Abstract
Cardiolipin (CL) is a unique mitochondrial phospholipid that, in skeletal muscle, is enriched with linoleic acid (18:2n6). Together, CL content and CL 18:2n6 composition are critical determinants of mitochondrial function. Skeletal muscle is comprised of slow and fast fibers that have high and low mitochondrial content, respectively. In response to overloading and unloading stimuli, these muscles undergo a fast-to-slow oxidative fiber type shift and a slow-to-fast glycolytic fiber type shift, respectively, with a concomitant change in mitochondrial content. Here, we examined changes in CL content and CL 18:2n6 composition under these conditions along with tafazzin (Taz) protein, which is a transacylase enzyme that generates CL lipids enriched with 18:2n6. Our results show that CL content, CL 18:2n6 composition, and Taz protein content increased with an overload stimulus in plantaris. Conversely, CL content and CL 18:2n6 composition was reduced with an unloaded stimulus in soleus. Interestingly, Taz protein was increased in the unloaded soleus, suggesting that Taz may provide some form of compensation for decreased CL content and CL 18:2n6 composition. Together, this study highlights the dynamic nature of CL and Taz in skeletal muscle, and future studies will examine the physiological significance behind the changes in CL content, CL 18:2n6 and Taz.
Highlights
Cardiolipin (CL) is a unique mitochondrial-specific dimeric phospholipid[1], that acts as a reliable marker of mitochondrial content[2]
In the present study we sought to characterize the dynamic nature of CL content, CL 18:2n6 composition and tafazzin gene (Taz) protein content in response to muscle overloading and unloading stimuli
In unloaded soleus induced by tenotomy, we hypothesized that the slow-to-fast fiber type shift, which have lower mitochondrial content, would correspond with a reduction in CL content, CL 18:2n6 composition, and Taz protein
Summary
Cardiolipin (CL) is a unique mitochondrial-specific dimeric phospholipid[1], that acts as a reliable marker of mitochondrial content[2]. CL’s fatty acid composition varies across tissue types[1], linoleic acid (18:2n6) is the dominate fatty acid bound to CL in cardiac and skeletal muscle[4, 10, 11] In these tissues, reductions in CL 18:2n6 composition can compromise mitochondrial function, as shown with impairments in cytochrome c oxidase activity[12,13,14]. Skeletal muscle fibers differ in their contractile speed and metabolic capacity, which allows for different tasks to be performed[18] Postural muscles, such as soleus, resist the downward pull of gravity and exhibit a more tonic activity pattern, and require more slow-twitch oxidative fibers that are fatigue resistant and abundant with mitochondria[18, 19]. On the other hand, unloading a predominantly slow-twitch muscle such as soleus induces muscle atrophy and a fiber type switch towards the fast-glycolytic phenotype[25, 26]
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