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Life sciences · Journal article
Acta Gymnica · September 15, 2026
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Background: Obesity is associated with metabolic dysregulation and impaired hemorheological function, which may affect oxygen delivery during exercise. However, how hemorheological properties change during submaximal exercise under controlled cardiovascular load remains unclear. Objective: This study compared hemorheological and metabolic responses during and after submaximal endurance exercise performed at a clamped heart rate (HR) in nonobese and obese Korean men. Methods: Twenty-four men participated: 12 in the obese group (OG; body mass index ≥ 25 kg/m2 and body fat percentage ≥ 25%) and 12 nonobese (NG) according to Korean adult obesity criteria. Participants completed 30 min of cycling at 75% of maximal HR, followed by 30 min of recovery. Metabolic and cardiorespiratory variables (relative and absolute oxygen uptake (VO2), relative and absolute carbon dioxide production (VCO2), ventilation, respiratory exchange ratio, blood lactate), substrate utilization (carbohydrate oxidation, fat oxidation, energy expenditure), and hemorheological parameters (red blood cell (RBC) aggregation index, RBC deformability at 3 Pa) were measured at baseline, during exercise, and during recovery. Results: Despite comparable HR and workload, relative VO2 and VCO2 were significantly lower in the OG during exercise (p <.001), whereas absolute VO2 and VCO2 showed no group differences. Ventilation, respiratory exchange ratio, blood lactate, and substrate utilization showed no group differences. The OG exhibited consistently RBC aggregation index and lower RBC deformability at 3 Pa across all time points (p <.01). Time-dependent changes in hemorheological variables were small, with only transient increases in AI observed. Conclusions: Under clamped HR submaximal exercise, individuals with obesity show lower oxygen consumption despite similar ventilatory and substrate utilization responses. Persistent hemorheological impairments in obesity may restrict peripheral oxygen delivery, contributing to reduced metabolic responses under equivalent cardiovascular load.