Hyperthermia Does Not Alter Baroreflex Control Of Heart Rate During Central Hypovolemia Associated With Simulated Hemorrhage. .

Baroreceptors modulate arterial blood pressure through neural control of cardiac output and peripheral vascular resistance. Hyperthermia reduces tolerance to central hypovolemia, however hyperthermia itself does not alter baroreflex control of heart rate or muscle sympathetic nerve activity. The combined influence of hyperthermia and profound central hypovolemia on baroreflex function remains unknown. This study tested the hypothesis that baroreflex sensitivity (as indexed from ∆ heart rate /∆ blood pressure) would be reduced in hyperthermia compared to normothermia during central hypovolemia. Twelve healthy males (32 ± 5 y) underwent central hypovolemia to pre-syncope, which was induced via progressive lower body negative pressure (LBNP), during normothermia and, on a separate day (randomized, counter balanced) during hyperthermia (+1.2 ± 0.1°C increase in internal temperature). Baroreflex sensitivity was assessed during the final full stage of LBNP completed, and during a 30 second period immediately preceding any bradycardia prior to pre-syncope. LBNP during hyperthermia reduced tolerance by ~58% relative to LBNP during normothermia (normothermia: 72mmHg ±20 vs hyperthermia: 42mmHg± 13; P\u3c0.001). During the final full LBNP stage, baroreflex sensitivity was not different between thermal conditions (hyperthermia: 1.9 ± 1.6 bpm/mmHg, normothermia: 2.4 ± 1.5 bpm/mmHg, p=0.46). Likewise, just prior to pre-syncope baroreflex sensitivity between thermal conditions was not different (hyperthermia: 1.0±1.3 bpm/mmHg, normothermia: 1.5±1.1 bpm/mmHg; p=0.10). These data indicate that during profound central hypovolemia baroreflex control of heart rate is unaffected by hyperthermia. Thus, reductions in the capacity to tolerate central hypovolemia while hyperthermic is not related to altered baroreflex control of heart rate

Renal Hemodynamics During Sympathetic Activation Following Aerobic and Anaerobic Exercise

We tested the hypotheses that prior aerobic (Study 1) or anaerobic (Study 2) exercise attenuates the increase in renal vascular resistance (RVR) during sympathetic stimulation. Ten healthy young adults (5 females) participated in both Study 1 (aerobic exercise) and Study 2 (anaerobic exercise). In Study 1, subjects completed three minutes of face cooling pre- and post- 30 min of moderate intensity aerobic exercise (68 ± 1% estimate maximal heart rate). In Study 2, subjects completed two minutes of the cold pressor test pre- and post- the completion of a 30 s maximal effort cycling test (Wingate Anaerobic Test). Both face cooling and the cold pressor test stimulate the sympathetic nervous system and elevate RVR. The primary dependent variable in both Studies was renal blood velocity, which was measured at baseline and every minute during sympathetic stimulation. Renal blood velocity was measured via the coronal approach at the distal segment of the right renal artery with pulsed wave Doppler ultrasound. RVR was calculated from the quotient of mean arterial pressure and renal blood velocity. In Study 1, renal blood velocity and RVR did not differ between pre- and post- aerobic exercise (P ≥ 0.24). Face cooling decreased renal blood velocity (P < 0.01) and the magnitude of this decrease did not differ between pre- and post- aerobic exercise (P = 0.52). RVR increased with face cooling (P < 0.01) and the extent of these increases did not differ between pre- and post- aerobic exercise (P = 0.74). In Study 2, renal blood velocity was 2 ± 2 cm/s lower post- anaerobic exercise (P = 0.02), but RVR did not differ (P = 0.08). The cold pressor test decreased renal blood velocity (P < 0.01) and the magnitude of this decrease did not differ between pre- and post- anaerobic exercise (P = 0.26). RVR increased with the cold pressor test (P < 0.01) and the extent of these increases did not differ between pre- and post- anaerobic exercise (P = 0.12). These data indicate that 30 min of moderate intensity aerobic exercise or 30 s of maximal effort anaerobic exercise does not affect the capacity to increase RVR during sympathetic stimulation following exercise

Heat Safety in the Workplace:Modified Delphi Consensus to Establish Strategies and Resources to Protect U.S Workers

The purpose of this consensus document was to develop feasible, evidence‐based occupational heat safety recommendations to protect the US workers that experience heat stress. Heat safety recommendations were created to protect worker health and to avoid productivity losses associated with occupational heat stress. Recommendations were tailored to be utilized by safety managers, industrial hygienists, and the employers who bear responsibility for implementing heat safety plans. An interdisciplinary roundtable comprised of 51 experts was assembled to create a narrative review summarizing current data and gaps in knowledge within eight heat safety topics: (a) heat hygiene, (b) hydration, (c) heat acclimatization, (d) environmental monitoring, (e) physiological monitoring, (f) body cooling, (g) textiles and personal protective gear, and (h) emergency action plan implementation. The consensus‐based recommendations for each topic were created using the Delphi method and evaluated based on scientific evidence, feasibility, and clarity. The current document presents 40 occupational heat safety recommendations across all eight topics. Establishing these recommendations will help organizations and employers create effective heat safety plans for their workplaces, address factors that limit the implementation of heat safety best‐practices and protect worker health and productivity

Human behavioral temperature regulation : an exercise approach : a thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy (Ph.D.), School of Sport and Exercise, Massey University, Palmerston North, New Zealand

Behavior represents our most preferred and effective modality by which body temperature is regulated. However, knowledge concerning the control of this behavior in humans is relatively limited. Therefore, the overall purpose of this thesis was to further our understanding of the control of human thermoregulatory behavior. This was accomplished by firstly establishing self-paced exercise and heat stress as a thermal behavioral model, while secondly the control of this behavior was investigated. In the first part of this thesis, voluntary reductions in exercise intensity have been found to be associated with thermal discomfort and reductions in heat production, which presumably improved heat exchange between the body and the environment over time, and ultimately aided body temperature regulation. Thus, these experimental data associatively indicate that reductions in exercise intensity in the heat are thermoregulatory behaviors, suggesting that self-paced exercise in the heat is a valid model by which to evaluate human thermal behavior. The studies presented in the second part of this thesis systematically evaluated the control of this behavior. It was subsequently demonstrated that skin temperature and the accompanying alterations in thermal perception and the percentage of peak oxygen uptake elicited by a given exercise intensity are all modulators of exercise intensity, and thus thermal behavior, in the heat. Notably, reductions in peak oxygen uptake appear to play a minimal role. Importantly, these studies strengthened the associations observed in the first part of this thesis by specifically establishing a causative relationship between exercise intensity and temperature regulation. Furthermore, the experimental observations also indicated that thermal behavior during self-paced exercise is ultimately initiated by the perception of effort response. In conclusion, the findings presented in this thesis suggest that a voluntary reduction in exercise intensity occurring in the heat is a thermoregulatory behavior, and that this behavior can be directly elicited by changes associated with elevations in skin temperature. During such instances, thermal perception and the percentage of peak oxygen uptake elicited by a given exercise intensity have been uniquely identified as contributors to this behavior. The findings of this thesis improve our understanding of the control of human thermoregulatory behavior

Age-related changes to cardiac systolic and diastolic function during whole-body passive hyperthermia

The effect of ageing on hyperthermia-induced changes in cardiac function is unknown. This study tested the hypothesis that hyperthermia-induced changes in left ventricular systolic and diastolic function are attenuated in older adults when compared with young adults. Eight older (71 ± 5 years old) and eight young adults (29 ± 5 years old), matched for sex, physical activity and body mass index, underwent whole-body passive hyperthermia. Mean arterial pressure (Finometer Pro), heart rate, forearm vascular conductance (venous occlusion plethysmography) and echocardiographic indices of diastolic and systolic function were measured during a normothermic supine period and again after an increase in internal temperature of ~1.0 °C. Hyperthermia decreased mean arterial pressure and left ventricular end-diastolic volumes and increased heart rate to a similar extent in both groups (P > 0.05). Ageing did not alter the magnitude of hyperthermia-induced changes in indices of systolic (lateral mitral annular S′ velocity) or diastolic function (lateral mitral annular E′ velocity, peak early diastolic filling and isovolumic relaxation time; P > 0.05). However, with hyperthermia the global longitudinal systolic strain increased in the older group, but was unchanged in the young group (P = 0.03). Also, older adults were unable to augment late diastolic ventricular filling [i.e. E/A ratio and A/(A + E) ratio] during hyperthermia, unlike the young (P <0.05). These findings indicate that older adults depend on a greater systolic contribution (global longitudinal systolic strain) to meet hyperthermic demand and that the atrial contribution to diastolic filling was not further augmented in older adults when compared with young adults

Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermia-induced hyperventilation

Postprint, author's accepted manuscriptThis study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end-tidal partial pressure of carbon dioxide (PET,CO2) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by ~1.8°C) to cause a sustained increase in ventilation and reduction in PET,CO2. Upon attaining hyperthermic hyperventilation, in protocol 1 (n = 10; three females) a bolus (19 ± 2 ml kg−1) of warm (~38°C) isotonic saline was rapidly (5–10 min) infused intravenously to restore reductions in central venous pressure, whereas in protocol 2 (n = 11; five females) phenylephrine was infused intravenously (60–120 μg min−1) to return mean arterial pressure to normothermic levels. In protocol 1, hyperthermia increased ventilation (by 2.2 ± 1.7 l min−1, P 0.05). In protocol 2, hyperthermia increased ventilation (by 5.0 ± 2.7l min−1, P 0.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre-hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans

Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage

Postprint, author's accepted manuscriptHyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature ∼1.1°C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAvmean), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAvmean (P = 0.001) by 12 ± 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 ± 1.4 l/min (P < 0.001), but did not alter MCAvmean (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 ± 0.9 l/min; P < 0.001), MAP (by 5 ± 6 mmHg; P = 0.004), and MCAvmean (by 12 ± 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans