71 research outputs found

    Exercise during growth: compelling evidence for the primary prevention of osteoporosis?

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    The effect of exercise and nutrition on the mechanostat

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    In this review, we discuss the effect of increased and decreased loading and nutrition deficiency on muscle and bone mass and strength (and bone length and architecture) independently and combined. Both exercise and nutrition are integral components of the mechanostat model but both have distinctly different roles. Mechanical strain imparted by muscle action is responsible for the development of the external size and shape of the bone and subsequently the bone strength. In contrast, immobilization during growth results in reduced growth in bone length and a loss of bone strength due to large losses in bone mass (a result of endosteal resorption in cortical bone and trabecular thinning) and changes in geometry (bone shafts do not develop their characteristic shape but rather develop a rounded default shape). The use of surrogate measures for peak muscle forces acting on bone (muscle strength, size, or mass) limits our ability to confirm a cause-and-effect relationship between peak muscle force acting on bone and changes in bone strength. However, the examples presented in this review support the notion that under adequate nutrition, exercise has the potential to increase peak muscle forces acting on bone and thus can lead to a proportional increase in bone strength. In contrast, nutrition alone does not influence muscle or bone in a dose-dependent manner. Muscle and bone are only influenced when there is nutritional deficiency &ndash; and in this case the effect is profound. Similar to immobilization, the immediate effect of malnutrition is a reduction in longitudinal growth. More specifically, protein and energy malnutrition results in massive bone loss due to endosteal resorption in cortical bone and trabecular thinning. Unlike loading however, there is indirect evidence that severe malnutrition when associated with menstrual dysfunction can shift the mechanostat set point upward, thus leading to less bone accrual for a given amount of bone strain.<br /

    Does elite competition inhibit growth and delay maturation in some gymnasts? quite possibly

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    Today, elite young gymnasts undertake training programs of progressive volume and intensity from an early age. For example, talented young female gymnasts often commence training at age 5 or 6 and train more than 20 to 30 hours per week year-round throughout childhood and adolescence. Despite the &quot;normal&quot; short stature of top-level gymnasts and the obvious health benefits of physical activity during growth, there is concern that elite level or those gymnasts involved in heavy training regimens may be at risk for adverse effects on growth and maturation. This concern has been the source of much debate in the literature and is complicated by the difficulties in distinguishing between the genetic predisposition to short stature and late or delayed maturation, and the effect of environmental factors such as nutrition and exercise that may influence growth and maturation. The effect of gymnastics training on growth and maturation is often reported as averaged data: an approach that does not identify individual growth patterns. Finding no difference between groups is not proof that there is &quot;in fact&quot; no difference. Accepting the null hypothesis without the appropriate critical review of both the methodological and statistical power to detect differences is a flawed endeavor. We believe there is compelling &quot;circumstantial&quot; evidence to build a case that preparation for advanced gymnastics competition may place some children and youth at risk of reduced growth and delayed maturation.<br /

    Asymptomatic Achilles tendon pathology is associated with a central fat distribution in men and a peripheral fat distribution in women: a cross sectional study of 298 individuals

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    <p>Abstract</p> <p>Background</p> <p>Adiposity is a modifiable factor that has been implicated in tendinopathy. As tendon pain reduces physical activity levels and can lead to weight gain, associations between tendon pathology and adiposity must be studied in individuals without tendon pain. Therefore, the purpose of this study was to determine whether fat distribution was associated with asymptomatic Achilles tendon pathology.</p> <p>Methods</p> <p>The Achilles tendons of 298 individuals were categorised as normal or pathological using diagnostic ultrasound. Fat distribution was determined using anthropometry (waist circumference, waist hip ratio [WHR]) and dual-energy x-ray absorptiometry.</p> <p>Results</p> <p>Asymptomatic Achilles tendon pathology was more evident in men (13%) than women (5%) (p = 0.007). Men with tendon pathology were older (50.9 ± 10.4, 36.3 ± 11.3, p < 0.001), had greater WHR (0.926 ± 0.091, 0.875 ± 0.065, p = 0.039), higher android/gynoid fat mass ratio (0.616 ± 0.186, 0.519 ± 0.142, p = 0.014) and higher upper-body/lower body fat mass ratio (2.346 ± 0.630, 2.022 ± 0.467, p = 0.013). Men older than 40 years with a waist circumference >83 cm had the greatest prevalence of tendon pathology (33%). Women with tendon pathology were older (47.4 ± 10.0, 36.0 ± 10.3, p = 0.008), had less total fat (17196 ± 3173 g, 21626 ± 7882 g, p = 0.009), trunk fat (7367 ± 1662 g, 10087 ± 4152 g, p = 0.003) and android fat (1117 ± 324 g, 1616 ± 811 g, p = 0.005). They had lower central/peripheral fat mass ratios (0.711 ± 0.321 g, 0.922 ± 0.194 g, p = 0.004) than women with normal tendons. Women with tendon pathology were more often menopausal (63%, 13%, p = 0.002).</p> <p>Conclusions</p> <p>Men with Achilles tendon pathology were older and had a central fat distribution. Women with tendon pathology were older and had a peripheral fat distribution. An interaction between age and waist circumference was observed among men.</p

    The structural adaptations of cortical bone to loading during different stages of maturation

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    Thermoregulation in young athletes exercising in hot environments.

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    Children are less efficient thermoregulators than are adults. During exercise, sweat evaporation is the most important physiological means of cooling the body. The sweat response in children, however, is less efficient than in adults, so children dissipate less heat though evaporative sweating and more through convection (the loss of heat through the skin) plus radiation. Children and adolescents with high levels of body fat and heavy builds are more susceptible to heat stress because they dissipate body heat less efficiently. Maintaining adequate hydration is crucial for preventing heat stress, Although water is often described as the best choice of fluid, studies on voluntary drinking habits and flavor preferences in children and adolescents suggest that greater consumption occurs when sports drinks are offered instead of water. Although a child\u27s sweat contains less sodium and chloride than an adult\u27s does, there appears to be no evidence that a child\u27s performance improves when given beverages more diluted than those currently recommended for adults, More information is necessary to identify the optimal electrolyte and carbohydrate content of sports drinks for young athletes.<br /

    Exercise to prevent and treat osteoporosis

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    An algorithm to guide exercise prescription for the prevention and management of osteoporosis

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    Menstrual dysfunction and bone health in female athletes

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    Female athletes are generally considered to be at Iow risk of osteoporosis because of the skeletal loading associated with sports participation. Sites that are exposed to long-term high-impact loading are consistently reported to be higher than the same sites in their sedentary peers. However, weight-bearing exercise does not always ensure that athletes will have high bone-mineral density, as the hormonal environment, dietary factors, and loading history all influence bone-mineral density, In particular, menstrual dysfunction, which can occur with intense training or disordered eating, is a significant risk factor for Iow bone-mineral density. Exercise history before menstrual dysfunction is likely to offer some protection for Iow bone-mineral density, particularly at the hip, Resumption of menses is unlikely to restore bone-mineral density to levels reported in eumenorrheic athletes or even sedentary peers, Athletes at risk of amenorrhea should be identified and their training loads and energy intakes monitored to ensure normal menstrual function, Athletes who remain amenorrheic should be counseled about the possible negative effects of amenorrhea and monitored for bone loss. Early intervention is recommended for amenorrheic athletes with Iow bone-mineral density.<br /
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