The Physiological Regulation of Skeletal Muscle Fatty Acid Supply and Oxidation During Moderate-Intensity Exercise.

Gerrit Van Hall

doi:10.1007/s40279-015-0394-8

Abstract

Energy substrates that are important to the working muscle at moderate intensities are the non-esterified fatty acids (NEFAs) taken up from the circulation and NEFAs originating from lipolysis of the intramuscular triacylglycerol (IMTAG). Moreover, NEFA from lipolysis via lipoprotein lipase (LPL) in the muscle of the very-low-density lipoproteins and in the (semi) post-prandial state chylomicrons may also contribute. In this review, the NEFA fluxes and oxidation by skeletal muscle during prolonged moderate-intensity exercise are described in terms of the integration of physiological systems. Steps involved in the regulation of the active muscle NEFA uptake include (1) increased energy demand; (2) delivery of NEFA to the muscle; (3) transport of NEFA into the muscle by NEFA transporters; and (4) activation of the NEFAs and either oxidation or re-esterification into IMTAG. The increased metabolic demand of the exercising muscle is the main driving force for all physiological regulatory processes. It elicits functional hyperemia, increasing the recruitment of capillaries and muscle blood flow resulting in increased NEFA delivery and accessibility to NEFA transporters and LPL. It also releases epinephrine that augments adipose tissue NEFA release and thereby NEFA delivery to the active muscle. Moreover, NEFA transporters translocate to the plasma membrane, further increasing the NEFA uptake. The majority of the NEFAs taken up by the active muscle is oxidized and a minor portion is re-esterified to IMTAG. Net IMTAG lipolysis occurs; however, the IMTAG contribution to total fat oxidation is rather limited compared to plasma-derived NEFA oxidation, suggesting a complex role and regulation of IMTAG utilization.

Highlights

Limitation of carbohydrate and lipid transfer from the microvascular system to the muscle cell occurs at the onset of exercise when the delivery and transport systems are not optimal and during continuous exercise above moderate intensities of 50 % of maximal pulmonary oxygen uptake (VO2max)
During very highintensity exercise the concept of symmorphosis is put to the test as it is the active muscle that sets the aerobic demand because more than 90 % of energy is spent in the active muscle
intramuscular triacylglycerol (IMTAG) is utilized during moderate-intensity exercise, but in substantially lower quantities than plasma non-esterified fatty acids (NEFAs) oxidation

Summary

Introduction

Limitation of carbohydrate and lipid transfer from the microvascular system to the muscle cell occurs at the onset of exercise when the delivery and transport systems are not optimal and during continuous exercise above moderate intensities of 50 % of maximal pulmonary oxygen uptake (VO2max). The well-described human in vivo increase in NEFA oxidation with exercise duration and the close linear relationship between NEFA delivery and uptake into the active muscle suggests that NEFA uptake is not solely controlled by the rate of sarcolemmal transport. This does not exclude an important regulatory role for fatty acid transporters and translocation of resting muscle NEFA uptake and its role in NEFA clearance from the circulation, after food ingestion and during exercise in untrained individuals or patients with, for example, type 2 diabetes mellitus. NEFA oxidation shows that the NEFA oxidation capacity of mitochondria is not limiting for IMTAG utilization

Skeletal Muscle NEFA Supply from Adipose Tissue Fat Lipolysis During Exercise

Findings

Discussion