Impact of obesity and type 2 diabetes on muscle power, quality, and force–velocity, and their relation to functional capacity

Background Obesity and type 2 diabetes (T2D) increase the risk of sarcopenia and mobility decline, yet the underlying muscle contractile alterations remain poorly understood. This study investigated how severe obesity and T2D affect muscle power, force–velocity relationships, and muscle quality. Methods In this cross-sectional study, 45 middle-aged individuals were categorized as non-obesity (Non-O; BMI 18.5–30 kg/m 2 ), obesity (O; BMI ≥ 35 kg/m 2 ), and obesity with T2D (O + T2D; BMI ≥ 35 kg/m 2 ). Isokinetic torque and power of knee extensors (KE) and dorsiflexors (DF) were measured (DF: 0–120°/s; KE: 0–270°/s). Muscle volume and fat infiltration (FF, %) were quantified using MRI. Outcomes included absolute, specific (relative to muscle volume), and normalized (relative to body weight) power. Functional capacity was assessed with five-times sit-to-stand (5xSTS) and 10-m walk (10MWT) tests. Results KE power was 51W lower in O + T2D than O (P = 0.008) with larger deficits at higher velocities (interaction, P = 0.027). O and O + T2D exhibited lower normalized KE power (–0.8 and –1.1 W/kg vs. Non-O; both P < 0.001). KE FF was higher in O (5%) than Non-O (3%, P = 0.003), and highest in O + T2D (7%, P = 0.023). DF torque declined faster with velocity in O and O + T2D (P ≤ 0.012). Specific power did not differ. KE normalized power was the strongest predictor of performance (5xSTS: R 2 = 0.57,P = 0.003; 10MWT: R 2 = 0.71,P < 0.001). Conclusions Severe obesity impairs normalized muscle power, with T2D exacerbating KE power deficits and fatty infiltration. These muscle contractile impairments may contribute to functional decline already in middle-aged individuals.