This commentary argues that skeletal muscle strength, physical function, and exercise capacity should be treated as formal clinical and research outcomes in type 1 diabetes (T1D) care — complementing, not replacing, glycaemic metrics.
Evidence suggests people with T1D show reduced muscle strength, impaired mitochondrial function, altered muscle morphology, and lower exercise capacity — consistent with accelerated neuromuscular ageing even without major overt complications. Resistance training trials in both adults and youth with T1D show strength gains without increasing adverse glycaemic events.
- This is an expert commentary, not a systematic review; no new primary data are presented. - Proposed biological mechanisms (cGAS–STING, AMPK/SIRT1/PGC-1α, Piezo1) remain largely preclinical and unproven specifically in T1D. - Whether improvements in muscle outcomes translate to long-term cardiometabolic or glycaemic benefit has not been established.
Consider adding simple muscle function assessments — such as handgrip dynamometry and sit-to-stand tests — to routine T1D care, especially in older adults, those with neuropathy, or patients with poor body composition despite acceptable HbA1c. Resistance training is already guideline-recommended; the gap is that muscle strength and physical function are rarely *measured* or *treated* as therapeutic targets.
