New trial: Mitoquinol (MitoQ) lifted resting and stress PCr/ATP ratios and improved diastolic function in adults with type 2 diabetes.

A placebo-controlled crossover trial found that four weeks of MitoQ supplementation improved 8 km cycling time trial performance and power output while reducing exercise-induced oxidative stress.

A clinical trial found that women who experience menopause later in life have better vascular endothelial function and lower mitochondrial oxidative stress. These findings suggest that mitochondrial health may help explain why later menopause is associated with lower cardiovascular disease risk.

A controlled trial examining whether a single 80 mg dose of Mitoquinol improves claudication onset, maximal walking time, and leg artery dilation in patients with peripheral artery disease, and what these findings reveal about the mitochondrial contribution to PAD-related mobility impairment.

A randomised crossover trial in older adults found that Mitoquinol supplementation improved leg-extension power without affecting strength, endurance, or aerobic capacity.

A randomised crossover trial in older adults found that Mitoquinol supplementation improved leg-extension power without affecting strength, endurance, or aerobic capacity. These findings suggest mitochondrial-targeted antioxidants may support specific aspects of physical function linked to mobility and ageing.

A controlled crossover study found that MitoQ reduced pain and improved working memory in fibromyalgia, but showed no benefit in ME/CFS beyond placebo. These findings highlight condition-specific responses to mitochondrial-targeted antioxidants and the importance of study design.

Mitoquinol improved oxidative stress biomarkers in septic shock but did not significantly change organ recovery or mortality, underscoring the complexity of translating redox modulation into clinical benefit.

A randomised controlled trial in older adults found that MitoQ reduced mitochondrial reactive oxygen species but did not restore exercise-induced redox signalling or adaptation. These findings suggest that age-related impairments in muscle adaptation may extend beyond oxidative stress alone.

A randomised controlled trial in healthy men found that MitoQ supplementation did not enhance or impair endurance training adaptations, including VO₂max and mitochondrial capacity. These findings suggest that mitochondria-targeted antioxidants do not disrupt exercise-driven adaptations in low-risk populations.

A randomised controlled trial in women with multiple sclerosis found that MitoQ supplementation, particularly when combined with exercise, modulated inflammatory and immune signalling pathways. These findings support a role for mitochondrial-targeted interventions in influencing neuroinflammation, although clinical benefits require longer-term investigation.

A clinical trial in type 2 diabetes found that MitoQ improved cardiac energetics and diastolic function without altering structural heart measures. These findings highlight mitochondrial dysfunction as an early, modifiable driver of diabetic cardiomyopathy.

A randomised controlled trial found that MitoQ supplementation enhanced exercise-induced PGC‑1α signalling and improved peak power, without affecting VO₂peak or mitochondrial adaptation. These findings highlight a role for mitochondrial-targeted antioxidants in modulating early training responses rather than maximal aerobic performance.

A controlled study in trained cyclists found that MitoQ supplementation improved oxygen uptake kinetics and reduced oxidative stress, without changing maximal performance outcomes. These findings highlight a role for mitochondrial-targeted antioxidants in enhancing exercise efficiency rather than peak capacity.

A randomised controlled trial in trained cyclists found that MitoQ supplementation reduced oxidative stress and influenced vascular signalling pathways, but did not improve VO₂max over four weeks. These findings highlight a disconnect between molecular adaptation and measurable performance outcomes in short-term studies.

A randomised controlled trial in hypertensive adults found that MitoQ supplementation reduced blood pressure, improved cardiac structure, and lowered oxidative stress and inflammation. Effects were strongest when combined with exercise, supporting mitochondrial oxidative stress as a modifiable driver of cardiovascular dysfunction.

A randomised crossover study in healthy young adults found that acute MitoQ supplementation did not improve blood pressure, arterial stiffness, or oxidative stress markers. These findings suggest that mitochondria‑targeted antioxidants are unlikely to influence vascular function in populations with low baseline oxidative stress.

A placebo-controlled trial found that mitochondria-targeted antioxidant supplementation with MitoQ did not improve muscle recovery or reduce soreness following exercise-induced muscle damage in untrained men.

A placebo-controlled pilot trial in stage 3–4 chronic kidney disease found that the mitochondria-targeted antioxidant MitoQ improved endothelial function and stabilised vascular haemodynamics over four weeks.

While mitochondrial oxidative stress remains a key mechanistic target in Parkinson’s disease (PD), the findings of this double-blind clinical trial in early PD highlight the challenges of translating this biology into effective treatment at the point of diagnosis.