M7(2) Ventilation Threshold

metabolic CO2

CO₂ produced from normal aerobic metabolism

non-metabolic CO2

CO₂ produced when bicarbonate buffers H⁺ from lactic acid

HCO₃ + H⁺ → H₂CO₃ → CO₂ + H₂O

ventilatory threshold

point during incremental exercise at which ventilation (breathing) starts to increase disproportionately to oxygen consumption (VO₂)

• largely due to non-metabolic CO₂ produced when bicarbonate buffers H⁺ from accumulating lactic acid

• reflects a shift to anaerobic metabolism

non steady state response

3 phases

• Light to Moderate Intensity

• Heavy Intensity

• Severe Intensity

light to moderate intensity

Ventilation (VE) rises linearly with oxygen consumption (VO₂).

• The main mechanism: increased tidal volume (TV).

  • Breathing becomes deeper rather than faster at first

  • VE/VO₂ ratio remains fairly stable

heavy intensity

(>60–70% VO₂ max)

VE begins to increase more dramatically relative to VO₂.

• Both breathing rate and tidal volume increase.

• VE/VO₂ rises above ~25 L/min per L/min VO₂.

• associated with:

  • Lactate accumulation → metabolic acidosis

  • Buffering by bicarbonate → extra CO₂ production

  • Hyperventilation (ventilatory threshold) to expel CO₂ and maintain pH

severe intensity

VE rises sharply.

• Ventilation increases disproportionately to VO₂ and VCO₂.

• Often exceeds the body’s ability to maintain pH and gas exchange completely

H+ driven buffering

when more H⁺ ions are present (during intense exercise):

• excess protons (H⁺) from lactic acid push the bicarbonate reaction toward producing CO₂ to buffer the acid

assessing VT

2 ways to assess ventilatory threshold

• assessment method 1: plotting VE vs VO₂

• assessment method 2: plotting VE/VO₂ and VE/VCO₂ vs VO₂

• assessment method 3: plotting VCO₂ vs VO₂

plotting VE vs VO2

at low-to-moderate exercise intensities: VE rises roughly linearly with VO₂

as exercise intensity increases two key points appear

• ventilatory threshold 1

• ventilatory threshold 2

A1VT1

ventilatory threshold 1 / aerobic threshold; the start of anaerobic metabolism

• VE starts to rise disproportionately to VO₂

• caused by CO₂ produced from bicarbonate buffering H⁺ (from lactic acid)

A1VT2

ventilatory threshold 2 / respiratory compensation point

• VE rises even more sharply

• blood acidosis is stronger and additional CO₂ from H+ buffering + acid-base response triggers hyperventilation

• indicates high intensity exercise approaching maximal effort

plotting VE/VO2 and VE/VCO2 vs VO2

• VE/VO₂ = Ventilatory equivalent for oxygen (how much air you need to breathe to take in 1 L of O₂).

• VE/VCO₂ = Ventilatory equivalent for carbon dioxide (how much air you need to breathe to exhale 1 L of CO₂).

A2VT1

ventilatory threshold 1 / aerobic threshold

• VE/VO₂ increases, while

• VE/VCO₂ stays stable (or slightly decreases).

• This happens because extra ventilation is needed to blow off CO₂ from H⁺ buffering as lactate starts to build.

• Marker of the aerobic threshold (transition from light to moderate intensity)

A2VT2

ventilatory threshold 2 / respiratory compensation point; the start of anaerobic metabolism

• Both VE/VO₂ and VE/VCO₂ increase sharply.

• Indicates metabolic acidosis is significant → extra H⁺ accumulation.

• Ventilation rises disproportionately as the body tries to compensate.

• Marker of high-intensity threshold (near-max effort).

plotting VCO2 vs VO2

VO₂ and VCO₂ rise linearly, with ~1:1 slope (CO₂ is coming from aerobic metabolism)

• VO₂ = oxygen uptake

• VCO₂ = carbon dioxide output

A3V1

At Ventilatory Threshold 1 (VT1)

• VCO₂ begins to rise disproportionately faster than VO₂.

• This reflects extra CO₂ being produced from bicarbonate buffering of H⁺ as lactate starts to accumulate.

A3V2

At Ventilatory Threshold 2 (VT2 / RCP)

• The slope steepens further, reflecting even more CO₂ from acid–base imbalance and respiratory compensation.

mechanism driving VT/RCP

although the classic explanation for VT/RCP is lactic acidosis, the evidence isn’t quite so neat

1. glycogen depletion

2. McArdle’s Syndrome

3. carotid chemoreceptor excision

glycogen depletion

If you deplete glycogen, you reduce lactate production.

• But the ventilatory threshold still appears at about the same point.

• → Suggests lactate alone can’t be the sole trigger.

McArdle’s syndrome

These patients cannot perform glycolysis properly → no lactate production.

• Yet, they still show a ventilatory threshold response.

• → Again, challenges the idea that lactate/H⁺ is the main signal.

carotid chemoreceptor excision

Carotid bodies sense blood gases (O₂, CO₂, H⁺).

• If you remove them, you’d expect less ventilatory drive.

• Instead, animals show a greater hyperventilatory response during exercise.

• → Suggests multiple redundant mechanisms beyond carotid chemoreceptors.

lactate threshold

the highest VO₂ or exercise intensity before blood lactate rises more than ~1.0 mM above baseline

• It’s an early marker of when lactate production starts to exceed clearance.

• Occurs at moderate exercise intensities

onset of blood lactate accumulation

A more standardized marker.

• Defined as the exercise intensity when blood lactate reaches ~4.0 mM.

• This level indicates a more systematic and rapid accumulation of lactate.

• Usually occurs at a higher intensity than LT.

LT and OBLA

Both LT and OBLA are strong predictors of endurance performance (sometimes even more so than VO₂max).

• Training can shift these thresholds to higher intensities → you can sustain harder work before hitting fatigue

LT and VT relationship

LT and VT are linked because

• lactate accumulation → H⁺ production → CO₂ release → hyperventilation

but the relationship isn’t perfect

LT and VT imperfect relationship

LT and VT often happen close together but not always at the exact same workload.

• Why? Other signals can also trigger ventilation (catecholamines, potassium, temperature, central command).

• So VT is a useful non-invasive estimate of LT, but not a direct measurement.

blood lactate at finish line

If you exercise near or above LT/OBLA:

• Lactate accumulates in the blood.

• At the finish line, blood lactate is often elevated because:

  • Production > clearance during high-intensity effort

  • Post-exercise, lactate gradually clears (minutes to hours) via oxidation or gluconeogenesis