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PURPOSE: To identify physiological, psychological, and skill characteristics that explain performance in downhill (DH) mountain-bike racing. METHODS: Four studies were used to (1) identify factors potentially contributing to DH performance (using an expert focus group), (2) develop and validate a measure of rider skill (using video analysis and expert judge evaluation), (3) evaluate whether physiological, psychological, and skill variables contribute to performance at a DH competition, and (4) test the specific contribution of aerobic capacity to DH performance. RESULTS: STUDY 1 identified aerobic capacity, handgrip endurance, anaerobic power, rider skill, and self-confidence as potentially important for DH. In study 2 the rider-skill measure displayed good interrater reliability. Study 3 found that rider skill and handgrip endurance were significantly related to DH ride time (β = -0.76 and -0.14, respectively; R2 = .73), with exploratory analyses suggesting that DH ride time may also be influenced by self-confidence and aerobic capacity. Study 4 confirmed aerobic capacity as an important variable influencing DH performance (for a DH ride, mean oxygen uptake was 49 ± 5 mL • kg-1 • min-1, and 90% of the ride was completed above the 1st ventilatory threshold). CONCLUSIONS: In order of importance, rider skill, handgrip endurance, self-confidence, and aerobic capacity were identified as variables influencing DH performance. Practically, this study provides a novel assessment of rider skill that could be used by coaches to monitor training and identify talent. Novel intervention targets to enhance DH performance were also identified, including self-confidence and aerobic capacity. [ABSTRACT FROM AUTHOR]

Local changes in cerebral blood flow are thought to match changes in neuronal activity, a phenomenon termed neurovascular coupling. Hypoxia increases global resting cerebral blood flow, but regional cerebral blood flow (rCBF) changes are non-uniform. Hypoxia decreases baseline rCBF to the default mode network (DMN), which could reflect either decreased neuronal activity or altered neurovascular coupling. To distinguish between these hypotheses, we characterized the effects of hypoxia on baseline rCBF, task performance, and the hemodynamic (BOLD) response to task activity. During hypoxia, baseline CBF increased across most of the brain, but decreased in DMN regions. Performance on memory recall and motion detection tasks was not diminished, suggesting task-relevant neuronal activity was unaffected. Hypoxia reversed both positive and negative task-evoked BOLD responses in the DMN, suggesting hypoxia reverses neurovascular coupling in the DMN of healthy adults. The reversal of the BOLD response was specific to the DMN. Hypoxia produced modest increases in activations in the visual attention network (VAN) during the motion detection task, and had no effect on activations in the visual cortex during visual stimulation. This regional specificity may be particularly pertinent to clinical populations characterized by hypoxemia and may enhance understanding of regional specificity in neurodegenerative disease pathology. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? It is widely reported that non-painful, local warming of the skin elicits highly reproducible vasodilatation in young healthy individuals. Systemic hypoxia also elicits cutaneous vasodilatation, although this is modest in comparison to that elicited by skin heating. The interaction of simultaneous cutaneous local thermal hyperaemia and systemic hypoxia has not been investigated., What is the main finding and its importance? When compared with normoxia, systemic hypoxaemia enhances skin vasodilator capacity in response to local skin warming. This finding has important implications for understanding the physiology of skin microvascular reactivity in individuals exposed to systemic hypoxia or with a hypoxic microenvironment of the skin., The primary aim of this study was to investigate the effect of systemic poikilocapnic hypoxia on forearm cutaneous thermal hyperaemia. A secondary aim was to examine the relationship between the individual susceptibility to oxygen desaturation and cutaneous vasodilator capacity. Twelve healthy participants (seven male) were exposed to 9 h of normoxia and 12% poikilocapnic hypoxia in a temperature- and humidity-controlled environmental chamber. Skin blood flow was assessed at the ventral forearm using laser Doppler flowmetry combined with rapid local heating. After 6 min at baseline (skin temperature clamped at 33°C), local skin temperature was elevated at a rate of 0.5°C every 5 s up to 42°C to elicit a sensory axon response and then held constant for 30 min to cause a plateau. Skin blood flow was calculated as cutaneous vascular conductance [CVC; in perfusion units/mean arterial blood pressure (APU mmHg−1)] and expressed in raw format and relative to heating at 44°C in normoxia (%CVC44). During hypoxaemia, vasodilatation was greater during the initial peak (raw, Δ0.35 APU mmHg−1, P = 0.09; %CVC44, Δ18%, P = 0.05) and the plateau phase (raw, Δ0.55 APU mmHg−1, P = 0.03; %CVC44, Δ26%, P = 0.02). The rate of rise in cutaneous blood flow during the initial peak was significantly greater during poikilocapnic hypoxia ( P < 0.01). We observed a negative relationship between oxygen saturation in poikilocapnic hypoxia and the change in baseline ( P = 0.06), initial peak ( P = 0.01) and plateau phase of thermal hyperaemia ( P = 0.01). Prolonged poikilocapnic hypoxia causes robust increases in CVC during both phases of thermal hyperaemia that are dependent on the oxygen saturation of the individual. [ABSTRACT FROM AUTHOR]

Background/Aims: According to mathematical modeling, intradialytic exercise of sufficient intensity and duration implemented in the second half of dialysis should be as efficacious as increasing dialysis time for dialysis adequacy. This assumption has not been tested in vivo. Methods: In this controlled trial, 11 hemodialysis (HD) patients (mean (SD) age 56 (13) years) were recruited. Each patient completed three trial arms in a randomized order: routine care (CONT), increased HD time of 30 min (TIME), and intradialytic exercise (EXER), 60 min of cycling at 90% of the lactate threshold in the last 90 min of HD. The primary outcome was eKt/Vurea. Secondary outcomes included reduction and rebound ratios of urea, creatinine, phosphate and β2-microglobulin.Outcomes were calculated from blood sampling collected pre-, post- and 30 min post-HD and confirmed with dialysate sampling. Results: Exercise was not as efficacious as increased HD time for eKt/Vurea (EXER vs. CONT, mean change (95% CI): 0.03 (-0.05 to 0.12); TIME vs. CONT: 0.15 (0.05-0.26)). Exercise was less efficacious at improving reduction ratios of urea and creatinine. However, exercise was more efficacious than increased dialysis time for phosphate reduction ratio (EXER vs. CONT: 8.6% (0.5-16.7); TIME vs. CONT: 5.0% (-1.0 to 11.1)). Conclusion: This study utilized a rigorously controlled in vivo design to test mathematical models and assumptions regarding dialysis adequacy. Intradialytic exercise towards the end of HD cannot replace the prescription of increased HD time for dialysis adequacy, but may be an adjunctive therapy for serum phosphate control. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Junglee NA, Di Felice U, Dolci A, Fortes MB, Jibani MM, Lemmey AB, Walsh NP, Macdonald JH. Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function. Am J Physiol Renal Physiol 305: F813-F820, 2013. First published July 3, 2013; doi:10.1152/ajprenal.00091.2013.--Unaccustomed strenuous physical exertion in hot environments can result in heat stroke and acute kidney injury (AKI). Both exercise-induced muscle damage and AKI are associated with the release of interleukin- 6, but whether muscle damage causes AKI in the heat is unknown. We hypothesized that muscle-damaging exercise, before exercise in the heat, would increase kidney stress. Ten healthy euhydrated men underwent a randomized, crossover trial involving both a 60-min downhill muscle-damaging run (exercise-induced muscle damage; EIMD), and an exercise intensity-matched non-muscle-damaging flat run (CON), in random order separated by 2 wk. Both treatments were followed by heat stress elicited by a 40-min run at 33°C. Urine and blood were sampled at baseline, after treatment, and after subjects ran in the heat. By design, EIMD induced higher plasma creatine kinase and interleukin-6 than CON. EIMD elevated kidney injury biomarkers (e.g., urinary neutrophil gelatinase-associated lipocalin (NGAL) after a run in the heat: EIMD-CON, mean difference [95% CI]: 12 [5, 19] ng/ml) and reduced kidney function (e.g., plasma creatinine after a run in the heat: EIMD-CON, mean difference [95% CI]: 0.2 [0.1, 0.3] mg/dl), where CI is the confidence interval. Plasma interleukin-6 was positively correlated with plasma NGAL (r 0.9, P 0.001). Moreover, following EIMD, 5 of 10 participants met AKIN criteria for AKI. Thus for the first time we demonstrate that muscle-damaging exercise before running in the heat results in a greater inflammatory state and kidney stress compared with non-muscle-damaging exercise. Muscle damage should therefore be considered a risk factor for AKI when performing exercise in hot environments. [ABSTRACT FROM AUTHOR]

AbstractOliver, Samuel J., Jamie H. Macdonald, Adam D. Harper Smith, Justin S. Lawley, Carla A. Gallagher, Umberto di Felice, and Neil P.Walsh. High altitude impairs in vivoimmunity in humans. High Alt Med Biol14:144–149, 2013.—The aim was to assess the effect of high altitude on the development of new immune memory (induction) using a contact sensitization model of in vivoimmunity. We hypothesized that high-altitude exposure would impair induction of the in vivoimmune response to a novel antigen, diphenylcyclopropenone (DPCP). DPCP was applied (sensitization) to the lower back of 27 rested controls at sea level and to ten rested mountaineers 28 hours after passive ascent to 3777 m. After sensitization, mountaineers avoided strenuous exercise for a further 24 hours, after which they completed alpine activities for 11–18 days. Exactly 4 weeks after sensitization, the strength of immune memory induction was quantified in rested mountaineers and controls at sea level, by measuring the response to a low, dose-series DPCP challenge, read at 48 hours as skin measures of edema (skinfold thickness) and redness (erythema). Compared with control responses, skinfold thickness and erythema were reduced in the mountaineers (skinfold thickness,−52%, p=0.01, d=0.86; erythema, −36%, p=0.02, d=0.77). These changes in skinfold thickness and erythema were related to arterial oxygen saturation (r=0.7, p=0.04), but not cortisol (r0.79), at sensitization. In conclusion, this is the first study to show, using a contact sensitization model of in vivoimmunity, that high altitude exposure impairs the development of new immunity in humans. [ABSTRACT FROM AUTHOR]

Aim: We sought to determine if an acute kidney injury biomarker, neutrophil gelatinaseassociated lipocalin (NGAL), would be up-regulated by high-intensity proteinuria-inducing exercise. Methods: A prospective cohort design was utilised. 100 healthy, active adults (mean age 24 ± 4 (SD) years) were screened for post-exercise proteinuria (PeP); 10 PeP positive and 10 PeP negative participants then completed a high-intensity exercise protocol involving an 800 meter sprint. Plasma and urinary NGAL, urinary creatinine, urinary albumin and urine volume were obtained at the following time points: pre-run, immediately post-, 25 minutes, one hour and two hours post-run. Results: Following high-intensity exercise, 64% of participants had urinary NGAL concentrations above the normal range, particularly at 25 minutes post (P = 0.002). However, there was no difference in NGAL response between PeP positive and negative groups and plasma NGAL was decreased, not elevated, following exercise (P = 0.002). In some individuals normalizing urinary NGAL for urinary creatinine attenuated elevations. Urinary NGAL was also negatively correlated with urine volume (r = -0.701, P = 0.005). Conclusion: Proteinuria susceptibility did not influence an acute injury biomarker response to exercise. Nevertheless, urinary NGAL was elevated by exercise, possibly due to increased production by the proximal tubule, increased plasma clearance (given the decrease in plasma NGAL) and/or a concentrating effect of exercise-induced oliguria. Until correct normalisation of urinary biomarkers is determined, NGAL should be interpreted cautiously in exercise and acute kidney injury-induced oliguria. The inter-individual NGAL response to exercise also warrants further investigation. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective To determine the effect of 6 years of routine management on body composition, physical functioning, and quality of life, and their interrelationships, in men with idiopathic vertebral fracture. Methods Twenty men with idiopathic vertebral fracture (patients: mean ± SD age 58 ± 6 years) were age and height matched to 28 healthy controls with no known disease. The primary outcome was skeletal muscle mass (appendicular lean mass by dual x-ray absorptiometry) assessed at 2 visits (0 and 6 years). Physical functioning and quality of life domains were assessed by the Senior Fitness Test and Short Form 36 (SF-36) questionnaire at visit 2 only. Data were analyzed by repeated-measures analysis of variance, independent t-tests, and correlation. Results At visit 1, appendicular lean mass was 9% lower in patients than controls. Although patients better maintained appendicular lean mass between visits (interaction P = 0.016), at visit 2 appendicular lean mass remained 5% lower in patients than controls. Furthermore, patients' appendicular lean mass change was correlated with femoral neck bone density change (r = 0.507, P = 0.023). Physical function tests were 13-27% lower in patients compared with controls ( P = 0.056 to 0.003), as were SF-36 quality of life physical domains (13-26% lower; P = 0.028 to <0.001). Conclusion Despite an association between changes in muscle mass and bone density, routine management of men with idiopathic vertebral fracture does not address muscle loss. Combined with the observation of reduced physical functioning and quality of life, this study identifies novel targets for intervention in men with idiopathic vertebral fracture. [ABSTRACT FROM AUTHOR]