The mitochondrial profile in women with polycystic ovary syndrome: impact of exercise

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting pre-menopausal women, and involves metabolic dysregulation. Despite the high prevalence of insulin resistance, the existence of mitochondrial dysregulation and its role in the pathogenesis of PCOS is not clear. Exercise is recommended as first-line therapy for women with PCOS. In particular, high-intensity interval training (HIIT) is known to improve metabolic health and enhance mitochondria characteristics. In this narrative review the existing knowledge of mitochondrial characteristics in skeletal muscle and adipose tissue of women with PCOS, and the effect of exercise interventions in ameliorating metabolic and mitochondrial health in these women are discussed. Even though the evidence on mitochondrial dysfunction in PCOS is limited, some studies point to aberrant mitochondrial functions mostly in skeletal muscle, while there is very little research in adipose tissue. Although most exercise intervention studies in PCOS report improvements in metabolic health, they show diverse and inconclusive findings in relation to mitochondrial characteristics. A limitation of the current studies are the lack of comprehensive mitochondrial analyses and the diversity in exercise modalities, with only one study investigating the impact of HIIT alone. Therefore, further comprehensive large-scale exercise intervention studies are required to understand the association between metabolic dysfunction and aberrant mitochondrial profile, and the molecular mechanisms underlying the exercise-induced metabolic adaptations in women with PCOS.

Validation of mitochondrial biomarkers and immune dynamics in polycystic ovary syndrome

“…New research highlighted a direct link between PCOS incidence and mitochondrial dysfunction. 31,32 In our study, MitoDEGs were selected from among the three datasets mitochondrial-related genes that overlapped with the previously described DEGs. Figure 4A shows the overall number of MitoDEGs, which included 21 upregulated and 17 downregulated genes.…”

Modulation of the Inflammatory Response in Polycystic Ovary Syndrome (PCOS)—Searching for Epigenetic Factors

“…It has been demonstrated that mtDNMT1 expression in the mitochondrial matrix is upregulated by the transcription factors involved in mitochondrial biogenesis that activate the expression of nuclear-encoded mitochondrial genes in response to hypoxia and loss of p53, such as nuclear respiratory factor 1 (NRF-1), peroxisome proliferator activated receptor gamma coactivator-1 alpha (PGC-1α), and mitochondrial transcription factor A (TFAM) [ 101 ]. Thus, polymorphisms in the NRF-1, PGC-1α, and TFAM genes may be associated with different mitochondrial biogenesis in women with PCOS and therefore epigenetically modulate the pattern of response to oxidative stress [ 106 , 107 ].…”

Metabolic and Molecular Mechanisms of Diet and Physical Exercise in the Management of Polycystic Ovarian Syndrome

“…In PCOS women, the mitochondrial DNA copy number is lower compared to women not affected by PCOS, and several mtDNA mutations occur in response to the insulin resistance and hyperandrogenism which enhance the oxidative stress, causing mtDNA abnormalities [ 160 ]. Different kinds of training protocols have demonstrated that exercise improves mitochondrial biogenesis and respiration upregulating PGC-1α expression [ 161 ] that is crucial for the transcriptional control of mitochondrial functions [ 162 ], even though further studies are needed to evaluate the effective role of exercise on mitochondria in PCOS.…”