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so which exercises actually get you in ketosis faster legitimately okay like scientifically back which exercises are gonna allow your liver to produce more ketones ultimately getting you through the keto flu getting you through the hump and creating those precious ketones the fastest okay we’re gonna break it all down because a lot of people think that it’s all about just depleting your glycogen burning up as many carbs as you possibly can so you have no carbs left and ultimately start burning fat it’s not quite that simple because we can burn fat and carbs at the same time even when we’re in ketosis so which exercises truely do get you into keto faster we’re gonna break it all down okay we’ve got new videos coming out just about every single day right now 7:30 a.m. Pacific time nobody’s got to speed when it comes down to how much good quality content we’re putting out so make sure you’re hitting that subscribe button and then hit that Bell icon to turn on notifications so you never miss a beat I also want to make sure you check out pili hunters I’ve talked about peeling nuts before pili nuts are the highest fat lowest carb nut that just out there it’s a Filipino nut and these guys have absolutely crushed it when it comes down to the quality so we’re talking 22 grams of a really healthy saturated fat that’s in these nuts and totally sprouted so they’re gonna digest and absorb so I wanna make sure you check them out after you watch this video they’ve got some really cool nut butters – they’ve got like a matcha peeling nut butter which just tastes amazing so anyway after we get through all this check them out down below in the description anyhow let’s get down to the science of how this all works the first thing we have to look at is aerobic activity okay that’s going for a walk going for a run okay aerobic activity is generally occurring anywhere between like 25 percent and 60 percent of our maximum heart rate okay it’s that low intensity range now the reason that aerobic activity utilizes fat so much is because essentially it has time to take fat and combine it with oxygen now I don’t want to like over complicate anything here I want to get down into the Nitty Gritty of these other things and this is going to be a somewhat complex video anyway because it’s a complex topic so when you’re working at a low intensity it likes 25 to 40% or so of your maximum heart rate your body is pulling fatty acids that are already flowing through the blood so fatty acids that have already kind of moved around and mobilized and they’re now in the blood your body starts using those 400 okay but when you start increasing the intensity up to about 60% the fat ends up getting pulled from what are called intra Maya cellular triglycerides okay it’s getting pulled from fatty tissue or fatty acids that are in the skeletal muscle tissue so the point is is 25 to 60 percent we’re burning fat we’re using fat as a fuel source it’s getting mobilized once we start getting upwards of 60 we get up to like 70 75 percent that goes down the amount of fat we’re using for fuel actually goes down okay now additionally what ends up happening is as we start increasing in intensity like when we’re weight training or we’re sprinting we also have the utilization of carbohydrates that comes into the mix we start using carbs whether it’s from stored glycogen or from carbs that we ate now when this comes into supply energy it of course takes away from fatty acid mobilization because our body’s like a we have carbs we don’t need the fats now so higher intensity equals carbohydrate metabolism and lower intensity equals fat metabolism that makes it pretty simple right it makes sense that okay at that rate we want to do cardio because we just want to mobilize fat well let me explain things a little bit more because it gets a little bit hairier than this when we’re at a high intensity blood flow ends up getting shuttled away from the fat tissue okay so that’s one of the reasons why we don’t burn as much fat during a workout itself now we can burn fat long term doing high-intensity work don’t get me wrong I love high-intensity work and it does burn a lot of fat but it comes down to mobilizing fatty acids and creating ketones from those it’s all about the slow burn and getting that stuff to the liver so I can create ketones we want those fats to come from the body into the bloodstream into the liver to create ketones and when we do high-intensity work what happens is blood flow gets shuttled away from the adipose tissue to actually move the muscle to move those muscle cells and to move the core and to move the vital organs that are pumping a lot of blood right pumping blood through them so that means that fat gets kind of stuck and gets kind of stuck in the adipocytes it gets stuck in the fat cell level okay so that’s a big reason why high intensity doesn’t move as much fat the other thing is something that has to do with CP t1 enzymes okay the enzyme CP t1 is involved in the carnitine transport shuttle that whole process of carnitine allowing fat into the mitochondria so carnitine is kind of like a bus that allows fat into the cell now if CP t1 then we don’t move as much fat into the mitochondria during high-intensity work CPT one down regulates high-intensity work slows down CPT one and it makes sense right why would we want to be shuttling fat into the cell when the cell is predominantly using carbs when it’s burning hot when it’s running really fast and we’re doing high-intensity work okay so CPT one is now down regulated now additionally once carbohydrates are being used it also up regulates something known as Mel and all coenzyme a I know I’m getting complex and I promise I’ll make some sense of it I’m just I have to explain it for those that are into the super nerdy stuff the malleable coenzyme a also inhibits CPT one so basically long story short is when you do cardio fat is being mobilized more as soon as the intensity gets high then you’re using carbohydrates and the fats aren’t being mobilized so that begs the question now we have two glaring things that are still opposing on one side we say okay well low intensity is great because it’s mobilizing fat perfect that’s the answer right then on the other hand we have people saying well ketones can’t be produced unless we drain our glycogen stores or for those of you that don’t know glycogen is what’s the carbs that are stored in our muscle so people have always told us you have to sniff the burn through the glycogen stores first and once those are burned then you can produce ketones I don’t necessarily think that’s the case okay and I’ll explain with some legit science that backs it up I think it has more to do with the aerobic side of things here’s why if we look at Jeff Bullock’s study Jeff Bullock published a very famous study that takes a look at athletes that are either low carb or high carb and he found that when they do endurance work the low-carb group burns 2.3 times more fat during their workout in the high carb group and at the end of the workout had the same amount of stored muscle glycogen as the high carb group the low-carb group and the high carb group had the same amount of stored muscle glycogen yet the low-carb group burned 2.3 times more fat so what does that tell us it tells us that glycogen doesn’t really matter because you can be on a keto diet and still have high amounts of glycogen so I firmly believe that you do not have to drain glycogen to produce ketones there could be a correlation but it’s not causation and what I mean by that is it could be a correlation that maybe the amount of time it takes to drain our glycogen stores could roughly be about the same amount of time it takes for Gita Genesis to occur meaning it takes roughly that amount of time to start producing ketones maybe it’s just a coincidence okay because this is pretty interesting then we start diving in a little bit deeper and start making some more sense of this the journal Cell published a study that found that when it came down to mobilizing lipids and ultimately creating ketones leptin was just as important as insulin and just as important as anything else meaning we weren’t able to really burn or mobilize fat unless leptin levels were low and insulin levels were low now leptin is like the cheap meal hormone okay leptin is what communicates from the fat cell to the brain to let the brain know that there’s enough fat on hand so when leptin levels start to go down and insulin levels go down fat can get mobilized high-intensity exercise has no effect on leptin so high intensity exercise all it really does is activate what’s called the hypothalamic-pituitary-adrenal axis and it basically gets catecholamines going so it basically makes it so that your body is revving up the metabolism because Adrenaline’s going epinephrine is going and this and that it does not mean that you’re automatically burning carbs or burning fat especially if leptin is an elevator so there’s other hormonal systems at play here high intensity exercise actually makes it so that leptin doesn’t drop at all like it doesn’t have a big effect there now this is wild stuff and I know I might be losing you but I know some of you guys are hanging in there and I will make some total sense of this so please just listen to all this jargon okay I beg of you some of you might be wondering okay well what about doing eccentric work okay what about trying to burn up as much glycogen as I can but not through high intensity okay there are ways that you can burn up muscle glycogen without doing super high intensity work for example eccentric contractions where you take a weight and you just move really slow on the eccentric okay and you break down the muscles that used to be what I thought would be the trick I used to tell people that I to say that’s the best way to get into ketosis cuz you burn up glycogen but you’re not going super super highly anaerobic you’re just burning up the glycogen there’s a study that was published in the Journal of applied physiology that shed some light on that it took a look at individuals that did 75 minutes of cycling followed by either eccentric work or concentric work meaning they focused on doing reps where they focus on the concentric movement or the eccentric movement and then they measured their glycogen resynthesis rates like how long it took and how easily they were able to restore glycogen on day one both groups were able to restore glycogen at the same rate on day three the group that did the II centric work the group that did the slow repetitions had 25 percent less and glycogen uptake why they did just as much damage they worked out just as hard just one did slower repetitions down one did more repetitions up and what it turns out happens is when you’re doing eccentric work you do a lot of structural damage to the cell so it turns out the sarcoplasm actually gets damaged okay so the muscle cell gets damaged to the point where it physically blocks glycogen from being able to come in what does this mean in the world of ketosis where is Thomas going trust me I’m not crazy I just I’m just wild on this stuff okay what that tells us is something simple when we are trying to recover from a knee centric workout the demand is still there okay our muscles are still demanding recovery from glycogen they want it they need it but the structural blockade is preventing it from happening which frustrates the body because it’s still trying it’s like okay let me produce more glycogen and give you more glycogen give you can work like a gin but it’s not even getting into the cell it’s not getting there because it’s damaged because he did so much damage with your workout it can’t get in okay where does this matter with keto if you are not eating carbohydrates that means that because gluconeogenesis is demand-driven because your body needs the carbohydrates it’s going to pull them from protein and normally that’s not that much of an issue but when you’re first trying to get into ketosis then it makes it so that your body is having to break down lots and lots and lots of protein creating excess glucose because it can’t get into the sell that excess glucose could thereby prevent you from going into ketosis or slow down the process in which your liver creates ketones so the whole simple point of all of this to summarize for everybody is my hypothesis on all this based on the research is that aerobic activity going for a simple walk or a run at fifty to sixty percent of your maximum heart rate is going to get your fats mobilize and get you a nikkie ptosis much faster than weight training does that mean that you shouldn’t wait trained not at all I think you should but your ultimate go-to and for what you should tell your friends and family that are doing the keto diet they should be doing simple aerobic activity it’s gonna get them into ketosis faster than anything else in the safest most effective way without any ambiguity and without any of this crazy nonsensical scientific jargon that I just threw at you so as always make sure you’re keeping it locked in here in my channel and I apologize for all the complexity of this one re watch it a couple times be happy see you soon
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Which Exercise Gets You Into Keto Fastest? – Thomas DeLauer
Aerobic Activity to generate ketones via Beta Oxidation
Maximal fat oxidation occurs at low to moderate intensity (between 25% and 60% of maximal oxygen consumption (VO2max)
At lower exercise intensities, most of the fatty acids used during exercise come from the blood
As exercise increases to moderate intensity (around 60% of VO2max) the majority of fatty acids oxidized appear to come from IMTAG
At higher exercise intensities (greater than 70 % VO2max), total fat oxidation is reduced to levels lower than that of moderate intensity
This reduced rate of fatty acid oxidation is coupled with an increase in carbohydrate breakdown to meet the energy demands of the exercise
This counterintuitive drop in fat utilization during high intensity exercise is caused by several factors
One factor is related to blood flow to adipose tissue and thus reduced fatty acid supply to the muscle
At high exercise intensity, blood flow is shunted (or directed) away from adipose tissue so that fatty acids released from adipose tissue become “trapped” in the adipose capillary beds, and are not carried to the muscle to be used
Another reason for reduced fat usage at high exercise intensities is related to the enzyme CPT1
CPT1 is important in the carnitine shuttle that moves fatty acids into the mitochondria for oxidation – the activity of CPT1 can be reduced under conditions of high intensity exercise.
As mentioned, with increasing exercise intensity fatty acid oxidation drops while carbohydrate oxidation increases
The increased usage of carbohydrate leads to increased levels of a molecule called malonyl CoA inside the cell – Malonyl CoA can bind to and inhibit the activity of CPT1
An inverse relationship of FA carbon chain length and oxidation exists where the longer the FA chain the slower the oxidation
The slowed oxidation of long chain FAs (LCFAs) (more than 12 carbons) are due to the requirement of a mitochondrial transport protein for LCFA transport
The transport protein known as carnitine palmitoyltransferase-1 (CPT-1) is located on the outer mitochondrial membrane and is responsible for the transportation of LCFAs into the mitochondria
CPT-1 is necessary for LCFA transport, a product of free carnitine, and is found in both the cytosol and mitochondrial matrix
CPT-1 catalyzes the transfer of a FA acyl group from acyl-CoA and free carnitine across the outer mitochondrial membrane forming acyl-carnitine
Once in the intermembrane space, translocase facilitates the transport of acyl-carnitine via CPT-II across the inner mitochondrial membrane at which point carnitine is liberated
During high intensity exercise however, large quantities of acetyl-CoA are also produced via fast glycolysis which enter the mitochondrial matrix and supersede TCA cycle (tricarboxylic acid/citric acid) cycle utilization
The result of the abundant glycolytic derived acetyl-CoA forms acetyl-carnitine and monopolizes the available free carnitine limiting FA derived acyl-CoA transport.
Thus, free carnitine is used to buffer excess glycolytic derived acetyl-CoA by forming acetyl-carnitine, and therefore the limited concentration of free carnitine is a rate limiting step in FA transport/oxidation
**CPT-1 is a product of free carnitine, but during high intensities free carnitine is used to buffer excess glycolytic derived acetyl-CoA, therefore limiting CPT-1’s ability to transport fatty acids into the cell**
Study – Nutrition
“Maximal rates of fat oxidation have been shown to be reached at intensities between 59% and 64% of maximum oxygen consumption in trained individuals and between 47% and 52% of maximum oxygen consumption in a large sample of the general population.”