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Lawley J.S.,Bangor University | Lawley J.S.,Institute for Exercise and Environmental Medicine | Oliver S.J.,Bangor University | Mullins P.G.,Bangor University | MacDonald J.H.,Bangor University
Journal of Cerebral Blood Flow and Metabolism | Year: 2013

Elevated brain water is a common finding in individuals with severe forms of altitude illness. However, the location, nature, and a causative link between brain edema and symptoms of acute mountain sickness such as headache remains unknown. We examined indices of brain white matter water mobility in 13 participants after 2 and 10 hours in normoxia (21% O2) and hypoxia (12% O2) using magnetic resonance imaging. Using a whole-brain analysis (tract-based spatial statistics (TBSS)), mean diffusivity was reduced in the left posterior hemisphere after 2 hours and globally reduced throughout cerebral white matter by 10 hours in hypoxia. However, no changes in T 2 relaxation time (T2) or fractional anisotropy were observed. The TBSS identified an association between changes in mean diffusivity, fractional anisotropy, and T2 both supra and subtentorially after 2 and 10 hours, with headache score after 10 hours in hypoxia. Region of interest-based analyses generally confirmed these results. These data indicate that acute periods of hypoxemia cause a shift of water into the intracellular space within the cerebral white matter, whereas no evidence of brain edema (a volumetric enlargement) is identifiable. Furthermore, these changes in brain water mobility are related to the intensity of high-altitude headache. © 2013 ISCBFM. Source


McLean S.P.,Southwestern University | Palmer D.,Institute for Exercise and Environmental Medicine | Ice G.,Southwestern University | Truijens M.,Institute for Fundamental and Clinical Human Movement science | Smith J.C.,Southwestern University
Medicine and Science in Sports and Exercise | Year: 2010

During gait, humans choose a combination of step length and step rate that minimizes V⊙O2. However, little work has been reported on the existence of such optimization in swimming. Purpose: The purpose of this study was to examine the manipulation of stroke rate on V⊙O2 in submaximal, constant speed freestyle swimming. Methods: Preferred stroke rate for swimming freestyle at 1.0 m⊙s-1 in a flume was determined for 10 competitive swimmers (mean ± SD: age = 33.3 ± 13.6 yr, height = 175.3 ± 8.6 cm, weight = 74.9 ± 12.2 kg). Participants then completed flume swims at 1.0 m⊙s-1 with stroke rates equal to j20%, j10%, 0%, +10%, and +20% of their preferred stroke rate in a randomized order during which V⊙O2 was continuously monitored. Each trial continued for 1 min after steady-state V⊙O2 was verified (∼4-5 min). During the final minute of each trial, V⊙O2 was measured using the Douglas bag technique, HR was recorded, and kick rate (KR) was computed using the time needed to complete 30 kicks. RPE was reported immediately after each trial. Results: V⊙O2 increased 11%-16% (P<0.05) when stroke rate was reduced but was nominally affected when stroke rate was increased. Likewise, HR increased 4%-6% (P<0.05), and RPE increased 15%-30% (P<0.05) when stroke rate was reduced but not affected when stroke rate was increased. Conclusions: These data suggest that these swimmers preferred to swim freestyle at the lowest stroke rate (or the longest stroke length) that did not require an increase in V⊙O2. © 2010 by the American College of Sports Medicine. Source


Bhella P.S.,The Texas Institute | Hastings J.L.,The Texas Institute | Fujimoto N.,The Texas Institute | Shibata S.,The Texas Institute | And 7 more authors.
Journal of the American College of Cardiology | Year: 2014

BACKGROUND: Sedentary aging has deleterious effects on the cardiovascular system, including decreased left ventricular compliance and distensibility (LVCD). Conversely, Masters level athletes, who train intensively throughout adulthood, retain youthful LVCD.OBJECTIVES: The purpose of this study was to test the hypothesis that preservation of LVCD may be possible with moderate lifelong exercise training.METHODS: Healthy seniors (n = 102) were recruited from predefined populations, screened for lifelong patterns of exercise training, and stratified into 4 groups: "sedentary" (<2 sessions/week); "casual" (2 to 3 sessions/week); "committed" (4 to 5 sessions/week); and "competitive" Masters level athletes (6 to 7 sessions/week). Right heart catheterization and echocardiography were performed while preload was manipulated using lower body negative pressure and rapid saline infusion to define LV pressure-volume relationships and Frank-Starling curves.CONCLUSIONS: Low doses of casual, lifelong exercise do not prevent the decreased compliance and distensibility observed with healthy, sedentary aging. In contrast, 4 to 5 exercise sessions/week throughout adulthood prevent most of these age-related changes. As LV stiffening has been implicated in the pathophysiology of many cardiovascular conditions affecting the elderly, this "dose" of exercise training may have important implications for prevention of cardiovascular disease.RESULTS: Peak oxygen uptake and LV mass increased with escalating doses of lifelong exercise, with little change in systolic function. At baseline, LV distensibility was greater in committed (21%) and competitive (36%) exercisers than in sedentary subjects. Group LV stiffness constants (sedentary: 0.062 ± 0.039; casual: 0.079 ± 0.052; committed: 0.055 ± 0.033; and competitive: 0.035 ± 0.033) revealed: 1) increased stiffness in sedentary subjects compared to competitive athletes, whereas lifelong casual exercise had no effect; and 2) greater compliance in committed exercisers than in sedentary or casual exercisers. © 2014 by the American College of Cardiology Foundation. Source


van Beek A.H.E.A.,Radboud University Nijmegen | Lagro J.,Radboud University Nijmegen | Olde-Rikkert M.G.M.,Radboud University Nijmegen | Zhang R.,Institute for Exercise and Environmental Medicine | Claassen J.A.H.R.,Radboud University Nijmegen
Neurobiology of Aging | Year: 2012

In Alzheimer's disease (AD) cerebrovascular function is at risk. Transcranial Doppler, near-infrared spectroscopy, and photoplethysmography are noninvasive methods to continuously measure changes in cerebral blood flow velocity (CBFV), cerebral cortical oxygenated hemoglobin (O 2Hb), and blood pressure (BP). In 21 patients with mild to moderate AD and 20 age-matched controls, we investigated how oscillations in cerebral blood flow velocity (CBFV) and O 2Hb are associated with spontaneous and induced oscillations in blood pressure (BP) at the very low (VLF = 0.05 Hz) and low frequencies (LF = 0.1 Hz). We applied spectral and transfer function analysis to quantify dynamic cerebral autoregulation and brain tissue oxygenation. In AD, cerebrovascular resistance was substantially higher (34%, AD vs. control: δ = 0.69 (0.25) mm Hg/cm/second, p = 0.012) and the transmission of very low frequency (VLF) cerebral blood flow (CBF) oscillations into O 2Hb differed, with increased phase lag and gain (δ phase 0.32 [0.15] rad; δ gain 0.049 [0.014] μmol/cm/second, p both < 0.05). The altered transfer of CBF to cortical oxygenation in AD indicates that properties of the cerebral microvasculature are changed in this disease. © 2012 Elsevier Inc. Source


Crandall C.G.,Institute for Exercise and Environmental Medicine | Crandall C.G.,University of Texas Southwestern Medical Center | Wilson T.E.,Heritage University | Marving J.,Copenhagen University | And 6 more authors.
Journal of Physiology | Year: 2012

Heat stress results in profound reductions in the capacity to withstand a simulated haemorrhagic challenge; however, this capacity is normalized if the individual is volume loaded prior to the challenge. The present study tested the hypothesis that volume loading during passive heat stress attenuates the reduction in regional blood volumes during a simulated haemorrhagic challenge imposed via lower-body negative pressure (LBNP). Seven subjects underwent 30 mmHg LBNP while normothermic, during passive heat stress (increased internal temperature ∼1°C), and while continuing to be heated after intravenous colloid volume loading (11 ml kg -1). Relative changes in torso and regional blood volumes were determined by gamma camera imaging with technetium-99m labelled erythrocytes. Heat stress reduced blood volume in all regions (ranging from 7 to 16%), while subsequent volume loading returned those values to normothermic levels. While normothermic, LBNP reduced blood volume in all regions (torso: 22 ± 8%; heart: 18 ± 6%; spleen: 15 ± 8%). During LBNP while heat stressed, the reductions in blood volume in each region were markedly greater when compared to LBNP while normothermic (torso: 73 ± 2%; heart: 72 ± 3%; spleen: 72 ± 5%, all P < 0.001 relative to normothermia). Volume loading during heat stress did not alter the extent of the reduction in these blood volumes to LBNP relative to heat stress alone (torso: 73 ± 1%; heart: 72 ± 2%; spleen: 74 ± 3%, all P > 0.05 relative to heat stress alone). These data suggest that blood volume loading during passive heat stress (via 11 ml kg -1 of a colloid solution) normalizes regional blood volumes in the torso, but does not mitigate the reduction in central blood volume during a simulated haemorrhagic challenge combined with heat stress. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society. Source

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