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Craig G Crandall - One of the best experts on this subject based on the ideXlab platform.
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mechanisms of orthostatic intolerance during Heat Stress
Autonomic Neuroscience: Basic and Clinical, 2016Co-Authors: Zachary J Schlader, Thad E. Wilson, Craig G CrandallAbstract:Heat Stress profoundly and unanimously reduces orthostatic tolerance. This review aims to provide an overview of the numerous and multifactorial mechanisms by which this occurs in humans. Potential causal factors include changes in arterial and venous vascular resistance and blood distribution, and the modulation of cardiac output, all of which contribute to the inability to maintain cerebral perfusion during Heat and orthostatic Stress. A number of countermeasures have been established to improve orthostatic tolerance during Heat Stress, which alleviate Heat Stress induced central hypovolemia (e.g., volume expansion) and/or increase peripheral vascular resistance (e.g., skin cooling). Unfortunately, these countermeasures can often be cumbersome to use with populations prone to syncopal episodes. Identifying the mechanisms of inter-individual differences in orthostatic intolerance during Heat Stress has proven elusive, but could provide greater insights into the development of novel and personalized countermeasures for maintaining or improving orthostatic tolerance during Heat Stress. This development will be especially impactful in occuational settings and clinical situations that present with orthostatic intolerance and/or central hypovolemia. Such investigations should be considered of vital importance given the impending increased incidence of Heat events, and associated cardiovascular challenges that are predicted to occur with the ensuing changes in climate.
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sympathetic activity during passive Heat Stress in healthy aged humans
The Journal of Physiology, 2015Co-Authors: Daniel Gagnon, Zachary J Schlader, Craig G CrandallAbstract:Key points Cardiovascular adjustments to Heat Stress are attenuated in healthy aged individuals, which could contribute to their greater prevalence of Heat-related illnesses and deaths during Heat waves. The attenuated cardiovascular adjustments in the aged could be due to lower increases in sympathetic nerve activity during Heat Stress. We examined muscle sympathetic nerve activity (MSNA) and plasma catecholamine concentrations in healthy young and aged individuals during whole-body passive Heat Stress. The main finding of this study is that increases in MSNA and plasma catecholamine concentrations did not differ between young and aged healthy individuals during passive Heating. Furthermore, the increase in these variables did not differ when a cold pressor test and lower body negative pressure were superimposed upon Heating. These findings suggest that attenuated cardiovascular adjustments to Heat Stress in healthy aged individuals are unlikely to be related to attenuated increases in sympathetic activity. Abstract Cardiovascular adjustments during Heat Stress are generally attenuated in healthy aged humans, which could be due to lower increases in sympathetic activity compared to the young. We compared muscle sympathetic nerve activity (MSNA) between 11 young (Y: 28 ± 4 years) and 10 aged (A: 70 ± 5 years) subjects prior to and during passive Heating. Furthermore, MSNA responses were compared when a cold pressor test (CPT) and lower body negative pressure (LBNP) were superimposed upon Heating. Baseline MSNA burst frequency (Y: 15 ± 4 vs. A: 31 ± 3 bursts min−1, P ≤ 0.01) and burst incidence (Y: 26 ± 8 vs. A: 50 ± 7 bursts (100 cardiac cycles (CC))−1, P ≤ 0.01) were greater in the aged. Heat Stress increased core temperature to a similar extent in both groups (Y: +1.2 ± 0.1 vs. A: +1.2 ± 0.0°C, P = 0.99). Absolute levels of MSNA remained greater in the aged during Heat Stress (burst frequency: Y: 47 ± 6 vs. A: 63 ± 11 bursts min−1, P ≤ 0.01; burst incidence: Y: 48 ± 8 vs. A: 67 ± 9 bursts (100 CC)−1, P ≤ 0.01); however, the increase in both variables was similar between groups (both P ≥ 0.1). The CPT and LBNP further increased MSNA burst frequency and burst incidence, although the magnitude of increase was similar between groups (both P ≥ 0.07). These results suggest that increases in sympathetic activity during Heat Stress are not attenuated in healthy aged humans.
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human cardiovascular responses to passive Heat Stress
Comprehensive Physiology, 2014Co-Authors: Craig G Crandall, Thad E. WilsonAbstract:Heat Stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the Stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to Heat Stress that are necessary for Heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during Heat Stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, Heat Stress conditions. Central hypovolemia is another cardiovascular challenge brought about by Heat Stress, which if added to a subsequent central volumetric Stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined Stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in Heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe Heat events that are predicted to occur.
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Heat Stress induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during Heat Stress
Journal of Applied Physiology, 2011Co-Authors: Craig G Crandall, David M Keller, Jonathan E Wingo, Matthew S GanioAbstract:The extent to which Heat Stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while Heat Stressed, while others are relatively tolerant. Heat Stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to Heat Stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and Heat-Stress conditions. Tolerance to LBNP was quantified using a cumulative Stress index (CSI), and the difference between normothermic CSI and Heat-Stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and Heat-Stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of Heat Stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the Heat Stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during Heat Stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the Heat-Stress-induced reductions in central venous pressure.
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acute volume expansion preserves orthostatic tolerance during whole body Heat Stress in humans
The Journal of Physiology, 2009Co-Authors: Craig G Crandall, David M Keller, Jonathan E Wingo, David A Low, Jeffrey L Hastings, Scott L DavisAbstract:Whole-body Heat Stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies Heat Stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates Heat Stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 +/- 10 years: mean +/- S.D.), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative Stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body Heating, and whole-body Heating + acute volume expansion. For the whole-body Heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-Heat Stress values. Whole-body Heat Stress alone reduced orthostatic tolerance by approximately 80% compared to normothermia (938 +/- 152 versus 182 +/- 57 CSI; mean +/- S.E.M., P < 0.001). Acute volume expansion during whole-body Heating completely ameliorated the Heat Stress-induced reduction in orthostatic tolerance (1110 +/- 69 CSI, P < 0.001). Although Heat Stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the Heat-Stressed human.
David M Keller - One of the best experts on this subject based on the ideXlab platform.
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Heat Stress induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during Heat Stress
Journal of Applied Physiology, 2011Co-Authors: Craig G Crandall, David M Keller, Jonathan E Wingo, Matthew S GanioAbstract:The extent to which Heat Stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while Heat Stressed, while others are relatively tolerant. Heat Stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to Heat Stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and Heat-Stress conditions. Tolerance to LBNP was quantified using a cumulative Stress index (CSI), and the difference between normothermic CSI and Heat-Stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and Heat-Stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of Heat Stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the Heat Stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during Heat Stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the Heat-Stress-induced reductions in central venous pressure.
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acute volume expansion preserves orthostatic tolerance during whole body Heat Stress in humans
The Journal of Physiology, 2009Co-Authors: Craig G Crandall, David M Keller, Jonathan E Wingo, David A Low, Jeffrey L Hastings, Scott L DavisAbstract:Whole-body Heat Stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies Heat Stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates Heat Stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 +/- 10 years: mean +/- S.D.), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative Stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body Heating, and whole-body Heating + acute volume expansion. For the whole-body Heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-Heat Stress values. Whole-body Heat Stress alone reduced orthostatic tolerance by approximately 80% compared to normothermia (938 +/- 152 versus 182 +/- 57 CSI; mean +/- S.E.M., P < 0.001). Acute volume expansion during whole-body Heating completely ameliorated the Heat Stress-induced reduction in orthostatic tolerance (1110 +/- 69 CSI, P < 0.001). Although Heat Stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the Heat-Stressed human.
Kadambot H M Siddique - One of the best experts on this subject based on the ideXlab platform.
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Heat Stress in grain legumes during reproductive and grain filling phases
Crop & Pasture Science, 2017Co-Authors: Muhammad Farooq, Faisal Nadeem, Nirmali Gogoi, Aman Ullah, Salem S Alghamdi, Harsh Nayyar, Kadambot H M SiddiqueAbstract:Thermal Stress during reproductive development and grain-filling phases is a serious threat to the quality and productivity of grain legumes. The optimum temperature range for grain legume crops is 10−36°C, above which severe losses in grain yield can occur. Various climatic models have simulated that the temperature near the earth’s surface will increase (by up to 4°C) by the end of this century, which will intensify the chances of Heat Stress in crop plants. The magnitude of damage or injury posed by a high-temperature Stress mainly depends on the defence response of the crop and the specific growth stage of the crop at the time of exposure to the high temperature. Heat Stress affects grain development in grain legumes because it disintegrates the tapetum layer, which reduces nutrient supply to microspores leading to premature anther dehiscence; hampers the synthesis and distribution of carbohydrates to grain, curtailing the grain-filling duration leading to low grain weight; induces poor pod development and fractured embryos; all of which ultimately reduce grain yield. The most prominent effects of Heat Stress include a substantial reduction in net photosynthetic rate, disintegration of photosynthetic apparatus and increased leaf senescence. To curb the catastrophic effect of Heat Stress, it is important to improve Heat tolerance in grain legumes through improved breeding and genetic engineering tools and crop management strategies. In this review, we discuss the impact of Heat Stress on leaf senescence, photosynthetic machinery, assimilate translocation, water relations, grain quality and development processes. Furthermore, innovative breeding, genetic, molecular and management strategies are discussed to improve the tolerance against Heat Stress in grain legumes.
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Heat Stress in wHeat during reproductive and grain filling phases
Critical Reviews in Plant Sciences, 2011Co-Authors: Muhammad Farooq, Helen Bramley, Jairo A Palta, Kadambot H M SiddiqueAbstract:Ambient temperatures have increased since the beginning of the century and are predicted to continue rising under climate change. Such increases in temperature can cause Heat Stress: a severe threat to wHeat production in many countries, particularly when it occurs during reproductive and grain-filling phases. Heat Stress reduces plant photosynthetic capacity through metabolic limitations and oxidative damage to chloroplasts, with concomitant reductions in dry matter accumulation and grain yield. Genotypes expressing Heat shock proteins are better able to withstand Heat Stress as they protect proteins from Heat-induced damage. Heat tolerance can be improved by selecting and developing wHeat genotypes with Heat resistance. WHeat pre-breeding and breeding may be based on secondary traits like membrane stability, photosynthetic rate and grain weight under Heat Stress. Nonetheless, improvement in grain yield under Heat Stress implies selecting genotypes for grain size and rate of grain filling. Integrating ph...
Muhammad Farooq - One of the best experts on this subject based on the ideXlab platform.
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Heat Stress in grain legumes during reproductive and grain filling phases
Crop & Pasture Science, 2017Co-Authors: Muhammad Farooq, Faisal Nadeem, Nirmali Gogoi, Aman Ullah, Salem S Alghamdi, Harsh Nayyar, Kadambot H M SiddiqueAbstract:Thermal Stress during reproductive development and grain-filling phases is a serious threat to the quality and productivity of grain legumes. The optimum temperature range for grain legume crops is 10−36°C, above which severe losses in grain yield can occur. Various climatic models have simulated that the temperature near the earth’s surface will increase (by up to 4°C) by the end of this century, which will intensify the chances of Heat Stress in crop plants. The magnitude of damage or injury posed by a high-temperature Stress mainly depends on the defence response of the crop and the specific growth stage of the crop at the time of exposure to the high temperature. Heat Stress affects grain development in grain legumes because it disintegrates the tapetum layer, which reduces nutrient supply to microspores leading to premature anther dehiscence; hampers the synthesis and distribution of carbohydrates to grain, curtailing the grain-filling duration leading to low grain weight; induces poor pod development and fractured embryos; all of which ultimately reduce grain yield. The most prominent effects of Heat Stress include a substantial reduction in net photosynthetic rate, disintegration of photosynthetic apparatus and increased leaf senescence. To curb the catastrophic effect of Heat Stress, it is important to improve Heat tolerance in grain legumes through improved breeding and genetic engineering tools and crop management strategies. In this review, we discuss the impact of Heat Stress on leaf senescence, photosynthetic machinery, assimilate translocation, water relations, grain quality and development processes. Furthermore, innovative breeding, genetic, molecular and management strategies are discussed to improve the tolerance against Heat Stress in grain legumes.
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Heat Stress in wHeat during reproductive and grain filling phases
Critical Reviews in Plant Sciences, 2011Co-Authors: Muhammad Farooq, Helen Bramley, Jairo A Palta, Kadambot H M SiddiqueAbstract:Ambient temperatures have increased since the beginning of the century and are predicted to continue rising under climate change. Such increases in temperature can cause Heat Stress: a severe threat to wHeat production in many countries, particularly when it occurs during reproductive and grain-filling phases. Heat Stress reduces plant photosynthetic capacity through metabolic limitations and oxidative damage to chloroplasts, with concomitant reductions in dry matter accumulation and grain yield. Genotypes expressing Heat shock proteins are better able to withstand Heat Stress as they protect proteins from Heat-induced damage. Heat tolerance can be improved by selecting and developing wHeat genotypes with Heat resistance. WHeat pre-breeding and breeding may be based on secondary traits like membrane stability, photosynthetic rate and grain weight under Heat Stress. Nonetheless, improvement in grain yield under Heat Stress implies selecting genotypes for grain size and rate of grain filling. Integrating ph...
Marina A. G. Von Keyserlingk - One of the best experts on this subject based on the ideXlab platform.
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Invited review: Effects of Heat Stress on dairy cattle welfare
Journal of Dairy Science, 2017Co-Authors: Liam Polsky, Marina A. G. Von KeyserlingkAbstract:The effects of high ambient temperatures on production animals, once thought to be limited to tropical areas, has extended into northern latitudes in response to the increasing global temperature. The number of days where the temperature-humidity index (THI) exceeds the comfort threshold (>72) is increasing in the northern United States, Canada, and Europe. Compounded by the increasing number of dairy animals and the intensification of production, Heat Stress has become one of the most important challenges facing the dairy industry today. The objectives of this review were to present an overview of the effects of Heat Stress on dairy cattle welfare and highlight important research gaps in the literature. We will also briefly discuss current Heat abatement strategies, as well as the sustainability of future Heat Stress management. Heat Stress has negative effects on the health and biological functioning of dairy cows through depressed milk production and reduced reproductive performance. Heat Stress can also compromise the affective state of dairy cows by inducing feelings of hunger and thirst, and we have highlighted the need for research efforts to examine the potential relationship between Heat Stress, frustration, aggression, and pain. Little work has examined how Heat Stress affects an animal's natural coping behaviors, as well as how the animal's evolutionary adaptations for thermoregulation are managed in modern dairy systems. More research is needed to identify improved comprehensive cow-side measurements that can indicate real-time responses to elevated ambient temperatures and that could be incorporated into Heat abatement management decisions.
