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High-intensity interval training increase mitochondrial performance.

vitamin D improves mitochondrial function through improved oxidative phosporylation.

T3 increases mitochondrial oxidative phosphorylation. This has huge impacts on which hypothyroidism is currently managed (only evaluate TSH and T4) and disease implication. We know that decoupling of oxidative phosporylation and a shift to glycolysis and glutaminolysis (substrate-level phosphorylation) results in genomic mutability and cancer, then a low T3 has implications in cancer prevention

Testosterone and insulin resistance.  Testosterone improves insulin sensitivity and mitochondrial function.

T3 induces beneficial oxidative changes in muscles through its interaction with mitochondrial receptors.  PGC-1alpha and PPAR-gamma were involved in this process.  The important point here is that T3 is increasing oxidative function of muscle through interaction with mitochondria.

NAD found to slow mitochondrial decline associated with aging.  SIRT1 is involved; interesting of note is the inverse association with HIF-1alpha

NAD in the form of nicotinamide riboside found to be effective in treating mitochondrial myopathy in animal model.

Testosterone improves insulin resistance and mitochondrial function in those men with low Testosterone.

Bioidentical progesterone shown to reduce post TBI mitochondrial dysfunction. This has significant implications on the ability of the damaged brain to heal and recover, thus limiting post-injury cognitive deficits.

TCE shown to mitochondrial toxic and risk factor for Parkinson's disease

study links mitochondrial dysfunction to Parkinson's disease. 

Huperzine A, a natural acetylcholinesterase inhibitor, provides neuroprotection through increase mitochondrial function and decrease in accumulated amyloid Beta protein.

T3 is major regulator of mitochondrial activity; not T4

mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis

Omega-3 improves mitochondrial function and thus chronic fatigue

Discussion of the mitochondrial role in chronic fatigue syndrome.  As the authors conclude, there is dysfunction, but whether the cause is primary or secondary or likely varies from individual to individual is yet undetermined.

very helpful post!

Only abstract available.  Loss of glutathione leads to loss in mitochondrial DNA.

DCA works in synergy, augments, effects of anti-mitochondrial chemo agents cisplatin and topetecan

More recent study finds that ivermectin induces apoptosis in leukemia cell lines via oxidative stress and mitochondrial disruption.