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      HIIT'ing or MISS'ing the Optimal Management of Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis of High- Versus Moderate-Intensity Exercise Prescription

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          Abstract

          Introduction: Polycystic Ovary syndrome (PCOS) is a metabolic disorder associated with increased cardiovascular disease risk. Exercise is an effective treatment strategy to manage symptoms and reduce long-term health risk. High-intensity interval training (HIIT) has been suggested as a more efficient exercise mode in PCOS; however, it is not clear whether HIIT is superior to moderate intensity steady state exercise (MISS).

          Methods: We synthesized available data through a systematic review and meta-analysis to compare the effectiveness of isolated HIIT and MISS exercise interventions. Our primary outcome measures were cardiorespiratory fitness and insulin resistance, measured using V ˙ O 2max and HOMA-IR respectively.

          Results: A total of 16 studies were included. Moderate-quality evidence from 16 studies identified significant improvements in V ˙ O 2max following MISS (Δ = 1.081 ml/kg/min, p < 0.001, n = 194), but not HIIT (Δ = 0.641 ml/kg/min, p = 0.128, n = 28). Neither HIIT nor MISS improved HOMA-IR [(Δ = −0.257, p = 0.374, n = 60) and (Δ = −0.341, p = 0.078, n = 159), respectively].

          Discussion: A significant improvement in V ˙ O 2max was evident following MISS, but not HIIT exercise in women with PCOS. This contrasts with previous literature in healthy and clinical cohorts that report superior benefits of HIIT. Therefore, based on available moderate-quality evidence, HIIT exercise does not provide superior outcomes in V ˙ O 2max compared with MISS, although larger high-quality interventions are needed to fully address this. Additional dietary/pharmacological interventions may be required in conjunction with exercise to improve insulin sensitivity.

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          Most cited references73

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          Meta-analysis in clinical trials

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            Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

            Abstract Aims To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD). Methods and results We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects. Conclusion Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
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              Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS)

              (2004)
              Since the 1990 NIH-sponsored conference on polycystic ovary syndrome (PCOS), it has become appreciated that the syndrome encompasses a broader spectrum of signs and symptoms of ovarian dysfunction than those defined by the original diagnostic criteria. The 2003 Rotterdam consensus workshop concluded that PCOS is a syndrome of ovarian dysfunction along with the cardinal features hyperandrogenism and polycystic ovary (PCO) morphology. PCOS remains a syndrome and, as such, no single diagnostic criterion (such as hyperandrogenism or PCO) is sufficient for clinical diagnosis. Its clinical manifestations may include: menstrual irregularities, signs of androgen excess, and obesity. Insulin resistance and elevated serum LH levels are also common features in PCOS. PCOS is associated with an increased risk of type 2 diabetes and cardiovascular events.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                16 August 2021
                2021
                : 12
                : 715881
                Affiliations
                [1] 1School of Sport and Health Sciences, Cardiff Metropolitan University , Cardiff, United Kingdom
                [2] 2Program for Pregnancy and Postpartum Health, Faculty of Kinesiology, Sport, and Recreation, Women and Children's Health Research Institute, Alberta Diabetes Institute, University of Alberta , Edmonton, AB, Canada
                [3] 3Neuroscience and Mental Health Research Institute, School of Medicine, Cardiff University , Cardiff, United Kingdom
                Author notes

                Edited by: Trine Moholdt, Norwegian University of Science and Technology, Norway

                Reviewed by: Rhiannon Kate Patten, Victoria University, Australia; Jamie Benham, University of Calgary Cumming School of Medicine, Canada

                *Correspondence: Rachel N. Lord rnlord@ 123456cardiffmet.ac.uk

                This article was submitted to Exercise Physiology, a section of the journal Frontiers in Physiology

                Article
                10.3389/fphys.2021.715881
                8415631
                09006d0f-cb56-4370-be8a-6368353fa150
                Copyright © 2021 Richards, Meah, James, Rees and Lord.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 27 May 2021
                : 19 July 2021
                Page count
                Figures: 5, Tables: 2, Equations: 2, References: 74, Pages: 14, Words: 9353
                Funding
                Funded by: Waterloo Foundation 10.13039/100012107
                Categories
                Physiology
                Systematic Review

                Anatomy & Physiology
                pcos,exercise,moderate-intensity,high-intensity,insulin resistance,cardiorespiratory fitness,cardiometabolic risk

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