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Showing 2 results for Fatty Acid

Mr Aidin Zarifi, Dr Hamid Rajabi, Dr Sadegh Hasan Nia, Dr Mohamadreza Dehkhoda, Dr Babak Mirsoltani,
Volume 13, Issue 10 (10-2015)
Abstract

High-intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that
resemble traditional endurance training despite a low total exercise volume. On the other hand, fatty acid
oxidation is increases in skeletal muscle with endurance training. This process is regulated in several sites,
including the transport of fatty acids across the plasma membrane. The transportation across this membrane is
recognized to be primarily protein mediated. Therefore, the purpose of this study was to determine the effect of
low-volume high intensity interval training on protein content of sarcolemmal fatty acids transporters (FAT/CD36
and FABPpm) in young men. Twenty recreationally active young men were assigned to a HIT (n=10, 19.3 yr old,
67.2 kg body wt, and 172.7 cm ht) or Control (n=10, 19.7 yr old, 65.9 kg body wt, and 174.4 cm ht) group. HIT
group performed three training sessions per week over 4 weeks. Each session consisted of 8-11×60 s intervals
at ∼100% of peak power output elicited during a ramp VO2peak test separated by 75 s of recovery. Skeletal
muscle (vastus lateralis) biopsy samples were obtained before and after training. HIT increased (17.5%)VO2peak (p<0.05). Also, after 4 weeks low-volume HIT, sarcolemmal content of CD36 and FABPpm increased
14 and 25 percent ,respectively (p<0.05). Therefore, the results showed that the practical model of low-volume
HIT could increase aerobic capacity and sarcolemmal content of CD36 and FABPpm. The increase indicates
that the facilitation of in muscle fatty acid transportation can be adapted which in turn increases the fat oxidation
capacity.


Dr Malihe Aveseh, Dr Maryam Koushkie Jahromi, Dr Javad Nemati, Dr Saeed Esmaeili Mahani,
Volume 21, Issue 25 (9-2023)
Abstract

Lactate has been recently considered as a signaling factor involved in metabolism. The aim of this study was to investigate the role of lactate entrance into the brain on endurance training-induced adaptations in lipid oxidation. 
24 male rats (age: 8 weeks, weight: 197 ± 21 g) were divided into control (C), trained (T), and traind+4-CIN (T+4-CIN, which experienced the inhibition of lactate entrance into the brain during exercise). All animals performed a single session of acute endurance exercise following their 12-weeks training protocol.  Free fatty acids (FFA) and triglyceride content in plasma and adipose tissue and cAMP and Inositol triphosphate (PI3) content in epididymal fat were measured immediately after acute exercise using ELISA and were compared among the groups by one-way analysis of variance (ANOVA).
Acute exercise significantly increased lactate concentration in cerebrospinal fluid (SCF) in both T and T+4-CIN compared to the C group. Lactate concentration was slightly lower in T + 4-CIN compared to the T.  Immediately after acute endurance training, a significant decrease of 61 and 31% in plasma triglyceride levels, a significant decrease of 39 and 26% in adipose tissue triglyceride levels, a significant increase of 125 and 56% in plasma FFA levels, a significant increase of 217 and 125% increase in FFA plasma levels, a significant increase of 87 and 41% in adipose tissue cAMP levels, and a significant increase of 90 and 49% in adipose tissue inositol triphosphate levels was observed in the T and T+4-CIN compared to the control group, respectively (all P < 0.01). Plasma triglyceride and adipose tissue levels in the 4-CIN + training group were significantly higher and plasma and adipose tissue FFA levels were significantly lower (all P < 0.05) than the values found in the T group.  In conclusion, the results of the present study showed that lactate can be effective on endurance training-induced adaptations in lipid oxidation due to its action in the brain.


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