Category Archives: Medical Research

The Physiology of the G.O.A.T. (Part 1- endocrine)

Who is the G.O.A.T.?

Figure 1 shows the main life events that took place since the G.O.A.T. was born. Lionel Andres Messi Cuccittini (Leo) was born on the 24th of June 1987, in the city of Rosario, Santa Fé province, Argentina. In 1992, when he was 4 years old, his grandmother suggested that he should play for local club “Abanderado Grandoli”. Even at that young age, his agility and soccer skills were quickly noticed, and he signed into the historic professional soccer team in Rosario, called Newell’s Old Boys, in the youth ranks in 1995. Newell’s Old Boys is notorious for being one of the few professional clubs from outside of Buenos Aires, Argentina, that has dominated the national scenes of the sport. Many great Argentinean players and tacticians have emerged from this club.

In 1998, unfortunate news came to Leo with his diagnosis of growth hormone deficiency (GHD), he immediately started the treatment, but his family struggled to find the means to pay for the treatment. Regardless, he continued to play soccer, and his father, continued looking for a club for Messi, as his talent was very evident. A scout from Barcelona, Spain, received a tip about a boy in Argentina called Messi. He had been watching videos of this player and knew about the need of the young player for GHD treatment, but everybody thought he was too young and little (2). Nevertheless, because of Messi’s extraordinary skills, a trial for the 11-year-old was arranged in Barcelona. The scout, and everybody present, were surprised to see the talented, and unusually small 11- year-old playing a game, and tried to sign him immediately. However, there was a delay that felt like an eternity, and Messi’s father told Barcelona’s scout that they needed to return to Argentina, and they couldn’t keep waiting for a decision. And right there, the scout was in such a rush to sign Messi that he wouldn’t wait to have a written contract, and did not want to lose such talent, so they signed an agreement on a napkin (https://www.espn.com/soccer/barcelona/story/4263107/barcelonalionel-messi-and-the-napkin-oral-history-of-his-transferarranged-20-years-ago).  In 2000, Messi joined “La Masia, FC Barcelona’s youth academy” and Messi and his father moved to Spain. Part of the contract included paying for Messi’s GHD treatment.

Messi made his debut with Barcelona in 2004, against city rivals Espanyol. Two years later, in 2006, Messi played at his first World Cup for Argentina. Two years after that, he won the Olympic gold medal with Argentina at the 2008 Beijing Olympics. By 2009, Leo had proven his mettle, and was voted the FIFA’s Ballon d’Or winner, the best player in the world, and received this prestigious award six more times. In 2022, Messi achieved his lifelong dream, and won the world cup with Argentina, and unofficially became the G.O.A.T. In early March 2023, Messi was voted yet again as the FIFA best men’s player, in other words, now Messi is “officially” the G.O.A.T.

Size matters, but it is not the main problem!

Messi was 1.32m (4ft 4in) tall at the age of 11 and he had not grown in a couple of years [1]. So, yes height was an issue, but not the biggest issue. Messi suffered from growth hormone deficiency-GHD. According to the Endocrine Society, GHD is a rare condition affecting 1 in 4,000- 1in 10,000 cases [2], and unfortunately, Messi was one of these rare cases. When children have GHD the normal growth of bone and muscle is impaired. GHD can be congenital or acquired, but the consequences of it go well beyond the obvious slowing in growth and short stature. It can cause serious systemic problems, including glucose [3] and fat metabolism [4], cardiovascular complications [5], depression [6], and all of these also lead to fatigue and  exercise intolerance.

Figure 3 illustrates how the secretion of GH occurs, and its actions on various target organs. Under normal healthy conditions, there is a fluctuation in GH secretion during the day, with a marked increase in its secretion during sleep, most precisely about an hour after the onset of deep sleep. Inputs such as exercise, stress, hypoglycemia signal the hypothalamus to secrete growth hormone releasing hormone (GHRH), this hormone travels to the anterior pituitary gland where ultimately, GH is secreted.  Somatropes are the cells in the anterior pituitary gland that secrete GH, which travels systemically to the liver, where insulin-like growth factor 1 is secreted (IGF-I). IGFs act on target cells that cause growth of bone and soft tissues. Since Messi had GHD, the levels of IGF-I were probably lower, slowing his growth during pre-pubertal years before the growth spurt. Other factors affect the levels of IGF-I, most specifically, inadequate nutrition negatively affects its levels in the blood. Fortunately, Messi received treatment before puberty, allowing him to grow to be 170 cm tall (5’7”). However, not only the lack of growth in bone and soft tissues could have halted his amazing athletic career, GHD also results in metabolic complications not related to growth that could have affected his tolerance to exercise.

Give me the sugar!

As illustrated in figure 3, GH acts directly on skeletal muscle, the liver, and adipose tissue. The overall action of GH is to maintain glucose homeostasis. In other words, GH increases the levels of circulating blood glucose, critical to produce adenosine triphosphate (ATP) for energy at rest, and most importantly during exercise. The action of GH on the muscle is to inhibit the glucose uptake by the muscle, thus, increasing the levels of circulating glucose to be later used for ATP production. Additionally, to further spare glucose in the blood stream, GH mobilizes fat stores by breaking down triglycerides, increasing fatty acid levels in blood. In the liver, GH also promotes gluconeogenesis, or the formation of glucose from non-carbohydrate substrates. All these actions can occur simultaneously and depend on the intensity and duration of exercise. With GHD, athletes can be more easily fatigued, and Messi probably would have been unable to perform to the level he did, and becoming the G.O.A.T.

We need glucose to create ATP, during exercise, especially at high intensities as humans depend on the ability to spare glucose, the only fuel for the central nervous system. Your brain is like a selfish boss, everybody (in this case every organ) must work to keep it happy and functioning. To keep your brain “happy” the rest of your organs need to make sure enough glucose is in the blood for the brain to have the energy for all of its intricate functions.

This glucose homeostasis happens by the orchestrated actions of several hormones including glucagon, cortisol, catecholamines and GH. One of the major adaptations of training is the decrease reliance on carbohydrates for energy and a shift to fat metabolism. At rest and low intensity exercise, we use mostly fats as “fuel” however, when we go above 50-60% of the maximum, we switch to carbohydrates for metabolism. This phenomenon is called the “crossover point”. Endurance exercise training shifts this crossover point to higher intensities, sparing glucose and decreasing the accumulation of lactic acid. When a person exercises and experience the “hit the wall” phenomenon (i.e., the sudden loss of energy during an endurance event like a race) it is due to low blood glucose levels. GHD probably could have played a role on Messi’s metabolism if not treated.

What else makes the G.O.A.T the best?

There is much to talk about Messi, from the endocrine system to his extraordinary neural activity that makes him very fast and coordinated. From his tolerance to fatigue, high maximal oxygen consumption and lactate threshold to the muscle fiber type to motor unit recruitment and synchronization, we are going to focus only on the metabolic adaptations of training of this elite athlete, and we promise a part 2 of this blog post to talk about the rest of the adaptations of training that makes the G.O.A.T the best!

Maximal Oxygen Consumption (VO2max)

Oxygen consumption refers to the amount of oxygen being taken up by the tissues per minute to oxidize substrates (like carbohydrates and fats). Maximal oxygen consumption (or VO2max) refers to the amount of oxygen used during an incremental exercise to exhaustion. The higher the VO2max the higher the endurance capacity of the person, and their “fuel” utilization. This oxygen is being taken up by skeletal muscle and used in the mitochondria to create ATP. One adaptation of endurance training is having higher VO2max values. While sedentary males range between 25- 45 ml/kg/min, and distance runners could be between 65- 85 ml/kg/min,  the values for professional soccer players can range between 59.2 to 63.2 ml/kg/min, and mid-fielders and attackers have higher values than defenders and goalies [7].

A limitation of this test is that it is conducted in standardized conditions in a laboratory, and fails to replicate the actual consumption, often supra-maximal, that occurs during a game. Nevertheless, this is the gold standard measurement for cardiovascular fitness, and we speculate that the G.O.A.T. may have high VO2max values. We also think that Messi has a high lactate threshold, or the point in which lactate production exceeds clearance during this incremental maximal exercise test to exhaustion. High lactate threshold and crossover point can be related, as the endurance-trained person has better ability to spare glucose (carb reserves) and thus creates less lactic acid. Also, higher oxidative metabolism results in higher ability to oxidize lactate during the athletic event and use it as fuel.  Athletes like Messi usually have all the biochemical adaptations that make their skeletal muscle fibers more resistant to fatigue. This is due to mitochondrial proliferation and capillary recruitment. Messi is also a very explosive and fast player, due to a combination of nature (his genetic makeup) and nurture (his training), probably with a high number of Type II fast-oxidative muscle fibers with high levels of Myosin-ATPase activity. These fibers have intermediate resistance to fatigue, high oxidative phosphorylation capacity, fast speed of contraction, many capillaries and mitochondria and high myoglobin content.

Why is Messi the G.O.A.T?

The chances of a young boy from the countryside of Argentina with GHD to be even considered for any major international soccer club are very slim. This is because in Argentina everybody plays soccer and there are numerous soccer players and too much competition. In fact, Messi was rejected from giant club “River Plate” in Buenos Aires, Argentina, before signing his agreement on a napkin with Barcelona.  The economic disparities also play a role on the odds of any young player to become a professional soccer player if any medical treatment is needed. However, there was something special about this boy, and it only took a trained eye to envision a wonderful professional career. Without the hormonal supplementation, Messi would have probably never had a shot. Fortunately for soccer fans all over the world, advances in biomedical research made it possible for Messi to reach his full potential and become this phenomenon adored by all.

References:

  1. Hawkey, I. Lionel Messi on a mission. 2008 [cited 2023 March 5]; Available from: http://www.timesonline.co.uk/tol/sport/football/european_football/article3779961.ece.
  2. Endocrine_Society. Growth Hormone Deficiency. 2023 [cited 2023 March 6th]; Available from: https://www.endocrine.org/patient-engagement/endocrine-library/growth-hormone-deficiency.
  3. Hew, F.L., et al., Growth hormone deficiency and cardiovascular risk. Baillieres Clin Endocrinol Metab, 1998. 12(2): p. 199-216.
  4. Gertner, J.M., Growth hormone actions on fat distribution and metabolism. Horm Res, 1992. 38 Suppl 2: p. 41-3.
  5. Lombardi, G., et al., The cardiovascular system in growth hormone excess and growth hormone deficiency. J Endocrinol Invest, 2012. 35(11): p. 1021-9.
  6. Karachaliou, F.H., et al., Association of growth hormone deficiency (GHD) with anxiety and depression: experimental data and evidence from GHD children and adolescents. Hormones (Athens), 2021. 20(4): p. 679-689.
  7. Slimani, M., et al., Maximum Oxygen Uptake of Male Soccer Players According to their Competitive Level, Playing Position and Age Group: Implication from a Network Meta-Analysis. J Hum Kinet, 2019. 66: p. 233-245.
Benjamin Puppato is a junior in the International Baccalaureate program at Floyd Central High School. He loves playing soccer, and also he is interested in statistics and facts about soccer, particularly of Argentinean players and teams.

 

 

 

 

Dr. Terson de Paleville is an associate professor of Physiology at the University of Louisville’s School of Medicine. She teaches Exercise Physiology and Human Physiology courses. Dr. Terson de Paleville has investigated the effects of activity-based therapy on respiratory muscles, body composition and autonomic function after spinal cord injury. Additional research project involves research on best practices for teaching physiology.
Protecting yourself means more than a mask; should classes be moved outside?
Mari K. Hopper, PhD
Associate Dean for Biomedical Science
Sam Houston State University College of Osteopathic Medicine

Disruption sparks creativity and innovation. For example, in hopes of curbing viral spread by moving classroom instruction outdoors, one Texas University recently purchased “circus tents” to use as temporary outdoor classrooms.

Although circus tents may be a creative solution… solving one problem may inadvertently create another. Moving events outdoors may be effective in reducing viral spread, but it also increases the skin’s exposure to harmful ultraviolet (UV) radiation from the sun. The skin, our body’s largest organ by weight, is vulnerable to injury. For the skin to remain effective in its role of protecting us from pollutants, microbes, and excessive fluid loss – we must protect it.

It is well known that UV radiation, including UVA and UVB, has deleterious effects including sunburn, premature wrinkling and age spots, and most importantly an increased risk of developing skin cancer.

Although most of the solar radiation passing through the earth’s atmosphere is UVA, both UVA and UVB cause damage. This damage includes disruption of DNA resulting in the formation of dimers and generation of a DNA repair response. This response may include apoptosis of cells and the release of a number of inflammatory markers such as prostaglandins, histamine, reactive oxygen species, and bradykinin. This classic inflammatory response promotes vasodilation, edema, and the red, hot, and painful condition we refer to as “sun burn.”1,2

Prevention of sunburn is relatively easy and inexpensive. Best practice is to apply broad spectrum sunscreen (blocks both UVA and UVB) 30 minutes before exposure, and reapply every 90 minutes. Most dermatologists recommend using SPF (sun protection factor) of at least 30. Generally speaking, an SPF of 30 will prevent redness for approximately 30 times longer than without the sunscreen. An important point is that the sunscreen must be reapplied to maintain its protection.

There are two basic formulations for sunscreen:  chemical and physical. Chemical formulations are designed to be easier to rub into the skin. Chemical sunscreens act similar to a sponge as they “absorb” UV radiation and initiate a chemical reaction which transforms energy from UV rays into heat. Heat generated is then released from the skin.3  This type of sunscreen product typically contains one or more of the following active ingredient organic compounds: oxybenzone, avobenzone, octisalate, octocrylene, homosalate, and octinoxate. Physical sunscreens work by acting as a shield. This type of sunscreen sits on the surface of the skin and deflects the UV rays. Active ingredients zinc oxide and/or titanium dioxide act in this way.4  It’s interesting to note that some sunscreens include an expiration date – and others do not. It is reassuring that the FDA requires sunscreen to retain their original “strength” for three or more years.

In addition to sunscreen, clothing is effective in blocking UV skin exposure. Darker fabrics with denser weaves are effective, and so too are today’s specially designed fabrics. These special fabrics are tested in the laboratory to determine the ultraviolet protection factor (UPF) which is similar to SPF for sunscreen.  A fabric must carry a UPF rating of at least 30 to qualify for the Skin Cancer Foundation’s Seal of Recommendation. A UPF of 50 allows just 1/50th of the UV rays to penetrate (effectively blocking 98%). Some articles of clothing are produced with a finish that will wash out over time. Other fabrics have inherent properties that block UV rays and remain relatively unchanged due to washing (some loss of protection over time is unavoidable) – be careful to read the clothing label.

Some individuals prefer relying on protective clothing instead of sunscreen due to concerns about vitamin D synthesis. Vitamin D activation in the body includes an important chemical conversion stimulated by UV exposure in the skin – and there is concern that sunscreen interferes with this conversion. However, several studies, including a recent review by Neale, et al., concluded that use of sunscreen in natural conditions is NOT associated with vitamin D deficiency.5,6 The authors did go on to note that at the time of publication, they could not find trials testing the high SPF sunscreens that are widely available today (current products available for purchase include SPFs over 100).

Additional concern about use of sunscreens includes systemic absorption of potentially toxic chemicals found in sunscreen. A recent randomized clinical trial conducted by Matta and colleagues investigated the systemic absorption and pharmacokinetics of six active sunscreen ingredients under single and maximal use conditions. Seven Product formulations included lotion, aerosol spray, non-aerosol spray, and pump spray. Their study found that in response to repeat application over 75% of the body surface area, all 6 of the tested active ingredients were absorbed systemically. In this study, plasma concentrations surpassed the current FDA threshold for potentially waiving some of the additional safety studies for sunscreen. The authors went on to note that the data is difficult to translate to common use and further studies are needed. It is important to note that the authors also conclude that due to associated risk for development of skin cancer, we should continue to use sunscreen.

Yet another concern for using sunscreen is the potential for harmful environmental and human health impact. Sunscreen products that include organic UV filters have been implicated in adverse reactions in coral and fish, allergic reactions, and possible endocrine disruption.8,9 In some areas, specific sunscreen products are now being banned (for example, beginning January of 2021, Hawaii will ban products that include oxybenzone and octinoxate). As there are alternatives to the use of various organic compounds, there is a need to continue to monitor and weigh the benefit verses the potential negative effects.

Although the use of sunscreen is being questioned, there is the potential for a decline in use to be associated with an increase in skin cancer. Skin cancer, although on the decline in recent years, is the most common type of cancer in the U.S. It is estimated that more than 3 million people in the United States are diagnosed with skin cancers each year (cancer.net). Although this is fewer than the current number of Americans diagnosed with COVID-19 (Centers for Disease Control and Prevention, July 20, 2020) – changes in human behavior during the pandemic (spending more time outdoors) may inadvertently result in an increase in the number of skin cancer cases in future years.  

While we responsibly counter the impact of COVID-19 by wearing masks, socially distancing, and congregating outdoors – we must also continue to protect ourselves from damaging effects of the sun. As physiologists, we are called upon to continue to investigate the physiological impacts of various sunscreen delivery modes (lotion, aerosol, non-aerosol spray, and pumps) and SPF formulations. We are also challenged to investigate inadvertent and potentially negative impacts of sunscreen including altered Vitamin D metabolism, systemic absorption of organic chemicals, and potentially adverse environmental and health outcomes.

Again, solving one problem may create another challenge – the work of a physiologist is never done!

Stay safe friends!

Mari

References:

  1. Lopes DM, McMahon SB. Ultraviolet radiation on the skin: a painful experience? CNS neuroscience & therapeutics. 2016;22(2):118-126.
  2. Dawes JM, Calvo M, Perkins JR, et al. CXCL5 mediates UVB irradiation–induced pain. Science translational medicine. 2011;3(90):90ra60-90ra60.
  3. Kimbrough DR. The photochemistry of sunscreens. Journal of chemical education. 1997;74(1):51.
  4. Tsuzuki T, Nearn M, Trotter G. Substantially visibly transparent topical physical sunscreen formulation. In: Google Patents; 2003.
  5. Passeron T, Bouillon R, Callender V, et al. Sunscreen photoprotection and vitamin D status. British Journal of Dermatology. 2019;181(5):916-931.
  6. Neale RE, Khan SR, Lucas RM, Waterhouse M, Whiteman DC, Olsen CM. The effect of sunscreen on vitamin D: a review. British Journal of Dermatology. 2019;181(5):907-915.
  7. Matta MK, Florian J, Zusterzeel R, et al. Effect of sunscreen application on plasma concentration of sunscreen active ingredients: a randomized clinical trial. Jama. 2020;323(3):256-267.
  8. Schneider SL, Lim HW. Review of environmental effects of oxybenzone and other sunscreen active ingredients. Journal of the American Academy of Dermatology. 2019;80(1):266-271.
  9. DiNardo JC, Downs CA. Dermatological and environmental toxicological impact of the sunscreen ingredient oxybenzone/benzophenone‐3. Journal of cosmetic dermatology. 2018;17(1):15-19.

    All images from:
    Royalty Free Stock Pictures – Public Domain Images
    www.dreamstime.com/

Prior to accepting the Dean’s positon at Sam Houston State University, Dr Hopper taught physiology and served as the Director of Student Research and Scholarly Work at Indiana University School of Medicine (IUSM). Dr Hopper earned tenure at IUSM and was twice awarded the Trustees Teaching Award. Based on her experience in developing curriculum, addressing accreditation and teaching and mentoring of medical students, she was selected to help build a new program of Osteopathic Medicine at SHSU. Active in a number of professional organizations, Dr. Hopper is past chair of the Chapter Advisory Council Chair for the American Physiological Society, the HAPS Conference Site Selection Committee, and Past-President of the Indiana Physiological Society.

Lighting the Spark: Engaging Medical Students in Renal Physiology
Jessica Dominguez Rieg, PhD
Department of Molecular Pharmacology and Physiology
University of South Florida Morsani College of Medicine

Recently, I spent some time reflecting on the way we teach physiology at my institution. One thing that kept coming to my mind- why does renal physiology get such a bad reputation? We often hear medical students commenting that renal physiology was the hardest topic of the first year, that there’s too much math involved, and concepts like acid-base and electrolyte disorders are too difficult to grasp. Does a negative attitude about renal physiology really matter in the long run? If the students can successfully pass USMLE Step 1, can I rest easy knowing they are competent in understanding how the kidneys function? Or can I, a basic science faculty, make a bigger impact on how these students view the renal system?

Chronic kidney disease is a growing public health concern in the United States, affecting roughly 40 million adults. Given the increasing burden of disease, an aging population, and modern medicine that is keeping patients with end-stage kidney disease alive longer, we need a robust workforce in nephrology. However, the field of nephrology is in the middle of a major crisis, and there is significant concern that there will not be an adequate workforce to meet the healthcare needs of patients afflicted with kidney disease. Only 62% of available nephrology fellowship positions were filled in the 2019 National Resident Matching Program match and less than 45% of positions were filled by U.S. MD graduates, making nephrology one of the least competitive subspecialties1. When does the waning interest in nephrology begin? Many think it starts early in a medical student’s academic journey.

I recently surveyed our medical students at the University of South Florida Morsani College of Medicine (250 respondents) and found that 60% of students agreed or strongly agreed that the topic of nephrology is interesting and yet close to one-third of them agreed or strongly agreed that renal pathophysiology is too complex and challenging for them. When asked what makes the biggest impact on their future career choice, 60% indicated that having role models and mentors in the specialty field was high impact; however, less than half of the students felt they had been exposed to encouraging role models or mentors in nephrology. Students ranked rotations during clerkships as having the highest impact in career choice; and yet our students are first exposed to nephrology during their Internal Medicine clerkship in their 3rd year, which only last 8 weeks. Not surprisingly, students ranked didactics in the preclinical years as having the lowest impact on career choice. What if we can change that? Perhaps there is too little done too late- and we just can’t get enough momentum going to gain a critical mass of students interested in nephrology. Is there anything that we, as medical physiology educators, can do to help? We can light the spark!

1. Make it matter. The complexity of renal physiology must be taught with meaningful clinical context. Students need to understand the clinical importance of what they are learning or there is a high chance they will get turned off from the very beginning. One of the best ways I have found to make it matter, is to work closely with my clinical colleagues. Not only can they provide (and co-teach) examples of how to

2. Make it digestible. Students often get overwhelmed by the level of detail that is expected in the renal block. We must ensure we are giving them the important content in bite-sized pieces so they have time to think about it, apply it, and understand it. I give our students a blank nephron map2 at the beginning of the renal block and ask that they work together to fill it out. On the last day of the renal block, we go through the maps together as a summary of renal function. Students like having all the transporters, hormones and key characteristics about each region of the nephron in one place. It helps them organize their knowledge and also gives them something to refer to in Year 2 and beyond.

3. Make it relatable. At our institution, students get renal physiology at the end of Year 1, so they’ve had all other organ systems besides reproductive physiology. I use many analogies throughout the renal system and always to try to highlight the similarities with the intestinal tract, which they are more familiar with at that point in time. After all, the nephron is like a “mini-intestine”, with similar histological features and transporter profiles. By relating the new renal content to something they’ve seen before, it can help make it a little easier to understand (and allows them to make systemic connections).

4. Make it stick. Students struggle with grasping acid-base disturbances. Consistent repetition and practice problems is key! Many times, students learn multiple ways to approach interpreting acid-base disturbances (different formulas, different values for expected compensatory responses, etc.) depending on who is teaching. This can be frustrating and confusing for students. We have found that having all faculty that teach some aspect of acid-base balance use a single resource, a step-by-step guide to interpreting acid-base disturbances3, has been very helpful in ensuring consistency in what we teach. Students also work through many practice problems in interpretation of arterial blood gases, starting in Year 1, again in Year 2, and again during the clerkships. The result is that students have gone from scoring less than 50% on NBME acid-base questions, to close to 90%- it’s sticking!

5. Make it fun! One of the notoriously challenging lectures in our preclinical years is integration of acid-base, volume, and electrolyte disorders. Traditionally, it was a lecture given by a nephrologist and was very technical and clinically oriented. However, students were lost and overwhelmed. So, I partnered with an internal medicine physician and we revamped the session into a fun, interactive series of cases where we co-facilitated discussion. Students were introduced to the 14th book of Lemony Snicket’s A Series of Unfortunate Events: The Hazardous Hospital, where they were asked to investigate the mysterious health issues of Sir Cornelius. The cases we presented were challenging and framed with very relevant basic science concepts, and students loved it! Not only did they have fun while learning, but they really appreciated having a basic scientist and clinician teaching together.

In conclusion, renal physiology is challenging and may be contributing to a lack of interest in a career in nephrology. As medical physiology educators, we have the ability to work with our clinical colleagues and revamp how we teach the renal system. We can get students engaged and excited about renal physiology by making the content clinically relevant, digestible, relatable and fun. After all, there needs to be a spark to light the fire!

References:

  1. National Resident Matching Program, Results and Data: Specialties Matching Service 2019 Appointment Year. National Resident Matching Program, Washington, DC. 2019
  2. Robinson PG, Newman D, Reitz CL, Vaynberg LZ, Bahga DK, Levitt MH. A large drawing of a nephron for teaching medical students renal physiology, histology, and pharmacology. Advances in Physiology Education. 42:2, 192-199, 2018.
  3. DeWaay D, Gordon J. The ABC’s of ABGs: teaching arterial blood gases to adult learners. MedEdPORTAL. 2011;7:9038.

Dr. Dominguez Rieg is a faculty member in the Department of Molecular Pharmacology & Physiology at the University of South Florida Morsani College of Medicine. She is the Course Director for the Gastrointestinal, Endocrine, Renal and Reproductive Systems block and the Physiology Integration Director that is responsible for mapping physiology content objectives across the entire curriculum. She teaches endocrine, renal and reproductive physiology and renal pathophysiology in multiple courses in the pre-clerkship years. She received her PhD in Physiological Sciences from the University of Arizona. Her research interests are kidney-intestine crosstalk and intestinal function in the context of systemic diseases such as obesity and diabetes. When she’s not at work, she is enjoying time with her young daughter and four German Shepherds.

Backward planning of lab course to enhance students’ critical thinking
Zhiyong Cheng, PhD
Food Science and Human Nutrition Department
The University of Florida

Development of critical thinking and problem-solving skills hallmarks effective teaching and learning [1-2]. Physiology serves as a fundamental subject for students in various majors, particularly for bioscience and pre-professional students [1-8]. Whether they plan on careers in science or healthcare, critical thinking and problem-solving skills will be keys to their success [1-8].

Backwards course design is increasingly employed in higher education. To effectively accomplish specific learning goals, instructions are to begin course development with setting learning objectives, then backwardly create assessment methods, and lastly design and deliver teaching and learning activities pertaining to the learning objectives and assessment methods. In terms of development of critical thinking and problem-solving skills, a lab course constitutes an excellent option to provide opportunities for instructors and students to explore innovative paths to their desired destinations, i.e., to accomplish specific learning goals.

In a traditional “cookbook” lab setting, detailed procedures are provided for the students to follow like cooking with a recipe. Students are usually told what to do step-by-step and what to expect at the end of the experiment. As such, finishing a procedure might become the expected goal of a lab course to the students who passively followed the “cookbook”, and the opportunity for developing critical thinking skills is limited. In a backwards design of a lab course; however, the instructor may engage the students in a series of active learning/critical thinking activities, including literature research, hypothesis formulation, study design, experimental planning, hands-on skill training, and project execution. Practically, the instructor may provide a well-defined context and questions to address. Students are asked to delve into the literature, map existing connections and identify missing links for their project to bridge. With the instructor’s guidance, students work together in groups on hypothesis development and study design. In this scenario, students’ focus is no longer on finishing a procedure but on a whole picture with intensive synthesis of information and critical thinking (i.e., projecting from generic context to literature search and evaluation, development of hypothesis and research strategy, and testing the hypothesis by doing experiments).

An example is this lab on the physiology of fasting-feeding transitions. The transition from fasting to feeding state is associated with increased blood glucose concentration. Students are informed of the potential contributors to elevated blood glucose, i.e., dietary carbohydrates, glycogen breakdown (glycogenolysis), and de novo glucose production (gluconeogenesis) in the liver. Based on the context information, students are asked to formulate a hypothesis on whether and how hepatic gluconeogenesis contributes to postprandial blood glucose levels. The hypothesis must be supported by evidence-based rationales and will be tested by experiments proposed by students with the instructor’s guidance. Development of the hypothesis and rationales as well as study design requires students to do intensive information extraction and processing, thereby building critical thinking and problem-solving skills. Students also need to make sound judgments and right decisions for their research plans to be feasible. For instance, most students tend to propose to employ the hyper-insulinemic-euglycemic clamp because the literature ranks it as a “gold standard” method to directly measure hepatic gluconeogenesis. However, the equipment is expensive and not readily accessible, and students have to find alternative approaches to address these questions. With the instructor’s guidance, students adjust their approaches and adopt more accessible techniques like qPCR (quantitative polymerase chain reaction) and Western blotting to analyze key gluconeogenic regulators or enzymes. Engaging students in the evaluation of research methods and selection helps them navigate the problem-solving procedure, increasing their motivation (or eagerness) and dedication to learning new techniques and testing their hypotheses. Whether their hypotheses are validated or disproved by the results they acquire in the end, they become skillful in thinking critically and problem solving in addition to hands-on experience in qPCR and Western blotting.

Evidently, students can benefit from backwards planning in different ways because it engages them in problem-based, inquiry-based, and collaborative learning — all targeted to build student problem solving skills [1-8]. For a typical lab course with pre-lab lectures; however, there is only 3-6 hours to plan activities. As such, time and resources could be the top challenges to implement backwards planning in a lab course. To address this, the following strategies will be of great value: (i) implementing a flipped classroom model to promote students’ pre- and after-class learning activities, (ii) delivering lectures in the lab setting (other than in a traditional classroom), where, with all the lab resources accessible, the instructor and students have more flexibility to plan activities, and (iii) offering “boot camp” sessions in the summer, when students have less pressure from other classes and more time to concentrate on the lab training of critical thinking and problem solving skills. However, I believe that this is a worthwhile investment for training and developing next-generation professionals and leaders.

References and further reading

[1] Abraham RR, Upadhya S, Torke S, Ramnarayan K. Clinically oriented physiology teaching: strategy for developing critical-thinking skills in undergraduate medical students. Adv Physiol Educ. 2004 Dec;28(1-4):102-4.

[2] Brahler CJ, Quitadamo IJ, Johnson EC. Student critical thinking is enhanced by developing exercise prescriptions using online learning modules. Adv Physiol Educ. 2002 Dec;26(1-4):210-21.

[3] McNeal AP, Mierson S. Teaching critical thinking skills in physiology. Am J Physiol. 1999 Dec;277(6 Pt 2):S268-9.

[4] Hayes MM, Chatterjee S, Schwartzstein RM. Critical Thinking in Critical Care: Five Strategies to Improve Teaching and Learning in the Intensive Care Unit. Ann Am Thorac Soc. 2017 Apr;14(4):569-575.

[5] Nguyen K, Ben Khallouq B, Schuster A, Beevers C, Dil N, Kay D, Kibble JD, Harris DM. Developing a tool for observing group critical thinking skills in first-year medical students: a pilot study using physiology-based, high-fidelity patient simulations. Adv Physiol Educ. 2017 Dec 1;41(4):604-611.

[6] Bruce RM. The control of ventilation during exercise: a lesson in critical thinking. Adv Physiol Educ. 2017 Dec 1;41(4):539-547.

[7] Greenwald RR, Quitadamo IJ. A Mind of Their Own: Using Inquiry-based Teaching to Build Critical Thinking Skills and Intellectual Engagement in an Undergraduate Neuroanatomy Course. J Undergrad Neurosci Educ. 2014 Mar 15;12(2):A100-6.

[8] Peters MW, Smith MF, Smith GW. Use of critical interactive thinking exercises in teaching reproductive physiology to undergraduate students. J Anim Sci. 2002 Mar;80(3):862-5.

Dr. Cheng received his PhD in Analytical Biochemistry from Peking University, after which he conducted postdoctoral research at the University of Michigan (Ann Arbor) and Harvard Medical School. Dr. Cheng is now an Assistant Professor of Nutritional Science at the University of Florida. He has taught several undergraduate- and graduate-level courses (lectures and lab) in human nutrition and metabolism (including metabolic physiology). As the principal investigator in a research lab studying metabolic diseases (obesity and type 2 diabetes), Dr. Cheng has been actively developing and implementing new pedagogical approaches to build students’ critical thinking and problem-solving skills.