Impact of Type 1 Diabetes on Exercise Capacity and the Maximum Level of Peripheral Fatigue Tolerated

Background: Type 1 diabetes (T1D) is associated with metabolic and neuromuscular impairments that may influence fatigue mechanisms and limit exercise tolerance. Although previous investigations have characterized muscle performance in T1D, the peripheral fatigue threshold, defined as the maximal sustainable level of peripheral fatigue, remains poorly understood in this population. This study aimed to compare the amplitude of the maximal peripheral fatigue threshold between individuals with T1D and healthy controls to elucidate the effects of T1D on neuromuscular function. Methods: Twenty-two participants (11 with T1D and 11 healthy controls) completed two randomized experimental sessions. In each session, 60 quadriceps maximal voluntary contractions (MVCs) were completed, performed for 3 s with 2 s of rest between contractions. One session was conducted under a non-fatigued control condition (CTRL), and the other followed a fatiguing neuromuscular electrical stimulation (FNMES) protocol. Central and peripheral fatigue were evaluated from the pre- to post-exercise changes in potentiated twitch force (ΔPtw) and voluntary activation (ΔVA), respectively. Critical torque (CT) was calculated as the average torque produced during the last 12 contractions, whereas the curvature constant of the torque-duration relationship (W') was quantified as the area above CT. Results: Although both groups exhibited a decline in pre-exercise Ptw following the FNMES condition, no significant within-group differences in ΔPtw were observed between sessions (T1D: p = 0.34; controls: p = 0.23). Nevertheless, the extent of peripheral fatigue was significantly lower in participants with T1D than in controls (ΔPtw = -38 ± 11% vs. -52 ± 17%; p < 0.05). Additionally, W' values were reduced by 24% in the T1D group relative to controls during the CTRL condition (p = 0.02), and CT was significantly lower in T1D participants (262 ± 49 N) compared to controls (353 ± 71 N; p < 0.01). A significant positive correlation was observed between ΔPtw and W' across groups (r² = 0.62, p < 0.001), suggesting a mechanistic link between peripheral fatigue tolerance and work capacity. Conclusions: The present results indicate that, although individuals with T1D retain the capacity to develop peripheral fatigue, their fatigue threshold and critical torque are markedly attenuated relative to those of healthy individuals. This reduction reflects impaired neuromuscular efficiency and diminished tolerance to sustained contractile activity. The strong relationship between peripheral fatigue and work capacity underscores the contribution of peripheral mechanisms to exercise intolerance in T1D. These results enhance current understanding of fatigue physiology in diabetes and emphasize the need for tailored exercise and rehabilitation strategies to improve fatigue resistance and functional performance in this population.