Assigned group work is associated with increased student motivation and perceptions of belonging in an asynchronous online physiology laboratory course.

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.

Firefighter Health: A Narrative Review of Occupational Threats and Countermeasures.

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.

Effect of reflex and mechanical decreases in skin perfusion on thermal- and agonist-induced eccrine sweating in humans.

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 venoarteriolar 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 pilocarpine doses (ED50 and EMAX) increased SkBF and sweat rate. Each mechanical perturbation resulted in decreased SkBF but minimal 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 balance during changes in body posture, limb position, or blood flow restrictive conditions.

Effect of sensory blockade and rate of sensory stimulation on local heating induced axon reflex response in facial skin.

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.

Gastrointestinal jabberwocky to bioengineering design: using function diagrams to teach physiology.

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.

Role of Bradykinin Type 2 Receptors in Human Sweat Secretion: Translational Evidence Does Not Support a Functional Relationship.

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 nonhuman 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/cm2/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/cm2/min); again no differences were observed with B2R antagonism. Last, 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.

Skin tattooing impairs sweating during passive whole body heating.

Tattooing of the skin involves repeated needle insertions to deposit ink into the dermal layer of the skin, potentially damaging eccrine sweat glands and the cutaneous vasculature. This study tested the hypothesis that reflex increases in sweat rate (SR) and cutaneous vasodilation are blunted in tattooed skin (TAT) compared with adjacent healthy skin (CON) during a passive whole body heat stress (WBH). Ten individuals (5 males and 5 females) with a sufficient area of tattooed skin participated in the study. Intestinal temperature (Tint), skin temperature (Tskin), skin blood flow (laser Doppler flux; LDF), and SR were continuously measured during normothermic baseline (34°C water perfusing a tube-lined suit) and WBH (increased Tint 1.0°C via 48°C water perfusing suit). SR throughout WBH was lower for TAT compared with CON (P = 0.033). Accumulated sweating responses during WBH (area under curve) were attenuated in TAT relative to CON (23.1 ± 12.9, 26.9 ± 14.5 mg/cm2, P = 0.043). Sweating threshold, expressed as the onset of sweating in time or Tint from the initiation of WBH, was not different between TAT and CON. Tattooing impeded the ability to obtain LDF measurements. These data suggest that tattooing functionally damages secretion mechanisms, affecting the reflex capacity of the gland to produce sweat, but does not appear to affect neural signaling to initiate sweating. Decreased sweating could impact heat dissipation especially when tattooing covers a higher percentage of body surface area and could be considered a potential long-term clinical side effect of tattooing.NEW & NOTEWORTHY This study is the first to assess the reflex control of sweating in tattooed skin. The novel findings are twofold. First, attenuated increases in sweat rate were observed in tattooed skin compared with adjacent healthy non-tattooed skin in response to a moderate increase (1.0°C) in internal temperature during a passive whole body heat stress. Second, reduced sweating in tattooed skin is likely related to functional damage to the secretory mechanisms of eccrine sweat glands, rendering it less responsive to cholinergic stimulation.

Opportunistic physiology: inserting physiology and pathophysiology content into virtually delivered clinical rotations.

It is important to reinforce physiology and pathophysiology concepts during clinical rotations, which traditionally occur after the foundational sciences in the US medical school system. We took an opportunistic approach when the COVID-19 pandemic forced our content into virtual delivery mode, as clinical medical education required a shift to nonpatient contact. We describe our experience in building a 2-wk course that consisted of online small groups during week 1 and panels and cases during week 2. The physiology content involved faculty-vetted resources, along with both discrete and open-ended focus questions for each learning objective. The course also included mechanical ventilation, and the physiologist utilized discussion points and developed a formative quiz to emphasize the physiology correlates, in addition to the very clinical aspects of mechanical ventilation. There were pathophysiology opportunities with pneumonia, acute respiratory distress syndrome, systemic inflammatory response syndrome, and multiple-organ system dysfunction among the clinical correlates. Review and recall of the foundational sciences occurred, allowing links between the pre-clerkship and clerkship years that were previously undiscovered in our institution. This virtually delivered medical curriculum related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 is timely, carries high student interest, and can benefit medical students and the communities they serve.

Effect of Suboccipital Release on Pain Perception and Autonomic Reflex Responses to Ischemic and Cold Pain.

OBJECTIVE/SUBJECTS: To determine the autonomic effects of suboccipital release (SOR) during experimentally induced pain, 16 healthy subjects (eight women, eight men) experienced ischemic (forearm postexercise muscle ischemia [PEMI]) and cold (cold pressor test [CPT]) pain. DESIGN: Beat-to-beat heart rate (electrocardiogram), mean arterial blood pressure (finger photoplethysmography), baroreflex sensitivity (transfer function analysis), and pain perception were measured. SOR or a sham (modified yaw; 30 cycles/min) was performed in minute 2 of pain. RESULTS: PEMI increased blood pressure by 23 ± 2 and 20 ± 2 mmHg; no differences occurred between SOR or yaw. PEMI modestly elevated heart rate during ischemia, followed by significant reduction from baseline with SOR (-3 ± 2 bpm) and yaw (-4 ± 2 bpm); no differences were observed between treatments. CPT increased blood pressure (SOR = 11 ± 1, yaw = 9 ± 2 mmHg) and heart rate (SOR = 10 ± 2, yaw = 8 ± 3 bpm) before SOR and yaw. Neither treatment nor sham blunted blood pressure increases (SOR = 25 ± 2, yaw = 22 ± 2 mmHg) during CPT; both decreased heart rate (SOR = -3 ± 2, yaw = -2 ± 2 bpm) from baseline. PEMI and CPT caused increased pain without treatment modulation. Following pain and manual intervention, SOR increased baroreflex sensitivity in the 0.15-0.35 Hz range and decreased R-R interval power spectral density in the 0.03-0.5 Hz range compared with yaw. To probe potential mechanisms and interactions between manual treatment and a prototypic analgesic, oral aspirin (967 mg) was given 60 minutes before testing to reduce prostaglandin synthesis. Aspirin slightly attenuated pain but neither altered cardiovascular changes to PEMI nor interacted with SOR or yaw. CONCLUSIONS: SOR has the capacity to modulate pain-induced autonomic control and regulation.

Heat exhaustion.

Heat exhaustion is part of a spectrum of heat-related illnesses that can affect all individuals, although children, older adults, and those with chronic disease are particularly vulnerable due to their impaired ability to dissipate heat. If left uninterrupted, there can be progression of symptoms to heatstroke, a life-threatening emergency. Signs and symptoms of heat exhaustion may develop suddenly or over time. Exposure to a hot environment for a prolonged period and performing exercise or work in the heat can overwhelm the body's ability to cool itself, causing heat exhaustion. Heat exhaustion can be worsened by dehydration due to inadequate access to water or insufficient fluid replacement. Heat exhaustion can be managed by the immediate reduction of heat gain by discontinuing exercise and reducing radiative heat source exposure. The individual should be encouraged to drink cool fluids and remove or loosen clothing to facilitate heat loss. In more extreme situations, more aggressive cooling strategies (e.g., cold shower, application of wet towels) to lower core temperature should be employed. Heat-related illnesses such as heat exhaustion can be prevented by increasing public awareness of the risks associated with exposure to high temperatures and prolonged exercise.

Thermoregulatory dysfunction in multiple sclerosis.

Multiple sclerosis (MS) is a progressive neurologic disorder that disrupts axonal myelin in the central nervous system. Demyelination produces alterations in saltatory conduction, slowed conduction velocity, and a predisposition to conduction block. An estimated 60-80% of MS patients experience temporary worsening of clinical signs and neurologic symptoms with heat exposure (Uhthoff's phenomenon). This heat intolerance in MS is related to the detrimental effects of increased temperature on action potential propagation in demyelinated axons, resulting in conduction slowing and/or block. Additionally, MS may produce impaired neural control of autonomic and endocrine functions. Isolating and interpreting mechanisms responsible for autonomic dysfunction due to MS can be difficult as it may involve sensory impairments, altered neural integration within the central nervous system, impaired effector responses, or combinations of all of these factors. MS lesions occur in areas of the brain responsible for the control and regulation of body temperature and thermoregulatory effector responses, resulting in impaired neural control of sudomotor pathways or neural-induced changes in eccrine sweat glands, as evidenced by observations of reduced sweating responses in MS patients. Although not comprehensive, some evidence exists concerning treatments (cooling, precooling, and pharmacologic) for the MS patient to preserve function and decrease symptom worsening during heat stress. This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS: (1) heat intolerance; (2) central regulation of body temperature; (3) thermoregulatory effector responses; and (4) countermeasures to improve or maintain function during thermal stress.

Renal sympathetic nerve, blood flow, and epithelial transport responses to thermal stress.

Thermal stress is a profound sympathetic stress in humans; kidney responses involve altered renal sympathetic nerve activity (RSNA), renal blood flow, and renal epithelial transport. During mild cold stress, RSNA spectral power but not total activity is altered, renal blood flow is maintained or decreased, and epithelial transport is altered consistent with a sympathetic stress coupled with central volume loaded state. Hypothermia decreases RSNA, renal blood flow, and epithelial transport. During mild heat stress, RSNA is increased, renal blood flow is decreased, and epithelial transport is increased consistent with a sympathetic stress coupled with a central volume unloaded state. Hyperthermia extends these directional changes, until heat illness results. Because kidney responses are very difficult to study in humans in vivo, this review describes and qualitatively evaluates an in vivo human skin model of sympathetically regulated epithelial tissue compared to that of the nephron. This model utilizes skin responses to thermal stress, involving 1) increased skin sympathetic nerve activity (SSNA), decreased skin blood flow, and suppressed eccrine epithelial transport during cold stress; and 2) increased SSNA, skin blood flow, and eccrine epithelial transport during heat stress. This model appears to mimic aspects of the renal responses. Investigations of skin responses, which parallel certain renal responses, may aid understanding of epithelial-sympathetic nervous system interactions during cold and heat stress.

Mechanisms of orthostatic intolerance during heat stress.

Heat stress profoundly and unanimously reduces orthostatic tolerance. This review aims to provide an overview of the numerous and multifactorial mechanisms by which this occurs in humans. Potential causal factors include changes in arterial and venous vascular resistance and blood distribution, and the modulation of cardiac output, all of which contribute to the inability to maintain cerebral perfusion during heat and orthostatic stress. A number of countermeasures have been established to improve orthostatic tolerance during heat stress, which alleviate heat stress induced central hypovolemia (e.g., volume expansion) and/or increase peripheral vascular resistance (e.g., skin cooling). Unfortunately, these countermeasures can often be cumbersome to use with populations prone to syncopal episodes. Identifying the mechanisms of inter-individual differences in orthostatic intolerance during heat stress has proven elusive, but could provide greater insights into the development of novel and personalized countermeasures for maintaining or improving orthostatic tolerance during heat stress. This development will be especially impactful in occuational settings and clinical situations that present with orthostatic intolerance and/or central hypovolemia. Such investigations should be considered of vital importance given the impending increased incidence of heat events, and associated cardiovascular challenges that are predicted to occur with the ensuing changes in climate.

Augmented supraorbital skin sympathetic nerve activity responses to symptom trigger events in rosacea patients.

Facial flushing in rosacea is often induced by trigger events. However, trigger causation mechanisms are currently unclear. This study tested the central hypothesis that rosacea causes sympathetic and axon reflex-mediated alterations resulting in trigger-induced symptomatology. Twenty rosacea patients and age/sex-matched controls participated in one or a combination of symptom triggering stressors. In protocol 1, forehead skin sympathetic nerve activity (SSNA; supraorbital microneurography) was measured during sympathoexcitatory mental (2-min serial subtraction of novel numbers) and physical (2-min isometric handgrip) stress. In protocol 2, forehead skin blood flow (laser-Doppler flowmetry) and transepithelial water loss/sweat rate (capacitance hygrometry) were measured during sympathoexcitatory heat stress (whole body heating by perfusing 50°C water through a tube-lined suit). In protocol 3, cheek, forehead, forearm, and palm skin blood flow were measured during nonpainful local heating to induce axon reflex vasodilation. Heart rate (HR) and mean arterial pressure (MAP) were recorded via finger photoplethysmography to calculate cutaneous vascular conductance (CVC; flux·100/MAP). Higher patient transepithelial water loss was observed (rosacea 0.20 ± 0.02 vs. control 0.10 ± 0.01 mg·cm(-2)·min(-1), P < 0.05). HR and MAP changes were not different between groups during sympathoexcitatory stressors or local heating. SSNA during early mental (32 ± 9 and 9 ± 4% increase) and physical (25 ± 4 and 5 ± 1% increase, rosacea and controls, respectively) stress was augmented in rosacea (both P < 0.05). Heat stress induced more rapid sweating and cutaneous vasodilation onset in rosacea compared with controls. No axon reflex vasodilation differences were observed between groups. These data indicate that rosacea affects SSNA and that hyperresponsiveness to trigger events appears to have a sympathetic component.

Human cardiovascular responses to passive heat stress.

Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe heat events that are predicted to occur.

Use of beat-to-beat cardiovascular variability data to determine the validity of sham therapy as the placebo control in osteopathic manipulative medicine research.

Osteopathic manipulative medicine researchers often use sham therapy as the placebo control during clinical trials. Optimally, the sham therapy should be a hands-on procedure that is perceptually indistinguishable from osteopathic manipulative treatment, does not create an effect on its own, and is not a treatment intervention. However, the sham therapy itself may often influence the outcome. The use of cardiovascular variability (eg, beat-to-beat heart rate variability) as a surrogate for the autonomic nervous system is one objective method by which to identify such an effect. By monitoring cardiovascular variability, investigators can assess autonomic nervous system activity as a response to the sham therapy and quickly determine whether or not the selected sham therapy is a true placebo control. The authors provide evidence for assessment of beat-to-beat heart rate variability as one method for assuring objectivity of sham therapy as a placebo control in osteopathic manipulative medicine research.