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      Monitoring rowers to determine under-performance

      abstract
      2 , , 2 , 2 , 2 , 1 , 1 , 2 , 2
      BMC Sports Science, Medicine and Rehabilitation
      BioMed Central
      World's Leading Rowing Sport Science and Medicine Conference - "Improving Performance Naturally"
      22-25 January 2015

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          Abstract

          Introduction Over the past few years, training load and performance in competition has continuously increased and is fraught with risk to result in the accumulation of fatiguing conditions. The coach determines training success by controlling boat speed, performance, power and soft parameters like stability of rowing technique, capacity to teamwork, and mood state. However, in team sports like rowing, monitoring of individual rowers fatigue to optimize regeneration is difficult. While training should voluntarily cause acute fatigue, the accumulation of training leads to more severe fatigue, which is called “overreaching”. When fatigue is more prolonged and recovery is impaired, the condition is defined as “non-functional overreaching” ending in a primarily unexplained, long-term, and unplanned decreasing performance, a condition defined as “Unexplained Underperformance Syndrome” (UUPS) or “overtraining syndrome” (OTS). Good standards and appropriate markers for diagnosis and treatment are currently lacking. Clinical signs of UUPS / OTS Athletes present with the key symptoms of prolonged underperformance and/or reduced trainability or disturbed regeneration following a period of heavy training load. Mood disturbances like fatigue, lethargy, exhaustion, sleep disturbances, and increased susceptibility to infections are present; athletes experience increased levels of perceived stress, decreased levels of regeneration and burnout. Often, athletes report about previous upper-respiratory-tract infections. Physical signs include muscle pain, non-specific irritation of the mucous membranes, increased heart rate at rest and during a given workload, performance, and maximum oxygen uptake and maximum lactate levels are decreased. Pathogenesis The syndrome has been linked to carbohydrate metabolism, decreased levels of peripheral hormones like catecholamines, and immune malfunction; however, until now, the diagnostic approaches are very limited. Virus reactivation and signs of inflammation are also common in severely overtrained athletes. Carbohydrate metabolism is involved with insulin resistance and increased catabolic hormones like cortisol. Signs of disturbed carbohydrate metabolism are low leptin levels, insulin resistance and reduced maximum lactate. The stress hormones like cortisol or catecholamines are increased in acute situations, however, when fatiguing, the peripheral tissues decrease hormonal receptors which is counter-regulated by increased levels of hypothalamic release hormones, in severe cases the hypothalamic-peripheral axes are disturbed. Metabolic stress will reduce early sex hormone levels like estrogens and testosterone and the release hormones FSH and LH, peripheral thyroid hormones are down regulated as well as TSH. There are parallels between the molecular mechanisms of ‘overtraining syndrome’ and systemic inflammatory reactions in trauma or sepsis. In healthy athletes, training induces a state of acute inflammation, which is rapidly counter-regulated by anti-inflammatory mechanisms. In the fatigued athlete, these mechanisms are disturbed and this leads to chronic inflammation and reduced immune function. Training induces so-called “damage-associated molecular patterns” (damps). These include molecules like free DNA, heat-shock-proteins or uric acid, which are released from the damaged muscle, oxidative stress and immunological signaling of so-called “pattern recognition receptors” (PRRs). These processes can be analyzed in blood samples by measuring inflammatory cytokines IL-1β, IL-8 and TNF-α, whereas a typical anti-inflammatory cytokine is represented by IL-10. Practical approaches We now understand much more of the training processes. In general, this knowledge should lead to an improved performance/recovery balance in athletes and therefore less underperformance and injury, which is the primary goal of any diagnosis. The immunological hypothesis has gained more importance; however, practical measurements in the training process are very limited due to laboratory needs and costs. Therefore, key symptoms of UUPS or OTS are underperformance and/or reduced trainability and disturbed regeneration following a period of heavy training load. Mood and sleep disturbances can be evaluated with questionnaires. Physiological signs are increased heart rate at rest and during a given workload. Rest and recovery measures are the most important treatment in early cases of UUPS/OTS. When the problems are prolonged, a clinical workup including selected blood parameters should be performed.

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          Most cited references3

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          Prevention, diagnosis, and treatment of the overtraining syndrome: joint consensus statement of the European College of Sport Science and the American College of Sports Medicine.

          Successful training not only must involve overload but also must avoid the combination of excessive overload plus inadequate recovery. Athletes can experience short-term performance decrement without severe psychological or lasting other negative symptoms. This functional overreaching will eventually lead to an improvement in performance after recovery. When athletes do not sufficiently respect the balance between training and recovery, nonfunctional overreaching (NFOR) can occur. The distinction between NFOR and overtraining syndrome (OTS) is very difficult and will depend on the clinical outcome and exclusion diagnosis. The athlete will often show the same clinical, hormonal, and other signs and symptoms. A keyword in the recognition of OTS might be "prolonged maladaptation" not only of the athlete but also of several biological, neurochemical, and hormonal regulation mechanisms. It is generally thought that symptoms of OTS, such as fatigue, performance decline, and mood disturbances, are more severe than those of NFOR. However, there is no scientific evidence to either confirm or refute this suggestion. One approach to understanding the etiology of OTS involves the exclusion of organic diseases or infections and factors such as dietary caloric restriction (negative energy balance) and insufficient carbohydrate and/or protein intake, iron deficiency, magnesium deficiency, allergies, and others together with identification of initiating events or triggers. In this article, we provide the recent status of possible markers for the detection of OTS. Currently, several markers (hormones, performance tests, psychological tests, and biochemical and immune markers) are used, but none of them meet all the criteria to make their use generally accepted.
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            Exercise is a potent stimulus for enhancing circulating DNase activity.

            To elucidate cell free DNA (cfDNA) clearance kinetics following an acute bout of high intensity exercise by measuring circulating DNase activity reduction (AR).
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              Thyroid hormones, cytokines, physical training and metabolic control.

              During the acute training response, peripheral cellular mechanisms are mainly metabolostatic to achieve energy supply. During prolonged training, glycogen deficiency occurs; this is associated with increased expression of local cytokines, and decreased insulin secretion and beta-adrenergic stimulation and lipolysis in adipose tissue which looses energy. This is indicated by decrease of adipocyte hormone leptin, which has inhibitory effects on excitatory hypothalamic neurons. Leptin, insulin, and cytokines such as interleukin 6 (IL-6) contribute to the metabolic error signal to the hypothalamus which result in decrease of hypothalamic release hormones and sympathoadrenergic stimulation. Thyroid stimulating hormone (TSH) is correlated to the metabolic hormones leptin and insulin, and may be used as indicator of metabolic control. Because the hypothalamus integrates various error signals (metabolic, hormonal, sensory afferents, and central stimuli), the pituitary's releasing hormones represent the functional status of an athlete. Long-term overtraining will lead to downregulation of hypothalamic hormonal and sympathoadrenergic responses, catabolism, and fatigue. These changes contribute to myopathy with predominant expression of slow muscle fiber type and inadequacy in performance. Thyroid hormones are closely involved in the training response and metabolic control.
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                Author and article information

                Conference
                BMC Sports Sci Med Rehabil
                BMC Sports Sci Med Rehabil
                BMC Sports Science, Medicine and Rehabilitation
                BioMed Central
                2052-1847
                2015
                11 August 2015
                : 7
                : Suppl 1
                : O15
                Affiliations
                [1 ]Division of Experimental Anesthesiology; University of Ulm, Ulm, Germany
                [2 ]Division of Sports- und Rehabilitation Medicine, University of Ulm, Ulm, Germany
                Article
                2052-1847-7-S1-O15
                10.1186/2052-1847-7-S1-O15
                4535195
                cc5c2c6b-cee0-445e-bb96-44663a4053e1
                Copyright © 2015 Steinacker et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                World's Leading Rowing Sport Science and Medicine Conference - "Improving Performance Naturally"
                Marlow, UK
                22-25 January 2015
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