Impairment in maximal lactate steady state after carbon monoxide inhalation is related to training status

What is the central question of this study? What is the effect of an elevated carboxyhaemoglobin (COHb) concentration following carbon monoxide inhalation on the maximal lactate steady state (MLSS) in humans and is this effect dependent on aerobic fitness? What is the main finding and its importance? An elevated COHb concentration intensified physiological responses to exercise at the MLSS - including heart rate, ventilation and peripheral fatigue - in general and reduced the MLSS (i.e., destabilized the blood lactate concentration) in trained but not untrained males and females.

This study investigated whether a lower effective [Hb], induced by carbon monoxide (CO) inhalation, reduces the peak oxygen uptake ( $$ ) and the maximal lactate steady state (MLSS) and whether training status explains individual variation in these impairments. Healthy young participants completed two ramp incremental tests (n = 20, 10 female) and two trials at MLSS (n = 16, eight female) following CO rebreathe tests and sham procedures (SHAM) in random orders. All fitness variables were normalized to fat-free mass (FFM) to account for sex-related differences in body composition, and males and females were matched for aerobic fitness. The $$ (mean (SD): -4.2 (3.7)%), peak power output (PPO) (-3.3 (2.2)%) and respiratory compensation point (RCP) (-6.3 (4.5)%) were reduced in CO compared with SHAM (P < 0.001 for all), but the gas exchange threshold (-3.3 (7.1)%) was not (P = 0.077). Decreases in $$ (r = -0.45; P = 0.047) and PPO (r = -0.49; P = 0.029) in CO were correlated with baseline aerobic fitness. Compared to SHAM, physiological and perceptual indicators of exercise-related stress were exacerbated by CO while cycling at MLSS. Notably, the mean blood lactate concentration ([La]) increased (i.e., Δ[La] >1.0 mM) between 10 min (5.5 (1.4) mM) and 30 min (6.8 (1.3) mM; P = 0.026) in CO, with 9/16 participants classified as unstable. These unstable participants had a higher $$ (66.2 (8.5) vs. 56.4 (8.8) ml kg FFM^-1  min^-1 , P = 0.042) and $$ at MLSS (55.8 (7.0) vs. 44.3 (7.0) ml kg FFM^-1  min^-1 , P = 0.006) compared to the stable group. In conclusion, a reduced O₂ -carrying capacity decreased maximal and submaximal exercise performance, with higher aerobic fitness associated with greater impairments in both.