exercise physiology Flashcards
- Describe how fat and carbohydrates are used by skeletal muscle at different exercise intensities in order to synthesize ATP.
low intensity fats are used, high intensity carbs are used
- Describe the role of catecholamines in the regulation of fat and carbohydrates during exercise.
epi goes up with intensity of exercise
epi causes lipolysis and glycogenolysis. however at high intensity vasoconstriction from epi will not allow blood flow to fat and this energy source is not utilized
- Describe the importance of mitochondria function in sports performance and how a mitochondrial dysfunction can cause important metabolic problems involved in some chronic diseases like type 2 diabetes.
people who are trained have more mitochondria
- Describe the role of lactate as a regulator of glucose metabolism.
The higher the glucose flux into the cell the higher the lactate production.
The second important function of lactate is to release the saturation of the enzyme pyruvate dehydrogenase (PDH). When the rate of pyruvate formation due to excessive glycolytic flux exceeds the rate of oxidation by the enzyme pyruvate dehydrogenase (PDH) lactate is then formed. Pyruvate then will be reduced to lactate by Lactate dehydrogenase (LDH) which will result in increases in lactate concentration during higher exercise intensities when glycolytic flux elicits a high production of pyruvate which exceeds the oxidative activity of pyruvate dehydrogenase. This lactate then can be converted to pyruvate in adjacent skeletal muscle cells and enter the TCA cycle.
- Describe the main mechanisms involved in the adaptations in substrate utilization caused by training and how some metabolic diseases patients like Type 2 diabetes or insulin resistant individuals could benefit from exercise programs.
more mitochondria, more mitochondria near fat and glycogen stores, better lactate clearance, more beta ox and lypolysis.
it will lower glucose in an insulin indeopendent fashion form Ca2+ levels, it drives lypolysis
Type 2 diabetic patients and obese insulin resistant individuals have difficulties in carbohydrate utilization and have difficulties with fatty acid oxidation which suggests “metabolic inflexibility” unlike normal and athletic individuals who can adapt to substrate availability and different needs for substrate oxidation (“metabolic flexibility”). This metabolic inflexibility is probably caused by some defects in pathways controlling glucose and energy homeostasis which suggest mitochondrial dysfunction implicated in insulin resistance and in disease progression into Type 2 diabetes.