News, Photos and Information about Los Angeles Times. These web pages provide a plain language summary of Australian Indigenous health. They include facts about common health problems and risk factors among Aboriginal. Given this study, and the press its getting, I will be writing the post on observational epidemiology next week. However, Im going to ask you all to undertake a little homework assignment. Before next week I would suggest you read this article by Gary Taubes from the New York Times Magazine in 2. I confirmed this week that someone i. On two consecutive nights I ate about 4 or 5 bowls of the stuff. Holy cow did I feel like hell for a few hours. The amazing part is that I did this on two consecutive nights. Talk about addictive potential. Dont say I didnt warn youOK, back to the purpose of this post How is ketosis impacting my ability to exerciseLearn about kidney cancer renal cell cancer signs and symptoms, including include blood in the urine, pain, fever and weight loss. Read about kidney cancer survival. Here is the summary of the results from my personal experiment Lets take a closer look at what may have been going on in each workout and see what we can learn. Swimming. This workout probably produced the most lactate of the three workouts we dont know for sure because I only measured immediate pre and post levels without measuring in workout levels. My glucose level rose by nearly 4. I did not consume anything. How does this happen Our bodies store glucose in the liver and in muscles in a storage form a long chain of joined glucose molecules called glycogen. Read about bile duct cancer cholangiocarcinoma life expectancy, survival rate, symptoms, treatment, stages, prognosis, causes, and risk factors. Cholangiocarcinoma. Doctors order bladder ultrasounds when theres a concern about bladder problems, such as difficulty urinating or daytime wetting. GLUT1 Deficiency Syndrome and the Ketogenic Diet What to Do When Your Child Grows Up and Still Needs the Diet Continuing to Combat the Fear of High. Whenever our bodies cannot access sufficient cellular oxygen, our metabolism shifts to a less efficient form of energy acquisition called anaerobic catabolism. During these periods of activity, we cannot oxidize fat or glycogen i. I will be writing in much more detail about these ideas in the next month or so, so dont worry if these ideas seem a bit foreign right now. Just know that sometimes our bodies can convert fat or glucose to energy efficiently, and sometimes we can only convert glucose to energy inefficiently. Because of my ketosis, and the metabolic flexibility that accompanies it for an overview of these changes look at my previous post on how ketosis impacted my performance, and in particular look at the table, I only require that my body turn to glucose for energy under the most stressful forms of exercise like I was doing a lot of during this workout. But keep in mind, my muscles CANNOT export one gram of the glucose they store, so any glucose in my bloodstream is either ingested which I didnt do or coming from my liver, which CAN export glucose. Furthermore, the stress of a workout like this results in my adrenal glands releasing a set of chemicals called catecholamines, which cause my liver to export even more of its stored glucose via a process called hepatic glucose output HGO. As an aside, one of the major defects in type 2 diabetes is the inability of insulin to suppress HGO. In other words, even when not under the catecholamine stress that should lead to HGO, their livers constantly export glucose, which contributes to elevated blood glucose levels. The very popular drug, metformin, used often in type 2 diabetes, blocks this process. While I did experience a pretty large rise in lactate almost 3x, my ketones still went up a bit. This could imply a few things Elevated lactate levels do not directly inhibit beta hydroxybutyrate B OHBMild elevations in glucose do not directly inhibit B OHBMild elevations in glucose do not directly inhibit B OHB, if insulin is being suppressed as is the case during vigorous exerciseB OHB was suppressed, but we are only appreciating the net effect, which was a small increase i. Descent Journey In The Dark Second Edition Rules Of Cricket. MCT oil and activity, B OHB levels were rising dramatically, but the rise was blunted by some other factor, such as HGO, insulin, andor lactateMore questions than answers from this workout, so on to the next workout. Cycling. Despite this being a tough ride at several points, on average it was less stressful than the other two workouts and I spent the greater fraction of time in my aerobic to tempo zone 2 to zone 3 zones. A ride like this, however, is a great example of the advantages of improved metabolic flexibility that accompanies nutritional ketosis. My average heart rate during this 6 hour ride was 1. Prior to becoming ketotic, at a HR of 1. RQ was about 0. 9. I was almost 1. 00 dependent on glycogen glucose for energy. Today, at a HR of 1. RQ is about 0. 7 to 0. HR and same power output as prior to ketosis, I now rely on glycogen for only about 1. This is an important point. I will devote future posts to this topic in more detail, but I wanted to use this opportunity to mention it. So what happened physiologically on this rideMy glucose levels fell, probably because I was slowly accessing glycogen stores for peak efforts recall from my RQ performance data, once my HR reaches 1. I become 5. 0 dependent on glycogen throughout the ride e. I was finished. B OHB levels increased by about 2. M, which is pretty high for me. My highest recorded B OHB level was 5. M also after a long ride. This confirms what my RQ data indicate my body almost entirely relies on fat oxidation for energy for activity at this intensity. In the process, B OHB is generated in large quantities, both for my brain and also my skeletal muscles e. In reality, cardiac myocytes heart muscle cells also like B OHB more than glucose and probably also access it when it is abundant. Lactate levels by the end of the ride were effectively unchanged though. Based on feel, I suspect I hit peak lactate levels of 8 to 1. M on this ride during peak efforts, but I had ample time to clear it. A few observations I consumed 6. Generation UCANs super starch, yet this did not appear to negatively impact my ability to generate ketones. Technically, we cant be sure this is the case, since I would have needed a control to know this e. I did, but without the consumption of super starch andor without the bike ride. Its possible that super starch did slightly inhibit ketosis and that my B OHB level would have been, say, 5. M instead of 4. 4 m. M. Metabolic studies of super starch show that it has a minimal impact on insulin secretion and blood glucose levels, hence the name super starch. Whatever impact peak levels of lactate production and hepatic glucose output had during the ride, they seem blunted by the end of the ride and the ride did finish with a modestly difficult 1. I rode at a HR of about 1. Since neither lactate levels nor glucose levels nor insulin levels by extension were elevated, I cant really draw any conclusion about whether one factor, more than any other, suppressed production of B OHB, so on to the next workout. High intensity training. This sort of workout spans the creatine phosphate CP system and the anaerobic energy system, and probably involves the aerobic energy system the least. Ill write a lot about these later, but for now just know the CP system is good for very short bursts of energy say 1. In other words, this is the type of workout where my nutritional state of ketosis offers the least advantage. An example of this sort of exercise is shown in the video in the post my pet peeve. This workout saw the greatest increase in glucose level, about 7. It is important to recall that during this workout I ingested water with a small amount of branched chain amino acids BCAAs valine, leucine, isoleucine and super starch, about 4 gm and 1.