20 research outputs found
Initial orthostatic hypotension at high altitude
No full textThomas, Kate N., Keith R. Burgess, Rishi Basnyat, Samuel J.E. Lucas, James D. Cotter, Jui-Lin Fan, Karen C. Peebles, Rebekah A.I. Lucas, Philip N. Ainslie. Initial orthostatic hypotension at high altitude. High Alt. Med. Biol. 11:163-167, 2010.-There are several reports on syncope occurring following standing at high altitude (HA), yet description of the detailed physiological responses to standing at HA are lacking. We examined the hypothesis that appropriate physiological adjustments to upright posture would be compromised at HA (5050m). Ten healthy volunteers stood up rapidly from supine rest, for 3min, at sea level and at 5050m. Beat-to-beat mean arterial blood pressure (MAP, Finometer), middle cerebral artery blood velocity (MCAv, Transcranial Doppler), end-tidal PCO2and PO2, and heart rate (ECG) were recorded continuously. After 14 days at HA, baseline MAP and MCAv were not different to sea level, although HR was elevated. Neither the magnitude of initial (0.05). By 3min of standing, MAP was restored to supine values both at sea level (-3±12mmHg) and HA (4±10mmHg), although there was more complete recovery of HR at sea level (+13±10b/min, p=0.02 vs.+23±10b/min, p=0.01). Reduced MCAv at 3min was comparable at sea level and altitude (both-16%). These data indicate that initial cardiovascular and cerebrovascular responses to standing are unaltered when partially acclimatized to HA
Cerebral vasomotor reactivity: Steady-state versus transient changes in carbon dioxide tension
No full textInfluence of indomethacin on ventilatory and cerebrovascular responsiveness to CO<sub>2</sub> and breathing stability:the influence of Pco<sub>2</sub> gradients
No full textIndomethacin (INDO), a reversible cyclooxygenase inhibitor, is a useful tool for assessing the role of cerebrovascular reactivity on ventilatory control. Despite this, the effect of INDO on breathing stability during wakefulness has yet to be examined. Although the effect of reductions in cerebrovascular CO reactivity on ventilatory CO sensitivity is likely dependent upon the method used, no studies have compared the effect of INDO on steady-state and modified rebreathing estimates of ventilatory CO sensitivity. The latter method includes the influence of PCO gradients and cerebral perfusion, whereas the former does not. We examined the hypothesis that INDO-induced reduction in cerebrovascular CO reactivity would 1) cause unstable breathing in conscious humans and 2) increase ventilatory CO sensitivity during the steady-state method but not during rebreathing methods. We measured arterial blood gases, ventilation (V̇E), and middle cerebral artery velocity (MCAv) before and 90 min following INDO ingestion (100 mg) or placebo in 12 healthy participants. There were no changes in resting arterial blood gases or V̇E following either intervention. INDO increased the magnitude of V̇E variability (index of breathing stability) during spontaneous air breathing (+4.3 ± 5.2 Δl/min, P = 0.01) and reduced MCAv (-25 ± 19%, P <0.01) and MCAv-CO reactivity during steady-state (-47 ± 27%, P <0.01) and rebreathing (-32 ± 25%, P <0.01). The V̇E-CO sensitivity during the steady-state method was increased with INDO (+0.5 ± 0.5 l·min·mmHg, P <0.01), while no changes were observed during rebreathing (P > 0.05). These data indicate that the net effect of INDO on ventilatory control is an enhanced ventilatory loop gain resulting in increased breathing instability. Our findings also highlight important methodological and physiological considerations when assessing the effect of INDO on ventilatory CO sensitivity, whereby the effect of INDO-induced reduction of cerebrovascular CO reactivity on ventilatory CO sensitivity is unmasked with the rebreathing method
Influence of indomethacin on the ventilatory and cerebrovascular responsiveness to hypoxia
No full textIndomethacin (INDO) has the potential to be a useful tool to explore the influence of cerebral blood flow and its responses to CO2 on ventilatory control. However, the effect of INDO on the cerebrovascular and ventilatory response to hypoxia remains unclear; therefore, we examined the effect of INDO on ventilatory and cerebrovascular sensitivity to hypoxia and hypercapnia. We measured end-tidal gases, ventilation (V̇E), and middle cerebral artery velocity (MCAv) before and 90 min following INDO (100 mg) in 12 healthy participants at rest and during hyperoxic hypercapnia and isocapnic hypoxia. Following INDO, resting V̇E and end-tidal gases were unaltered (P > 0.05), whilst MCAv was lowered by 25 ± 19% (P <0.001). INDO ingestion reduced MCAv-CO2 reactivity by 46 ± 29% (2.9 ± 0.9 vs. 1.7 ± 0.9 cm/s/mmHg; P <0.001) and enhanced the V̇E-CO2 sensitivity by 0.5 ± 0.5 L min / mmHg (1.9 ± 1.5 vs. 2.3 ± 1.6 L min/mmHg; P <0.05). No changes were observed in either the MCAv or V̇E responsiveness to isocapnic hypoxia following INDO ingestion (P > 0.05). These findings indicate that INDO does not alter cerebrovascular and ventilatory responsiveness to hypoxia, indicating a preserved peripheral chemoreflex in response to this pharmacological agent
Brain charts for the human lifespan [Elektronisk resurs]
No full textOver the past few decades, neuroimaging has become a ubiquitous tool in basic research and clinical studies of the human brain. However, no reference standards currently exist to quantify individual differences in neuroimaging metrics over time, in contrast to growth charts for anthropometric traits such as height and weight1. Here we assemble an interactive open resource to benchmark brain morphology derived from any current or future sample of MRI data ( http://www.brainchart.io/ ). With the goal of basing these reference charts on the largest and most inclusive dataset available, acknowledging limitations due to known biases of MRI studies relative to the diversity of the global population, we aggregated 123,984 MRI scans, across more than 100 primary studies, from 101,457 human participants between 115 days post-conception to 100 years of age. MRI metrics were quantified by centile scores, relative to non-linear trajectories2 of brain structural changes, and rates of change, over the lifespan. Brain charts identified previously unreported neurodevelopmental milestones3, showed high stability of individuals across longitudinal assessments, and demonstrated robustness to technical and methodological differences between primary studies. Centile scores showed increased heritability compared with non-centiled MRI phenotypes, and provided a standardized measure of atypical brain structure that revealed patterns of neuroanatomical variation across neurological and psychiatric disorders. In summary, brain charts are an essential step towards robust quantification of individual variation benchmarked to normative trajectories in multiple, commonly used neuroimaging phenotypes. © 2022. The Author(s)
Brain charts for the human lifespan
No full textOver the past few decades, neuroimaging has become a ubiquitous tool in basic research and clinical studies of the human brain. However, no reference standards currently exist to quantify individual differences in neuroimaging metrics over time, in contrast to growth charts for anthropometric traits such as height and weight1. Here we assemble an interactive open resource to benchmark brain morphology derived from any current or future sample of MRI data ( http://www.brainchart.io/ ). With the goal of basing these reference charts on the largest and most inclusive dataset available, acknowledging limitations due to known biases of MRI studies relative to the diversity of the global population, we aggregated 123,984 MRI scans, across more than 100 primary studies, from 101,457 human participants between 115 days post-conception to 100 years of age. MRI metrics were quantified by centile scores, relative to non-linear trajectories2 of brain structural changes, and rates of change, over the lifespan. Brain charts identified previously unreported neurodevelopmental milestones3, showed high stability of individuals across longitudinal assessments, and demonstrated robustness to technical and methodological differences between primary studies. Centile scores showed increased heritability compared with non-centiled MRI phenotypes, and provided a standardized measure of atypical brain structure that revealed patterns of neuroanatomical variation across neurological and psychiatric disorders. In summary, brain charts are an essential step towards robust quantification of individual variation benchmarked to normative trajectories in multiple, commonly used neuroimaging phenotypes. © 2022. The Author(s)
Excessive occupational heat exposure: a significant ergonomic challenge and health risk for current and future workers
No full textOccupational heat exposure threatens the health of a worker not only when heat illness occurs but also when a worker's performance and work capacity is impaired. Occupational contexts that involve hot and humid climatic conditions, heavy physical workloads and/or protective clothing create a strenuous and potentially dangerous thermal load for a worker. There are recognized heat prevention strategies and international thermal ergonomic standards to protect the worker. However, such standards have been developed largely in temperate western settings, and their validity and relevance is questionable for some geographical, cultural and socioeconomic contexts where the risk of excessive heat exposure can be high. There is evidence from low- and middle-income tropical countries that excessive heat exposure remains a significant issue for occupational health. Workers in these countries are likely to be at high risk of excessive heat exposure as they are densely populated, have large informal work sectors and are expected to experience substantial increases in temperature due to global climate change. The aim of this paper is to discuss current and future ergonomic risks associated with working in the heat as well as potential methods for maintaining the health and productivity of workers, particularly those most vulnerable to excessive heat exposure.
Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge
Get PDFPostprint, author's accepted manuscriptPassive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress
Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated hemorrhagic challenge
Get PDFPostprint, author's accepted manuscriptTolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin) and core temperatures (Tcore) on LBNP tolerance. We hypothesized that elevations in Tskin as well as Tcore would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskin and Tcore were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i) control, with neutral Tskin (34.3 ± 0.5°C) and Tcore (36.8 ± 0.2°C); (ii) primarily skin hyperthermia, with high Tskin (37.6 ± 0.2°C) and neutral Tcore (37.1 ± 0.2°C); (iii) primarily core hyperthermia, with neutral Tskin (35.0 ± 0.5°C) and high Tcore (38.3 ± 0.2°C); and (iv) combined skin and core hyperthermia, with high Tskin (38.8 ± 0.6°C) and high Tcore (38.1 ± 0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury × minutes). The LBNP tolerance was reduced during the skin hyperthermia (569 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; both P < 0.05). However, LBNP tolerance did not differ between skin hyperthermia and core hyperthermia trials (P = 0.92). The lowest LBNP tolerance was observed during combined skin and core hyperthermia(257±106mmHgmin;P<0.05 relative to all other trials). These data indicate that elevated skin temperature, as well as elevated core temperature, can both contribute to reductions in LBNP tolerance in heat-stressed individuals. However, heat stress-induced reductions in LBNP tolerance are greatest in conditions when both skin and core temperatures are elevated
Influence of high altitude on cerebrovascular and ventilatory responsiveness to CO<sub>2</sub>
No full textAn altered acid–base balance following ascent to high altitude has been well established. Such changes in pH buffering could potentially account for the observed increase in ventilatory CO2 sensitivity at high altitude. Likewise, if [H+] is the main determinant of cerebrovascular tone, then an alteration in pH buffering may also enhance the cerebral blood flow (CBF) responsiveness to CO2 (termed cerebrovascular CO2 reactivity). However, the effect altered acid–base balance associated with high altitude ascent on cerebrovascular and ventilatory responsiveness to CO2 remains unclear. We measured ventilation (V̇E), middle cerebral artery velocity (MCAv; index of CBF) and arterial blood gases at sea level and following ascent to 5050 m in 17 healthy participants during modified hyperoxic rebreathing. At 5050 m, resting V̇E, MCAv and pH were higher (P < 0.01), while bicarbonate concentration and partial pressures of arterial O2 and CO2 were lower (P < 0.01) compared to sea level. Ascent to 5050 m also increased the hypercapnic MCAv CO2 reactivity (2.9 ± 1.1 vs. 4.8 ± 1.4% mmHg−1; P < 0.01) and V̇E CO2 sensitivity (3.6 ± 2.3 vs. 5.1 ± 1.7 l min−1 mmHg−1; P < 0.01). Likewise, the hypocapnic MCAv CO2 reactivity was increased at 5050 m (4.2 ± 1.0 vs. 2.0 ± 0.6% mmHg−1; P < 0.01). The hypercapnic MCAv CO2 reactivity correlated with resting pH at high altitude (R2= 0.4; P < 0.01) while the central chemoreflex threshold correlated with bicarbonate concentration (R2= 0.7; P < 0.01). These findings indicate that (1) ascent to high altitude increases the ventilatory CO2 sensitivity and elevates the cerebrovascular responsiveness to hypercapnia and hypocapnia, and (2) alterations in cerebrovascular CO2 reactivity and central chemoreflex may be partly attributed to an acid–base balance associated with high altitude ascent. Collectively, our findings provide new insights into the influence of high altitude on cerebrovascular function and highlight the potential role of alterations in acid–base balance in the regulation in CBF and ventilatory control
