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Muscle Failure / Severe Obesity / Type 2 Diabetes · Journal article
Journal of Diabetes and Metabolic Disorders · July 3, 2026
Reinforces what was already believed, rather than introducing something new.
This cross-sectional study of 45 middle-aged adults demonstrates that severe obesity reduces normalized knee extensor power by 0.8 W/kg and obesity with T2D by 1.1 W/kg compared to non-obese controls, with T2D further impairing absolute power and increasing fatty infiltration. Normalized knee extensor power emerged as a strong predictor of functional performance (5xSTS R² = 0.57, 10MWT R² = 0.71), suggesting muscle contractile impairment may underlie mobility decline in this population.
Cross-sectional observational study. 45 middle-aged individuals: non-obesity (BMI 18.5–30 kg/m²), obesity (BMI ≥ 35 kg/m²), and obesity with type 2 diabetes (BMI ≥ 35 kg/m²).. Intervention: Measurement of knee extensor and dorsiflexor power and torque across velocities; MRI assessment of muscle volume and fat infiltration.. Compared with: Three-way comparison among non-obesity, obesity, and obesity with T2D groups.. n = 45.
Knee extensor power 51 W lower in obesity + T2D versus obesity alone (P = 0.008), with larger deficits at higher velocities (interaction P = 0.027) Normalized knee extensor power reduced in obesity (−0.8 W/kg, P < 0.001) and obesity + T2D (−1.1 W/kg, P < 0.001) versus non-obesity Knee extensor fat infiltration 5% in obesity versus 3% in non-obesity (P = 0.003), and 7% in obesity + T2D (P = 0.023)
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Clinicians should recognize that normalized muscle power impairment, particularly in knee extensors, is a quantifiable marker of functional decline in obese and diabetic middle-aged adults and may guide identification of individuals at risk for sarcopenia and mobility loss. The strong predictive association (R² = 0.71) between normalized knee power and walking speed suggests that muscle quality assessment could inform early intervention strategies.
Cross-sectional study demonstrating that obesity and T2D impair normalized muscle power and quality in middle-aged adults, with quantified deficits and functional associations, but lacks a comparator intervention and cannot establish causation.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should recognize that normalized muscle power impairment, particularly in knee extensors, is a quantifiable marker of functional decline in obese and diabetic middle-aged adults and may guide identification of individuals at risk for sarcopenia and mobility loss. The strong predictive association (R² = 0.71) between normalized knee power and walking speed suggests that muscle quality assessment could inform early intervention strategies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
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/m2), obesity (O; BMI ≥ 35 kg/m2), and obesity with T2D (O + T2D; BMI ≥ 35 kg/m2). 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: R2 = 0.57,P = 0.003; 10MWT: R2 = 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.
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