Chapter 6 — Quiz

Twenty questions. Attempt before opening.

Multiple Choice

1. Cells directly spend which molecule as energy?

  • a) Glucose
  • b) Fatty acids
  • c) ATP
  • d) Glycogen
Answer **c.** Everything else is a way of *making* ATP. Cash in your pocket; glycogen is the current account, body fat the pension.

2. Approximately how do total body fat stores compare with total glycogen stores?

  • a) Roughly equal
  • b) Fat is about twice as large
  • c) Fat is about forty times or more larger
  • d) Glycogen is larger
Answer **c.** ~90,000+ kcal of fat in a lean adult versus ~2,000 kcal of glycogen. **You cannot run out of fat** in any circumstance a person survives.

3. Muscle glycogen cannot raise blood glucose because:

  • a) It is chemically different from liver glycogen
  • b) Muscle cells lack the enzyme needed to release glucose into the blood
  • c) It is used up too quickly
  • d) It is stored as fat instead
Answer **b.** Your quadriceps cannot lend glucose to your brain. Only **liver** glycogen — about 100 g — is the strategic reserve; muscle glycogen is a local fuel tank.

4. Which statement about protein storage is correct?

  • a) Excess protein is stored in muscle for later use
  • b) There is no protein store; using protein for energy dismantles functional tissue
  • c) Protein is stored in the liver alongside glycogen
  • d) Protein is converted to glycogen and stored
Answer **b.** Every gram of body protein is doing a job. There's a small circulating amino acid pool and nothing else. Not spending savings — selling furniture.

5. Lactate is best described as:

  • a) A waste product causing next-day muscle soreness
  • b) A fuel that can be used by heart and muscle and converted back to glucose by the liver
  • c) An acid that permanently damages muscle
  • d) A signal that you have exceeded your fat-burning zone
Answer **b.** The Cori cycle. Elite athletes are better at *clearing and using* lactate, not at avoiding it. Next-day soreness is mechanical damage and repair; lactate is long gone.

6. Oxygen's specific role in the mitochondrion is to:

  • a) Break down glucose
  • b) Transport fatty acids across the membrane
  • c) Act as the final electron acceptor at the end of the electron transport chain
  • d) Activate the citric acid cycle
Answer **c.** In the dam analogy, oxygen is the drainage channel at the bottom. Without it the reservoir backs up, the pumps stall, and everything stops — which is why minutes without breathing is fatal regardless of how much fuel you have. (b) is carnitine.

7. Carbohydrate and fat converge in metabolism at:

  • a) Pyruvate
  • b) Acetyl-CoA
  • c) Lactate
  • d) Glycogen
Answer **b.** Both become acetyl-CoA and feed the same citric acid cycle and the same dam. **This convergence is why there's nothing to switch between.**

8. A respiratory quotient of 0.80 in a resting person indicates approximately:

  • a) 100% fat oxidation
  • b) 100% carbohydrate oxidation
  • c) About two-thirds fat, one-third carbohydrate
  • d) A measurement error
Answer **c.** Not 0.7 and not 1.0. **You have never been in a fat-burning mode and never been out of one.**

9. In the fat-burning-zone comparison, a 30-minute run (400 kcal, 35% from fat) versus a 30-minute walk (150 kcal, 60% from fat) oxidizes:

  • a) Less fat, because the proportion is lower
  • b) The same amount of fat
  • c) More fat — about 140 kcal worth versus 90
  • d) No fat at all
Answer **c.** 400 × 0.35 = 140 vs. 150 × 0.60 = 90. A smaller *proportion* and a larger *amount*. And the deeper point: fat loss over weeks tracks energy balance, not which substrate you oxidized during a half hour.

10. Gluconeogenesis can make glucose from all of the following EXCEPT:

  • a) Lactate
  • b) Glycerol
  • c) Amino acids
  • d) Fatty acids
Answer **d.** The chemistry runs one way: glucose can become fat, but the bulk of fat cannot become glucose. Only the small glycerol backbone can. This is why not eating carbohydrate raises your protein requirement.

11. The key difference between nutritional ketosis and diabetic ketoacidosis is:

  • a) The type of ketone produced
  • b) Insulin — present and acting as a brake in ketosis, effectively absent in DKA
  • c) Whether the person is exercising
  • d) The time of day
Answer **b.** In nutritional ketosis (~0.5–3 mmol/L) insulin is low but present and limits ketone production. In DKA (often >10–15 mmol/L) that brake is gone, ketones rise without limit, and blood pH falls. **These are different situations, not points on one scale.**

12. mTOR and AMPK, respectively, drive:

  • a) Fat storage and fat burning
  • b) Building/anabolism and breakdown/autophagy
  • c) Digestion and absorption
  • d) Ketosis and gluconeogenesis
Answer **b.** mTOR is activated by amino acids (especially leucine), insulin, and plentiful energy. AMPK is activated by energy stress — exercise, fasting. **You want both, at different times**, which is why "permanently inhibit mTOR for longevity" is a poor idea.

13. Roughly how much of your own protein do you break down and rebuild each day?

  • a) 5–10 g
  • b) 40–50 g
  • c) 200–300 g
  • d) 2–3 kg
Answer **c.** Far more than anyone eats. This constant turnover is quality control — and because the amino acid pool is small and nitrogen loss is one-way, it's why protein is a *daily* requirement in a way carbohydrate and fat are not.

True / False

One-line justification.

14. You must eat carbohydrate because your brain runs on glucose.

Answer **False.** The premises are true; the conclusion doesn't follow, because gluconeogenesis can supply glucose from lactate, glycerol, and amino acids, and ketones can substitute for much of the brain's requirement. **But it isn't free** — the cost is paid in protein, which is why very-low-carbohydrate diets need higher protein intakes.

15. Being in ketosis means you are losing body fat.

Answer **False.** It means you are *oxidizing* a lot of fat, which is substrate availability, not fat loss. Eat mostly fat and you burn mostly fat. Body fat only decreases if you oxidize more than you consume. A person can be deeply ketotic and gaining weight.

16. L-carnitine supplementation increases fat burning in healthy people.

Answer **False.** The mechanism is real — carnitine genuinely shuttles fatty acids into mitochondria — but it isn't rate-limiting in healthy people, and muscle carnitine isn't readily raised by oral supplements. Genuine deficiency exists in specific clinical situations, and there it matters a great deal.

17. Fasting for 16 hours has been shown in human trials to activate autophagy and extend lifespan.

Answer **False.** The mechanism is real and Nobel-recognized; the *human* outcome data isn't there. Autophagy is hard to measure in living humans, most data is indirect, and the specific hour-thresholds circulating online derive largely from rodent work. **Mice have a metabolic rate roughly seven times ours** — anyone quoting you an hour figure is quoting a mouse. Verdict: ⚗️ **Untested**, which is not the same as false.

18. Exogenous ketone supplements accelerate body-fat loss.

Answer **False**, and the logic is backwards. Your body makes ketones *because* it's drawing on fat stores; supplying them from outside provides an additional fuel and if anything reduces the demand on your own fat. The marketing confuses a **marker** with a **mechanism**.

Short Answer

19. Explain the threshold concept of this chapter in your own words, and give the single strongest piece of evidence for it.

Answer **There is no fuel switch.** You are always oxidizing both carbohydrate and fat, in a continuously shifting ratio governed by exercise intensity, time since eating, glycogen status, training status, and habitual carbohydrate intake. It's a mixing board, not a gearbox. **Strongest evidence:** the respiratory quotient of a resting human is about **0.80** — neither 0.7 (pure fat) nor 1.0 (pure carbohydrate). This is a direct, routine measurement, not an inference. The mechanistic reason is that both fuels converge on **acetyl-CoA** and feed the same citric acid cycle, so there is no separate machinery to switch between.

20. Explain the reasoning pattern the chapter identifies in the L-carnitine verdict, and why it recurs so often.

Answer **"X is required for Y, therefore more X increases Y."** It recurs because the first half is usually true and verifiable, which makes the whole thing feel established. But biological pathways have a **rate-limiting step**, and it's rarely the ingredient being sold — often because the body already has plenty, or regulates the level tightly, or the bottleneck is somewhere else entirely. The chapter's image: a road being *required* to reach a city doesn't mean widening it gets you there faster if the traffic jam is at the bridge. The same structure appears in the BCAA/leucine claim (§6.10 cost check), in most vitamin claims (Chapter 13), and in a large fraction of the supplement aisle generally.

Applied Scenario

21. A client tells you: "I do fasted cardio at 65% max heart rate for 45 minutes every morning because that's the fat-burning zone, and I'm on keto so I'm already in fat-burning mode. My ketones read 1.6. But I've lost nothing in five weeks and my gym performance has collapsed."

Address every claim. Then say what you'd change.

Answer **"Fat-burning zone."** Real physiology, wrong conclusion. At 65% a higher *proportion* of energy comes from fat, but total energy expenditure is lower, and substrate use during the session is largely irrelevant to fat loss over weeks — which tracks energy balance (Ch 4). **"Fasted."** Fasted training does shift the mix toward fat during the session. Studies comparing fasted and fed training at matched energy expenditure generally find little difference in fat-loss outcomes, and fasted training often reduces the intensity you can sustain — which may be part of the performance problem. **"Already in fat-burning mode."** There is no mode. RQ is always between 0.7 and 1.0. Ketosis raises fat oxidation, which is a substrate observation, not a fat-loss observation. **"Ketones read 1.6."** That confirms they're in nutritional ketosis. It says **nothing** about whether they're in an energy deficit. The meter measures a slider position, not the account balance. **"Lost nothing in five weeks."** The likely explanation is not metabolic — it's that they're eating at or near maintenance. Ketogenic diets are energy-dense and it is entirely possible to overeat them. Chapter 4 §4.7's error bars apply: their intake estimate is probably low. The next step is measurement, not further restriction. **"Performance collapsed."** Expected. Muscle glycogen (§6.2) is the fuel for higher-intensity work, and it's chronically low on a ketogenic diet. Fat cannot supply ATP at the required *rate* (§6.5). There's often partial adaptation over weeks, but high-intensity performance typically remains reduced. **What I'd change, in order:** (1) **Measure intake for three days** before changing anything — the plateau is almost certainly an energy question. (2) **Stop optimizing the zone**; train at an intensity they enjoy and can recover from, and consider raising it, since total expenditure is what matters. (3) **Decide whether keto is serving them** — if performance matters to them, it may not be the right tool, and it has no metabolic advantage to trade against that cost (Chapter 10). (4) **Put the ketone meter away.** It's measuring something real and irrelevant to their goal, and it's giving them false confirmation that things are working.

Scoring

Score Reading
18–21 Excellent, and this is the hardest chapter in Part I.
14–17 Solid. Reread §6.6 (the mixing board) and §6.2 (the stores).
10–13 Focus on §6.1, §6.2, §6.6 — the three Fast Track sections carry most of the value.
Under 10 Reread the Fast Track sections only, then move on. Chapters 7–12 will reinforce this material in context, and it lands better the second time.

Part I is complete. Before Chapter 7, check: have you done the belief inventory, the claim filter card, the digestion log, the three-day diary, your own RMR, and the fuel-mix reflection? Six components. Phase 1 of the Framework is finished if you have.