exercise physiology exam 1

What is the primary tissue disposal unit for glucose and the largest reservoir of glycolytic enzymes?

skeletal muscle (cite 1)

Which enzyme catalyzes Step 1 of glycolysis, and what does it do?

Hexokinase (HK)[cite: 1]; converts Glucose to Glucose-6-phosphate (G-6-P) using 1 ATP (thermodynamically favorable reaction)[cite: 1].

What enzyme is the major control point of glycolysis in skeletal muscle, and which reaction does it catalyze?

Phosphofructokinase (PFK)[cite: 1, 2]; catalyzes Step 3: Fructose-6-phosphate (F-6-P) -> Fructose 1,6-diphosphate (F-1,6-DP) using 1 ATP[cite: 1].

What are the allosteric activators and inhibitors of Phosphofructokinase (PFK)?

Activators: ADP, AMP, and F-6-P[cite: 2]. Inhibitors: ATP, citrate, and fatty acids[cite: 2].

Why is Step 6 of glycolysis (GAPDH) critical, and what does it produce?

Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) forms the first high-energy intermediate (NADH) by reducing NAD+[cite: 1]. This NADH is either used for lactate production or shuttled to the mitochondria for the electron transport chain[cite: 1].

Why must lactate dehydrogenase (LDH) convert pyruvate to lactate during intense anaerobic exercise?

To re-oxidize NADH back to NAD+, which is required to keep Step 6 (GAPDH) running and sustain glycolysis[cite: 2].

What are the two types of LDH subunits and where do they predominate?

M-type (muscle) predominates in anaerobic tissues (muscle, liver) favoring lactate formation; H-type (heart) predominates in aerobic tissues favoring pyruvate oxidation[cite: 2].

Why is skeletal muscle NOT a gluconeogenic tissue?

Muscle lacks Glucose-6-phosphatase, an enzyme unique to the liver and kidneys that is needed to dephosphorylate G-6-P into free glucose for release into the blood[cite: 4].

How does glucose enter muscle cells at rest versus during exercise/insulin stimulation?

Resting muscle: predominantly non-insulin-mediated GLUT-1 transporters[cite: 4]. Exercise / Insulin: GLUT-4 transporters translocate to the plasma membrane (muscle contraction has an "insulin-like" effect that increases GLUT-4 even when circulating insulin drops)[cite: 4, 5].

What is the precursor step to the Krebs cycle, its enzyme, and what inhibits it?

Pyruvate -> Acetyl-CoA + NADH via Pyruvate Dehydrogenase (PDH)[cite: 5]. It is inhibited by high [ATP] and high [Acetyl-CoA][cite: 5].

What is the rate-limiting enzyme of the Krebs cycle, and what reaction does it catalyze?

Isocitrate dehydrogenase[cite: 6]; catalyzes Isocitrate -> alpha-Ketoglutarate and yields the cycle's first NADH[cite: 6].

What are the 4 key regulatory checkpoints of the Krebs cycle?

1. Pyruvate dehydrogenase (PDH), 2. Citrate synthase (CS), 3. Isocitrate dehydrogenase (rate-limiting), 4. alpha-Ketoglutarate dehydrogenase[cite: 6].

Where does the Malate-Aspartate shuttle operate, how many ATPs does it yield, and does it adapt to endurance training?

Heart; yields 3 ATP per cytoplasmic NADH (more efficient)[cite: 6, 7]; YES, cytoplasmic and mitochondrial malate dehydrogenase (MDH) activity increases up to 50% with aerobic training[cite: 10, 13].

Where does the Glycerol-Phosphate shuttle operate, how many ATPs does it yield, and does it adapt to endurance training?

Skeletal muscle; yields 2 ATP per cytoplasmic NADH (transfers electrons to FAD)[cite: 6, 7]; NO, cytosolic glycerol phosphate dehydrogenase does not adapt to aerobic training[cite: 10, 13].

In the ETC, where do NADH and FADH2 donate electrons, and what mobile carriers shuttle them?

NADH enters Complex I (yields 3 ATP)[cite: 7, 8]; FADH2 enters Complex II (yields 2 ATP; no ATP generated at Complex II)[cite: 7, 8]. Coenzyme Q shuttles electrons from Complexes I & II to Complex III; Cytochrome C shuttles electrons from Complex III to Complex IV[cite: 8].

What inhibits Complex I and Complex IV of the Electron Transport Chain?

Complex I is inhibited by Rotenone or Amytal; Complex IV is inhibited by Cyanide (CN-)[cite: 7].

What is the total net ATP yield from 1 mole of glucose oxidized completely to CO2 and H2O?

36 to 38 ATP (net: 2 ATP + 2 NADH from glycolysis; 2 NADH from PDH; 2 ATP + 6 NADH + 2 FADH2 from Krebs)[cite: 8].

Does endurance exercise training increase the specific activity of mitochondria?

No. Enzymatic activity per unit of mitochondria does not change; training simply increases total mitochondrial mass (volume/density)[cite: 11].

What is the Intracellular Lactate Shuttle mechanism?

Cytosolic LDH produces lactate from rapid glycolysis -> lactate enters mitochondria via Monocarboxylate Transporters (MCT) -> mitochondrial LDH oxidizes lactate to pyruvate + NADH -> pyruvate enters Krebs[cite: 14]. Cytosolic LDH produces lactate; mitochondrial LDH consumes it[cite: 15].

How does endurance training affect blood lactate appearance (Ra) vs. clearance (Rd)?

Training has NO effect on blood lactate appearance rate (Ra)[cite: 15]; it causes a significant increase in the metabolic clearance rate (Rd), leading to lower blood lactate levels at any workload[cite: 16, 17].

What are the 4 steps of the Carnitine Shuttle for fatty acid transport into mitochondria?

1. Acyl group transferred from cytosolic acyl-CoA to carnitine by Carnitine acyltransferase-1 (CAT-1)[cite: 17]. 2. Acyl-carnitine transported into matrix by translocase[cite: 17]. 3. Acyl group transferred back to mitochondrial CoA by CAT-2[cite: 17]. 4. Free carnitine recycled back to cytosol[cite: 17].

What is the Glucose-Fatty Acid Cycle (Randle Cycle) and how does fat oxidation suppress glycolysis?

High beta-oxidation produces excess Acetyl-CoA and Citrate[cite: 18, 19]. 1) Citrate inhibits PFK (Step 3)[cite: 18, 19]; 2) Backlog of G-6-P inhibits Hexokinase (Step 1)[cite: 19]; 3) High Acetyl-CoA inhibits Pyruvate Dehydrogenase (PDH)[cite: 19].

What is the primary determinant of substrate utilization during exercise?

Workload / power output (diet, training status, and sex are secondary)[cite: 20].

What is the Crossover Concept and how does endurance training alter it?

As exercise intensity increases, energy reliance shifts from lipid oxidation toward carbohydrate oxidation[cite: 20]. Endurance training shifts the crossover point upwards and to the right, meaning a higher workload can be sustained using fat before relying on carbohydrate[cite: 20].

What is McArdle's syndrome?

A genetic disorder characterized by a lack of the enzyme glycogen phosphorylase, preventing the breakdown of muscle glycogen[cite: 3, 17].