Purpose: To examine a diagnosis of unexplained underperformance syndrome (UUPS, or overtraining syndrome) in an international rower describing a full recovery and return to elite competition the same year.
Methods: On diagnosis and 4 and 14 mo postdiagnosis, detailed assessments including physiological, nutritional, and biomarkers were made.
Results: Clinical examination and laboratory results for hematology, biochemistry, thyroid function, immunology, vitamins, and minerals were unremarkable and did not explain the presentation and diagnosis. Redox biomarkers including hydroperoxides, plasma antioxidant capacity, red blood cell glutathione, superoxide dismutase, coenzyme Q10, vitamin E (α- and γ-tocopherol), and carotenoids (lutein, α-carotene, β-carotene) provided evidence of altered redox homeostasis. The recovery strategy began with 12 d of training abstinence and nutritional interventions, followed by 6 wk of modified training. At 4 mo postintervention, performance had recovered strongly, resulting in the athlete's becoming European champion that same year. Further improvements in physiological and performance indices were observed at 14 mo postintervention. Physiologically relevant increases in concentrations of carotenoids were achieved at each postintervention time point, exceeding the reported critical-difference values.
Conclusions: Increasing athlete phytonutrient intake may enhance recovery and tolerance of training and environmental stressors, reducing the risk of unexplained UUPS. Alterations in redox homeostasis should be considered as part of the medical management in UUPS. This is the first reported case study of an elite athlete with alterations in redox homeostasis in conjunction with a diagnosis of UUPS.
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http://dx.doi.org/10.1123/ijspp.2016-0777 | DOI Listing |
Int J Biol Macromol
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College of Chemistry & Pharmacy, Northwest A&F University, Yangling, Shaanxi 712100, PR China. Electronic address:
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Department of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain; Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, 08028 Barcelona, Spain. Electronic address:
The redox state of proteins is essential for their function and guarantees cell fitness. Peroxiredoxins protect cells against oxidative stress, maintain redox homeostasis, act as chaperones, and transmit hydrogen peroxide signals to redox regulators. Despite the profound structural and functional knowledge of peroxiredoxins action, information on how the different functions are concerted is still scarce.
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January 2025
Instituto de Matemática e Estatística, Departamento de Ciência da Computação, Universidade de São Paulo, Rua do Matão 1010, São Paulo 05508-090, SP, Brazil.
The tumor suppressor p53, in its wild-type form, plays a central role in cellular homeostasis by regulating senescence, apoptosis, and autophagy within the DNA damage response (DDR). Recent findings suggest that wild-type p53 also governs ferroptosis, an iron-dependent cell death process driven by lipid peroxidation. Post-translational modifications of p53 generate proteoforms that significantly enhance its functional diversity in regulating these mechanisms.
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Laboratory of Biochemistry and Vascular Biology, Center for Biologics Evaluation and Research, Food and Drug Administration (FDA), Silver Spring, Maryland, USA.
The mitochondria play a key role in maintaining oxygen homeostasis under normal oxygen tension (normoxia) and during oxygen deprivation (hypoxia). This is a critical balancing act between the oxygen content of the blood, the tissue oxygen sensing mechanisms, and the mitochondria, which ultimately consume most oxygen for energy production. We describe the well-defined role of the mitochondria in oxygen metabolism with a special focus on the impact on blood physiology and pathophysiology.
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Department of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang 261031, Shandong Province, China.
Pancreatic Cancer (PC) is a devastating malignancy with a poor prognosis and in-creasing morbidity. Current treatment strategies have limited efficacy in improving patient survival. Metabolic reprogramming is a hallmark of cancer and plays a key role in the pro-gression and maintenance of PC.
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