Changes in mitochondrial perilipin 3 and perilipin 5 protein content in rat skeletal muscle following endurance training and acute stimulated contraction

Abstract

New Findings r What is the central question of this study?The aim was to determine whether mitochondrial protein content of perilipin 3 (PLIN3) and perilipin 5 (PLIN5) is increased following endurance training and whether mitochondrial PLIN5 protein is increased to a greater extent in endurance-trained rats when compared with sedentary rats following acute contraction. r What is the main finding and its importance?Mitochondrial PLIN3 but not PLIN5 protein was increased in endurance-trained compared with sedentary rats, suggesting a mitochondrial role for PLIN3 due to chronic exercise. Contrary to our hypothesis, acute mitochondrial PLIN5 protein was similar in both sedentary and endurance-trained rats.Endurance training results in an increased association between skeletal muscle lipid droplets and mitochondria. This association is likely to be important for the expected increase in intramuscular fatty acid oxidation that occurs with endurance training. The perilipin family of lipid droplet proteins, PLIN(2-5), are thought to play a role in skeletal muscle lipolysis. Recently, results from our laboratory demonstrated that skeletal muscle mitochondria contain PLIN3 and PLIN5 protein. Furthermore, 30 min of stimulated contraction induces an increased mitochondrial PLIN5 content. To determine whether mitochondrial content of PLIN3 and PLIN5 is altered with endurance training, Sprague-Dawley rats were randomized into sedentary or endurance-trained groups for 8 weeks of treadmill running followed by an acute (30 min) sciatic nerve stimulation to induce lipolysis. Mitochondrial PLIN3 protein was ß1.5-fold higher in red gastrocnemius of endurance-trained rats compared with sedentary animals, with no change in mitochondrial PLIN5 protein. In addition, there was an increase in plantaris intramuscular lipid storage. Acute electrically stimulated contraction in red gastrocnemius from sedentary and endurance-trained rats resulted in a similar increase of mitochondrial PLIN5 between these two groups, with no net change in PLIN3 in either group. Plantaris intramuscular lipid content decreased to a similar extent in sedentary and endurance-trained rats. These results suggest that while total mitochondrial PLIN5 content is not altered by endurance training, PLIN5 does have an acute role in the mitochondrial fraction during muscle contraction. Conversely, mitochondrial PLIN3 does not change acutely with muscle contraction, but PLIN3 content IntroductionThe physiological adaptations to endurance training in skeletal muscle include, but are not limited to, increased oxidative capacity, intramuscular triglyceride storage and an increase in the proteins and enzymes involved in regulating oxidative phosphorylation (Davies et al. 1981;Hoppeler et al. 1985). These are important adaptations because they lead to an improvement in the ability of muscles to use stored triglycerides efficiently. An increased reliance on intramuscular triglycerides as a fuel source after endurance training has been demonstrated in both rodent (Molé et al. 19...

Increases in skeletal muscle ATGL and its inhibitor G0S2 following 8 weeks of endurance training in metabolically different rat skeletal muscles

“…With the use of the plantaris muscle, we were able to determine IMTG content and that there was an increase in stored muscle lipids with training and no inhibition of lipolysis (as witnessed by the delta of the rested vs. stimulated leg), despite the apparent increase in G0S2 content. Whereas there was not a significant increase in IMTG use, these data demonstrate that despite the increase in G0S2 content, there was no inhibition of lipolysis (32). This suggests that lipolysis is under more complex regulation by G0S2 and not simply by G0S2 content.…”

“…Therefore, the purpose of our study was to characterize whole skeletal muscle and isolated mitochondrial G0S2 content in response to muscle contraction and endurance training in three skeletal muscles with varying oxidative capacities and metabolic profiles (SOL, RG, and WG). Our specific aims were the following: 1) to determine if endurance training would increase the capacity for lipolysis through alterations in muscle ATGL, CGI-58, and G0S2 protein content; 2) to determine if an acute, electrically stimulated contraction, which induced significant muscle lipolysis in whole muscle (30,32), would decrease G0S2 relative to ATGL and CGI-58 to regulate lipolysis acutely; and 3) to examine whether mitochondrial G0S2 content would increase with acute muscle contraction and endurance training to increase energy production.…”

Training alters the distribution of perilipin proteins in muscle following acute free fatty acid exposure

“…) and PLIN3 is observed in the mitochondrial fraction of sedentary and endurance‐trained rats (Ramos et al . ), suggesting that PLIN3 plays a role in IMTG oxidation. Taken together, these data suggest that redistributing PLIN2, PLIN3 and PLIN5 in response to acute FFA elevation would confer a metabolic advantage by maintaining a metabolically flexible intramuscular LD pool.…”

Muscle Lipid Metabolism: Role of Lipid Droplets and Perilipins

“…Conversely, PLIN3 levels in muscle biopsies from healthy patients are positively correlated with whole-body oxidative capacity, while PLIN3 knockdown results in decreased FA oxidation [81]. Subcellular localization of PLIN3 may play a role in its function, as it has been observed that endurance training, but not electrically induced contraction, induces PLIN3 expression and its association with mitochondria in rats (Figure 1(c)) [82]. Whether species-specific function or intracellular localization is responsible for this discrepancy is still unknown.…”