5 resultados para cryotherapy

em Deakin Research Online - Australia


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Background: External genital warts are a common sexually transmitted viral disease. We describe the patterns of treatment for initial presentations of external genital warts (EGWs) in Australian sexual health centers.
Methods: This was a retrospective audit of 489 case notes from consecutive individuals who presented with a new diagnosis of EGWs to 1 of 5 major sexual health clinics in Australia. Eligibility criteria were consecutive patients aged 18 to 45 years inclusively, presenting with first ever episode of EGWs from January 1, 2004. Exclusion criteria were patients who were immunocompromised, including HIV infection, or enrollment in a treatment study for EGWs.
Results: The median age at presentation of women was 23.2 years and of men 26.8 years. One quarter (n = 127) of patients had another sexually transmitted infection diagnosed at presentation. Nearly half of the patients (n = 224) presented only once for treatment. Most often, patients were treated with a monotherapy (n = 382/489; 78%), usually cryotherapy (257; 53%). Staff applied treatment in 361 (74%) cases. There was wide variation across sites, possibly reflecting local policies and budgets. We found no difference in wart resolution (n = 292; 60%) by initial treatment chosen.
Conclusions:
The diagnosis and treatment of genital warts constitute a sizable proportion of clinical visits to the audited sexual health services and require a large input of staff time to manage, including the application of topical treatments. Our results help complete the picture of the burden of EGWs on Australian sexual health centers before the introduction of the HPV vaccine.

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Purpose: Given the widespread use of water immersion during recovery from exercise, we aimed to investigate the effect of contrast water immersion on recovery of sprint cycling performance, HR and, blood lactate.

Methods: Two groups completed high-intensity sprint exercise before and after a 30-min randomized recovery. The Wingate group (n = 8) performed 3 x 30-s Wingate tests (4-min rest periods). The repeated intermittent sprint group (n = 8) cycled for alternating 30-s periods at 40% of predetermined maximum power and 120% maximum power, until exhaustion. Both groups completed three trials using a different recovery treatment for each trial (balanced randomized application). Recovery treatments were passive rest, 1:1 contrast water immersion (2.5 min of cold (8-C) to 2.5 min of hot (40-C)), and 1:4 contrast water immersion (1 min of cold to 4 min of hot). Blood lactate and HR were recorded throughout, and peak power and total work for pre- and postrecovery Wingate performance and exercise time and total work for repeated sprinting were recorded.

Results: Recovery of Wingate peak power was 8% greater after 1:4 contrast water immersion than after passive rest, whereas both contrast water immersion ratios provided a greater recovery of exercise time (È10%) and total work (È14%) for repeated sprinting than for passive rest. Blood lactate was similar between trials. Compared with passive rest, HR initially declined more slowly during contrast water immersion but increased with each transition to a cold immersion phase.

Conclusions: These data support contrast water immersion being effective in maintaining performance during a short-term recovery from sprint exercise. This effect needs further investigation but is likely explained by cardiovascular mechanisms, shown here by an elevation in HR upon each cold immersion.

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Achieving an appropriate balance between training and competition stresses and recovery is important in maximising the performance of athletes. A wide range of recovery modalities are now used as integral parts of the training programmes of elite athletes to help attain this balance. This review examined the evidence available as to the efficacy of these recovery modalities in enhancing between-training session recovery in elite athletes. Recovery modalities have largely been investigated with regard to their ability to enhance the rate of blood lactate removal following high-intensity exercise or to reduce the severity and duration of exercise-induced muscle injury and delayed onset muscle soreness (DOMS). Neither of these reflects the circumstances of between-training session recovery in elite athletes. After high-intensity exercise, rest alone will return blood lactate to baseline levels well within the normal time period between the training sessions of athletes. The majority of studies examining exercise-induced muscle injury and DOMS have used untrained subjects undertaking large amounts of unfamiliar eccentric exercise. This model is unlikely to closely reflect the circumstances of elite athletes. Even without considering the above limitations, there is no substantial scientific evidence to support the use of the recovery modalities reviewed to enhance the between-training session recovery of elite athletes. Modalities reviewed were massage, active recovery, cryotherapy, contrast temperature water immersion therapy, hyperbaric oxygen therapy, nonsteroidal anti-inflammatory drugs, compression garments, stretching, electromyostimulation and combination modalities. Experimental models designed to reflect the circumstances of elite athletes are needed to further investigate the efficacy of various recovery modalities for elite athletes. Other potentially important factors associated with recovery, such as the rate of post-exercise glycogen synthesis and the role of inflammation in the recovery and adaptation process, also need to be considered in this future assessment.

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

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Cold water immersion (CWI) and active recovery (ACT) are frequently used as postexercise recovery strategies. However, the physiological effects of CWI and ACT after resistance exercise are not well characterized. We examined the effects of CWI and ACT on cardiac output (Q̇), muscle oxygenation (SmO2), blood volume (tHb), muscle temperature (Tmuscle), and isometric strength after resistance exercise. On separate days, 10 men performed resistance exercise, followed by 10 min CWI at 10°C or 10 min ACT (low-intensity cycling). Q̇ (7.9 ± 2.7 l) and Tmuscle (2.2 ± 0.8°C) increased, whereas SmO2 (-21.5 ± 8.8%) and tHb (-10.1 ± 7.7 μM) decreased after exercise (P < 0.05). During CWI, Q̇ (-1.1 ± 0.7 l) and Tmuscle (-6.6 ± 5.3°C) decreased, while tHb (121 ± 77 μM) increased (P < 0.05). In the hour after CWI, Q̇ and Tmuscle remained low, while tHb also decreased (P < 0.05). By contrast, during ACT, Q̇ (3.9 ± 2.3 l), Tmuscle (2.2 ± 0.5°C), SmO2 (17.1 ± 5.7%), and tHb (91 ± 66 μM) all increased (P < 0.05). In the hour after ACT, Tmuscle, and tHb remained high (P < 0.05). Peak isometric strength during 10-s maximum voluntary contractions (MVCs) did not change significantly after CWI, whereas it decreased after ACT (-30 to -45 Nm; P < 0.05). Muscle deoxygenation time during MVCs increased after ACT (P < 0.05), but not after CWI. Muscle reoxygenation time after MVCs tended to increase after CWI (P = 0.052). These findings suggest first that hemodynamics and muscle temperature after resistance exercise are dependent on ambient temperature and metabolic demands with skeletal muscle, and second, that recovery of strength after resistance exercise is independent of changes in hemodynamics and muscle temperature.