Can sleep be used as an indicator of overreaching and overtraining in athletes?

Heales, LJ ORCiD: 0000-0002-4510-3324; Lastella, AM ORCiD: 0000-0003-1793-3811; Sargent, C ORCiD: 0000-0001-5340-4701; Vincent, GE ORCiD: 0000-0002-7036-7823To achieve optimal athletic performance and competition readiness, it is crucial to balance the highest appropriate training stimulus with sufficient recovery. Excessive and/or progressive increases in training load are integral to improving athletic performance (Halson, 2014). However, increased training loads and/or inadequate recovery can result in maladaptation to training, and if continued, can lead to the development of overreaching/overtraining (Meeusen et al., 2013; Cadegiani and Kater, 2017). In terms of recovery, sleep is an essential component of an athlete’s recuperation due to its physiological and psychological restorative effects (Dinges et al., 1997; Pejovic et al., 2013). Sleep quantity and quality declines following augmented increases (+30%) in training load (Hausswirth et al., 2014), and poor sleep is a common complaint among overreached and/or overtrained athletes (Wall et al., 2003). Regardless of whether reduced sleep is a cause or effect of overreaching and/or overtraining, it is possible that measures of sleep could serve as an indicator of the presence of overreaching and/or overtraining. This opinion article will examine the current research underpinning the relationship between insufficient sleep and the development of overreaching/overtraining, describe the implications for practitioners (e.g., sport and exercise scientists, coaches), and identify areas for future research

PINK1 Is Necessary for Long Term Survival and Mitochondrial Function in Human Dopaminergic Neurons

Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to investigate the role of PINK1 in Parkinson's disease, we studied PINK1 loss of function in human and primary mouse neurons. Using RNAi, we created stable PINK1 knockdown in human dopaminergic neurons differentiated from foetal ventral mesencephalon stem cells, as well as in an immortalised human neuroblastoma cell line. We sought to validate our findings in primary neurons derived from a transgenic PINK1 knockout mouse. For the first time we demonstrate an age dependent neurodegenerative phenotype in human and mouse neurons. PINK1 deficiency leads to reduced long-term viability in human neurons, which die via the mitochondrial apoptosis pathway. Human neurons lacking PINK1 demonstrate features of marked oxidative stress with widespread mitochondrial dysfunction and abnormal mitochondrial morphology. We report that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine. In addition we provide evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in PINK1 deficiency. The phenotypic effects of PINK1 loss-of-function described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD

Saltwater ecotoxicology of Ag, Au, CuO, TiO2, ZnO and C60 engineered nanoparticles: An overview

This review paper examined 529 papers reporting experimental nanoecotoxicological original data. Only 126 papers referred to saltwater environments (water column and sediment) including a huge variety of species (n=51), their relative endpoints and engineered nanoparticles (ENPs) (n=38). Wetried to provide a synthetic overview of the ecotoxicological effects of ENPs from existing data, refining papers on the basis of cross-cutting selection criteria and supporting a “mind the gap” approach stressing on missing data for hazard and risk assessment. After a codified selection procedure, attention was paid to Ag, Au, CuO, TiO2, ZnO and C60 ENPs, evidencing and comparing the observed nanoecotoxicity range of effect. Several criticisms were evidenced: i) some model organisms are overexploited like microalgae and molluscs compared to annelids, echinoderms and fish; ii) underexploited model organisms: mainly bacteria and fish; iii) exposure scenario variability: high speciesspecific and ENP scenarios including organismlife stage and way of administration/spiking of toxicants; iv) scarce comparability between results due to exposure scenario variability; v) micro- and mesocosms substantially unexplored; vi) mixture effects: few examples are available only for ENPs and traditional pollutants; mixtures of ENPs have not been investigated yet; vii) effects of ions and ENPs: nAg, nCuO and nZnO toxicity aetiology is still a matter of discussion; viii) size and morphology effects of ENPs: scarcely investigated, justified and understood. Toxicity results evidenced that: nAu N nZnO N nAg N nCuO N nTiO2 N C60

Diagnostic ultrasound imaging for lateral epicondylalgia: A case-control study

Heales, LJ ORCiD: 0000-0002-4510-3324Copyright © 2014 by the American College of Sports Medicine.Introduction: Lateral epicondylalgia (LE) is clinically diagnosed as pain over the lateral elbow that is provoked by gripping. Usually, LE responds well to conservative intervention; however, those who fail such treatment require further evaluation, including musculoskeletal ultrasound. Previous studies of musculoskeletal ultrasound have methodological flaws, such as lack of assessor blinding and failure to control for participant age, sex, and arm dominance. The purpose of this study was to assess the diagnostic use of blinded ultrasound imaging in people with clinically diagnosed LE compared with that in a control group matched for age, sex, and arm dominance.Methods: Participants (30 with LE and 30 controls) underwent clinical examination as the criterion standard test. Unilateral LE was defined as pain over the lateral epicondyle, which was provoked by palpation, resisted wrist and finger extension, and gripping. Controls without symptoms were matched for age, sex, and arm dominance. Ultrasound investigations were performed by two sonographers using a standardized protocol. Grayscale images were assessed for signs of tendon pathology and rated on a four-point ordinal scale. Power Doppler was used to assess neovascularity and rated on a five-point ordinal scale.Results: The combination of grayscale and power Doppler imaging revealed an overall sensitivity of 90% and specificity of 47%. The positive and negative likelihood ratios for combined grayscale and power Doppler imaging were 1.69 and 0.21, respectively.Conclusions: Although ultrasound imaging helps confirm the absence of LE, when findings are negative for tendinopathic changes, the high prevalence of tendinopathic changes in pain-free controls challenges the specificity of the measure. The validity of ultrasound imaging to confirm tendon pathology in clinically diagnosed LE requires further study with strong methodology

Spectrum of movement disorders and neurotransmitter abnormalities in paediatric POLG disease

Objectives To describe the spectrum of movement disorders and cerebrospinal fluid (CSF) neurotransmitter profiles in paediatric patients with POLG disease. Methods We identified children with genetically confirmed POLG disease, in whom CSF neurotransmitter analysis had been undertaken. Clinical data were collected retrospectively. CSF neurotransmitter levels were compared to both standardised age‐related reference ranges and to non‐POLG patients presenting with status epilepticus. Results Forty‐one patients with POLG disease were identified. Almost 50% of the patients had documented evidence of a movement disorder, including non‐epileptic myoclonus, choreoathetosis and ataxia. CSF neurotransmitter analysis was undertaken in 15 cases and abnormalities were seen in the majority (87%) of cases tested. In many patients, distinctive patterns were evident, including raised neopterin, homovanillic acid and 5‐hydroxyindoleacetic acid levels. Conclusions Children with POLG mutations can manifest with a wide spectrum of abnormal movements, which are often prominent features of the clinical syndrome. Underlying pathophysiology is probably multifactorial, and aberrant monoamine metabolism is likely to play a role.</p

Spectrum of movement disorders and neurotransmitter abnormalities in paediatric POLG disease

Objectives To describe the spectrum of movement disorders and cerebrospinal fluid (CSF) neurotransmitter profiles in paediatric patients withandnbsp;POLGandnbsp;disease. Methods We identified children with genetically confirmedandnbsp;POLGandnbsp;disease, in whom CSF neurotransmitter analysis had been undertaken. Clinical data were collected retrospectively. CSF neurotransmitter levels were compared to both standardised age‐related reference ranges and to non‐POLGandnbsp;patients presenting with status epilepticus. Results Forty‐one patients withandnbsp;POLGandnbsp;disease were identified. Almost 50% of the patients had documented evidence of a movement disorder, including non‐epileptic myoclonus, choreoathetosis and ataxia. CSF neurotransmitter analysis was undertaken in 15 cases and abnormalities were seen in the majority (87%) of cases tested. In many patients, distinctive patterns were evident, including raised neopterin, homovanillic acid and 5‐hydroxyindoleacetic acid levels. Conclusions Children withandnbsp;POLGandnbsp;mutations can manifest with a wide spectrum of abnormal movements, which are often prominent features of the clinical syndrome. Underlying pathophysiology is probably multifactorial, and aberrant monoamine metabolism is likely to play a role.</p

Normal rates of whole-body fat oxidation and gluconeogenesis after overnight fasting and moderate-intensity exercise in patients with medium-chain acyl-CoA dehydrogenase deficiency.

BACKGROUND: Impairments in gluconeogenesis have been implicated in the pathophysiology of fasting hypoglycemia in medium-chain acyl-CoA dehydrogenase deficiency. However, whole body glucose and fat metabolism have never been studied in vivo. METHODS: Stable isotope methodology was applied to compare fat and glucose metabolism between four adult patients with MCADD and four matched controls both at rest and during 1.5 h of moderate-intensity exercise. Additionally, intramyocellular lipid and glycogen content and intramyocellular acylcarnitines were assessed in muscle biopsies collected prior to and immediately after cessation of exercise. RESULTS: At rest, plasma FFA turnover was significantly higher in patients with MCADD, whereas the plasma FFA concentrations did not differ between patients and controls. Blood glucose kinetics did not differ between groups both at rest and during exercise. Palmitate and FFA turnover, total fat and carbohydrate oxidation rates, the use of muscle glycogen and muscle derived triglycerides during exercise did not differ between patients and controls. Plasma FFA oxidation rates were significantly lower in patients at the latter stages of exercise. Free carnitine levels in muscle were lower in patients, whereas no differences were detected in muscle acetylcarnitine levels. CONCLUSIONS: Whole-body or skeletal muscle glucose and fat metabolism were not impaired in adult patients with MCADD. This implies that MCADD is not rate limiting for energy production under the conditions studied. In addition, patients with MCADD have a higher FFA turnover rate after overnight fasting, which may stimulate ectopic lipid deposition and, as such, make them more susceptible for developing insulin resistance