My road to become an IFBB Pro

I thought I’d share my story with you guys, how I got here where I am now.

My prep actually started end of February. I was 79kg, and I was getting ready for the Nabba Worlds in June in Italy. I was very keen, had the passion burning inside me. I wanted to win! Last year I finished 2nd at the Nabba Worlds in Russia and I really wanted to prove myself this year. Athletes would know that a contest prep is not easy, but you can always step it up when you’re keen, so I went all in.

So June came, and I went to Italy to compete. Finished 2nd again - not gonna lie, I was pissed off. We planned another competition a couple of weeks after that, Portugal or Spain, but I said no. I knew what improvements I had to make and I needed a bit more time to make them happen.

So after my first comp mid June I went straight into prepping for the second one in November. First I wanted to go to Poland but then we learnt that the @ironrebelshow was gonna be organised again in November - and we went there with @abe.superman In May when he competed, so I changed my mind and I registered for Denmark.

I had to bring up my shoulders, especially my rear delts, so I started training them 3x a week. My glutes and hammies needed more shape, so that meant glutes and hammies 2x a week, and quads/full legs with glutes 1x a week. Are you keeping score? That meant Ꭵ hᎪᎠ ᏆᎾ ᏆᏒᎪᎥᏁ ᏆᎳᎥᏟᎬ Ꭺ ᎠᎪᎽ ᏆᎳᎥᏟᎬ Ꭺ ᎳᎬᎬᏦ... and this is exactly what I did for 6 months to get into the shape I needed for the @ironrebelshow in Denmark last weekend.

The first pic was taken 2 weeks into my prep in March. The second pic was 1 week before the second comp last weekend. I’m proud of this package, I’m proud of the improvements I’ve made and the condition I’ve got myself into. I know there’s more to come, but so far that was my best ever shape.

About diabetes – part 1

There are 3 main types of diabetes mellitus:

  • Type 1 Diabetes: results from the pancreas failing to produce enough insulin
  • Type 2 Diabetes: a condition of defective insulin signalling
  • Gestational Diabetes: a condition where women without previously diagnose diabetes exhibit high blood glucose levels during pregnancy.

When insulin isn’t produced or acts ineffectively, glucose remains circulating in the blood, leading to a condition known as hyperglycemia. Long term hyperglycemia can result in the dysfunction and failure of various organs and systems, including the eyes, kidneys, nerves, heart and blood vessels.

The key players in diabetes are the pancreas and the liver.

The pancreas is both an endocrine and exocrine gland.

Exocrine means that it’s a gland that release its contents through a tube from inside to outside the body. It helps with digestion by producing important enzymes that break down food, which allows the body to absorb the nutrients.

The endocrine function primarily involves the secretion of the 2 primary hormones relevant to diabetes management: insulin and glucagon.

Insulin increases the storage of glucose, fatty acids and amino acids in cells and tissues and is considered an anabolic hormone. Insulin is a key player in the storage and use of fuels within the body.

Disorders in insulin production and signalling have widespread and devastating effects on the body’s organs and tissues. Glucagon is a peptide hormone produced by alpha cells in the pancreas. The pancreas releases glucagon when blood sugar levels fall too low. It opposes the action of insulin by raising the concentration of glucose in the blood.

Dietary carbs are not essential, however, the body needs glucose. The brain typically needs about 130 gr of glucose every day. Not all glucose has to come from the diet because the liver has the ability to synthesise it.

The liver serves as a warehouse for glucose storage and production. It can also produce fatty acids under certain conditions.

As blood glucose and insulin levels increase, the liver increases its absorption of glucose. Glucose is stored as glycogen. The amount of glycogen stored depends on circulating insulin and glucose levels. When blood glucose levels drop, insulin production falls. The shortage of insulin signals the liver to release its assets by sending glucose back into the blood to keep the body nourished.

When carb intake is restricted, it lowers blood sugar and insulin levels. As insulin levels fall and energy is needed, fatty acids leave their respected fat cells and enter the bloodstream. From here they’re taken up by specific cells and metabolised. Ketone bodies are molecules created in the liver, that are pushed into the blood stream where they’re utilised by skeletal and heart muscles cells as fuel. Also, the brain begins to use ketones as an alternate fuel source when blood levels are high enough to cross the blood-brain barrier. When this happens a person is said to be in nutritional ketosis.

Ketogenic diets are very popular because they suppress insulin and that seems to be very effective in the treatment and management of obesity and T2D. However the severe restriction of carbs (often below 30 gr) may increase the potential for hypoglycaemia of people with T1D.

Lipogenesis is creating fat within the body from glucose or other substrates. It takes place mostly in the liver. Lipogenesis occurs in the liver during times of calorific excess and overfeeding. The liver converts excess glucose to fatty acids. These fatty acids can be stored in the liver or transported via lipoproteins (carriers) to muscle and fat tissue for future fuel use or storage. The ratio that is stored or used is highly dependent on energy intake vs. energy expenditure.

In a healthy liver, insulin halts the production of glucose and instead promotes glycogen storage or generates fatty acids during times of energy excess.

The liver of a person with T1D has no internal break system. Insulin deficiency allows glucose production in the liver to go uncontrolled leading to hyperglycaemia and ketoacidosis if unmanaged. When there’s not enough insulin available, glucose cannot enter the cells for use as energy. Therefore the liver produces even more glucose in an attempt to provide energy for the starved cells, but because insulin is not available, none of this glucose can enter the cells. It builds up and starves the cells even further. Consequently, administration of insulin medication is needed to facilitate the entry of glucose into cells.

Insulin increases glucose uptake in the liver by facilitating the creation of glycogen and decreases glucose output.

Prolonged elevations in insulin that result from an energy surplus increase the body’s ability to produce fat via the process of lipogenesis.

Source:

Phil Graham: Diabetic Muscle