Basics 2

What is VO2, and why is it important?

VO2 is the rate of oxygen consumption (L/min), and it is important as it is used to calculate energy expenditure.

How do liters of O₂ convert to kcal? Give an example?

By combusting a fuel (carb or fat) in 1 liter of O₂, it is equivalent to ~5 kcal.

• Eg. If VO₂ = 4 L/min for 60 min then 5 kcal/L × 4 L/min = 20 kcal/min → 20 × 60 = 1200 kcal/hour

What are RER and RQ?

• RER (Respiratory Exchange Ratio) = VCO₂ / VO₂ measured at the mouth (lungs).

• RQ (Respiratory Quotient) happens inside the mitochondria, the “true” cellular measure. Cellular respiration and ETC occur in the mitochondria.

• They are conceptually the same ratio but differ in where they are measured

What does RER tell you?

It tells you whether you are burning more carbs or fat.

• RER = 1.0 → pure carbohydrate metabolism.

• RER = 0.7 → pure fat metabolism.

• Values in between (e.g., 0.85) mean a mix of carbs and fat.  

Why RER and RQ can differ

• RQ (mitochondrial) is the gold standard, but we can’t measure it directly.

• RER (mouth/lungs) is what we can actually measure — but it can be distorted by:

  • Acid-base balance (e.g., during heavy exercise, extra CO₂ is produced from buffering lactic acid).

  • Other disturbances → cause RER to rise above 1.0 or not reflect true substrate use.

The numbers are real, but they no longer represent what is happening in the mitochondria. Instead, they reflect a shift in the blood’s acid–base balance and the body’s attempt to correct it through hyperventilation. Give or take 75% is accurate for measuring RER, and 80% in an untrained state.

In what situations can RER differ from true RQ, and why?

• High-intensity exercise → lactic acid buffering makes extra CO₂ (acidic) → hyperventilation.

• Metabolic acidosis (e.g., DKA) → excess H⁺ buffered, more CO₂ blown off.

• Anxiety/voluntary hyperventilation → chemoreceptor-driven CO₂ loss.

• High altitude → hypoxia triggers hyperventilation.

What is the common endpoint of carbohydrate and fat metabolism before the Krebs cycle?

Both glucose (via glycolysis/pyruvate) and fatty acids (via beta-oxidation) are oxidized to acetyl-CoA, which enters the Krebs cycle.

Why can’t we distinguish between carb and fat metabolism once acetyl-CoA enters the Krebs cycle?

Because from acetyl-CoA onward, metabolism is identical: both substrates generate NADH, FADH₂, and CO₂ in the Krebs cycle → feed into the electron transport chain.

Where does the key difference in CO₂ production occur between carbs and fats?

In carbohydrate metabolism, the pyruvate dehydrogenase (PDH) step (pyruvate → acetyl-CoA) produces extra CO₂. Fatty acid beta-oxidation does not produce CO₂ before acetyl-CoA, so total CO₂ per O₂ is lower (RER ≈ 0.7 vs. 1.0).

How do you calculate energy expenditure using VO₂ and the RER table?

Energy (kcal) = (kcal per L O₂ from RER table) × (VO₂ in L/min) × (time in min)