Abstract
It is well recognized that whole-body fatty acid (FA) oxidation remains increased for several hours following aerobic endurance exercise, even despite carbohydrate intake. However, the mechanisms involved herein have hitherto not been subject to a thorough evaluation. In immediate and early recovery (0–4 h), plasma FA availability is high, which seems mainly to be a result of hormonal factors and increased adipose tissue blood flow. The increased circulating availability of adipose-derived FA, coupled with FA from lipoprotein lipase (LPL)-derived very-low density lipoprotein (VLDL)-triacylglycerol (TG) hydrolysis in skeletal muscle capillaries and hydrolysis of TG within the muscle together act as substrates for the increased mitochondrial FA oxidation post-exercise. Within the skeletal muscle cells, increased reliance on FA oxidation likely results from enhanced FA uptake into the mitochondria through the carnitine palmitoyltransferase (CPT) 1 reaction, and concomitant AMP-activated protein kinase (AMPK)-mediated pyruvate dehydrogenase (PDH) inhibition of glucose oxidation. Together this allows glucose taken up by the skeletal muscles to be directed towards the resynthesis of glycogen. Besides being oxidized, FAs also seem to be crucial signaling molecules for peroxisome proliferator-activated receptor (PPAR) signaling post-exercise, and thus for induction of the exercise-induced FA oxidative gene adaptation program in skeletal muscle following exercise. Collectively, a high FA turnover in recovery seems essential to regain whole-body substrate homeostasis.
Highlights
Exercise activities, especially of longer duration, cause large quantities of energy to be expended.This necessitates metabolic recovery processes to restore substrate stores in recovery
Arteriovenous fatty acid (FA) sampling and stable isotope-labeled palmitate measurements across the leg in recovery from 2 h one-legged knee extensor exercise at 65% of maximal leg power output [21] suggested that uptake of albumin-bound FAs into human skeletal muscle declines within the first hours of recovery, while leg FA oxidation remained at 44%, increased compared with resting levels
5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), in primary rat cardiomyocytes [76]. These findings point to that activation of AMPK during exercise is important for PDK4 induction and the inactivation of pyruvate dehydrogenase (PDH) leading to suppression of glucose relative to FA oxidation in skeletal muscle in recovery
Summary
Especially of longer duration, cause large quantities of energy to be expended This necessitates metabolic recovery processes to restore substrate stores in recovery. A plethora of metabolic changes occur in order to regain substrate homeostasis, especially in the previously active skeletal muscles, and in other organs such as adipose tissue and the liver. These processes are energy demanding and accompanied by enhanced post-exercise oxygen consumption (EPOC), of which the magnitude is dependent on exercise duration and intensity [1]. Physiological and molecular mechanisms underpinning the enhanced FA availability and the elevated FA oxidation in skeletal muscle during post-exercise recovery will be addressed, while we aim to discuss the concomitant gluco- and lipid metabolic consequences of the increased FA availability in recovery
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
