Lipid storage changes in human skeletal muscle during detraining

Abstract

Exercise training is known to increase intramuscular triglyceride content in both trained and untrained legs. The purpose of the study was to determine the changes of intramyocellular lipids (IMCL) and extramyocellular lipids (EMCL) of both trained and untrained legs during detraining. We measured both IMCL and EMCL levels in previously trained vs. untrained legs during 4-weeks of detraining after 6-weeks of strength training. Eight young men (aged 21.4 ± 1.4 years) trained their vastus lateralis muscle in one leg using a dynamometer, whereas the contralateral leg served as untrained control. Muscle cross-sectional area (CSA), IMCL, EMCL, total creatine (creatine + phophocreatine) of extensor (vastus lateralis) muscles were assessed using magnetic resonance imaging (MRI) and proton magnetic resonance spectra (1H-MRS) before training, 3 days after and 28 days after the last bout of training. CSA was increased in both legs by Day 3 after training, and was still high at Day 28 post-training; IMCL increased in both legs by Day 3 after training, then decreased at Day 28 post-training only in the untrained leg; EMCL shows no significant change by Day 3 after training, but at Day 28 post-training has increased in the trained leg and decreased in the untrained leg; total creatine did not change significantly.Conclusion: Decreases of IMCL and EMCL storages in previously untrained leg during detraining indicates an ectopic influence on tissue lipid storage by different metabolic demand among tissues in the same human body.

Exercise training‐induced visceral fat loss in obese women: The role of training intensity and modality

“…28 Apart from the possible greater elevations of post-exercise EE and associated fat oxidation, high-intensity exercise-induced hydrocarbon source redistribution might have also potentially contributed to the greater reductions in AVFA observed in SITs and HIIT relative to that in MICT. 29,30 Indirect evidences have suggested that following exercise active muscles may transiently increase competition with adipose tissues, including abdominal fat depots, for circulating postprandial hydrocarbons from multiple sources (fat, carbohydrate, and protein) for tissue reconstruction, 31,32 and the extent of competition appears to be dependent upon exercise intensity. 29,30 The resultant greater partitioning of postprandial hydrocarbon-based nutrients into the active muscles may create apparent negative energy balance in the abdominal fat cells and promote the fat reduction.…”

Quantification of muscle triglyceride synthesis rate requires an adjustment for total triglyceride content

“…The existence of these two pools is well established; however, their individual significance in skeletal muscle physiology is still not clear. Studies utilizing MRS demonstrated that different physiological states or interventions can affect the distribution -and perhaps the physiology -of imTG and emTG pools (28)(29)(30). Training resulted in a significant increase in imTG content with no change in emTG, while detraining resulted in a return of imTG content to the baseline with increased emTG content (29).…”

“…Studies utilizing MRS demonstrated that different physiological states or interventions can affect the distribution -and perhaps the physiology -of imTG and emTG pools (28)(29)(30). Training resulted in a significant increase in imTG content with no change in emTG, while detraining resulted in a return of imTG content to the baseline with increased emTG content (29). Rosiglitazone therapy decreased the imTG/emTG ratio by increasing the emTG pool size (30).…”

Muscle function and architecture in children with juvenile idiopathic arthritis

“…In the present study, we found a significantly lower ratio of IMAT 19 During detraining, the trained muscle also kept a higher myocellular lipid storage than untrained muscle. 20 In a previous study, we showed that children with JIA have a lower lipid oxidation rate during submaximal exercise than healthy peers. 21 Consequently, the lower IMAT content in children with JIA than in healthy children could be explained by a lower level of physical activity and a weakened oxidative metabolism.…”