Fat Metabolism During Exercise


Learn how carbohydrate and fat metabolism influence exercise intensity and how to utilize fatty acids for fuel in exercise to enhance sports performance training and manage body fat.


Exercise Physiology | Muscle Contraction | Muscle Fibers | Muscle Adaptations | Exercise Fuels | CHO Metabolism | Fat Metabolism | Oxygen Uptake | Cardiovascular Exercise | Respiratory Responses | VO2 Max | Temperature Regulation | Heat | Fluid Balance | Fatigue | Sprinting | Endurance | Genes | Practical Case Example


Fat Metabolism 


Learn about fat metabolism as a fuel source. Fatty acids are stored in the muscle and in the adipose tissue. Learn about the interactions between fatty acids from the bloodstream plasma and muscle. Study lipase, hormone-sensitive lipase, and the breakdown of triglycerides. The lecture will cover important aspects of interactions between fatty acids and other fuel sources as utilized and influenced by increasing or decreasing exercise intensity.

In this lecture, we’re going to focus on how the muscle uses fat during exercise. These fatty acids can come either from the bloodstream, which has been derived from the adipose tissue triglyceride stores or from the triglycerides that are stored within the muscle. The fatty acids from outside the muscle, first of all, have to cross the Sarcolemma or the plasma membrane of the muscle. They have to, then, diffuse through the cytosol, cross the mitochondrial membrane before they’re oxidized within the mitochondria. The breakdown or the conversion of fatty acyl-CoA to a single CoA Is referred to as beta-oxidation and this occurs in the mitochondria.


Sections 

  1. Fat Metabolism During Exercise
  2. Interactions Between Muscle TG & Plasma FFA Oxidation
  3. TG Lipases in Adipose Tissue & Skeletal Muscle
  4. Regulation of Adipose Tissue Lipolysis During Exercise
  5. Regulation of Skeletal Muscle Lipolysis During Exercise
  6. Determinants of Skeletal Muscle FA Uptake During Exercise
  7. Carnitine – at the Crossroads of CHO & Fat Metabolism
  8. Carnitine – at the Crossroads of CHO & Fat Metabolism
  9. FFA Oxidation During Exercise Related to Intramuscular
    Beta-Oxidative Capacity (HAD)
  10. Exercise Intensity and Lipid Oxidation
  11. Why is fat oxidation reduced with increased exercise intensity?
  12. Training and Lipid Metabolism During Exercise
  13. Training and Muscle FA Uptake During Exercise
  14. Overview of Exercise Metabolism

Fat Metabolism During Exercise 


During prolonged exercise, we see changes in a number of aspects of fat metabolism. These studies have involved traces, again, labeling fatty acids and glycerol. To estimate the rates of lipolysis, which is the breakdown of triglyceride, the rates of fatty acid uptake, and the rates of fatty acid oxidation. You can see in this slide during quite prolonged exercise, lasting about 4 hours, the progressive increase in the rates of lipolysis, and this will come from both adipose tissue and potentially also from muscle triglycerides, the increase in fatty acid uptake from the blood by the contracting muscle largely and the increase in fatty acid oxidation.

Interactions Between Muscle TG & Plasma FFA Oxidation 


This is a somewhat complex slide but it demonstrates the interactions between the oxidation effects from the blood and fatty acids derived from the muscle. In a normal situation, over time, as I showed you in the previous slide, you can see a progressive increase in fat oxidation of fatty acids derived from the plasma. That’s associated with a breakdown of fossil triglycerides, which then declines as the increase in fatty acid oxidation from the plasma occurs. If you give the subjects a drug, which blocks the mobilization of fatty acids from their adipose tissue, you don’t see the same increase in fatty acid oxidation from these plasma sources. Under those circumstances, you can see an increased reliance on the intra-muscular triglyceride stores. I should add, under this condition of low free fatty acid availability, as I mentioned in the previous lecture, that will influence the right of blockage and breakdown. So not only is there an increase in muscle triglyceride utilization, but there’s also an increase in muscle glycogen utilization under these conditions to compensate for the reduced plasma fatty acid availability.

TG Lipases in Adipose Tissue & Skeletal Muscle 


The breakdown of triglycerides in both skeletal muscle and adipose tissue is referred to as lipolysis, and the enzymes that break down these triglycerides are referred to as lipases. There are two key lipases that have been identified, both in adipose tissue and in skeletal muscle that are important in regulating the breakdown of triglycerides during exercise. The first is known as adipose tissue triglyceride lipase, and although it was initially identified in adipose tissue, it’s also been found in skeletal muscle. The second important enzyme is a lipase known as Hormone Sensitive Lipase and as the name implies, it’s regulated by a number of key hormones. It’s been shown, that in the breakdown of triglycerides, that ATGL, is primarily involved in breaking down triglycerides, and the whole non-sensitive lipase seems to attack the diglycerides. Both enzymes are activated in adipose tissue and in the muscle during exercise to break down the triglycerides, mobilize the fatty acids, and make them available for either transporting the blood. In the case of adipose tissue, or transporting the cytosol of the muscle across to the mitochondria.

Regulation of Adipose Tissue Lipolysis During Exercise 


If we first look at adipose tissue lipolysis during exercise, there are a number of important regulatory factors. As I said it’s mediated by the lipases, ATGL, and hormone-sensitive lipase, or HSL, and an important activator of these lipases in Adipose tissue is the sympathetic nervous system, circulating adrenaline, acting through beta receptors. One of the side effects of taking beta-blockers, and a number of cardiovascular patients do that, is that they see inhibition of the mobilization of fatty acids during exercise. And that can sometimes be associated with muscle fatigue, probably because of an increase in glycogen use and that needs to be managed if you’re employing exercise in cardiac patients who might also be on these beta-blocker agents. The decrease in plasma insulin, which is important for the mobilization of liver glucose is also important for the mobilization of fatty acids. Insulin is known to have potent antilipolytic effects. And so it’s reduction during exercise is important in allowing a normal increase in free fatty acid mobilization. The adipose tissue blood flow is an important parameter as well because it continues to flush out if you like, the fatty acids from the adipose tissue into the systemic circulation. It’s known at higher exercise intensity where there tends to be some vasoconstriction of the adipose tissue that can often limit the availability of free fatty acids to the contracting muscle.

Because free fatty acids (FFA) are hydrophobic, they have to be transported albumin, the major plasma protein. And the ratio of the binding of free fatty acids to albumin is also an important determinate of mobilization of free fatty acids from that opposed to tissue. The blood glucose concentration goes directly and also the viral effects on insulin can influence the immobilization of fatty acids. It’s also known that lactate can inhibit fatty acid mobilization or lipolysis in adipose tissue and perhaps in higher intensities when you see an increase in lactate, which might also contribute to a reduction in the availability in fatty acids. Interestingly one of the major metabolic effects in caffeine is to stimulate the mobilization of free fatty acids. So addition to any effects that caffeine has on the central nervous system, acting as a stimulus, it’s also known to increase free fatty acid levels, and that may contribute in part to ergogenic benefits of caffeine in drinks to help exercise.

Regulation of Skeletal Muscle Lipolysis During Exercise 


We turn our attention to skeletal muscle lipolysis. Then again, those two enzymes are involved, ATGL and Hormone-Sensitive Lipase. Again, the beta-adrenergic system and increase in adrenaline, acting through the protein kinase-A pathway will activate the Hormone-Sensitive Lipase. A calcium-dependent Kinase known as extracellular regulated Kinase, or ERK, is activated in response to calcium, which increases during muscle contraction, and that will stimulate lipolysis. The blood glucose concentration will tend to inhibit the hormone-sensitive lipolysis. And interestingly, the availability of free fatty acids, as I showed you in that earlier slide if free fatty acid availability is reduced, then there’ll be an increased reliance on intramuscular triglycerides.

Determinants of Skeletal Muscle FA Uptake During Exercise 


Now, for those plasma free fatty acids that need to be taken up by a contracting muscle. For many years it was thought this occurred by simple diffusion, and that by raising the plasma levels of free fatty acids that would automatically increase fatty acid (FA) uptake into muscle. To a large extent, that’s true but, it’s also been shown in recent years that an important part of free fatty acid uptake occurs by facilitated diffusion, in much the same way that we saw for glucose uptake. And so, the major determinants of skeletal muscle fatty acid uptake then, are the plasma level, the arterial concentration of those free fatty acids and the ability of the muscle to take up and oxidize those fatty acids, to maintain a diffusion gradient. There’s a number of sites, where fatty acid transporters are involved. A number of proteins have been identified, these include the fatty acid-binding protein, FABP. Another fatty acid-binding protein called CD36, and fatty acid transport protein or FATP. These proteins are involved in transporting fatty acids across the sarcolemma, across the largely aqueous environment of the cytosol inside a muscle, and also across the mitochondrial membrane. In relation to that latter process, these fatty acid transporters in particular CD36, do so in partnership with an important transport compound known as Carnitine and an enzyme that’s involved in that process known as CPT. Together these transporters facilitate the mitochondrial entry of fatty acids so that they can be oxidized. As I mentioned earlier, the process of beta-oxidation involves converting fatty-acyl-CoAs to acetyl-CoA and there’s a key enzyme called HAD found in the mitochondria. The amount of that that you have will determine how much you can oxidize the fatty acids.

Carnitine – at the Crossroads of CHO & Fat Metabolism 


I mentioned the compound Carnitine, and it has an important role in facilitating the transport of fatty acids into the mitochondria. It does indeed seed at the crossroads of carbohydrate and fat metabolism. You can see an interaction between the two here. And if there’s a very large increase in the rate of carbohydrate utilization and production of acetyl-CoA, then Carnitine can act as a buffer and you get increases in acetylCarnitine to buffer these increases in acetyl-CoA. One of the challenges then is the impact on the availability of Carnitine for fatty acid transport into mitochondria, and I’ll come back to this point in just a moment. But you can see here, in relation to the mitochondrial uptake of fatty acids, here is the long-chain fatty acid. The importance of Carnitine and the CPT1 enzyme complex which transports the long-chain fatty acid into the mitochondria where it can undertake beta-oxidation and enter the oxidative pathway. And so Carnitine has an important role And you may have noticed if you’ve been to some of the sports nutrition shops the promotion of Carnitine supplementation to promote the burning effect both for weight loss and also in bodybuilding. There’s been some research over the years to suggest that perhaps Carnitine supplementation can play a role. They’re equally some results suggesting not a major role. But again, the important role of Carnitine is to transport fatty acids into the mitochondria.

FFA Oxidation During Exercise Related to Intramuscular Beta-Oxidative Capacity (HAD) 


Finally how well a muscle can oxidize fatty acids is also a determinant of fatty acid uptake and this will maintain the diffusion radiant into the mitochondria. So here you can see the relationship between fatty acid oxidation, plasma fatty acid oxidation, and the concentration of that enzyme HAD, which is involved in beta-oxidation. If you increase the number of mitochondria in the muscle, you will get an increase in HAD. And as we saw in our muscle lectures, one of the muscle adaptations to endurance-type exercise is an increase in mitochondria and an increase in HAD. Therefore, the capacity to oxidize fatty acids.

Exercise Intensity & Lipid Oxidation 


Why is it then, that fatty acids and fat oxidation decrease at higher intensities? I showed you in one of the earlier graphs the increases in fat oxidation that occur at moderate intensity. But then the decrease in total fat oxidation as you go to higher intensities. You can see at the lowest intensity a heavy reliance on plasma fatty acids with a little contribution from muscle triglycerides. As you increase the exercise intensity the contribution from plasma free fatty acids becomes relatively less. There’s initially an increase in intramuscular triglyceride use, but then a decrease at the higher intensity.

Why is fat oxidation reduced with increased exercise intensity? 


Some of the factors that contribute to this, certainly in relation to plasma free fatty acid oxidation, a reduction in the availability in the delivery of fatty acids can contribute. Inside the muscle there are relationships partly related to Carnitine and CPT, that I showed you, that as you increase the rate of glycogen breakdown, as you increase adrenaline and sympathetic nerve activation, that is known to inhibit the activity of CPT and that will have a negative effect or inhibit the mitochondrial uptake of fatty acids. For the reasons that I outlined, Carnitine acting as a buffer of acetyl-CoA derived from carbohydrate, as you increase the exercise intensity and increase the production of acetyl-CoA from carbohydrate. That can often reduce the availability of Carnitine for fatty acid uptake. An interesting aspect of this, though, is that the oxidation of carbohydrate requires relatively less oxygen for a given amount of ATP production. So it makes good sense for the body to rely more on carbohydrate, as you become closer to you maximal oxygen uptake.

Training & Lipid Metabolism During Exercise 


In terms of training effects, on fatty acid, oxidation, and intramuscular triglyceride use, just as we saw a reduction in the reliance on carbohydrate metabolism after training, we see an increase in the reliance on fat. And so what we have here is the rate of fatty acid uptake, in the open bars, and the increase in fat oxidation. You can see both in untrained and trained an increase in both fatty acid uptake and fatty acid or fat oxidation. You’ll notice here that the increase in fat oxidation is somewhat higher than the increase in fatty acid uptake. And that reflects the increased reliance on intramuscular triglycerides, which you won’t measure in this parameter here. So exercise training increases the oxidation in both plasma free fatty acid and intramuscular triglycerides and the fatty acids that come from them.

Training & Muscle FA Uptake During Exercise 


In relation to the effects of training on muscle fatty acid uptake during exercise, we can see a relationship between free fatty acid uptake by the muscle, and the arterial free fatty acid concentration. You can see that in the non-trained muscle, there is a saturation of this process. And that’s consistent with the notion that there are these fatty acid transporters that are becoming fully saturated in terms of their ability to take up fatty acids. In contrast, when you look at the trained muscle, you can see the increase in free fatty acid uptake, with an increase in free fatty acid concentration. And so this reflects the training-induced increases in these transport proteins within skeletal muscle. Together with an increase in mitochondrial oxidative capacity and an increase in HAD and the beta-oxidative capacity, this will drive fatty acid uptake into the contracting muscle. And the increased stability of fat to be oxidized within the skeletal muscle is thought to contribute in part to why regular exercise helps in reducing body mass, in particular, body fat levels, because of this greater ability to oxidize fat in skeletal muscle, rather than to store that fat in adipose tissue.

Overview of Exercise Metabolism 


So as we come to the end of this module on fuels, hopefully, you’ve got an understanding of how carbohydrates, fats, and creatine phosphate can be utilized under various exercise conditions. If we look at aerobic type exercise, this slide summarizes the interaction between carbohydrate and fat utilization and the influence of increasing exercise intensity. If you have an understanding of the factors which influence the selection of carbohydrate and fat during this exercise that’s relevant for sports performance, it’s also relevant for exercise prescription to try and optimize the utilization of fat to manage body mass and body fat labels.[7].


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    Fat Metabolism During Exercise was last modified: October 12th, 2019 by Derek Curtice