Exercise and Regulation of Lipid Metabolism

Effect of Tai Chi exercise on blood lipid profiles: a meta-analysis of randomized controlled trials

“…The trials included in our meta-analysis were of relatively short duration, mostly within three months (Tsai et al, 2003;Zhang and Fu, 2008;Chen et al, 2010;Lu and Kuo, 2012). The results coincided with the fact that in comparison with TG, LDL-C and HDL-C needed a longer time to change by the means of exercise and complementary intervention (Franklin et al, 2014;Gordon et al, 2014;Noland, 2015). The baseline LDL-C and HDL-C levels were nearly normal, which increased the difficulty in evaluating the treatment effect of Tai Chi on dyslipidemias.…”

“…Beebe et al (2013) revealed that Tai Chi exercise was associated with improvements in LDL-C particle size in obese older women. Tai Chi practicing comprises aerobic exercise and resistance exercise, increasing the whole body fat oxidation, adipose tissue lipolysis and fatty acid utilization by skeletal muscle, mobilizing lipid from adipose tissue, liver and intramuscular reserves, dictating tissue fatty acid uptake, intracellular lipid delivery and mitochondrial β-oxidation, coordinating activation of the sympathetic nervous system and induction of energy deficit-sensing pathways, promoting energy expenditure via heightened TG/FA cycling, inducing energy-sensing pathways such as adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), activating peroxisome proliferator-activated receptor delta (PPARD)-mediated remodeling of lipid metabolism pathways in muscle, and increasing adiponectin level with strong anti-atherogenic and anti-inflammatory effects (Chang et al, 2011;Franklin et al, 2014;Gordon et al, 2014;Noland, 2015). The possibility that the change of body fat ratio and insulin resistance might have an influence on lipid profiles should also be considered (Kohno et al, 2000).…”

Maturation of human induced pluripotent stem cell-derived cardiomyocytes for modeling hypertrophic cardiomyopathy

“…CPT2 activity was similar between all groups of hiPSC-CMs, but was significantly increased only in MPAT hiPSC-CMs relative to hiPSCs. As CPT1 activity is considered to be the rate limiting step in long chain fatty acid oxidation 17 , increased CPT1 activity is consistent with increased use of long chain fatty acids, and is likely indicative of metabolic maturation.…”

Exercise, fasting, and mimetics: toward beneficial combinations?

“…For instance, knocking out both b1 and b2 subunits (57) results in marked exercise intolerance but the effect is not related to decreased glucose transporter (GLUT)-4 membrane translocation, but rather to decreased mitochondrial activity associated with decreased activity of the a1 and 2 subunits. It has become increasingly clear that the molecular adaptations to food withdrawal, exercise, or both vary over time (acute vs. longer term responses), as well as with the intensity of exercise (4,11). Very recently, it has been shown that ablation of the AMPK a1 and 2 subunits markedly enhances the acute activation of PGC-1a in response to exercise, but not the longer-term metabolic adaptations in mouse skeletal muscle (58), and that the running speed of mice during endurance runs is critical for AMPK activation and expression of SIRT1 and AMPK/SIRT1 target genes related to mitochondrial activity (59,60).…”

“…Food withdrawal and physical exercise trigger this flexibility, which leads to drastic metabolic changes that partially overlap and are prominent in skeletal muscle (for reviews, see refs. 4,5) but also in other organs, such as liver (5)(6)(7)(8), white adipose tissue (WAT) (5,6,(9)(10)(11), and brown adipose tissue (BAT) (9,12). Most studies focus on skeletal muscle, in which fasting/food withdrawal shifts metabolism toward fatty acid oxidation, oxidative metabolism, and slow myosin heavy chain expression (4), whereas exercise regimens have different metabolic consequences.…”