muscle contractions in diabetic rat skeletal muscles: fiber-type specific effects

“…If SR Ca 2ϩ handling in diabetes is not impaired, the mechanistic bases for diabetes-induced [Ca 2ϩ ] i dysregulation must reside elsewhere. Diabetes induces fiber-type-specific effects predominantly targeting fast-twitch fibers/muscles (55). These fibers/muscles are characterized by a very different microvascular partial pressure of oxygen (Pmv O 2 ) than their slow-twitch counterparts both during and following contractions (7,34), and it is therefore possible that the impaired SR-Ca 2ϩ handling in these fibers in diabetes is related to their Pmv O 2 profile.…”

Effect of 20-Hydroxyecdysone on Proteolytic Regulation in Skeletal Muscle Atrophy

“…The reason behind our selecting this animal model is that this type of atrophy is very commonly encountered by clinicians following orthopedic surgery or degenerative musculoskeletal diseases (18); moreover, tenotomy is reproducible in inducing muscle atrophy. Additionally, there is accumulating evidence that slow-twitch fibers are more sensitive to inactivity or microgravity than fast-twitch fibers (19,20), and 20E enhances muscle hypertrophy of different fiber types in a muscle-specific fashion (15). Thus, the second goal of this study was to evaluate whether 20E induces a fiber type-specific response of proteolytic regulation of tenotomy-induced muscle atrophy in slowdominant soleus and fast-dominant plantaris muscles.…”