973 resultados para resistance exercise


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Optimal bone metabolism is the result of hormonal, nutritional, and mechanical harmony, and a deficit in one area is usually impossible to overcome by improvements in others. Exercise during growth influences bone modeling locally at the regions being loaded, whereas calcium is thought to act systemically to influence bone remodeling. Despite acting through different mechanisms, a growing body of research suggests that exercise and calcium may not operate independently. Low dietary calcium intake or reduced bioavailability may minimize the adaptive response to exercise-induced bone loading. Conversely, adequate levels of calcium intake can maximize the positive effect of physical activity on bone health during the growth period of children and adolescents. Research also suggests that adequate levels of calcium intake can maximize bone density at the regions being loaded during exercise. Achieving optimal bone health and minimizing one’s risk of osteoporotic fracture later in life depend on a lifelong approach. This approach relies on the establishment of an optimum level of bone during the growth years, with a subsequent goal to maintain and slow the rate of age-related bone loss thereafter. Exercise, adequate nutrition, and optimal hormone levels are the components that influence the bone outcome. Making healthy nutritional choices, engaging in weight-bearing physical activity, and ensuring optimal hormone levels during growth provides a window of opportunity to build optimal bone mass, to reduce the risk of fracture later in life. Concurrent management of fracture risk with a physical activity prescription, adequate nutrition, and pharmacotherapy for osteoporosis when required offers the best approach to optimal bone health throughout adulthood.

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Hormesis enco 16 mpasses the notion that low levels of stress stimulate or upregulate 17 existing cellular and molecular pathways that improve the capacity of cells and organisms to 18 withstand greater stress. This notion underlies much of what we know about how exercise 19 conditions the body and induces long-term adaptations. During exercise, the body is 20 exposed to various forms of stress, including thermal, metabolic, hypoxic, oxidative, and 21 mechanical stress. These stressors activate biochemical messengers, which in turn activate 22 various signaling pathways that regulate gene expression and adaptive responses. 23 Historically, antioxidant supplements, nonsteroidal anti-inflammatory drugs, and 24 cryotherapy have been favored to attenuate or counteract exercise-induced oxidative stress 25 and inflammation. However, reactive oxygen species and inflammatory mediators are key 26 signaling molecules in muscle, and such strategies may mitigate adaptations to exercise. 27 Conversely, withholding dietary carbohydrate and restricting muscle blood flow during 28 exercise may augment adaptations to exercise. In this review article, we combine, integrate, 29 and apply knowledge about the fundamental mechanisms of exercise adaptation. We also 30 critically evaluate the rationale for using interventions that target these mechanisms under 31 the overarching concept of hormesis. There is currently insufficient evidence to establish 32 whether these treatments exert dose-dependent effects on muscle adaptation. However, 33 there appears to be some dissociation between the biochemical/molecular effects and 34 functional/performance outcomes of some of these treatments. Although several of these 35 treatments influence common kinases, transcription factors and proteins, it remains to be 36 determined if these interventions complement or negate each other, and whether such 37 effects are strong enough to influence adaptations to exercise.

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In spite of increasing gender diversity in employment roles, presumptions persist about the gender of people employed in particular occupations. Focusing on healthcare data collected in Australia and the United Kingdom within the past decade, we use Conversation Analysis (CA) to identify how presumptions about gender are displayed within social interaction through the use of gender-specific pronouns. We show how gender-specific pronouns are asymmetrically selected on the basis of a referent’s occupations, with gender-unspecified members of traditionally male occupations (e.g. doctors) referred to with masculine pronouns and gender-unspecified members of traditionally female occupations (e.g. nurses) referred to with feminine pronouns. We also explore ways people avoid making such presumptions. Our analysis therefore reveals a state of flux in contemporary social life, with instances in which gender presumptions persist as well as attempts to employ person references that reflect contemporary social dynamics.

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Cisplatin (cis-diamminedichloroplatinum (II)), is a platinum based chemotherapeutic employed in the clinic to treat patients with lung, ovarian, colorectal or head and neck cancers. Cisplatin acts to induce tumor cell death via multiple mechanisms. The best characterized mode of action is through irreversible DNA cross-links which activate DNA damage signals leading to cell death via the intrinsic mitochondrial apoptosis pathway. However, the primary issue with cisplatin is that while patients initially respond favorably, sustained cisplatin therapy often yields chemoresistance resulting in therapeutic failure. In this chapter, we review the DNA damage and repair pathways that contribute to cisplatin resistance. We also examine the cellular implications of cisplatin resistance that may lead to selection of subpopulations of cells within a tumor. In better understanding the mechanisms conferring cisplatin resistance, novel targets may be identified to restore drug sensitivity.

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This article conceptualises ‘participatory reluctance’ as a particular orientation to social media that problematises binarised notions of connection and disconnection in social networking sites. It qualitatively examines how the concept has functioned within gay men’s social networking service, Gaydar, among 18- to 28-year-old users of the site in Brisbane, Australia. Participatory reluctance is shown to be a central aspect of the culture of this space, fostered among the studied demographic by the convergence of the growing global push for marriage equality and increasing normalisation of the kinds of gay male identities commonly adopted among this group, with three key factors rooted primarily in Gaydar’s design: (1) young users’ perceptions of the site as a space for procuring casual sex; (2) their perceptions of the imagined user as embodying existing stereotypes of gay masculinity, and; (3) a lack of genuine alternatives in terms of niche digital spaces for gay men’s social networking.

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Increased concentrations of biomarkers reflecting myocardial stress such as cardiac troponin I and T and brain natriuretic peptide (BNP) have been observed following strenuous, long-lasting endurance exercise. The pathophysiological mechanisms are still not fully elucidated and the interpretations of increased post-exercise concentrations range from (i) evidence for exercise-induced myocardial damage to (ii) non-relevant spurious troponin elevations, presumably caused by assay imprecision or heterophilic antibodies. Several lines of evidence suggest that inflammatory processes or oxidative stress could be involved in the rise of NT-proBNP and Troponin observed in critically ill patients with sepsis or burn injury. We tested the hypothesis that inflammatory or oxidative stress is also responsible for exercise-induced cardiomyocyte strain in a large cohort of triathletes following an Ironman triathlon. However, the post-race increase in cardiac troponin T and NT-proBNP was not associated with several markers of exercise-induced inflammation, oxidative stress or antioxidant vitamins. Therefore, we clearly need more studies with other inflammatory markers and different designs to elucidate the scientific background for increases in myocardial stress markers following strenuous endurance events.

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Both a systemic inflammatory response as well as DNA damage has been observed following exhaustive endurance exercise. Hypothetically, exercise-induced DNA damage might either be a consequence of inflammatory processes or causally involved in inflammation and immunological alterations after strenuous prolonged exercise (e.g. by inducing lymphocyte apoptosis and lymphocytopenia). Nevertheless, up to now only few studies have addressed this issue and there is hardly any evidence regarding a direct relationship between DNA or chromosomal damage and inflammatory responses in the context of exercise. The most conclusive picture that emerges from available data is that reactive oxygen and nitrogen species (RONS) appear to be the key effectors which link inflammation with DNA damage. Considering the time-courses of inflammatory and oxidative stress responses on the one hand and DNA effects on the other the lack of correlations between these responses might also be explained by too short observation periods. This review summarizes and discusses the recent findings on this topic. Furthermore, data from our own study are presented that aimed to verify potential associations between several endpoints of genome stability and inflammatory, immune-endocrine and muscle damage parameters in competitors of an Ironman triathlon until 19 days into recovery. The current results indicate that DNA effects in lymphocytes are not responsible for exercise-induced inflammatory responses. Furthermore, this investigation shows that inflammatory processes, vice versa, do not promote DNA damage, neither directly nor via an increased formation of RONS derived from inflammatory cells. Oxidative DNA damage might have been counteracted by training- and exercise-induced antioxidant responses. However, further studies are needed that combine advanced -omics based techniques (transcriptomics, proteomics) with state-of-the-art biochemical biomarkers to gain more insights into the underlying mechanisms.

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Antioxidant requirements have neither been defined for endurance nor been defined for ultra-endurance athletes. To verify whether an acute bout of ultra-endurance exercise modifies the need for nutritive antioxidants, we aimed (1) to investigate the changes of endogenous and exogenous antioxidants in response to an Ironman triathlon; (2) to particularise the relevance of antioxidant responses to the indices of oxidatively damaged blood lipids, blood cell compounds and lymphocyte DNA and (3) to examine whether potential time-points of increased susceptibility to oxidative damage are associated with alterations in the antioxidant status. Blood that was collected from forty-two well-trained male athletes 2 d pre-race, immediately post-race, and 1, 5 and 19 d later was sampled. The key findings of the present study are as follows: (1) Immediately post-race, vitamin C, alpha-tocopherol, and levels of the Trolox equivalent antioxidant capacity, the ferric reducing ability of plasma and the oxygen radical absorbance capacity (ORAC) assays increased significantly. Exercise-induced changes in the plasma antioxidant capacity were associated with changes in uric acid, bilirubin and vitamin C. (2) Significant inverse correlations between ORAC levels and indices of oxidatively damaged DNA immediately and 1 d post-race suggest a protective role of the acute antioxidant responses in DNA stability. (3) Significant decreases in carotenoids and gamma-tocopherol 1 d post-race indicate that the antioxidant intake during the first 24 h of recovery following an acute ultra-endurance exercise requires specific attention. Furthermore, the present study illustrates the importance of a diversified and well-balanced diet to maintain a physiological antioxidant status in ultra-endurance athletes in reference to recommendations.

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It is commonly accepted that regular moderate intensity physical activity reduces the risk of developing many diseases. Counter intuitively, however, evidence also exists for oxidative stress resulting from acute and strenuous exercise. Enhanced formation of reactive oxygen and nitrogen species may lead to oxidatively modified lipids, proteins and nucleic acids and possibly disease. Currently, only a few studies have investigated the influence of exercise on DNA stability and damage with conflicting results, small study groups and the use of different sample matrices or methods and result units. This is the first review to address the effect of exercise of various intensities and durations on DNA stability, focusing on human population studies. Furthermore, this article describes the principles and limitations of commonly used methods for the assessment of oxidatively modified DNA and DNA stability. This review is structured according to the type of exercise conducted (field or laboratory based) and the intensity performed (i.e. competitive ultra/endurance exercise or maximal tests until exhaustion). The findings presented here suggest that competitive ultra-endurance exercise (>4h) does not induce persistent DNA damage. However, when considering the effects of endurance exercise (<4h), no clear conclusions could be drawn. Laboratory studies have shown equivocal results (increased or no oxidative stress) after endurance or exhaustive exercise. To clarify which components of exercise participation (i.e. duration, intensity and training status of subjects) have an impact on DNA stability and damage, additional carefully designed studies combining the measurement of DNA damage, gene expression and DNA repair mechanisms before, during and after exercise of differing intensities and durations are required.

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Regular moderate physical activity reduces the risk of several noncommunicable diseases. At the same time, evidence exists for oxidative stress resulting from acute and strenuous exercise by enhanced formation of reactive oxygen and nitrogen species, which may lead to oxidatively modified lipids, proteins, and possibly negative effects on DNA stability. The limited data on ultraendurance events such as an Ironman triathlon show no persistent DNA damage after the events. However, when considering the effects of endurance exercise comparable to a (half) marathon or a short triathlon distance, no clear conclusions could be drawn. In order to clarify which components of exercise participation, such as duration, intensity, frequency, or training status of the subjects, have an impact on DNA stability, more information is clearly needed that combines the measurement of DNA damage, gene expression, and DNA repair mechanisms before, during, and after exercise of differing intensities and durations.

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Chronic diseases are a leading cause of death and disability, largely attributable to modifiable lifestyle risk factors. Many midlife Australian are getting insufficient physical activity for health and face a range of barriers to exercise. Results of this study provide evidence that benefits and barriers are an important predictor of exercise behaviour in midlife women and, that a 12 week nurse led health promotion program can effectively promote benefits and increase physical activity. This study provides evidence about benefits and barriers to exercise that will inform health promotion practice for chronic disease risk factor reduction in midlife women.

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As the results of the latest Excellence in Research Australia (ERA) exercise come closer to being announced, universities around Australia are holding their collective breaths. The ERA claims to be an assessment of research strengths and quality at Australian universities. While it is not supposed to produce a set of league tables, ultimately that is what tends to happen...

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Aim The aim of this study was to analyse the effect of an 8-week multimodal physiotherapy programme (MPP), integrating physical land-based therapeutic exercise (TE), adapted swimming and health education, as a treatment for patients with chronic non-specific neck pain (CNSNP), on disability, general health/mental states and quality of life. Methods 175 CNSNP patients from a community-based centre were recruited to participate in this prospective study. Intervention: 60-minute session (30 minutes of land-based exercise dedicated to improving mobility, motor control, resistance and strengthening of the neck muscles, and 30 minutes of adapted swimming with aerobic exercise keeping a neutral neck position using a snorkel). Health education was provided using a decalogue on CNSNP and constant repetition of brief advice by the physiotherapist during the supervision of the exercises in each session. Study outcomes: primary: disability (Neck Disability Index); secondary: physical and mental health states and quality of life of patients (SF-12 and EuroQoL-5D respectively). Differences between baseline data and that at the 8-week follow-up were calculated for all outcome variables. Results Disability showed a significant improvement of 24.6% from a mean (SD) of 28.2 (13.08) at baseline to 16.88 (11.62) at the end of the 8-week intervention. All secondary outcome variables were observed to show significant, clinically relevant improvements with increase ranges between 13.0% and 16.3% from a mean of 0.70 (0.2) at baseline to 0.83 (0.2), for EuroQoL-5D, and from a mean of 40.6 (12.7) at baseline to 56.9 (9.5), for mental health state, at the end of the 8-week intervention. Conclusion After 8 weeks of a MPP that integrated land-based physical TE, health education and adapted swimming, clinically-relevant and statistically-significant improvements were observed for disability, physical and mental health states and quality of life in patients who suffer CNSNP. The clinical efficacy requires verification using a randomised controlled study design.

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Background Aquatic exercise has been widely used for rehabilitation and functional recovery due to its physical and physiological benefits. However, there is a high variability in reporting on the muscle activity from surface electromyographic (sEMG) signals. The aim of this study is to present an updated review of the literature on the state of the art of muscle activity recorded using sEMG during activities and exercise performed by humans in water. Methods A literature search was performed to identify studies of aquatic exercise movement. Results Twenty-one studies were selected for critical appraisal. Sample size, functional tasks analyzed, and muscles recorded were studied for each paper. The clinical contribution of the paper was evaluated. Conclusions Muscle activity tends to be lower in water-based compared to land-based activity; however more research is needed to understand why. Approaches from basic and applied sciences could support the understanding of relevant aspects for clinical practice.

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Non-motorised underwater treadmills are commonly used in fitness activities. However, no studies have examined physiological and biomechanical responses of walking on non-motorised treadmills at different intensities and depths. Fifteen middle-aged healthy women underwent two underwater walking tests at two different depths, immersed either up to the xiphoid process (deep water) or the iliac crest (shallow water), at 100, 110, 120, 130 step-per-minute (spm). Oxygen consumption (VO2), heart rate (HR), blood lactate concentration, perceived exertion and step length were determined. Compared to deep water, walking in shallow water exhibited, at all intensities, significantly higher VO2 (+13.5%, on average) and HR (+8.1%, on average) responses. Water depth did not influence lactate concentration, whereas perceived exertion was higher in shallow compared to deep water, solely at 120 (+40%) and 130 (+39.4%) spm. Average step length was reduced as the intensity increased (from 100 to 130 spm), irrespective of water depth. Expressed as a percentage of maximum, average VO2 and HR were: 64–76% of peak VO2 and 71–90% of maximum HR, respectively at both water depths. Accordingly, this form of exercise can be included in the “vigorous” range of exercise intensity, at any of the step frequencies used in this study.