Fat and Carbohydrate Exercise Physiology Flashcards
How are fat and carbohydrates used by skeletal muscle at different exercise intensities?
Fat is the preferred source of ATP at low intensities (less than 55% of VO2 max).
Carbohydrates are increasingly relied on for ATP generation at higher intensities (55%-75%), and almost exclusively by 100% of VO2 max.
Intensities greater than 100% VO2max are by definition anaerobic and must rely entirely on glycolysis in the cytosol, thus carbohydrates are the sole source of ATP generation.
Fat yields more ATP, but CHO is much faster. Thus CHO use increases roughly proportionately with intensity.
What is the role of epinephrine in regulating fat and CHO in exercise?
Epinephrine increases phosphorylase activity during exercise, leading to muscle glycogenolysis. Thus it is a major regulator of glucose metabolism in exercise. Epinephrine also increases the activity of hormone sensitive lipase, increasing the amount of FFA available. However, in high intensity exercise, epinephrine may also reduce blood flow to adipose tissue via vasoconstriction and reduce the availability of FFA.
What local factors regulate CHO metabolism in exercise?
Increased muscle contraction leads to increased intracellular calcium. This binds to calmodulin and stimulates phosphorylase to breakdown glycogen. I Type 1 diabetics, this use of glucose also results in glucose lowering even without added insulin, and they may use lower doses of insulin before exercising. High intensity exercise also results in decreased contraction time and higher power production which favor Type II muscle fiber recruitment. T-II fibers have higher glycolytic capacity and lower mitochondria, resulting in increased glucose consumption.
How do catecholamines regulate fat metabolism during exercise?
Catecholamines (primarily epinephrine and norepinephrine) bind b-adrenergic and a2-adrenergic receptors on adipocytes, stimulating cAMP -> PKA -> phosphorylated Hormone Sensitive Lipase -> increased FFA creation. FFA produce far more ATP than glucose and are preferred sources of energy at low intensities, but they are a slow source of energy so they are not used as much at high intensities. Also, catecholamines may cause vasoconstriction leading to decreased blood flow to adipose tissues. Thus they both stimulate and inhibit FFA metabolism in exercise.
How are FFA transported from adipocytes to the site of beta oxidation in the cells?
Adipose tissue blood flow is critical for supplying catecholamines for FFA formation as well as albumin for FFA binding in the blood. Albumin takes FFA to muscle cells where Sarcolemmal Fatty Acid Binding Protein (S-FABP) and another FABP transport the FFA into and through the cell. FFA are then activated to fatty acyl-CoA by attaching Coenzyme A, and the activated complex is then imported into the mitochondria by carnitine-palmitoyl transferase 1 (CPT-1). Beta-oxidation occurs in the mitochondrial matrix.
How does Lactate regulate glucose metabolism?
The creation of lactate from pyruvate regenerates NAD+ from NADH, allowing for the continuation of glycolysis and creation of more ATP.
Lactate also enters the Cori cycle to regenerate glucose
How does athletic training lead to a reduction in lactate production?
After training, glycolytic flux is decreased at the same intensity level, thus the trained athlete uses less glucose for the same work as an untrained athlete. This occurs via increased mitochondrial density allowing greater ATP generation via oxidative phosphorylation and a decreased reliance on glycolysis. Increased mitochondrial density can double the capacity to oxidize pyruvate and FFA.
How does athletic training lead to an increase in lactate clearance from the blood?
Endurance training has a large effect on lactate transporters called Metacarboxylates (MCTs) which facilitate lactate movement into and out of cells. MCT 1 are highly expressed in oxidative (Type 1) cells and facilitate transport of lactate into the cell and mitochondria for later oxidation. MCT 4 are expressed on glycolytic fibers and facilitate the export of lactate from these cells. Thus, trained athletes are more proficient in cycling lactate out of glycolytic cells and into oxidative cells, decreasing the amount of lactate in the blood stream.
What are the primary cellular differences between trained endurance athletes and those suffering from obesity and metabolic syndrome or T2D?
Trained athletes have much higher densities of mitochondria and thus increased oxidative capacity. This makes them very metabolically flexible, able to burn are quantities of fats or carbs efficiently.
Obese/metabolic syndrome/T2D patients have decreased mitochondrial density and lower oxidative capacity. Fats and pyruvate can only be oxidized in the mitochondria, and this decreased density greatly inhibits their metabolism, leading to metabolic inflexibility.
