Search

In Austria, exercise therapy is an accredited profession that requires academic training on a university’s master level. However, exercise therapy is not listed in the service plans of health and medical insurance funds and is therefore not reimbursed as a health service for patients. This position paper aims to compile the scientific evidence of the efficacy and effectiveness of exercise therapy as a treatment component in medical care. It also informs about the skills and competencies that exercise therapists acquire during their university education in sport science. Based on that, the necessity to include exercise therapy as a health service for patients is argued. Additionally, legal parity for exercise therapists within the healthcare professions offering evidence-based treatment methods is advocated. Numerous studies confirm that exercise therapy clearly leads to improvements in musculoskeletal, internal, neurological, psychiatric, and psychosomatic diseases. Exercise therapy is thus a highly evidence-based, low-sideeffect component of prevention, treatment, and rehabilitation measures for almost all chronic diseases. It has a positive impact on pathogenesis, symptoms, fitness, quality of life, morbidity, and mortality of patients. The five-year academic training in sport science for exercise therapists conveys medical, theoretical knowledge, and practical skills on training and exercise, communication-related, sports-, and movement-related skills, as well as a profound education in scientific methodology. Consequently, the integration of exercise as therapeutic treatment into the healthcare system is highly indicated from a medical, societal and economic perspective. A new legal framework offering self-employment regulations for exercise therapists is required. [ABSTRACT FROM AUTHOR]

This study aimed to test the effects of repeated short-term bouts of hyperoxia on maximal 5-minute cycling performance under acute hypoxic conditions (3,200 m). Seventeen healthy and recreationally trained individuals (7 women and 10 men) participated in this randomized placebo-controlled cross-over trial. The procedures included a maximal cycle ergometer test and 3 maximal 5-minute cycling time trials (TTs). TT1 took place in normoxia and served for habituation and reference. TT2 and TT3 were conducted in normobaric hypoxia (15.0% inspiratory fraction of oxygen). During TT2 and TT3, the subjects were breathing through a face mask during five 15-second periods. The face mask was connected through a nonrebreathing T valve to a 300-L bag filled with 100% oxygen (intermittent hyperoxia) or ambient hypoxic air (placebo). The main outcome was the mean power output during the TT. Statistical significance level was set at p < 0.05. The mean power output was higher in the intermittent hyperoxia compared with the placebo condition (255.5 ± 49.6Wvs. 247.4 ± 48.2 W, p = 0.001). Blood lactate concentration and ratings of perceived exertion were significantly lower by about 9.7 and 7.3%, respectively, in the intermittent hyperoxia compared with the placebo condition, whereas heart rate values were unchanged. IH application increased arterial oxygen saturation (82.9 ± 2.6% to 92.4 ± 3.3%, p < 0.001). Repeated 15-second bouts of hyperoxia, applied during high-intensity exercise in hypoxia, are sufficient to increase power output. Future studies should focus on potential dose-response effects and the involved mechanisms. [ABSTRACT FROM AUTHOR]

Objective: The development of breast cancer cells is linked to hypoxia. The hypoxiainduced factor HIF-1α influences metastasis through neovascularization. Hypoxia seems to decrease the responsiveness to hormonal treatment due to loss of estrogen receptors (ERs). Obesity is discussed to increase hypoxia in adipocytes, which promotes a favorable environment for tumor cells in mammary fat tissue, whereas, tumor cells profit from good oxygen supply and are influenced by its deprivation as target regions within tumors show. This review gives an overview of the current state on research of hypoxia and breast cancer in human adipose tissue. Methods: A systematic literature search was conducted on PubMed (2000–2016) by applying hypoxia and/or adipocytes and breast cancer as keywords. Review articles were excluded as well as languages other than English or German. There was no restriction regarding the study design or type of breast cancer. A total of 35 papers were found. Eight studies were excluded due to missing at least two of the three keywords. One paper was removed due to Russian language, and one was dismissed due to lack of adherence. Seven papers were identified as reviews. After applying exclusion criteria, 18 articles were eligible for inclusion. Results: Two articles describe the impairment of mammary epithelial cell polarization through hypoxic preconditioning. A high amount of adipocytes enhances cancer progression due to the increased expression of HIF-1α which causes the loss of ER α protein as stated in four articles. Four articles analyzed that increased activation of HIF's induces a series of transcriptions resulting in tumor angiogenesis. HIF inhibition, especially when combined with cytotoxic chemotherapy, holds strong potential for tumor suppression as stated in further four articles. In two articles there is evidence of a strong connection between hypoxia, oxidative stress and a poor prognosis for breast cancer via HIF regulated pathways. Acute hypoxia seems to normalize the microenvironment in breast cancer tissue and has proven to affect tumor growth positively as covered in two articles. Conclusion: This review indicates that the development of breast cancer is influenced by hypoxia. A high amount of adipocytes enhances cancer progression due to the increased expression of HIF-1α. [ABSTRACT FROM AUTHOR]

Simulated altitude (normobaric hypoxia, NH) is used to study physiologic hypoxia responses of altitude. However, several publications show differences in physiological responses between NH and hypobaric conditions at altitude (hypobaric hypoxia, HH). The causality for these differences is controversially discussed. One theory is that the lower air density and environmental pressure in HH compared to NH lead to lower alveolar pressure and therefore lower oxygen diffusion in the lung. We hypothesized that, if this theory is correct, due to physical laws (Hagen-Poiseuille, Boyle), resistance respectively air compression (Boyle) at expiration should be lower, expiratory flow higher, and therefore peak flow and maximum expiratory flow (MEF) 75–50 increased in hypobaric hypoxia (HH) vs. normobaric hypoxia (NH). To prove the hypothesis of differences in respiratory flow as a result of lower alveolar pressure between HH and NH, we performed spirography in NH at different simulated altitudes and the corresponding altitudes in HH. In a cross over study, 6 healthy subjects (2 f/4 m, 28.3 ± 8.2 years, BMI: 23.2 ± 1.9) performed spirography as part of spiroergometry in a normobaric hypoxic room at a simulated altitude of 2800 m and after a seven-hour hike on a treadmill (average incline 14%, average walking speed 1.6 km/h) to the simulated summit of Mauna Kea at 4200 m. After a two-month washout, we repeated the spirometry in HH on the start and top of the Mauna Kea hiking trail, HI/USA. Comparison of NH (simulated 4200 m) and HH at 4200 m resulted in increased pulmonary ventilation during exercise (VE) (11.5%, p < 0.01), breathing-frequency (7.8%, p < 0.01), peak expiratory flow PEF (13.4%, p = 0.028), and MEF50 (15.9%, p = 0.028) in HH compared to NH, whereas VO2max decreased by 2%. At 2800 m, differences were only trendy, and at no altitude were differences in volume parameters. Spirography expresses higher mid expiratory flows and peak flows in HH vs. NH. This supports the theory of lower alveolar and small airway pressure due to a lower air density resulting in a lower resistance. [ABSTRACT FROM AUTHOR]