I contend that getting in shape looks like this:

  1. Exercise
  2. Nutrient timing
  3. Supplements
  4. Macros


Here is more support for this. Exercise opens up Skeletal Muscle GLUT-4. This keeps the fat based GLUT-4 storage pathway closed! Thus, you can eat your junk food at that time and not store it as fat! That's the theory behind Carl's program. His training may look weird but it's about shock and awe of the body!

Odd that they used a high fat diet, which isn't the cause of obesity IMHO

Diabetes. 2016 Oct;65(10):2911-9. doi: 10.2337/db16-0305. Epub 2016 Jul 13.
Increased Skeletal Muscle GLUT4 Expression in Obese Mice After Voluntary Wheel Running Exercise Is Posttranscriptional.

Gurley JM1, Griesel BA1, Olson AL2.
Author information
Erratum in
Erratum. Increased Skeletal Muscle GLUT4 Expression in Obese Mice After Voluntary Wheel Running Exercise Is Posttranscriptional. Diabetes 2016;65:2911-2919. [Diabetes. 2016]
Abstract
Exercise promotes glucose clearance by increasing skeletal muscle GLUT4-mediated glucose uptake. Importantly, exercise upregulates muscle GLUT4 expression in an insulin-independent manner under conditions of insulin resistance, such as with type 2 diabetes. However, the insulin-independent mechanism responsible for rescued muscle GLUT4 expression is poorly understood. We used voluntary wheel running (VWR) in mice to test the prevailing hypothesis that insulin-independent upregulation of skeletal muscle GLUT4 protein expression with exercise is through increased Glut4 transcription. We demonstrate that 4 weeks of VWR exercise in obese mice rescued high-fat diet-induced decreased muscle GLUT4 protein and improved both fasting plasma insulin and hepatic triacylglyceride levels, but did not rescue muscle Glut4 mRNA. Persistent reduction in Glut4 mRNA suggests that a posttranscriptional mechanism regulated insulin-independent muscle GLUT4 protein expression in response to exercise in lean and obese mice. Reduction of GLUT4 protein in sedentary animals upon treatment with rapamycin revealed mTORC1-dependent GLUT4 regulation. However, no difference in GLUT4 protein expression was observed in VWR-exercised mice treated with either rapamycin or Torin 1, indicating that exercise-dependent regulation on GLUT4 was mTOR independent. The findings provide new insight into the mechanisms responsible for exercise-dependent regulation of GLUT4 in muscle.