Abstract
Background
Blood lactate accumulation during exercise has traditionally been associated with reduced oxygen availability and an increased reliance on glycolytic metabolism. However, lactate production is influenced by multiple processes beyond oxygen availability. Previous pilot work demonstrated that a standardized controlled breathing intervention produced intermittent reductions in peripheral oxygen saturation comparable to intermittent hypoxic training, but its effects on blood lactate had not been investigated. This crossover study compared normobaric hypoxia (NH) and controlled breathing (CB). We hypothesized that both interventions would increase blood lactate accumulation relative to control.
Methods
Fifteen healthy adults completed three laboratory visits using a within-subject crossover design. Participants performed an identical 30-minute functional exercise protocol during control (CON), NH (15% inspired oxygen), and CB. Blood lactate was measured at rest, after 10, 20, and 30 minutes of exercise, and after 10 minutes of recovery. Blood lactate AUC, maximum blood lactate, average HR, peripheral oxygen saturation (SpO
2
), and ratings of perceived exertion (RPE) were assessed. Data were analyzed using linear mixed-effects models with Tukey-adjusted pairwise comparisons.
Results
Contrary to hypothesis, NH and CB produced different metabolic responses despite reducing peripheral oxygen saturation. Blood lactate differed among conditions over time (condition × time interaction, p = 0.007), with CB demonstrating lower blood lactate than CON at 10, 20, 30 minutes, and recovery, and lower blood lactate than NH at 20 and 30 minutes. Maximum blood lactate (p = 0.002), blood lactate AUC (p 2
relative to CON. RPE did not differ among conditions (p = 0.371).
Conclusions
A standardized controlled breathing intervention was associated with lower blood lactate accumulation, cumulative lactate exposure, peak blood lactate concentration, and average HR despite significant reductions in peripheral oxygen saturation during moderate-intensity exercise. These exploratory findings suggest pulse oximetry-measured peripheral oxygen saturation may not fully predict metabolic responses to exercise. Because underlying mechanisms were not directly assessed, future mechanistic studies using direct measurements of skeletal muscle oxygenation, gas exchange, and metabolic regulation are warranted.