Introduction: A clearer understanding of how reproductive hormone concentrations affect temperature regulation is essential to expand our knowledge of female physiology. Resting core temperature fluctuates with changes in reproductive hormone levels. However, there is little to no evidence that these hormone fluctuations affect the output of heat loss responses during heat stress. Nonetheless, no studies have considered if variations in reproductive hormone concentrations affect the underlying neural control of heat loss responses. Objective & hypothesis: This study determined the effect of low vs. high reproductive hormone concentrations on the neural control of heat loss responses during heat stress in healthy female adults. Based on previous literature showing minimal effects of the output on heat loss responses, we hypothesized that the onset threshold for increases in skin sympathetic nerve activity (SSNA), local sweat rate (LSR), and cutaneous vascular conductance (CVC) do not differ between states of low and high reproductive hormone concentrations. Methods: Ten healthy females (20-35 years) were exposed to heat stress using a water-perfused suit (50°C) during states of low (days 1-7 post-menses [n=6], placebo phase of oral contraceptive use [n=3], or >12 weeks after intramuscular progestin injection [n=1]) and high (days 19-25 post-menses, active phase of contraceptive use, or < 12 weeks after progestin injection) reproductive hormone concentrations. Continuous measurements of SSNA (radial nerve), forearm LSR and CVC, were performed until esophageal temperature increased by 1.2°C. The mean body temperature (esophageal temperature × 0.8 + mean skin temperature × 0.2) onset threshold for SSNA, LSR, and CVC was determined using segmented linear regression. Data are presented as mean ± standard deviation or mean differences (high – low) with [95% confidence interval] and were analyzed with paired samples t-test (α of 0.05). Results: Estrogen (145 ± 55 pmol/L to 341 ± 242 pmol/L) and progesterone (1.6 ± 0.3 nmol/L to 12.0 ± 12.9 nmol/L) concentrations were greater (p< 0.05) during the high vs. low hormone phase. Baseline esophageal temperature was greater during the high (37.09 ± 0.24°C) vs. low (36.91 ± 0.30°C) hormone phase (0.18°C [0.01, 0.35], p=0.05). Baseline mean body temperature was 36.34 ± 0.31°C during the low phase and 36.54 ± 0.23°C during the high phase (0.20°C [-0.01, 0.40], p=0.06). The change in mean body temperature at the onset threshold for SSNA was 0.70 ± 0.31°C during the low phase and 0.74 ± 0.10°C during the high phase (-0.04°C [-0.23, 0.31], p=0.73). The onset threshold for forearm LSR and CVC was 0.80 ± 0.29°C and 0.81 ± 0.28°C during the low phase compared with 0.81 ± 0.12°C and 0.83 ± 0.19°C for the high phase (LSR: 0.00°C [-0.21, 0.22], p=0.98; CVC: -0.02°C [-0.19, 0.22], p=0.86). Conclusion: These results indicate that, despite resulting in a greater resting core temperature, a state of high reproductive hormone concentrations does not alter the neural control of heat loss responses during passive heat stress in healthy female adults. Funding: Natural Sciences and Engineering Research Council of Canada This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Function diagrams focus on physiological concepts rather than associated structures and can serve as elaboration tools and mnemonic aids. A function diagram prototype of the gastrointestinal system was recently described (Wilson TE, Barrett KE. Adv Physiol Educ 45: 264-268, 2021). In this article, a functional diagram of the glomerulus, nephron, urinary system, and bladder is proposed. Colloquially named "Nessie the Nephron" to loosely capture the looping structure and elusive understanding of renal blood flow, glomerular filtration, and epithelial transport for the student, not to mention the nearly mythical countercurrent multiplier. "Navigating the Lochs" references Nessie's possible habitat and more importantly the movement and storage of the modified ultrafiltrate from the nephron. The primary analogies that form the structure of this function diagram are Rain Barrel, Soaker Hose, and Hose Nozzle (afferent and efferent blood flow and filtration pressure); Water Purification System (glomerular filtration barrier forming multiple step filtration process involving the capillary, basement membrane, and podocytes); Mixed Recycling Machine (proximal tubule individual, co-, and bulk transport); Desiccator and Briner (thin descending limb removal of water and thin/thick ascending limb removal of salt); Conveyor Belt Picker (distal nephron selective ion transport); and Concentrator (collecting duct water and urea transport). The primary analogies that elaborate Navigating the Lochs are Aqueduct and Cistern System (fluid movement and collection); and Pressure Gauge, Syringe Bulb, and Two-Valve Plumbing (bladder storage and micturition). Complementing these analogies is the rich potential for inclusion of clinical and comparative applications and examples to link previous knowledge and strengthen memories for future retrieval.NEW & NOTEWORTHY Function diagrams put the focus on physiology and physiological concepts rather than the associated anatomy and can serve as elaboration tools and mnemonic aids. The function diagram of the nephron can provide analogies for glomerular filtration, bulk and selective epithelial transport, and overall ability to create concentrated or dilute urine. The function diagram of the urinary system and bladder can provide analogies for moving and storing urine and finally micturition.

How the renin-angiotensin-aldosterone system (RAAS) regulates fluid and electrolyte balance via cardiorenal modifications has been resolved. Humans are at risk for hypovolemia and electrolyte disorders during conditions causing high eccrine sweating. Heat adaptation protocols alter sweat rate and composition, which have been speculated to involve direct actions of RAAS on eccrine sweat glands. Sweat capacity varies between males and females, and it is unknown if RAAS differences between sexes play a role. Precise evidence and mechanisms remain unresolved. Male and female 8-12-week-old wildtype (C57BL/6J) mice were used for all experiments. A subset of mice had subcutaneously-implanted mini-osmotic pumps infusing angiotensin II (Ang II) (1000 ng/kg/min) for 28 days. Paw skin (containing sweat glands), tail skin (without sweat glands), and kidney tissue were harvested for RNA extraction and RT-qPCR. Gene targets include Ang II receptor-associated protein (Agtrap), epithelial sodium channel (ENaC), mineralocorticoid receptor (MR), and sodium-potassium ATPase (Na + /K + -ATPase); all of which have previously been observed in eccrine sweat glands using immunohistochemical staining and are known to play functional roles in ion transport. We hypothesized that Ang II infusion increases mRNA of Agtrap, ENaC, MR, and Na + /K + -ATPase in paws but not tails in both male and female mice due to paws containing eccrine sweat glands. Relative gene expression of Agtrap, ENaC, MR, and Na + /K + -ATPase was compared across time and between vehicle and Ang II infusion in paws, kidneys, and tails in each sex and between sexes via ANOVA. In paws, there was a main effect of sex (p = 0.0227) and an interaction (sex and infusion) of 0.0080 in Agtrap mRNA expression. It is shown in male mice that Agtrap mRNA increased between vehicle and Ang II infusion (p = 0.0057), but in females Agtrap mRNA expression decreased between vehicle and 28 days. Agtrap mRNA expression in males was higher than females after 28 days of Ang II infusion (p = 0.0024). ENaC mRNA expression did not exhibit significant fluctuations between vehicle and 28 days of Ang II infusion within or between male and female mice. There was a main effect of sex on MR mRNA (p = 0.0064). Vehicle female MR mRNA expression was greater than in male vehicle mice (p = 0.0034). MR mRNA expression also decreased in female mice between vehicle and Ang II infusion (p = 0.0314). Na + /K + -ATPase mRNA exhibited the same directional shifts between vehicle and Ang II infusion within and between male and female mice. In kidneys, Agtrap, ENaC, and MR expression decreased between vehicle and Ang II infusion in both male and female mice. There were no significant differences between male and female mice within vehicle or Ang II treatment. There was a main effect of sex (p = 0.0097) in mRNA expression of Na + /K + -ATPase. Na + /K + -ATPase mRNA expression decreased between vehicle and 28 days in both male and female mice. With no treatment, female mRNA expression was greater than in males (p = 0.0137). In tails, Agtrap mRNA gene expression revealed a main effect of treatment (p = 0.0406). Further, Agtrap, ENaC, MR, and Na + /K + -ATPase mRNA expression decreased between vehicle and Ang II infusion in both male and female mice. Our findings indicate chronic infusion of high-level Ang II increases gene expression of Agtrap in paws of male but not female mice. Ang II also decreases expression of MR in female, but not male mice. It remains to be resolved if functional changes correlate with altered gene expression. Combined, these data suggest that Ang-II distinctly regulates mRNA expression of RAAS-related receptors in female compared to male mice paws containing eccrine sweat glands, but not tail or kidney tissue. TL1TR001997 UL1TR001998 This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Cold-induced vasodilation (CIVD) is a counterintuitive focal increase in glabrous skin blood flow during cold exposure with unclear local and neural mechanisms. To understand this phenomenon, we tested 12 (8 men, 4 women) healthy subjects’ laser-Doppler flux (LDF) and arterial blood pressure (ABP) on a beat-by-beat basis. The experimental hand was exposed to warm (10 min 35°C water) and then cold (30 min 8°C water) water immersion and contralateral control hand experienced 22-23°C air throughout. Beat-by-beat oscillations in LDF (2 experimental and 1 control finger skin just proximal to the nailbed) and ABP were analyzed via a fast-Fourier transform (FFT) to obtain power spectral density and transfer function analysis (TFA) of LDF to ABP to obtain gain, phase, and coherence between the signals. Frequencies were normalized to total power and binned within very low (nVLF; 0.02-0.07), low (nLF; 0.07-0.20), and high (nHF; 0.20-0.35) Hz ranges. ABP power decreased from warm to cold immersion in the nVLF but no differences were observed in nLF and nHF. LDF power was greater in the control finger than immersed fingers in nVLF and nLF, but not different in nHF. There was an interaction in nLF where cooling decreased power in immersion sites but increased power in the control. There was also an interaction in nHF where cooling increased power in immersion sites but did not change power in the control. Average pooled TFA coherence between LDF and ABP were 0.5±0.2, 0.5±0.1, and 0.4±0.1 for warm and 0.5±0.2, 0.5±0.2, and 0.4±0.1 for cold for VLF, LF, and HF, respectively. TFA gain was lower during cooling for immersion but not control sites in the VLF and LF ranges. In contrast, HF gain was lower in both immersion and control sites. Cooling decreased phase (time-delay) of the LDF to ABP signal in the VLF during cooling immersion sites but these data were somewhat finger dependent. Data from this analysis approach confirms a significant effect of local vasoconstriction within sympathetic vasoconstriction as identified by changes in the VLF and LF, respectively. Comparing CIVD bins (LDF criteria, n=6) to general cutaneous vasoconstriction bins with no CIVD (n=6) yielded increases in nHF (P=0.02) and nLF (P=0.09) and decreases in nVLF (P=0.05) power with CIVD. TFA gain during CIVD did not yield differences across frequency bins compared to cutaneous vasoconstriction alone. Thus, the unique analysis of arterial blood pressure and the FFT-TFA approach appears to be beneficial in providing insights into CIVD events with a local release of vasoconstriction under the tonic sympathetic tone and local vasoconstriction and vasodilation balance. National Institute of Environmental Health Sciences (P30ES026529) awarded through UK Center for Appalachian Research in Environmental Sciences (UK-CARES) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

It is well-known how the systemic renin-angiotensin-aldosterone system (RAAS) regulates fluid and electrolyte balance via cardiovascular and renal modifications. Thermoregulatory eccrine sweating can also alter whole-body fluid and electrolyte balance, especially in conditions requiring evaporative cooling. Systemic adaptation protocols that augment RAAS and intradermal injections of aldosterone appear to alter sweat rate and composition; however, the precise mechanisms are unknown and it is difficult to know if these effects were a result of direct modifications to the sweat glands. To investigate how alterations in RAAS may impact eccrine sweat glands, RT-qPCR was performed on kidney tissue from WT mice only and excised tails (no sweat glands) and paws (contain eccrine sweat glands) from WT mice (n = 20) and mice with subcutaneous osmotic pumps (n=6) to continuously deliver angiotensin II (ang II) (1,000 ng/kg/min for 4 weeks). Genes targets include the ang II type 1 receptor (AGT1R), ENaC, mineralocorticoid receptor (MR), and Na + /K + -ATPase, which all have previously been observed in eccrine sweat glands via immunohistochemical techniques and have functional roles in ion transport. We hypothesized that gene targets would increase expression with systemic RAAS as induced by ang II infusion in paws but not tails due to paws containing eccrine sweat glands. One-way ANOVAs reveal increased gene expression in paws of ang II infusion mice in AGT1R (p<0.0001), MR (p<0.0001), and Na + /K + -ATPase (p<0.0001) vs paws of WT mice. Additionally, ang II infusion mice had greater gene expression of paws in targets AGT1R (P=0.0016), MR (P=0.0152) and Na + /K + -ATPase (p<0.0001) vs ang II infusion mice tails. Within WT mice, only AGT1R showed differences in expression between kidney tissue and paws (P = 0.0046) and kidney tissue and tails (P = 0.0147). No gene expression differences were found in any target between paws and tails in WT mice. In summary, RAAS genes expression of AGT1R, MR, and Na + /K + -ATPase in mice paws escalated with chronic systemic ang II infusion. These results suggest that enhanced systemic RAAS modifies tissue containing eccrine sweat glands to upregulate ion transport machinery. It remains to be resolved if direct functional changes will correlate to the altered gene expression. These observations provide some of the first data that eccrine sweat glands have the capacity to alter gene expression to a RAAS component as occurs in the nephron. TL1TR001997 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

The dissemination of discipline-focused educational scholarship advances theory and stimulates pedagogical application. The aim of Advances in Physiology Education is to publish manuscripts that advance knowledge and inform educators in the field. This primer is tailored for individuals new to manuscript reviewing, early in their careers, or experienced in reviewing research but not educational manuscripts. Peer reviewing for basic and applied science is akin to evaluating research questions and rigor in teaching and learning studies, with differences in approach and analysis similar to those between biophysics and molecular physiology or cell and integrated physiology. Our purpose is to provide an overview of the review process and expectations. The submission and peer review process involves several steps: authors submit a manuscript and the Editor assigns an Associate Editor, who then assigns peer Reviewers. Reviewers are contacted via email and can accept or decline the invitation. Reviewers evaluate the work's strengths and weaknesses and then independently submit comments and recommendations to the Associate Editor. After review, the Associate Editor collects and weighs Reviewers' comments, sometimes garners additional reviews and input, to make a recommendation to the Editor. The Editor reviews the process, comments, and recommendations to render a final decision. Both authors and Reviewers receive an email with the decision. The editorial staff assists with communication and helps track the overall process. Peer review is integral to scientific publishing, ensuring quality and rigor, and reviewing is both a privilege and a responsibility of all in the scientific community.NEW & NOTEWORTHY This mini-review offers a comprehensive and current overview of the peer review process and the qualifications required to serve as a journal reviewer for Advances in Physiology Education. The guidelines are specifically designed for early career professionals new to manuscript reviewing, as well as seasoned research manuscript reviewers who are new to educational manuscript evaluation. Peer review is a cornerstone of scientific publishing, ensuring both quality and rigor. It is both a privilege and a responsibility for all members of the scientific community.

Letter to the EditorPhysiological adaptation/phenotypic plasticity: a vital core concept from the medical and health care perspectiveThad E. Wilson and Kristen Metzler-WilsonThad E. WilsonDepartment of Physiology, University of Kentucky College of Medicine, Lexington, Kentucky, United StatesDepartment of Epidemiology & Environmental Health, University of Kentucky College of Public Health, Lexington, Kentucky, United States, andKristen Metzler-WilsonDepartment of Physical Therapy, University of Kentucky College of Health Sciences, Lexington, Kentucky, United StatesPublished Online:23 Jan 2024https://doi.org/10.1152/advan.00268.2023MoreSectionsPDF (207 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat The recent article by Estaphan et al. (1) eloquently unpacks the concept of physiological adaptation from a consensus process involving 25 Australian universities (2) and nicely illustrates a fundamental biological principle for individuals pursuing health care careers. Physiological adaptation, defined as "organisms adjust and adapt to acute and chronic changes in the internal and external environments across the lifespan" (1), has clear implications for health care. The authors' inclusion of adaptations to internal changes makes this concept particularly relevant to health care. Without the ability to adapt, processes like pathophysiology, disease signs and symptoms, medical treatments/rehabilitation, and disease prevention do not make sense. The lack of this concept in the current 14 Core Concepts in Physiology (3) can be viewed as a limitation to student fundamentals for those of us who teach physiology to medical and health professions students. Similar to how evolution allows understanding of biological changes across generations, phenotypic plasticity allows us to make sense of biological changes within an organism's lifetime. Phenotypic plasticity is the fundamental concept that an organism's genotype can produce diverse phenotypes in response to environmental conditions experienced by the organism (4). This conditional-induced plasticity can be acute or chronic, discrete or continuous, anabolic or catabolic, adaptative or maladaptive and can be involved in both health and disease. This concept fits neatly with the definition of physiological adaptation and the four themes and nine subthemes of Estaphan et al. (1).The term "phenotypic plasticity" is common for developmental, comparative, ecological, environmental, evolutionary, and plant physiologists (5–8) and even has crossover to popular science (9). "Physiological adaptation" (2) may be palatable to diverse users and educators, as phenotypic plasticity is not mentioned in the Australian Task Force articles. One potential problem with "adaptation" is its central use in evolution and genetics rather than being confined as in the earlier definition by Estaphan et al. (1). No matter the term, physiological adaptation or phenotypic plasticity, this concept is truly broad and inclusive enough to be a core concept in our discipline and is vital in health care. Health care examples include baroreceptor accommodation in hypertension, blood volume increases in heart failure, airway remodeling resulting in exaggerated cholinergic responses in asthma, lung parenchymal compliance changes in emphysema, skeletal muscle atrophy associated with limb immobilization, and sarcomere addition in hypertrophy after resistance training. We believe phenotypic plasticity should be listed separately from the other core concepts and that it per se is the foundation of several branches of physiology mentioned above, as well as conservation, exercise, and medical physiologies. The 14 core concepts proposed by Michael et al. (3) do not explicitly contain the important principles that include nongenetic physiological adaptation/phenotypic plasticity. This concept should be included in any revision of Core Concepts in Physiology (10) to allow for "bifocals," i.e., the multiple-lens approach of both evolution and phenotypic plasticity, to help us all "see" physiology better and relate it to the area where many of our students desire to apply their physiology knowledge, health care.DISCLOSURESNo conflicts of interest, financial or otherwise, are declared by the authors.AUTHOR CONTRIBUTIONST.E.W. conceived and designed research; T.E.W. and K.M. drafted manuscript; T.E.W. and K.M. edited and revised manuscript; T.E.W. and K.M. approved final version of manuscript.REFERENCES1. Estaphan S, Wadley GD, Todd G, Towstoless M, Hryciw DH, Lexis L, Hayes A, Tangalakis K; Task Force. Unpacking and validating the "physiological adaptation" core concept of physiology. Adv Physiol Educ 47: 831–837, 2023. doi:10.1152/advan.00083.2023. Link | ISI | Google Scholar2. Tangalakis K, Lexis L, Hryciw DH, Towstoless M, Bakker AJ, Beckett E, Brown D, Cameron M, Choate J, Chopin L, Cooke MB, Douglas T, Estaphan S, Etherington S, Gaganis V, Moorhouse A, Moro C, Paravicini T, Perry B, Phillips R, Scott C, Todd G, Uebergang T, Wadley G, Watt M, Hayes A. Establishing consensus for the core concepts of physiology in the Australian higher education context using the Delphi method. Adv Physiol Educ 47: 419–426, 2023. doi:10.1152/advan.00140.2022. Link | ISI | Google Scholar3. Michael J, Cliff W, McFarland J, Modell H, Wright A. The Core Concepts of Physiology: a New Paradigm for Teaching Physiology. New York: American Physiological Society & Springer Nature, 2017.Crossref | Google Scholar4. Kelly SA, Panhuis TM, Stoehr AM. Phenotypic plasticity: molecular mechanisms and adaptive significance. Compr Physiol 2: 1417–1439, 2012. doi:10.1002/cphy.c110008. Crossref | PubMed | ISI | Google Scholar5. Gomulkiewicz R, Stinchcombe JR. Phenotypic plasticity made simple, but not too simple. Am J Bot 109: 1519–1524, 2022. doi:10.1002/ajb2.16068. Crossref | PubMed | ISI | Google Scholar6. Hammond KA, Cardullo RA, Ghalambor CK. The role of developmental plasticity in comparative physiology: mechanism and process. In: Comparative Developmental Physiology: Contributions, Tools, and Trends, edited by Warburton SJ, Burggren WW, Pelster B, Reiber CL, Spicer J. New York: Oxford University Press, 2006, p. 71–82.Crossref | Google Scholar7. Horowitz M. Epigenetics and cytoprotection with heat acclimation. J Appl Physiol (1985) 120: 702–710, 2016. doi:10.1152/japplphysiol.00552.2015. Link | ISI | Google Scholar8. Sommer RJ. Phenotypic plasticity: from theory and genetics to current and future challenges. Genetics 215: 1–13, 2020. doi:10.1534/genetics.120.303163. Crossref | PubMed | ISI | Google Scholar9. Lieberman D. The Story of the Human Body: Evolution, Health, and Disease. New York: Vintage, 2014.Google Scholar10. Michael J, McFarland J. Another look at the core concepts of physiology: revisions and resources. Adv Physiol Educ 44: 752–762, 2020. doi:10.1152/advan.00114.2020. Link | ISI | Google ScholarAUTHOR NOTESCorrespondence: T. E. Wilson (Thad.Wilson@uky.edu). Download PDF Previous Back to Top FiguresReferencesRelatedInformation Related ArticlesUnpacking and validating the "physiological adaptation" core concept of physiology 09 Oct 2023Advances in Physiology Education More from this issue > Volume 48Issue 1March 2024Pages 112-113 Crossmark Copyright & PermissionsCopyright © 2024 the American Physiological Society.https://doi.org/10.1152/advan.00268.2023PubMed38259038History Received 19 December 2023 Accepted 20 December 2023 Published online 23 January 2024 Published in print 1 March 2024 KeywordsadaptationCore Concepts in Physiologymedical educationphysiological education Metrics

With the rise of online instruction, a better understanding of the factors that contribute to belonging and motivation in these contexts is essential to creating optimal learning environments. Although group work is known to be beneficial to student success, few studies have investigated its role in the context of asynchronous online courses. The present study addresses this gap through a survey of 146 undergraduate students in an asynchronous online physiology lab over two semesters, one with required group work and one without group work. Students were surveyed to evaluate the influence of group work on their motivation and sense of belonging, as well as their perceptions of inclusive and exclusive features of the course. Students assigned to groups had a higher sense of belonging (P = 0.006) and beliefs about their competence (P = 0.002) and perceived lower effort and psychological costs associated with the course (P = 0.04 and 0.04, respectively) compared to students not assigned to groups. Students assigned to groups reported that peer interactions made them feel included in the course (70% of coded responses) while those not assigned to groups valued instructor interactions (51% of coded responses) as inclusive. Negative peer interactions were commonly reported as exclusive by students assigned to groups (28% of coded responses) while a lack of peer interactions (23% of coded responses) made students not assigned to groups feel excluded. These data indicate that assigning groups in asynchronous online courses is an effective way to increase student motivation and perceptions of belonging.NEW & NOTEWORTHY This study explores the effect of assigned group work in an asynchronous online physiology laboratory course on student motivation and belonging. Students' perceptions of belonging and competence-related beliefs were higher, and effort and psychological costs were lower, when assigned to groups compared to students not assigned to groups. Students assigned to groups noted peer interactions as the most inclusive aspect of the course, whereas instructor interactions were noted as inclusive by those not assigned group work.

Structural firefighters are responsible for protecting properties and saving lives during emergency operations. Despite efforts to prepare firefighters for these hazardous occupational demands, the unfortunate reality is that the incidence of health morbidities is increasing within the fire service. Specifically, cardiovascular disease, cancer, and mental health disorders are among the most documented morbidities in firefighters. Pubmed and Google Scholar search engines were used to identify peer-reviewed English language manuscripts that evaluated firefighters' occupational health threats, allostatic factors associated with their occurrence, and evidence-based strategies to mitigate their impact. This narrative review provides fire departments, practitioners, and researchers with evidence-based practices to enhance firefighters' health.

PURPOSE:Cold limb immersion, a form of cryotherapy, can cause cardiovascular changes due to cold-pain induced autonomic reflexes. This cryotherapy treatment side effect has received less attention but could have direct implications for physical rehabilitation of individuals with cardiovascular comorbidities. METHODS:To test hypotheses related to the pressor effects of varied limb sites and surface areas of cryotherapy, two common lower limb injury sites (ankle and knee) were immersed into cold water (15 min, 1-3°C) and then referenced to a standard cold pressor test (CPT). Beat-by-beat arterial blood pressure (finger photoplethysmography), heart rate (ECG), systemic vascular conductance (SVC; Modelflow), and calf vascular conductance (VC) (venous occlusion plethysmography) were measured in 14 healthy participants. RESULTS:At 2 min, CPT increased mean arterial pressure (21 ± 4 mm Hg) more than either ankle or leg immersion (15 ± 4 and 15 ± 5 mm Hg, respectively; P = 0.015). Systemic vascular conductance and calf VC decreased but were not different across treatments ( P = 0.417 and P = 0.086). Mean arterial pressure and SVC were not different from 2 to 15 min of immersion ( P = 0.164 and P = 0.522), but calf VC decreased further by the end of immersion (3.1 ± 0.5 to 2.8 ± 0.4 and 2.7 ± 3 to 1.7 ± 0.2 units; P = 0.028). Mean arterial pressure increases with CPT were similar with solely CPT and when CPT followed ankle or leg immersion (27 ± 5 and 23 ± 4 mm Hg, respectively; P = 0.199). CONCLUSIONS:These data indicate robust pressor responses without autonomic reflex habituation and that cryotherapy immersion location but not surface area appears to mediate cardiovascular responses. This cryotherapy side effect may be an important consideration for patients with cardiovascular-related comorbidities.

Regional differences in skin barrier properties are common in mammals, as some exterior surfaces are fairly impermeable and others are leakier. Neural-induced changes in skin physiology and temperature have the potential to alter skin barrier properties, but the circumstances and mechanisms are unclear. We hypothesized that increasing methylcholine (MCh) or acetylcholine (ACh) concentration would decrease the transepithelial resistance (an index of the skin barrier) measured across mouse paw pad skin jacketed at neutral skin (32°C) or internal (37°C) temperature. Additionally, we hypothesized that paw pads would have lower transepithelial resistance compared to mouse tail skin, and subjecting samples to 40°C (local cutaneous heat stress) would lower transepithelial resistance compared to paw pad skin tested at 32°C. 30 C57BL/6 mouse rear paw pads (containing sweat glands) and 7 mouse tail skins (no sweat glands) were dissected and mounted into a vertical Ussing chamber filled with Kreb’s bicarbonate buffer, gassed with 95% O₂ & 5% CO₂, and encased in a temperature jacket. Transepithelial resistance utilized a current clamp and was measured with Ag-AgCl 2 electrodes placed in both epidermal and hypodermal baths during hypodermal-side-only cholinergic dosing (5 min/dose). ACh (0, 0.0833, 0.1666, 0.2499, 0.4166, 0.58323, and 0.74989 M) significantly decreased transepithelial resistance in paw pads clamped at 37°C in a dose-dependent manner. Tail skin had significantly higher transepithelial resistance than paw pad skin. However, transepithelial resistance decreased significantly with MCh (same dosing as ACh) at both skin sites. Increasing jacket temperature to 40°C did not alter the magnitude of decrease in transepithelial resistance to MCh in paw pads compared to 32°C. Transepithelial resistance observations were similar when data were expressed as absolute or relative changes to baseline. Increased ion movement in murine skin (signifying a leakier epithelium) occurred with cholinergic stimulation but not with local hyperthermia, suggesting that neural influences can suffciently affect skin function to directly alter regional skin barriers. P30ES026529 with additional support from TL1TR001997 and R25ES027684. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Students find pulmonary physiology difficult and complex. Information overload is a strong deterrent of learning and decreases motivation. Function diagrams are simplified renditions of a complex system that can house a series of analogies and mnemonics for the purpose of concept elaboration and knowledge retrieval. This lung function diagram uses the five lobes (3 of the right and 2 of the left) to link several analogies that when put together describes the major lung functions. The five lobes correspond to (i) Lung compliance & surface tension, (ii) Mechanics of breathing & airway resistance, (iii) Control of breathing, (iv) Gas diffusion and oxygen transport, and (v) Ventilation-perfusion matching. Each lobe serves as a memory palace location for one of the five items but the lobe housing an item has no anatomical relation. The first image is of someone doing a belly flop while holding a big, medium, and small balloon. The small balloon represents thick-walled hard-to-inflate balloon (analogy of fibrosed lung), the medium balloon medium-walled normally-inflated (analogy of normal lung), and the big balloon represents a thin-walled easily-inflated balloon (higher compliance). The belly flop represents water’s high surface tension. The second image is of a mechanic turning on a water spicket. Here the mechanic represents the mechanics involved in respiration. The flow of a liquid out the spicket represents narrow vs. wider aperture extrapolates to air flow and determinants of airway resistance, especially if different size hoses are attached. The third image is of a computer circuit board connected to a small motor. This represents the regulation of respiration, accepting inputs and back-and-forth circuitry with outputs to increase or decrease the speed of the motor or ventilation. The forth image is of a car filled with three commuters returning home (blood flow returning to the lungs) and soda cans and baking soda in the trunk. In this image the four-seat car represents hemoglobin with its four oxygen binding sites, each passenger is an oxygen. The soda represents dissolved carbon dioxide, baking soda represents bicarbonate, and the trunk is the hemoglobin site that binds to carbon dioxide. Passengers getting into of the car and soda cans and baking soda being unloaded from the trunk represents O2 and CO2 binding/unbinding. The final image of gas tanks traveling down a conveyer belt to be filled. Here the gas filling rate of partially filled cylinders represents ventilation, the speed of belt carrying these cylinders represents perfusion. Our overall premise is that simple witty memorable diagrams, function diagrams, that do not look like a detailed figures and graphs may facilitate elaboration and decrease perceived perplexity of learning difficult topics such as pulmonary physiology. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

In humans, skin blood flux (SkBF) and eccrine sweating are tightly coupled, suggesting common neural control and regulation. This study was designed to separate these two sympathetic nervous system end-organ responses via nonadrenergic SkBF-decreasing mechanical perturbations during heightened sudomotor drive. We induced sweating physiologically via whole body heat stress using a high-density tube-lined suit (protocol 1; 2 women, 4 men), and pharmacologically via forearm intradermal microdialysis of two steady-state doses of a cholinergic agonist, pilocarpine (protocol 2; 4 women, 3 men). During sweating induction, we decreased SkBF via three mechanical perturbations: arm and leg dependency to engage the cutaneous venoarter-iolar response (CVAR), limb venous occlusion to engage the CVAR and decrease perfusion pressure, and limb arterial occlusion to cause ischemia. In protocol 1, heat stress increased arm cutaneous vascular conductance and forearm sweat rate (capacitance hygrometry). During heat stress, despite decreases in SkBF during each of the acute (3 min) mechanical perturbations, eccrine sweat rate was unaffected. During heat stress with extended (10 min) ischemia, sweat rate decreased. In protocol 2, both pilocar-pine doses (ED50 and EMAX) increased SkBF and sweat rate. Each mechanical perturbation resulted in decreased SkBF but mini-mal changes in eccrine sweat rate. Taken together, these data indicate that a wide range of acute decreases in SkBF do not appear to proportionally decrease either physiologically-or pharmacologically induced eccrine sweating in peripheral skin. This preservation of evaporative cooling despite acutely decreased SkBF could have consequential impacts for heat storage and bal-ance during changes in body posture, limb position, or blood flow restrictive conditions.

Physiology concepts are often student‐perceived as difficult because of low knowledge transfer or background, inability to focus on what is most important, and difficulty visualizing concept elements. Elaboration is a learning science strategy that uses learning‐enhanced additions, constructions, or generations to improve mastery of novel material by leveraging the mental cues available for recall and application. Elaboration appears to be especially helpful for neurodivergent students. To connect acid‐base balance and disorders to something vivid and memorable, we developed a gnome hat color elaboration that is based on pH indicator strips ‐ where red is acidic, blue is basic, and yellow‐green is neutral. Acidosis was defined as the process of gnomes making red hats and implements and alkalosis as gnomes making blue hats and implements. Blood “battle grounds” were drawn with pH <7.35 and >7.45 for acidemia and alkalemia, respectively. The plasma neutral space (pH 7.35‐7.45) denotes yellow‐green gnomes’ habitat. This slightly basic starting point is unfair from the red gnome viewpoint and escalates acid‐base tensions. This elaboration can then be layered over acid‐base classification tools, such as acid‐base boxes (Dietz, Adv Physiol Educ, 35(4):454‐5, 2011), where the three gnome groups populate either inside the box (yellow‐green), left of the box (red), or right of the box (blue). Over the years, we have adapted the box limits to correspond to the normative laboratory values for HCO3‐ and PCO2used in national board exams (USMLE, COMLEX, etc.). Naming an acid‐base disorder then becomes a quick visual of gnome hat color, where names are derived when a second gnome emerges outside of the box – e.g., one red hat gnome for pH and another for HCO3‐ is metabolic acidosis. Compensation can also be identified, if the opposite color hatted gnome emerges out of the other side of the box. Based on data using USMLE Physiology© hosted by Lecturio™, which provided a convenience sample free from the power biases associated with respondents being direct, graded students of either author, 32% of polled respondents specifically mentioned gnomes helping them to learn, recall, or apply acid‐base information. Additionally, 57% specifically noted that the approach was clear, easy to follow, and recallable, often comparing it to their other acid‐base balance learning experiences. Of the 14 hosted acid‐base physiology podcasts, the gnome‐based approach layered with the acid‐base box received 2‐ to 8‐fold more comments than other podcasts. Overall, podcasts were well received with 96% of respondents rating 4‐5/5 stars (91% were 5/5 stars). It is difficult to identify the amount of variance accounted for by the gnome hat approach, but having nearly 1/3 of students mention this approach in non‐mandatory, non‐coerced, open‐ended feedback means that for some it was vivid and memorable. There appears to be a potential for imaginative and colorful concept elaboration efficacy in physiological education, even when the elaboration may seem a bit over‐the‐top and simplistic.

Bradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and non-human paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46-48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79±0.12 and vehicle = +0.64±0.10 mg/cm 2 /min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/ml) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38±0.16 and vehicle = +0.32±0.12 mg/cm 2 /min); again no differences were observed with B2R antagonism. Lastly, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically-or pharmacologically-induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

Local neuronal circuits in non-glabrous skin drive the initial increase of the biphasic cutaneous vasodilation response to fast non-noxious heating. Voltage-sensitive Na+ (NaV) channel inhibition blocks the afferent limb of the non-glabrous forearm cutaneous axon reflex. Slow local heating does not engage this response. These mechanisms have not been adequately investigated or extended into areas associated with flushing pathology. We hypothesized that despite regional differences in sensory afferents, both sensory blockade and slowing the heating rate would abate the cutaneous axon reflex-mediated vasodilator responses in facial skin. We measured skin blood flow responses (laser-Doppler flowmetry) of 6 healthy subjects (5 female) to non-noxious forearm, cheek, and forehead local heating, expressed as a percentage of cutaneous vascular conductance at plateau (CVC = flux/mean arterial pressure). We assessed CVC during fast (1 °C/30s) and slow (1 °C/10 min) local heating to 43 °C in both NaV inhibition (topical 2.5% lidocaine/prilocaine) and control conditions. NaV inhibition decreased forearm (control: 84 ± 4, block: 34 ± 9%plateau, p < 0.001) and trended toward decreased forehead (control: 90 ± 3, block: 68 ± 3%plateau, p = 0.057) initial CVC peaks but did not alter cheek responses (control: 90 ± 3, block: 92 ± 13%plateau, p = 0.862) to fast heating. Slow heating eliminated the initial CVC peak incidence for all locations, and we observed similar results with combined slow heating and NaV inhibition. Slower sensory afferent activation rate eliminated the axon reflex response in facial and non-glabrous skin, but topical sensory blockade did not block axon reflex responses in flushing-prone cheek skin. Thus, slower heating protocols are needed to abate facial, particularly cheek, axon reflex responses.

Function diagrams put the focus on physiology and physiological concepts rather than the associated anatomy. Function diagrams could potentially serve as an elaboration tool and memory aid (mnemonic) to improve learning and recall. The function diagram prototype of the gastrointestinal system can aid in the instruction of difficult gastrointestinal physiology topics using a sequential focus on fundamental gastrointestinal functions.