This study provides a detailed dynamometric assessment of multiple muscle contractile domains in two locomotor muscles of individuals with severe obesity, with and without T2D. A major strength of the study is the careful matching of groups and the comprehensive design, allowing us to isolate the added impact of T2D, independent of DPN, on muscle function in severe obesity. To date, this has been only sparsely investigated in this population. The key finding is a reduced ability of individuals with severe obesity and T2D to scale muscle power with increasing contraction velocity, particularly in KE. This indicates a diminished functional reserve, whereby the capacity to generate power under high-velocity conditions is impaired, despite preserved muscle strength and mass.

Consistently, deficits in both KE absolute and body weight–normalized power were more evident at higher contraction speeds, alongside greater fat infiltration in T2D compared to obesity alone. Moreover, normalized power deficits across all velocities were more pronounced in both KE and DF among groups with obesity, with and without T2D, compared to individuals without obesity. Importantly, normalized power emerged as the strongest predictor of physical performance (i.e., 5xSTS and 10MWT), even after adjusting for physical activity. These findings demonstrate that severe obesity combined with T2D impair muscle contractile function, beyond strength and size, highlighting the relevance of assessing muscle power alongside strength in middle-aged individuals and of expressing power relative to body weight for functional interpretation.

Impact of severe obesity on muscle function

Individuals with severe obesity without T2D demonstrated preserved or greater contractile strength and muscle volume in both KE and DF compared to those with T2D and individuals without obesity. These findings align with prior evidence suggesting that obesity may confer a protective effect on absolute muscle mass and strength, particularly in weight-bearing muscles such as the KE [47,48,49]. Similar effects have also been reported in the DF [50, 51].

Specific muscle power was preserved in obesity, though prior studies have reported conflicting results. Some studies report no change in torque or power normalized to muscle volume [35, 47, 52], while others describe reduced specific strength in this population [17, 48, 53]. These discrepancies are likely due to methodological differences in muscle volume assessment. Studies using bioimpedance or DEXA often report reduced specific strength without adequately accounting for myosteatosis [17, 48, 53]. In contrast, our study used MRI, providing more precise estimates of muscle volume and fat infiltration.

Across all contraction velocities, absolute power was preserved in both KE and DF, with a tendency toward greater KE power in individuals with obesity, indicating no impairment in sustaining absolute power production. While one study has examined muscle power using isokinetic dynamometry [47], others have derived power from jump tests [35] or examined hypergravity-trained athletes rather than directly assessing individuals with obesity [54]. Despite methodological differences, our results align with prior evidence suggesting that obesity does not compromise absolute muscle power and may even be associated with increased power output. However, this does not necessarily translate into functional benefits, as the excess mechanical and metabolic demands of obesity must be considered. Supporting this notion, individuals with obesity exhibited lower functional capacity in the 5xSTS and 10MWT, despite preserved absolute power. In contrast, muscle power normalized to body weight was significantly reduced in individuals with obesity for both KE and DF, consistent with studies showing that excess adiposity impairs normalized strength and power, even when absolute levels are maintained or enhanced [20].

Impact of T2D on muscle function

Compared to individuals with severe obesity alone, those with T2D exhibited additional impairments in muscle quality and function. Despite similar muscle volume, MRI revealed greater fatty infiltration in knee extensors of the T2D group, supporting the role of ectopic fat accumulation in muscle dysfunction. This finding aligns with frameworks to redefine obesity classification by incorporating measures of adiposity beyond BMI [55]. Fat infiltration, and associated lipotoxicity are linked to hyperglycemia, insulin resistance, dyslipidemia, and systemic inflammation [21, 56, 57], all of which were more pronounced in our T2D group.

Interestingly, specific power did not differ between groups when accounting for fat infiltration. This contrasts with population-based studies, where specific strength tends to decline more significantly than absolute strength and muscle volume in T2D cohorts [11, 12, 25, 26]. This discrepancy may partly reflect methodological differences, as discussed above, with our study providing a more detailed evaluation of specific power. Another explanation is that our T2D participants had well-controlled diabetes, as previous studies have suggested a stronger association between elevated HbA1c levels and reduced specific strength [11, 12]. Diminished specific strength may also reflect neuropathy-related impairments rather than T2D per se, as it has predominantly been reported in individuals with DPN [18, 28, 34, 46, 58]. Our detailed neuropathy screening rules out any contribution to the deficits by DPN. Moreover, normalization to contractile muscle volume primarily reflects macroscopic muscle properties and may not adequately capture intracellular or metabolic impairments. Consequently, specific power does not fully represent muscle quality in T2D, where intramuscular alterations associated with insulin resistance, such as mitochondrial dysfunction and intramyocellular lipid accumulation, are well described [29, 59], and may already present with obesity per se [60].

Beyond alterations in muscle composition, individuals with T2D exhibited a greater decline in both absolute and normalized KE power at higher contraction velocities, compared to those with obesity alone, and lower normalized KE and DF power than individuals without obesity. This suggests that T2D disrupts the power-velocity relationship, with minimal power advantages when transitioning from moderate to fast contraction speeds. This power plateau may partly explain their slower gait speed. In contrast, 5xSTS performance was comparable between obesity groups, consistent with findings that chair-stand performance plateaus at BMI levels above 30 kg/m2, which may reflect the more strength based nature of 5xSTS compared to gait speed [15]. Existing research on power output in T2D indicates lower absolute and specific power in DF, reduced normalized power at the knee, and a stronger association between power (rather than torque) and gait speed [31, 32, 34]. However, among these studies, only Volpato et al. accounted for neuropathy (regression analyses), leaving the direct effects of T2D on muscle power unclear. Our study addresses this gap by isolating the impact of T2D independent of neuropathy.

Overall, our findings suggest that muscle power deficits and fatty infiltration are exacerbated by the presence of T2D and its associated metabolic disturbances. This supports the notion that hyperglycemia, inflammation, and metabolic syndrome, rather than BMI, determine whether obesity preserves or harm functional muscle health [9, 21, 61].

Muscle-specific differences and underlying mechanisms

Comparisons between KE and DF revealed distinct patterns in muscle-specific impairments. KE power and quality were more affected by the presence of T2D, suggesting greater vulnerability to diabetes-related impairments. This aligns with the concept of accelerated muscle ageing in T2D, as KE function also tends to decline more than DF with ageing [44]. Despite this, KE force–velocity profiles remained unchanged, whereas DF exhibited a steeper decline at higher velocities in obesity, with no additional effect from T2D. Our findings contrast with those of Sacchetti et al. [33], who reported altered force–velocity curves in KE among sedentary and trained individuals with diabetes, with further decrements in the presence of DPN. However, their cohort included older adults with longer T2D duration and lower BMI, suggesting that KE impairments in force–velocity behavior may not manifest until later disease stages. Studies on DF force–velocity behavior in obesity and T2D are lacking, though slowed contractility has been reported in DF using twitch and voluntary force development tests [28, 62].

Several factors may explain the muscle-specific differences in function. KE, a large muscle group involved in high-intensity activities (e.g. sprinting and jumping), may be more susceptible to metabolic dysfunction. In contrast, DF are much smaller, richer in type I fibers, yet critical for gait [63, 64]. While KE could theoretically be affected by disuse due to their role in high-load movements, the relatively high physical activity levels in our cohort, where all groups met WHO physical activity recommendations, suggest that disuse alone is unlikely to explain the observed deficits. Moreover, the relatively high overall physical activity level in our cohort may have helped preserve DF function, buffering against the impact of T2D. Therefore, it is reasonable to conclude that physical activity differences had limited impact on muscle contractile function in our study. Furthermore, evaluating more sedentary individuals would likely disclose greater impairments across both KE and DF.

Mechanistically, obesity is associated with a shift toward fast-twitch glycolytic fibers, potentially enhancing strength and power, and contributing to the steeper force–velocity slope observed in DF [65]. In T2D, contractile function is thought to be impaired through multiple mechanisms including lipotoxicity [21], impaired insulin signaling [30], mitochondrial dysfunction [29], extracellular matrix disruption [66], and altered calcium handling [27], many of which disproportionately affect type II fibers [21, 30]. Given the knee extensors’ greater reliance on type II fibers, this muscle group may be particularly susceptible to contractile impairments. Moreover, the increased fat infiltration in KE observed in our study suggests the presence of greater metabolic strain and structural vulnerability compared to DF in T2D. Accordingly, KE appear especially vulnerable in individuals with T2D, helping to explain the more pronounced power deficits of KE observed in this group. Nevertheless, future studies linking specific intramuscular mechanisms with muscle functional deficits are warranted to further clarify the vulnerability of knee extensors in T2D.

Together these dual influences, obesity promoting force via fiber type shift, and T2D undermining contractility, may explain why obesity alone preserves muscle power, while its combination with T2D leads to power impairments.

Correlations to physical performance and clinical implications

Regression analyses demonstrated that lower limb muscle function, particularly knee extensor normalized power, was significantly associated with physical performance in both the 5xSTS and 10MWT. These findings underscore the critical role of muscle power in mobility-related tasks, particularly relative to body weight, reinforcing evidence that power is a stronger determinant of functional performance than strength alone [32, 67]. Notably, the task-specific distinction between the 5xSTS and 10MWT, with the latter relying more on rapid force production and movement velocity, may explain the stronger association between normalized power and gait speed observed in our study. Importantly, this association persisted after adjusting for MVPA, suggesting that functional impairments in obesity and T2D are not solely due to activity levels.

These results highlight the importance of early detection of muscle deficits, potentially using simple functional tests, especially velocity-sensitive tests such as 10MWT, before overt mobility limitations occur. Moreover, given the higher risk of functional decline in this population, our findings support interventional strategies that specifically target muscle power, not just strength, in combination with weight loss and glycemic control, as these strategies may be crucial for preserving mobility and reducing disability risk in individuals with severe obesity and T2D [5].

Limitations

Some limitations should be acknowledged. First, although groups were matched on age, sex, and height, one participant in the O group was unmatched on sex, which may have introduced minor variability. Second, despite similar self-reported activity levels at inclusion, differences in accelerometer-based MVPA levels persisted. Third, missing MRI and NCS data in a few individuals may have influenced group comparisons. Finally, the cross-sectional design impairs causal interpretation of the observed associations in muscle function and performance.