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      Heat and Dehydration Additively Enhance Cardiovascular Outcomes following Orthostatically-Stressful Calisthenics Exercise

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          Abstract

          Exercise and exogenous heat each stimulate multiple adaptations, but their roles are not well delineated, and that of the related stressor, dehydration, is largely unknown. While severe and prolonged hypohydration potentially “silences” the long-term heat acclimated phenotype, mild and transient dehydration may enhance cardiovascular and fluid-regulatory adaptations. We tested the hypothesis that exogenous heat stress and dehydration additively potentiate acute (24 h) cardiovascular and hematological outcomes following exercise. In a randomized crossover study, 10 physically-active volunteers (mean ± SD: 173 ± 11 cm; 72.1 ± 11.5 kg; 24 ± 3 year; 6 females) completed three trials of 90-min orthostatically-stressful calisthenics, in: (i) temperate conditions (22°C, 50% rh, no airflow; CON); (ii) heat (40°C, 60% rh) whilst euhydrated (HEAT), and (iii) heat with dehydration (no fluid ~16 h before and during exercise; HEAT+DEHY). Using linear mixed effects model analyses, core temperature (T CORE) rose 0.7°C more in HEAT than CON (95% CL: [0.5, 0.9]; p < 0.001), and another 0.4°C in HEAT+DEHY ([0.2, 0.5]; p < 0.001, vs. HEAT). Skin temperature also rose 1.2°C more in HEAT than CON ([0.6, 1.8]; p < 0.001), and similarly to HEAT+DEHY ( p = 0.922 vs. HEAT). Peak heart rate was 40 b·min −1 higher in HEAT than in CON ([28, 51]; p < 0.001), and another 15 b·min −1 higher in HEAT+DEHY ([3, 27]; p = 0.011, vs. HEAT). Mean arterial pressure at 24-h recovery was not consistently below baseline after CON or HEAT ( p ≥ 0.452), but was reduced 4 ± 1 mm Hg after HEAT+DEHY ([0, 8]; p = 0.020 vs. baseline). Plasma volume at 24 h after exercise increased in all trials; the 7% increase in HEAT was not reliably more than in CON (5%; p = 0.335), but was an additional 4% larger after HEAT+DEHY ([1, 8]; p = 0.005 vs. HEAT). Pooled-trial correlational analysis showed the rise in T CORE predicted the hypotension ( r = −0.4) and plasma volume expansion ( r = 0.6) at 24 h, with more hypotension reflecting more plasma expansion ( r = −0.5). In conclusion, transient dehydration with heat potentiates short-term (24-h) hematological (hypervolemic) and cardiovascular (hypotensive) outcomes following calisthenics.

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          Comfort and thermal sensations and associated physiological responses at various ambient temperatures

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            Exercise for Hypertension: A Prescription Update Integrating Existing Recommendations with Emerging Research

            Hypertension is the most common, costly, and preventable cardiovascular disease risk factor. Numerous professional organizations and committees recommend exercise as initial lifestyle therapy to prevent, treat, and control hypertension. Yet, these recommendations differ in the components of the Frequency, Intensity, Time, and Type (FITT) principle of exercise prescription (Ex Rx); the evidence upon which they are based is only of fair methodological quality; and the individual studies upon which they are based generally do not include people with hypertension, which are some of the limitations in this literature. The purposes of this review are to (1) overview the professional exercise recommendations for hypertension in terms of the FITT principle of Ex Rx; (2) discuss new and emerging research related to Ex Rx for hypertension; and (3) present an updated FITT Ex Rx for adults with hypertension that integrates the existing recommendations with this new and emerging research.
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              Integrated physiological mechanisms of exercise performance, adaptation, and maladaptation to heat stress.

              This article emphasizes significant recent advances regarding heat stress and its impact on exercise performance, adaptations, fluid electrolyte imbalances, and pathophysiology. During exercise-heat stress, the physiological burden of supporting high skin blood flow and high sweating rates can impose considerable cardiovascular strain and initiate a cascade of pathophysiological events leading to heat stroke. We examine the association between heat stress, particularly high skin temperature, on diminishing cardiovascular/aerobic reserves as well as increasing relative intensity and perceptual cues that degrade aerobic exercise performance. We discuss novel systemic (heat acclimation) and cellular (acquired thermal tolerance) adaptations that improve performance in hot and temperate environments and protect organs from heat stroke as well as other dissimilar stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia causing endotoxin release or the release of mitochondrial DNA fragments in response to cell necrosis, to mediate a systemic inflammatory syndrome inducing coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage and failure. We discuss how an inflammatory response that induces simultaneous fever and/or prior exposure to a pathogen (e.g., viral infection) that deactivates molecular protective mechanisms interacts synergistically with the hyperthermia of exercise to perhaps explain heat stroke cases reported in low-risk populations performing routine activities. Importantly, we question the "traditional" notion that high core temperature is the critical mediator of exercise performance degradation and heat stroke. Published 2011. This article is a U.S. Government work and is in the public domain in the USA.
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                Author and article information

                Contributors
                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                09 October 2017
                2017
                : 8
                : 756
                Affiliations
                [1] 1School of Physical Education, Sport and Exercise Sciences, Division of Sciences, University of Otago , Dunedin, New Zealand
                [2] 2Department of Physiology, Division of Health Sciences, University of Otago , Dunedin, New Zealand
                [3] 3School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham , Birmingham, United Kingdom
                Author notes

                Edited by: Gary W. Mack, Brigham Young University, United States

                Reviewed by: Thad E. Wilson, Osteopathic Medical School, Marian University, United States; Stephen Cheung, Brock University, Canada

                *Correspondence: James D. Cotter jim.cotter@ 123456otago.ac.nz

                This article was submitted to Exercise Physiology, a section of the journal Frontiers in Physiology

                Article
                10.3389/fphys.2017.00756
                5640974
                29062280
                525f7a8c-4566-44d9-8798-98110ab1aaf8
                Copyright © 2017 Akerman, Lucas, Katare and Cotter.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 15 May 2017
                : 19 September 2017
                Page count
                Figures: 9, Tables: 3, Equations: 2, References: 105, Pages: 17, Words: 13112
                Categories
                Physiology
                Original Research

                Anatomy & Physiology
                hypotension,hypervolemia,aldosterone,erythropoietin,calisthenics,adaptation,orthostasis,hypohydration

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