Association Between Acute Kidney Injury Hospital Visits and Environmental Heat Stress at a Nicaraguan Sugarcane Plantation.

BACKGROUND: Mesoamerican sugarcane cutters are at a high risk of chronic kidney disease of non-traditional origin, a disease likely linked to heat-related acute kidney injury (AKI). Studies in general populations have described a positive association between high environmental temperatures and clinically assessed kidney outcomes, but there are no studies in occupational settings. METHOD: We accessed routine records of clinically diagnosed AKI (AKI-CD) and wet bulb globe temperatures (WBGT) at a large Nicaraguan sugarcane plantation and modeled the relationship between these using negative binomial regression. A rest-shade-hydration intervention was gradually enhanced during the study period, and efforts were made to increase the referral of workers with suspected AKI to healthcare. RESULTS: Each 1°C WBGT was associated with an 18% (95% confidence interval [CI]: [4, 33%]) higher AKI-CD rate on the same day and a 14% (95% CI [-5, 37%]) higher rate over a week. AKI-CD rates and severity, and time between symptoms onset and diagnosis decreased during the study period, that is, with increasing rest-shade-hydration intervention. Symptoms and biochemical signs of systemic inflammation were common among AKI-CD cases. DISCUSSION: Occupational heat stress, resulting from heavy work in environmental heat, was associated with a higher rate of clinically diagnosed AKI in a population at risk of CKDnt. Promoting rest-shade-hydration may have contributed to reducing AKI rates during the study period. Occupational health and safety personnel have key roles to play in enforcing rest, shade, and hydration practices, referring workers with suspected AKI to healthcare as well as collecting and analyzing the data needed to support workplace heat stress interventions.

Impact of heat and a rest-shade-hydration intervention program on productivity of piece-paid industrial agricultural workers at risk of chronic kidney disease of nontraditional origin.

OBJECTIVES: Assess the impact of environmental heat and a rest-shade-hydration (RSH) intervention against heat stress on productivity of piece-paid Mesoamerican sugarcane cutters. These workers are at a high risk of chronic kidney disease of non-traditional origin (CKDnt), from the severe heat stress they experience due to heavy work under hot conditions. RSH interventions in these populations improve kidney health outcomes, but their impact on productivity has yet to be examined. METHODS: We accessed routine productivity data from seed (SC, N = 749) and burned (BCC, N = 535) sugarcane cutters observed over five harvest seasons with increasing RSH intervention at a large Nicaraguan sugarcane mill. Hourly field-site wet-bulb globe temperature (WBGT) was recorded by mill staff and summarized as a daily mean. Mixed linear regression was used to model daily productivity, adjusting for age (18-29, 30-44, and >45 years), sex, WBGT (<28, 28-29, 29-30, 30-31, and >31 °C) on the same and preceding day, harvest season (2017-18 to 2021-22), month, and acclimatization status (<1, 1-2, and >2 weeks). RESULTS: There was an inverse dose-response relationship between SC productivity and WBGT on the same and preceding days, decreasing by approximately 3%/°C WBGT. Productivity increased during the study period, i.e. coinciding with RSH scale-up, by approximately 19% in SC and 9% in BCC. CONCLUSION: Agricultural worker productivity was expected lower on hotter days, strengthening the interest in all stakeholders to mitigate increasing global temperatures and their impact. Despite decreasing the total time allocated for work each day, an RSH intervention appears to result in increased productivity and no apparent loss in productivity.

Exposure to passive heat and cold stress differentially modulates cerebrovascular-CO2 responsiveness.

Heat and cold stress influence cerebral blood flow (CBF) regulatory factors (e.g., arterial CO2 partial pressure). However, it is unclear whether the CBF response to a CO2 stimulus (i.e., cerebrovascular-CO2 responsiveness) is maintained under different thermal conditions. This study aimed to compare cerebrovascular-CO2 responsiveness between normothermia, passive heat, and cold stress conditions. Sixteen participants (8 females; 25 ± 7 yr) completed two experimental sessions (randomized) comprising normothermic and either passive heat or cold stress conditions. Middle and posterior cerebral artery velocity (MCAv, PCAv) were measured during rest, hypercapnia (5% CO2 inhalation), and hypocapnia (voluntary hyperventilation to an end-tidal CO2 of 30 mmHg). The linear slope of the cerebral blood velocity (CBv) response to changing end-tidal CO2 was calculated to measure cerebrovascular-CO2 responsiveness, and cerebrovascular conductance (CVC) was used to examine responsiveness independent of blood pressure. CBv-CVC-CO2 responsiveness to hypocapnia was greater during heat stress compared with cold stress (MCA: +0.05 ± 0.08 cm/s/mmHg/mmHg, P = 0.04; PCA: +0.02 ± 0.02 cm/s/mmHg/mmHg, P = 0.002). CBv-CO2 responsiveness to hypercapnia decreased during heat stress (MCA: -0.67 ± 0.89 cm/s/mmHg, P = 0.02; PCA: -0.64 ± 0.62 cm/s/mmHg; P = 0.01) and increased during cold stress (MCA: +0.98 ± 1.33 cm/s/mmHg, P = 0.03; PCA: +1.00 ± 0.82 cm/s/mmHg; P = 0.01) compared with normothermia. However, CBv-CVC-CO2 responsiveness to hypercapnia was not different between thermal conditions (P > 0.08). Overall, passive heat, but not cold, stress challenges the maintenance of cerebral perfusion. A greater cerebrovascular responsiveness to hypocapnia during heat stress likely reduces an already impaired cerebrovascular reserve capacity and may contribute to adverse events (e.g., syncope).NEW & NOTEWORTHY This study demonstrates that thermoregulatory-driven perfusion pressure changes, from either cold or heat stress, impact cerebrovascular responsiveness to hypercapnia. Compared with cold stress, heat stress poses a greater challenge to the maintenance of cerebral perfusion during hypocapnia, challenging cerebrovascular reserve capacity while increasing cerebrovascular-CO2 responsiveness. This likely exacerbates cerebral hypoperfusion during heat stress since hyperthermia-induced hyperventilation results in hypocapnia. No regional differences in middle and posterior cerebral artery responsiveness were found with thermal stress.

Targeting workload to ameliorate risk of heat stress in industrial sugarcane workers.

OBJECTIVE: The aim of this study was to quantify the physiological workload of manual laborers in industrial sugarcane and assess the effect of receiving a rest, shade, and hydration intervention to reduce heat stress exposure risk. METHODS: In an observational study, physiological workload was evaluated for burned cane cutters (BCC), seed cutters (SC) and drip irrigation repair workers (DIRW) using heart rate (HR) recorded continuously (Polar®) across a work shift. Workers' percentage of maximal HR (%HRmax), time spent in different HR zones, and estimated core temperature (ECTemp) were calculated. The effect of increasing rest across two harvests was evaluated for BCC and SC. RESULTS: A total of 162 workers participated in this study [52 BCC (all male), 71 SC (13 female) and 39 DIRW (16 female)]. Average %HRmax across a work shift was similar between BCC and SC (BCC: 58%, SC: 59%), but lower in DIRW (51%). BCC and SC spent similar proportions of work shifts at hard/very hard intensities (BCC: 13%, SC: 15%), versus DIRW who worked mostly at light (46%) or light-moderate (39%) intensities. SC maximum ECTemp reached 38.2°C, BCC 38.1°C; while DIRW only reached 37.7°C. Females performed at a higher %HRmax than males across work shifts (SC 64% versus 58%; DIRW 55% versus 49%). An additional rest period was associated with a lower average %HRmax across a work shift in BCC. CONCLUSION: In this setting, BCC and SC both undertake very physiologically demanding work. Females maintained a higher workload than male co-workers. Regulated rest periods each hour, with water and shade access, appears to reduce physiological workload/strain.

Non-pharmacological interventions for vascular health and the role of the endothelium.

The most common non-pharmacological intervention for both peripheral and cerebral vascular health is regular physical activity (e.g., exercise training), which improves function across a range of exercise intensities and modalities. Numerous non-exercising approaches have also been suggested to improved vascular function, including repeated ischemic preconditioning (IPC); heat therapy such as hot water bathing and sauna; and pneumatic compression. Chronic adaptive responses have been observed across a number of these approaches, yet the precise mechanisms that underlie these effects in humans are not fully understood. Acute increases in blood flow and circulating signalling factors that induce responses in endothelial function are likely to be key moderators driving these adaptations. While the impact on circulating factors and environmental mechanisms for adaptation may vary between approaches, in essence, they all centre around acutely elevating blood flow throughout the circulation and stimulating improved endothelium-dependent vascular function and ultimately vascular health. Here, we review our current understanding of the mechanisms driving endothelial adaptation to repeated exposure to elevated blood flow, and the interplay between this response and changes in circulating factors. In addition, we will consider the limitations in our current knowledge base and how these may be best addressed through the selection of more physiologically relevant experimental models and research. Ultimately, improving our understanding of the unique impact that non-pharmacological interventions have on the vasculature will allow us to develop superior strategies to tackle declining vascular function across the lifespan, prevent avoidable vascular-related disease, and alleviate dependency on drug-based interventions.

Impact of acute dynamic exercise and arterial shear rate modification on radial artery low-flow mediated constriction in young men.

PURPOSE: Leg cycling exercise acutely augments radial artery low-flow mediated constriction (L-FMC). Herein, we sought to determine whether this is associated with exercise-induced changes in arterial shear rate (SR). METHODS: Ten healthy and recreationally active young men (23 ± 2 years) participated in 30 min of incremental leg cycling exercise (50, 100, 150 Watts). Trials were repeated with (Exercise + WC) and without (Exercise) the use of a wrist cuff (75 mmHg) placed distal to the radial artery to increase local retrograde SR while reducing mean and anterograde SR. Radial artery characteristics were measured throughout the trial, and L-FMC and flow mediated dilatation (FMD) were assessed before and acutely (~ 10 min) after leg cycling. RESULTS: Exercise increased radial artery mean and anterograde SR, along with radial artery diameter, velocity, blood flow and conductance (P < 0.05). Exercise + WC attenuated the exercise-induced increase in mean and anterograde SR (P > 0.05) but also increased retrograde SR (P < 0.05). In addition, increases in radial artery blood flow and diameter were reduced during Exercise + WC (Exercise + WC vs. Exercise, P < 0.05). After Exercise, L-FMC was augmented (- 4.4 ± 1.4 vs. - 13.1 ± 1.6%, P < 0.05), compared to no change in L-FMC after Exercise + WC (- 5.2 ± 2.0 vs. - 3.0 ± 1.6%, P > 0.05). In contrast, no change in FMD was observed in either Exercise or Exercise + WC trials (P > 0.05). CONCLUSIONS: These findings indicate that increases in L-FMC following exercise are abolished by the prevention of increases radial artery diameter, mean and anterograde SR, and by elevation of retrograde SR, during exercise in young men.

Workplace Intervention for Heat Stress: Essential Elements of Design, Implementation, and Assessment.

Heat stress is associated with numerous health effects that potentially harm workers, especially in a warming world. This investigation occurred in a setting where laborers are confronted with occupational heat stress from physically demanding work in high environmental temperatures. Collaboration with a major Nicaraguan sugarcane producer offered the opportunity to study interventions to prevent occupational heat-stress-related kidney disease. Two aims for this study of a rest-shade-water intervention program were: (1) describe the evolving intervention, summarize findings that motivated proposed improvements, assess impact of those improvements, and identify challenges to successful implementation and (2) extract primary lessons learned about intervention research that have both general relevance to investigations of work-related disease prevention and specific relevance to this setting. The learning curve for the various stakeholders as well as the barriers to success demonstrate that effectiveness of an intervention cannot be adequately assessed without considerations of implementation. Designing, effectively implementing, and assessing both health impacts and implementation quality is a resource-intensive endeavor requiring a transdisciplinary approach. Both general and specific lessons learned are presented for decisions on study design and study elements, implementation assessment, and management engagement in understanding how productivity and health can be successfully balanced and for building effective communication between investigators and all levels of management.

Menstrual phase influences cerebrovascular responsiveness in females but may not affect sex differences.

Background and aims: Sex differences in the rate and occurrence of cerebrovascular diseases (e.g., stroke) indicate a role for female sex hormones (i.e., oestrogen and progesterone) in cerebrovascular function and regulation. However, it remains unclear how cerebrovascular function differs between the sexes, and between distinct phases of the menstrual cycle. This study aimed to compare cerebrovascular-CO2 responsiveness in 1) females during the early follicular (EF), ovulatory (O) and mid-luteal (ML) phases of their menstrual cycle; and 2) males compared to females during phases of lower oestrogen (EF) and higher oestrogen (O). Methods: Eleven females (25 ± 5 years) complete experimental sessions in the EF (n = 11), O (n = 9) and ML (n = 11) phases of the menstrual cycle. Nine males (22 ± 3 years) completed two experimental sessions, approximately 2 weeks apart for comparison to females. Middle and posterior cerebral artery velocity (MCAv, PCAv) was measured at rest, during two stages of hypercapnia (2% and 5% CO2 inhalation) and hypocapnia (voluntary hyperventilation to an end-tidal CO2 of 30 and 24 mmHg). The linear slope of the cerebral blood velocity response to changes in end-tidal CO2 was calculated to measure cerebrovascular-CO2 responsiveness.. Results: In females, MCAv-CO2 responsiveness to hypocapnia was lower during EF (-.78 ± .45 cm/s/mmHg) when compared to the O phase (-1.17 ± .52 cm/s/mmHg; p < .05) and the ML phase (-1.30 ± .82; p < .05). MCAv-CO2 responsiveness to hypercapnia and hypo-to-hypercapnia, and PCAv-CO2 responsiveness across the CO2 range were similar between menstrual phases (p ≥ .20). MCAv-CO2 responsiveness to hypo-to hypercapnia was greater in females compared to males (3.12 ± .91 cm/s/mmHg vs. 2.31 ± .46 cm/s/mmHg; p = .03), irrespective of menstrual phase (EF or O). Conclusion: Females during O and ML phases have an enhanced vasoconstrictive capacity of the MCA compared to the EF phase. Additionally, biological sex differences can influence cerebrovascular-CO2 responsiveness, dependent on the insonated vessel.

A Systematic Review and Meta-Analysis Examining Whether Changing Ovarian Sex Steroid Hormone Levels Influence Cerebrovascular Function.

Sex differences in cerebrovascular disease rates indicate a possible role for ovarian sex steroid hormones in cerebrovascular function. To synthesise and identify knowledge gaps, a systematic review and meta-analysis was conducted to assess how ovarian sex steroid hormone changes across the lifespan affect cerebrovascular function in women. Three databases (EMBASE, MEDLINE and Web of Science) were systematically searched for studies on adult cerebrovascular function and ovarian sex steroid hormones. Forty-five studies met pre-defined inclusion criteria. Studied hormone groups included hormone replacement therapy (HRT; n = 17), pregnancy (n = 12), menstrual cycle (n = 7), menopause (n = 5), oral contraception (n = 2), and ovarian hyperstimulation (n = 2). Outcome measures included pulsatility index (PI), cerebral blood flow/velocity (CBF), resistance index (RI), cerebral autoregulation, and cerebrovascular reactivity. Meta-analysis was carried out on HRT studies. PI significantly decreased [-0.05, 95% CI: (-0.10, -0.01); p = 0.01] in post-menopausal women undergoing HRT compared to post-menopausal women who were not, though there was considerable heterogeneity (I 2 = 96.8%). No effects of HRT were seen in CBF (p = 0.24) or RI (p = 0.77). This review indicates that HRT improves PI in post-menopausal women. However, there remains insufficient evidence to determine how changing ovarian sex steroid hormone levels affects cerebrovascular function in women during other hormonal phases (e.g., pregnancy, oral contraception).

Sex differences in adaptation to intermittent post-exercise sauna bathing in trained middle-distance runners.

BACKGROUND: The purpose of this study was to investigate the effect of sex on the efficacy of intermittent post-exercise sauna bathing to induce heat acclimation and improve markers of temperate exercise performance in trained athletes. METHODS: Twenty-six trained runners (16 female; mean ± SD, age 19 ± 1 years, V̇O2max F: 52.6 ± 6.9 mL⋅kg-1⋅min-1, M: 64.6 ± 2.4 mL⋅kg-1⋅min-1) performed a running heat tolerance test (30 min, 9 km⋅h-1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [V̇O2max] and lactate profile) pre and post 3 weeks of normal exercise training plus 29 ± 1 min post-exercise sauna bathing (101-108 °C) 3 ± 1 times per week. RESULTS: Females and males exhibited similar reductions (interactions p > 0.05) in peak rectal temperature (- 0.3 °C; p < 0.001), skin temperature (- 0.9 °C; p < 0.001) and heart rate (- 9 beats·min-1; p = 0.001) during the HTT at post- vs pre-intervention. Only females exhibited an increase in active sweat glands on the forearm (measured via modified iodine technique; F: + 57%, p < 0.001; M: + 1%, p = 0.47). Conversely, only males increased forearm blood flow (measured via venous occlusion plethysmography; F: + 31%, p = 0.61; M: + 123%; p < 0.001). Females and males showed similar (interactions p > 0.05) improvements in V̇O2max (+ 5%; p = 0.02) and running speed at 4 mmol·L-1 blood lactate concentration (+ 0.4 km·h-1; p = 0.001). CONCLUSIONS: Three weeks of post-exercise sauna bathing effectively induces heat acclimation in females and males, though possibly amid different thermoeffector adaptations. Post-exercise sauna bathing is also an effective ergogenic aid for both sexes.

Occupational heat exposure and the risk of chronic kidney disease of nontraditional origin in the United States.

Occupational heat exposure is linked to the development of kidney injury and disease in individuals who frequently perform physically demanding work in the heat. For instance, in Central America, an epidemic of chronic kidney disease of nontraditional origin (CKDnt) is occurring among manual laborers, whereas potentially related epidemics have emerged in India and Sri Lanka. There is growing concern that workers in the United States suffer with CKDnt, but reports are limited. One of the leading hypotheses is that repetitive kidney injury caused by physical work in the heat can progress to CKDnt. Whether heat stress is the primary causal agent or accelerates existing underlying pathology remains contested. However, the current evidence supports that heat stress induces tubular kidney injury, which is worsened by higher core temperatures, dehydration, longer work durations, muscle damaging exercise, and consumption of beverages containing high levels of fructose. The purpose of this narrative review is to identify occupations that may place US workers at greater risk of kidney injury and CKDnt. Specifically, we reviewed the scientific literature to characterize the demographics, environmental conditions, physiological strain (i.e., core temperature increase, dehydration, heart rate), and work durations in sectors typically experiencing occupational heat exposure, including farming, wildland firefighting, landscaping, and utilities. Overall, the surprisingly limited available evidence characterizing occupational heat exposure in US workers supports the need for future investigations to understand this risk of CKDnt.

Corrigendum: Cerebral Hemodynamic and Neurotrophic Factor Responses Are Dependent on the Type of Exercise.

[This corrects the article DOI: 10.3389/fphys.2020.609935.].

Intermittent post-exercise sauna bathing improves markers of exercise capacity in hot and temperate conditions in trained middle-distance runners.

PURPOSE: This study investigated whether intermittent post-exercise sauna bathing across three-weeks endurance training improves exercise heat tolerance and exercise performance markers in temperate conditions, compared to endurance training alone. The subsidiary aim was to determine whether exercise-heat tolerance would further improve following 7-Weeks post-exercise sauna bathing. METHODS: Twenty middle-distance runners (13 female; mean ± SD, age 20 ± 2 years, [Formula: see text]O2max 56.1 ± 8.7 ml kg-1 min-1) performed a running heat tolerance test (30-min, 9 km h-1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [[Formula: see text]O2max], speed at 4 mmol L-1 blood lactate concentration ([La-]) before (Pre) and following three-weeks (3-Weeks) normal training (CON; n = 8) or normal training with 28 ± 2 min post-exercise sauna bathing (101-108 °C, 5-10%RH) 3 ± 1 times per week (SAUNA; n = 12). Changes from Pre to 3-Weeks were compared between-groups using an analysis of co-variance. Six SAUNA participants continued the intervention for 7 weeks, completing an additional HTT (7-Weeks; data compared using a one-way repeated-measures analysis of variance). RESULTS: During the HTT, SAUNA reduced peak rectal temperature (Trec; - 0.2 °C), skin temperature (- 0.8 °C), and heart rate (- 11 beats min-1) more than CON at 3-Weeks compared to Pre (all p < 0.05). SAUNA also improved [Formula: see text]O2max (+ 0.27 L-1 min-1; p = 0.02) and speed at 4 mmol L-1 [La-] (+ 0.6 km h-1; p = 0.01) more than CON at 3-Weeks compared to Pre. Only peak Trec (- 0.1 °C; p = 0.03 decreased further from 3-Weeks to 7-Weeks in SAUNA (other physiological variables p > 0.05). CONCLUSIONS: Three-weeks post-exercise sauna bathing is an effective and pragmatic method of heat acclimation, and an effective ergogenic aid. Extending the intervention to seven weeks only marginally improved Trec.

Impact of whole body passive heat stress and arterial shear rate modification on radial artery function in young men.

We sought to determine how whole body heating acutely influences radial artery function, characterized using flow-mediated dilation (FMD) and low-flow-mediated constriction (L-FMC), and the mechanistic role of shear rate modification on radial artery functional characteristics during heating. Eleven young healthy men underwent whole body heating (water-perfused suit) sufficient to raise the core temperature by +1°C. Trials were repeated with (heat + WC) and without (heat) the application of a wrist cuff located distal to the radial artery examined, known to prevent increases in mean and anterograde shear rates but increase retrograde shear rate. Radial artery characteristics were assessed throughout each trial, with FMD and L-FMC assessed before and upon reaching the target core temperature. Heat markedly increased radial artery mean and anterograde shear rates, along with radial artery diameter and blood flow (P < 0.05). Heat + WC abolished the heat-induced increase in mean and anterograde shear rates (P > 0.05) but markedly increased retrograde shear rate (P < 0.05). Concomitantly, increases in radial artery diameter and blood flow were decreased (heat + WC vs. heat, P < 0.05). Heat attenuated FMD (8.6 ± 1.2% vs. 2.2 ± 1.4%, P < 0.05), whereas no change in FMD was observed in heat + WC (7.8 ± 1.2% vs. 10.8 ± 1.2%, P > 0.05). In contrast, L-FMC was not different in either trial (P > 0.05). In summary, acute whole body heating markedly elevates radial artery shear rate, diameter, and blood flow and diminishes FMD. However, marked radial artery vasodilation and diminished FMD are absent when these shear rate changes are prevented. Shear rate modifications underpin the radial artery response to acute whole body heat stress, but further endothelium-dependent vasodilation (FMD) is attenuated likely as the vasodilatory range limit is approached.NEW & NOTEWORTHY We observed that acute whole body heating elevates radial artery shear rate, diameter, and blood flow. This results in a diminished flow-meditated dilatation (FMD) but does not change low-flow-mediated constriction (L-FMC). Preventing shear rate changes during whole body heating reduces radial artery vasodilation and reverses FMD reductions but has no effect on L-FMC. These findings indicate that shear rate changes underpin conduit artery responses to acute whole body heat stress, but further endothelium-dependent flow-mediated vasodilation is attenuated as the vasodilatory range limit is approached.

Exercise-induced elevations in cerebral blood velocity are greater in running compared to cycling at higher intensities.

The optimal exercise intensity and modality for maximizing cerebral blood flow (CBF) and hence potential exposure to positive, hemodynamically derived cerebral adaptations is yet to be fully determined. This study compared CBF velocity responses between running and cycling across a range of exercise intensities. Twenty-six participants (12 females; age: 26 ± 8 years) completed four exercise sessions; two mode-specific maximal oxygen consumption (VO2max ) tests, followed by (order randomized) two incremental exercise protocols (3-min stages at 35%, 50%, 65%, 80%, 95% VO2max ). Continuous measures of middle cerebral artery velocity (MCAv), oxygen consumption, end-tidal CO2 (PET CO2 ), and heart rate were obtained. Modality-specific MCAv changes were observed for the whole group (interaction effect: p = .01). Exercise-induced increases in MCAvmean during cycling followed an inverted-U pattern, peaking at 65% VO2max (Δ12 ± 7 cm/s from rest), whereas MCAvmean during running increased linearly up to 95% VO2max (change from rest: Δ12 ± 13 vs. Δ7 ± 8 cm/s for running vs. cycling at 95% VO2max ; p = .01). In contrast, both modalities had an inverted-U pattern for PET CO2 changes, although peaked at different intensities (running: 50% VO2max , Δ6 ± 2 mmHg; cycling: 65% VO2max , Δ7 ± 2 mmHg; interaction effect: p = .01). Further subgroup analysis revealed that the running-specific linear MCAvmean response was fitness dependent (Fitness*modality*intensity interaction effect: p = .04). Above 65% VO2max , fitter participants (n = 16; male > 45 mL/min/kg and female > 40 mL/min/kg) increased MCAvmean up to 95% VO2max , whereas in unfit participants (n = 7, male < mL/min/kg and female < 35 mL/min/kg) MCAvmean returned toward resting values. Findings demonstrate that modality- and fitness-specific profiles for MCAvmean are seen at exercise intensities exceeding 65% VO2max .

Pathophysiological Mechanisms by which Heat Stress Potentially Induces Kidney Inflammation and Chronic Kidney Disease in Sugarcane Workers.

BACKGROUND: Chronic kidney disease of non-traditional origin (CKDnt) is common among Mesoamerican sugarcane workers. Recurrent heat stress and dehydration is a leading hypothesis. Evidence indicate a key role of inflammation. METHODS: Starting in sports and heat pathophysiology literature, we develop a theoretical framework of how strenuous work in heat could induce kidney inflammation. We describe the release of pro-inflammatory substances from a leaky gut and/or injured muscle, alone or in combination with tubular fructose and uric acid, aggravation by reduced renal blood flow and increased tubular metabolic demands. Then, we analyze longitudinal data from >800 sugarcane cutters followed across harvest and review the CKDnt literature to assess empirical support of the theoretical framework. RESULTS: Inflammation (CRP elevation and fever) and hyperuricemia was tightly linked to kidney injury. Rehydrating with sugary liquids and NSAID intake increased the risk of kidney injury, whereas electrolyte solution consumption was protective. Hypokalemia and hypomagnesemia were associated with kidney injury. DISCUSSION: Heat stress, muscle injury, reduced renal blood flow and fructose metabolism may induce kidney inflammation, the successful resolution of which may be impaired by daily repeating pro-inflammatory triggers. We outline further descriptive, experimental and intervention studies addressing the factors identified in this study.

Insulation and Evaporative Resistance of Clothing for Sugarcane Harvesters and Chemical Sprayers, and Their Application in PHS Model-Based Exposure Predictions.

Many workers are exposed to heat stress that can be exacerbated by the type of clothing they wear. The resulted heat strain can lead to short or long-term heat-related disorders. This study aimed to measure clothing properties of sugarcane field workers and evaluate the heat strain by an international standard, predicted heat strain model (PHS). The clothing thermal insulation and evaporative resistance values of sugarcane cutter and chemical sprayer outfits were acquired for the whole body, body regions and specific body parts via thermal manikin measurements. The detailed clothing insulation values of body parts can be utilized in advanced thermo-physiological models, while in this study, the values for the whole body together with weather data were used in PHS. Estimated duration limited exposure times (DLE) for an hour-by-hour prediction over a workday and for a range of high humidity scenarios were calculated. Such evaluation tools can be used for risk assessment and management to support organizational measures and prepare equipment and materials in the case of hot weather events in order to avoid dehydration and other heat-related disorders.

The CO2 stimulus duration and steady-state time point used for data extraction alters the cerebrovascular reactivity outcome measure.

NEW FINDINGS: What is the central question of this study? Cerebrovascular reactivity (CVR) is a common functional test to assess brain health, and impaired CVR has been associated with all-cause cardiovascular mortality: does the duration of the CO2 stimulus and the time point used for data extraction alter the CVR outcome measure? What is the main finding and its importance? This study demonstrated CVR measures calculated from 1 and 2 min CO2 stimulus durations were significantly higher than CVR calculated from a 4 min CO2 stimulus. CVRs calculated from the first 2 min of the CO2 stimulus were significantly higher than CVR values calculated from the final minute if the duration was ≥4 min. This study highlights the need for consistent methodological approaches. ABSTRACT: Cerebrovascular reactivity to carbon dioxide (CVR) is a common functional test to assess brain vascular health, though conflicting age and fitness effects have been reported. Studies have used different CO2 stimulus durations to induce CVR and extracted data from different time points for analysis. Therefore, this study examined whether these differences alter CVR and explain conflicting findings. Eighteen healthy volunteers (24 ± 5 years) inhaled CO2 for four stimulus durations (1, 2, 4 and 5 min) of 5% CO2 (in air) via the open-circuit Douglas bag method, in a randomized order. CVR data were derived from transcranial Doppler (TCD) measures of middle cerebral artery blood velocity (MCAv), with concurrent ventilatory sensitivity to the CO2 stimulus ( V̇E,CO2 ). Repeated measures ANOVAs compared CVR and V̇E,CO2 measures between stimulus durations and steady-state time points. An effect of stimulus duration was observed (P = 0.002, η² = 0.140), with 1 min (P = 0.010) and 2 min (P < 0.001) differing from 4 min, and 2 min differing from 5 min (P = 0.019) durations. V̇E,CO2 sensitivity increased ∼3-fold from 1 min to 4 and 5 min durations (P < 0.001, η² = 0.485). CVRs calculated from different steady-state time points within each stimulus duration were different (P < 0.001, η² = 0.454), specifically for 4 min (P = 0.001) and 5 min (P < 0.001), but not 2 min stimulus durations (P = 0.273). These findings demonstrate that methodological differences alter the CVR measure.

Cerebral Hemodynamic and Neurotrophic Factor Responses Are Dependent on the Type of Exercise.

This study examined acute cerebral hemodynamic and circulating neurotrophic factor responses to moderate intensity continuous exercise (MICT), guideline-based high intensity interval exercise (HIIT), and sprint interval exercise (SIT). We hypothesized that the pattern of middle cerebral artery velocity (MCAv) response would differ between interval and continuous exercise, with SIT inducing the smallest increase from rest, while increases in neurotrophic factors would be intensity-dependent. In a randomized crossover design, 24 healthy adults (nine females) performed three exercise protocols: (i) MICT (30 min), (ii) HIIT (4 × 4 min at 85% HRmax), and (iii) SIT (4 × 30 s supramaximal). MCAv significantly increased from rest across MICT (Δ13.1 ± 8.5 cm⋅s-1, p < 0.001) and all bouts of HIIT (Δ15.2 ± 9.8 cm⋅s-1, p < 0.001), but only for the initial bout of SIT (Δ17.3 ± 11.6 cm⋅s-1, p < 0.001). Immediately following each interval bout, MCAv increased (i.e., rebounded) for the SIT (9-14% above rest, p ≤ 0.04), but not HIIT protocol. SIT alone induced significant elevations from rest to end-exercise in vascular endothelial growth factor (VEGF; Δ28 ± 36%, p = 0.017) and brain-derived neurotrophic factor (BDNF, Δ149% ± 162%, p < 0.001) and there were greater increases in lactate than in either other protocol (>5-fold greater in SIT, p < 0.001), alongside a small significant reduction at the end of active recovery in insulin-like growth factor 1 (IGF-1, Δ22 ± 21%, p = 0.002). In conclusion, while the nature of the response may differ, both guideline-based and sprint-based interval exercise have the potential to induce significant changes in factors linked to improved cerebrovascular and brain health.

Is core temperature the trigger of a menopausal hot flush?

OBJECTIVE: Menopausal hot flushes negatively impact quality of life and may be a biomarker of cardiovascular and metabolic disease risk; therefore understanding the physiology of hot flushes is important. Current thinking is that a small elevation (∼0.03-0.05C) in core temperature surpasses a sweating threshold (that is reduced in the menopause), sweating is activated, and a hot flush ensues. Nevertheless, more recent studies examining thermoregulatory control question whether core temperature per se can explain the trigger for a hot flush. The primary aim of this study was to assess the contribution of increases in core temperature on the occurrence of menopausal hot flushes. METHODS: For this purpose, 108 hot flushes were objectively assessed in a laboratory setting in 72 symptomatic postmenopausal women (aged 45.8 ±â€Š5.1 years; body mass index 25.9 ±â€Š4.5 kg/m) from five previously reported studies. Women rested, wearing a tube-lined suit (or trousers), which was perfused with 34C water. A subset then underwent mild heat stress (48°C water). Sweat rate, skin blood flow, blood pressure, heart rate, skin, and core temperature were measured continuously throughout. A hot flush was objectively identified during rest (spontaneous hot flush) or mild heating as an abrupt increase in sternal sweat rate. Further, a subset of symptomatic postmenopausal women (n = 22) underwent whole-body passive heating for 60 minutes to identify core temperature thresholds and sensitivities for sweat rate and cutaneous vasodilation, which were compared to a subset of premenopausal women (n = 18). Data were analyzed using t tests and/or general linear modeling, and are presented as mean (95% confidence interval). RESULTS: In the 20 minutes before a spontaneous hot flush, core temperature increased by 0.03 ±â€Š0.12C (P < 0.05), but only 51% of hot flushes were preceded by an increase in core temperature. During mild heating, 76% of hot flushes were preceded by an increase in core temperature. The temperature thresholds for sweating were similar, but the vasodilatory threshold was higher in postmenopausal compared with premenopausal women (37.1 ±â€Š0.2 vs 36.8 ±â€Š0.3°C; P = 0.06). CONCLUSION: We provide new evidence that menopausal hot flushes are unlikely triggered by an increase in core temperature. These findings provide important information about the physiology of hot flushes that have implications for treatment and management options for menopausal hot flushes.