The Case for Coordinating Efforts to Establish Program Guidelines and Strengthen Physiology Undergraduate Degree Programs

Undergraduate degree programs named “Physiology” have existed for over 50 yr. The number of programs and enrolled students have been growing since ~2005 (5, 9). There are many thousands of students currently enrolled in physiology pro- grams across the United States and indeed across the world. Despite the long history and current popularity of the physiol- ogy major, there is no coordinated plan articulated for the design, administration, or assessment of degree programs in physiology at the undergraduate level. Although several professional societies have invested in under- graduate physiology education in various ways, none has under- taken the task of developing programmatic guidelines at the level of a degree program. This paper outlines the work being done by multiple stakeholders in physiology undergraduate education in the hopes of building a collaboration among interested parties. A large-scale collaboration could result in establishing consensus national programmatic guidelines. Through coordinated efforts, we ensure that entities with common educational interests are working together, and we collectively strengthen our programs to help our students succeed. The goals of this paper are to: 1) draw attention to the lack of national, program-level guidelines for physiology under- graduate degree programs; 2) share ongoing efforts by stake- holders in physiology undergraduate education; 3) suggest a mechanism for coordination among stakeholders; and 4) dis- cuss challenges and considerations for development of pro- grammatic guidelines for physiology programs

Differential Post-Exercise Blood Pressure Responses between Blacks and Caucasians

Post-exercise hypotension (PEH) is widely observed in Caucasians (CA) and is associated with histamine receptors 1- and 2- (H1R and H2R) mediated post-exercise vasodilation. However, it appears that blacks (BL) may not exhibit PEH following aerobic exercise. Hence, this study sought to determine the extent to which BL develop PEH, and the contri- bution of histamine receptors to PEH (or lack thereof) in this population. Forty-nine (22 BL, 27 CA) young and healthy subjects completed the study. Subjects were randomly assigned to take either a combined H1R and H2R antagonist (fexofenadine and ranitidine) or a con- trol placebo. Supine blood pressure (BP), cardiac output and peripheral vascular resistance measurements were obtained at baseline, as well as at 30 min, 60 min and 90 min after 45 min of treadmill exercise at 70% heart rate reserve. Exercise increased diastolic BP in young BL but not in CA. Post-exercise diastolic BP was also elevated in BL after exercise with histamine receptor blockade. Moreover, H1R and H2R blockade elicited differential responses in stroke volume between BL and CA at rest, and the difference remained follow- ing exercise. Our findings show differential BP responses following exercise in BL and CA, and a potential role of histamine receptors in mediating basal and post-exercise stroke vol- ume in BL. The heightened BP and vascular responses to exercise stimulus is consistent with the greater CVD risk in BL

Postexercise hypotension as a clinical tool: a “single brick” in the wall

After an exercise session, a reduction of blood pressure (BP) is expected, a phenomenon called postexercise hypotension (PEH). PEH as a predictor of chronic training responses for BP has been broadly explored. It suggests that when PEH occurs after each exercise sessions, its benefits may summate over time, contributing to the chronic adaptation. Thus, PEH is an important clinical tool, acting as a “single brick” in the wall, and building the chronic effect of decreasing BP. However, there is large variation in the literature regarding methodology and results, creating barriers for understanding comparisons among PEH studies. Thus, the differences among subjects' and exercise protocols’ characteristics observed in the studies investigating PEH must be considered when readers interpret the results. Furthermore, understanding of these factors of influence might be useful for avoiding misinterpretations in future comparisons and how the subjacent mechanisms contribute to the BP reduction after exercise

Comparison of morning versus evening aerobic-exercise training on heart rate recovery in treated hypertensive men: a randomized controlled trial

Heart rate recovery (HRR) is a marker of cardiac autonomic regulation and an independent predictor of mortality. Aerobic-exercise training conducted in the evening (evening training) produces greater improvement in resting cardiac autonomic control in hypertensives than morning training, suggesting it may also result in a faster autonomic restoration postexercise. This study compared the effects of morning training and evening training on HRR in treated hypertensive men. Forty-nine treated hypertensive men were randomly allocated into three groups: morning training, evening training and control. Training was conducted three times/week for 10 weeks. Training groups cycled (45 min, moderate intensity) while control group stretched (30 min). In the initial and final assessments of the study, HRR60s and HRR300s were evaluated during the active recovery (30 W) from cardiopulmonary exercise tests (CPET) conducted in the morning and evening. Between-within ANOVAs were applied (P ≤ 0.05). Only evening training increased HRR60s and HRR300 differently from control after morning CPET (+4 ± 5 and +7 ± 8 bpm, respectively, P < 0.05) and only evening training increased HRR300s differently from morning training and control after evening CPET (+8 ± 6 bpm, P < 0.05). Evening training improves HRR in treated hypertensive men, suggesting that this time of day is better for eliciting cardiac autonomic improvements via aerobic training in hypertensives

Effect of propranolol on sympathetically mediated leg vasoconstriction in humans

Sympatho-excitatory manoeuvres are used to study vascular responsiveness in humans, but it is unclear if circulating adrenaline attenuates peripheral vasoconstriction during these manoeuvres. We hypothesized that vasoconstrictor responses to three manoeuvres (neck pressure, unilateral thigh-cuff release and isometric handgrip) would be greater after the administration of the β-adrenergic blocker propranolol. Seven men and six women underwent these manoeuvres while beat-by-beat arterial pressure (finger photoplethysmography), femoral mean blood velocity (Doppler ultrasound) and femoral artery diameter (edge-detection software) were measured. Femoral vascular conductance was calculated as flow/pressure. Propranolol had no effect on baseline femoral vascular conductance (P > 0.05). As a result of neck pressure, femoral vascular conductance was reduced 23.9 ± 3.5% before vs. 33.2 ± 3.2% after infusion of propranolol (P = 0.033). After thigh-cuff release, femoral vascular conductance declined 50.2 ± 5.8% before vs. 57.4 ± 9.6% after propranolol infusion (P = 0.496). During handgrip, femoral vascular conductance was reduced 47.2 ± 9.6% before vs. 55.2 ± 9.2% after propranolol administration (P = 0.447). After handgrip, women had a greater rise in conductance than men (women: 153 ± 16.2%; men: 36.4 ± 10.6%; P < 0.001), which was blunted by 54.8% by propranolol (P < 0.001 vs. control), but unaffected by propranolol in men (P = 0.355 vs. control). The finding that β-adrenergic receptor-mediated vasodilatation minimally affects vascular responses to these sympatho-excitatory manoeuvres reinforces their utility in the investigation of sympathetic vascular regulation in humans. Interestingly, post-handgrip hyperaemia is greater in women than men and is, in part, β-adrenergic receptor mediated

Recovery from exercise: vulnerable state, window of opportunity, or crystal ball?

Why should we study the recovery from exercise as a discrete phenomenon from exercise itself? We identify three distinct (but not mutually exclusive) rationales that drive the need to investigate the physiology of recovery from exercise. 1) Some individuals are at a heightened risk of clinical outcomes in the immediate post-exercise period; thus the potential negative outcomes of this vulnerable state must be weighed against the numerous benefits of exercise training, and may be mitigated to reduce risk. 2) Many of the signaling mechanisms responsible for the beneficial effects of exercise training remain amplified during the exercise recovery period, and may present a window of opportunity that can be exploited by interventions to enhance the beneficial adaptations to exercise training, especially in clinical populations. 3) On an individual level, exercise recovery responses may provide investigators with a crystal ball ability to predict future clinical outcomes even in apparently healthy individuals. In short, the physiology of recovery is a multi-faceted and complex process, likely involving systems and pathways that are distinct from the physiology of exercise itself. For these reasons, it merits ongoing study