REF-1459 · Kontro et al., 2022 · Experimental Physiology · Paper · PubMed

Does raised carbon monoxide cost threshold work?

After CO rebreathing, 16 adults strained more at MLSS, lactate drifted in 9, the fitter; in 20, respiratory compensation point fell 6.3%. Not smoke; smoking status unstated. Abstract.

Main caveat: Abstract only; COHb reached, CO dose and the time from CO to exercise are not stated.
moderate evidenceMeasured on recreational to trained athletes

Kontro and colleagues (University of Calgary) asked whether a lower effective haemoglobin concentration, induced by CO inhalation, reduces VO2peak and MLSS, and whether training status explains who loses most.

Healthy young participants completed two ramp incremental tests (n = 20, 10 female) and two trials at MLSS (n = 16, eight female) after CO rebreathe tests and sham procedures in random orders; fitness values were normalised to fat-free mass and males and females were matched for aerobic fitness.

Against sham, CO lowered VO2peak by 4.2 (SD 3.7)%, peak power by 3.3 (2.2)% and the respiratory compensation point by 6.3 (4.5)% (all P < 0.001); the gas exchange threshold change of −3.3 (7.1)% was not significant (P = 0.077). Falls in VO2peak (r = −0.45) and peak power (r = −0.49) correlated with baseline aerobic fitness.

At MLSS, heart rate, ventilation, peripheral fatigue and perceived effort were all worse with CO, and mean lactate rose from 5.5 (1.4) mM at 10 min to 6.8 (1.3) mM at 30 min, with 9 of 16 classed as unstable. Those nine had the higher VO2peak and VO2 at MLSS.

Our reading: the clearest data in the base on what raised COHb does to the intensity athletes train at, and the fitter people lost more, with moderate correlations; it is a CO dose in a laboratory, not a cigarette.

Protocol

Participants: n = 20 for ramp tests (10 female) and n = 16 for MLSS trials (8 female); healthy and young; males and females matched for aerobic fitness.
Exposure: CO rebreathe tests or sham, in random order. COHb reached, CO dose and time to exercise are not in the abstract.
Tests: ramp incremental cycling for VO2peak, peak power, respiratory compensation point and gas exchange threshold; cycling at MLSS, with lactate at 10 and 30 min; instability defined as a lactate rise above 1.0 mM between those times.
Analysis: fitness variables normalised to fat-free mass; correlations with baseline aerobic fitness.
Funding and interests: PubMed lists non-US government support; the record names no funder and holds no conflict statement.

Key Results

Outcome, CO against shamMean change (SD)P
VO2peak−4.2 (3.7)%<0.001
Peak power−3.3 (2.2)%<0.001
Respiratory compensation point−6.3 (4.5)%<0.001
Gas exchange threshold−3.3 (7.1)%0.077
At MLSS with COUnstable, 9 of 16Stable, 7 of 16P
VO2peak (mL/kg FFM/min)66.2 (8.5)56.4 (8.8)0.042
VO2 at MLSS (mL/kg FFM/min)55.8 (7.0)44.3 (7.0)0.006
Lactate at MLSS with CO: 5.5 (1.4) mM at 10 min, 6.8 (1.3) mM at 30 min (P = 0.026).
Correlations with baseline fitness: VO2peak loss r = −0.45 (P = 0.047); peak power loss r = −0.49 (P = 0.029).

Mechanisms

Measured: lower peak values and respiratory compensation point after CO; higher heart rate, ventilation, peripheral fatigue and perceived effort at MLSS; lactate instability in the fitter participants.
Authors' interpretation: a reduced oxygen-carrying capacity decreased maximal and submaximal performance, with higher aerobic fitness associated with greater impairments in both.
Inference: fitter people run closer to their delivery limit (PHYS-09, established), which would fit a larger loss. Nothing in the abstract tests this mechanism, or says whether threshold is lost before VO2peak: the percentages were not compared formally in what is reported.

Practical Application

Does raised carbon monoxide cost threshold work? After CO rebreathing, 16 adults strained more at MLSS, lactate drifted in 9, the fitter; in 20, respiratory compensation point fell 6.3%. Not smoke; smoking status unstated. Abstract.
Fitness is no protection here: the fitter people lost more, at moderate correlations in about 20 people. Read it as "no reason to expect a fit athlete to be spared", not as a dose for any one athlete.
Heart rate and effort after CO: at the same MLSS work, heart rate, ventilation and perceptual strain rose with CO, so on a smoke day those numbers may not be comparable with a smoke-free day (PHYS-12; an inference from CO to smoke).
What it does not show: the effect of a cigarette or a hookah (see REF-1456, REF-1468); how many cigarettes equal this dose (no COHb in the abstract); how long the effect lasts; anything in smokers. Not from this paper; the base's own position: CO exposure is a cost, and nothing here supports it as a way to train the blood.

Limitations

Abstract only; COHb reached, CO dose and the time from CO to exercise are not stated.
CO by rebreathing is not smoke: no particles, no nicotine, no chronic exposure.
Who was measured: healthy young adults, not described as smokers or as competitive athletes.
Stable and unstable groups were split after the fact (9 vs 7), so the fitness link is observational within a crossover; correlations are moderate with P values near 0.05.
Blinding is not mentioned in the abstract; the sham procedure is its only stated control.
Funding and interests: non-US government support per PubMed; no statement in the record.
How this entry was checked and changed
Why this level

(from the abstract) — a controlled crossover with at least 15 participants and exercise performance outcomes (rubric B+); the exposure is CO by rebreathing, so its transfer to smoking is an inference