Impaired oxygen consumption kinetics and autonomic dysfunction contribute to increased fatigue in obese young males during sustained exercise

Obesity is associated with reduced exercise tolerance, yet the physiological mechanisms underlying this impairment remain unclear. This study examined whether oxygen uptake (V̇O₂) kinetics reflect autonomic regulation during prolonged moderate-intensity exercise in normal-weight and obese males. This cross-sectional study included nine normal-weight and nine obese males (aged 20-22) who performed 30 min of constant-load cycling at 70% of ventilatory threshold to assess V̇O₂ kinetics and heart rate variability (HRV) responses. V̇O₂ kinetics parameters-including the time constant (τ), which reflects the rate of cardiopulmonary and muscular adjustment to exercise, and the V̇O₂ drift slope-were analyzed. HRV was assessed at rest and during exercise. Changes in HRV and their correlations with V̇O₂ kinetics and perceived fatigue were evaluated. The obese group had a significantly longer τ than the normal-weight group, despite similar relative intensities. During exercise, HRV indices-including overall HRV, low-frequency, very low-frequency, and the standard deviation along the line of identity (SD2) -were significantly lower in the obese group, indicating attenuated autonomic responsiveness. In the normal-weight group, the slope was strongly correlated with the changes in the root mean square of successive differences, the high-frequency power, the standard deviation perpendicular to the line of identity (SD1), and SD1/SD2 (<i>r</i>=-0.769 to -0.857; <i>P</i><0.05), whereas these associations were absent in the obese group. These findings suggest that in normal-weight individuals, V̇O₂ kinetics are closely linked to autonomic modulation during prolonged exercise, whereas this link is disrupted in obesity, potentially leading to reduced aerobic efficiency and greater exercise intolerance.