I do things a little differently but here are some tips to add to your knowledge base:
• Vanilla beans straight out of the pods: adding a little of these to your diet helps put more mitochondria in your muscle tissue for weight maintenance in contrast to higher carbohydrate tolerance and greater metabolic speed.
• Doing squats helps build more upper body muscle. So you have to eat a more calories to speed up metabolic rate. The bigger the muscle volume, it then becomes effortless to not store fat.
• Cold Showers even for a minute or two (as long as can stand it, you start to tolerate it better the more you do it) will help with higher carbohydrate tolerance and greater metabolic speed. This also puts more mitochondria in white adipose tissue so when you do eat a carbohydrate it gets burned immediately for fuel. not stored.
The more muscle volume to fat ratio you have the better chances you have of burning anything you eat immediately. You over-eat protein or fat and bile will direct excess glucose to be stored in muscle tissue as glycogen (and maybe even the liver and adipose fat cells) and stored which blocks lipid droplets from being released from adipose cells and not released when you over-eat protein or fat.
When your not eating enough or over-eat you then gain the risk of gaining all the weight back if you ignore your hunger signaling after practicing fasting and time restricted eating, and caloric restriction quits working?
Bottom line muscle to fat ratio matters more than focusing on type of food sources and amount your eating in calories and if you ignore that, you will be eating 20 grams of carbs for the rest of your life? Not fun?
References:
[1] “… After exercise, the rate of glycogen synthesis is increased to replete glycogen stores, and blood glucose is the substrate. Indeed insulin-stimulated glucose uptake and glycogen synthesis is elevated after exercise, which, from an evolutional point of view, will favor glycogen repletion and preparation for new “fight or flight” events. In the modern society, the reduced glycogen stores in skeletal muscles after exercise allows carbohydrates to be stored as muscle glycogen and prevents that glucose is channeled to de novo lipid synthesis, which over time will causes ectopic fat accumulation and insulin resistance. The reduction of skeletal muscle glycogen after exercise allows a healthy storage of carbohydrates after meals and prevents development of type 2 diabetes. …” …More
[2] “…Further, unlike fat, muscle helps to burn calories and boost metabolism, even when at rest, according to the Mayo Clinic. This helps create lasting weight loss results. For this reason alone, the goal of losing “weight” in general is not desired if it means losing muscle. …” …More
[3] “…Years ago, scientists found that a pound of fat contains 3,500 calories of energy. However, burning one pound of body fat isn’t as simple as reducing your calories by that amount – your body loves to burn muscle too. Scott Laidler learned this from his own journey when he first started out in fitness. He said, “When I cut I took my calories too low and in the process worked off a lot of the muscle mass that I had gained. The phases would cross over for a few weeks, where I would look and feel good, but I wanted to be lean and muscular all year round. It really wasn’t satisfying.” …” …More
[4] “…Insulin resistance (IR) is the result of long-lasting positive energy balance and the imbalance between the uptake of energy rich substrates (glucose, lipids) and energy output. The defects in the metabolism of glucose in IR and type 2 diabetes are closely associated with the disturbances in the metabolism of lipids. In this review, we have summarized the evidence indicating that one of the important mechanisms underlying the development of IR is the impaired ability of skeletal muscle to oxidize fatty acids as a consequence of elevated glucose oxidation in the situation of hyperglycemia and hyperinsulinemia and the impaired ability to switch easily between glucose and fat oxidation in response to homeostatic signals. The decreased fat oxidation results into the accumulation of intermediates of fatty acid metabolism that are supposed to interfere with the insulin signaling cascade and in consequence negatively influence the glucose utilization. Pathologically elevated fatty acid concentration in serum is now accepted as an important risk factor leading to IR. Adipose tissue plays a crucial role in the regulation of fatty acid homeostasis. The adipose tissue may be the primary site where the early metabolic disturbances leading to the development of IR take place and the development of IR in other tissues follows. In this review we present recent evidence of mutual interaction between skeletal muscle and adipose tissue in the establishment of IR and type 2 diabetes. …” …More
