Selling Chris beforehand, my daughter just turned 21, and when she came down to visit us in Southern Florida a couple months ago, she said, Dad, you need a hair transplant and you need to dye your hair. It's too gray. So I appreciate being here. I'm actually one of the first people that started this course. I think it's, whatever, 14, 15 years old now. So it's been a whole lot of fun, and I always enjoy coming and certainly getting to see some familiar faces, as well as meet some new folks. So as Chris said, we've got about an hour here. These talks get pretty packed, as you know, and between myself and Dr. Borchers, we've got to cover all of the, quote, unquote, medical aspects for you guys. So just by way of introduction here, this is what we're going to cover over the next 55 minutes or so. As you can see, it's a broad range of things, including the pre-participation exam, the sort of highlights, of course, of the cardiac and pulmonary issues, and do some work with environmental exposure, altitude, talk a little bit about nutrition, and then finish up with the eating disorder slash female triad, as well as exercise and pregnancy. So to get us started, then, the purpose of the PPE, or the pre-participation evaluation, and again, this is really more historical, and as many of you may know, it's undergoing some close scrutiny right now in terms of what its real purpose is. Nevertheless, when it was started, it was intended to be, quote, unquote, gathering baseline data. Interestingly, we said it was to detect manageable medical conditions that may interfere with sport participation. More importantly, perhaps, is to determine any contraindications to participation, and as you'll see, very few athletes are disqualified based on the PPE. This is a real contentious topic now, and that is discovering predisposition to injury. Can we actually predict who's at risk for injury based upon, for example, the two-minute traditional musculoskeletal exam? And then, of course, one of the elephants on the wall is this whole idea about fulfilling legal and insurance requirements, which I'm sure we realize is probably not true. There's been some newer work, as you may know, looking at things like functional testing, and that's in the fourth edition of the pre-participation evaluation, so you may actually see that on the exam as a question, and the fifth edition is soon to come, and my understanding is, talking with Bill Roberts and Dave Bernhardt, the editors, that it may be released by the end of this year, if not early next year. So I think we were all trained, and it goes back to the history and the physical examination, right? So these are just some of the highlights here, and again, this is a fairly busy slide, but I want to draw your attention to a few things and some of the changes. So for example, we talked about immunizations, right? When I started 30 years ago, this was not something we really routinely assessed during the PPE, but as we know now, college athletes or college students in general are at high risk for things such as meningococcemia, so there's been some changes there. Meat illness is another topic, and we'll go into that in some detail and tie that into sickle cell testing, and then finally, some of the nutritional issues, which are again largely related to issues around the female triad. So again, it starts with the history, as we know. This is a real key slide, and we're going to expand upon this when we talk about the cardiac issues and what's really current about screening, because again, you'll hear a lot of information. It's like concussion. When I first started 30 years ago, a concussion visit was 10 minutes, and now they're 30 to 45 minutes, so I don't see concussions anymore. In any event, so this is a really key slide, and you need to know this for purposes of the exam. So at the end of the day, still in this country, it's the American Heart Association 17-point screening exam that's really the standard of care, if you will. We'll talk a little bit about EKGs and ECHOs, because you're going to see some stuff related to the athlete's heart, but for test-taking purposes, it's still the American Heart Association 14-point exam, history and physical, that you can see here. Here's another slide that you don't need to necessarily appreciate the details, but this is what drives our decision-making for athletes when we talk about disqualification from sport, right? And that's the Bethesda guidelines, the 36 Bethesda guidelines, and again, this is really important for test-taking purposes, that if nothing else, you understand what is involved with this and how we actually make decisions, and to make a long story short, the way I like to look at it is, if you have situations such as hypertrophic obstructive cardiomyopathy, and we'll talk in detail about that, these are the athletes that are really only allowed to participate in quote-unquote 1A sports, and as you can see, that means that they've got a low demand, if you will, on the strength side, as well as the cardiovascular side. So it's the Bethesda guidelines for test-taking purposes that you need to be familiar with. This slide's perhaps outdated, but it still comes up on the test, right? And that is, if you have athletes with a single organ, it used to be that they could be disqualified from sport, and of course, that's no longer the case, thanks to the American Disabilities Act, and we'll address that specifically with a question. Heat intolerance is something that comes up, and there's a few things that we need to know here. The problem is, we don't know a lot, right? And what I mean by that is, we understand risk factors and we understand treatment, but for actually returning athletes to sport, there are no standards yet that have really been established. So, if you see a question along those lines, recognize that we really don't have true standards of care yet. So, for example, if you have an athlete that has sustained, unfortunately, a heat stroke, you know, what's the guidelines, what's the recommendation, or more importantly, what's the evidence for returning him or her to sport? And it's very minimal right now, it's really just expert opinion. And just a couple of highlights here, there's a very nice article that was just published last year by Chad Asplen and Fran O'Connor, which I'd encourage you to take a look at, and as well, Doug Cazza from Connecticut has done a lot of work in this area. Since we're talking about the PPE, remember the spinal cord injured athlete? This does come up frequently, right? And what is it you need to know? Well, if you have a lesion at T6 or above, you lose sympathetic innervation, and so these athletes are at much higher risk for heat-related illness. And why is that? Well, they have a decreased cardiac output, and that's due to the fact that their stroke volume is decreased, but they have a minimal compensatory increase in their heart rate. So, back to a little bit of physiology 101, and this is something that you will see, and I'm sure everybody in this audience is certainly familiar with the Downs athlete and the risks for atlantoaxial instability and the minimal requirement for AP and lateral films, if not flexion extension as well. So I mentioned earlier all of the purposes to the PPE, but when you really start to look at it, and this literature is actually a bit dated and probably needs to be updated, frankly, but to make a long story short, as you can see here, very few athletes are actually disqualified. So when we talk about the PPE and what we think it does, it turns out it probably doesn't do a very good job, or alternatively, very few athletes are really truly disqualified. Hypertension is the one that you need to know, and I would encourage you to be familiar with the JNC guidelines, particularly for the pediatric literature, okay? That does come up on the test as well, knowing the criteria for blood pressure and monitoring. Just a couple of questions here. Let's start with, again, back to the PPE. It's designed to do what? Substitute for an adolescent's routine health exam, protect the institution from medical legal issues, identify athletes with coronary artery disease, detect any medical or musculoskeletal condition that predispose the athlete to injury or illness, and finally, to exclude participation. So the answer is D, of course, right? What we're really trying to do here is trying to identify, and as I said earlier, this is really I think an exciting area that needs a lot of work, and particularly on the musculoskeletal side, you know, what is it we can really predict in terms of injury? And it turns out probably previous injury is as good a predictor of subsequent injury as anything that we do on a musculoskeletal exam. Another question here, a football PPE reveals you have an athlete with a normal functioning single solitary kidney. After appropriate consultation and discussion with the parents and athlete, what should the team physician recommend? Number one, participation after explaining the risks of playing contact sport. Number two, participation in non-contact sport only. Participation avoiding NSAIDs and seeking nutritional counseling. Participation with the addition of special padding to protect the athlete's kidney. And finally, participation after modifying the weightlifting program, emphasizing core strength. And the answer is A, right? Athletes with a single kidney should be counseled regarding their condition. Although the incidence of renal injury is small, there may or may not be an increased risk of injury with contact sports. One final question, you perform PPE at your local high school. Which of the following conditions require further workup before clearing the athlete for participation in sport? Number one, infantile febrile seizures. Very common, right? And the risk for subsequent seizures is actually quite low. That's when you get into issues regarding what sports athletes can be cleared if they have a known seizure disorder. Sickle cell trait, we probably know that's wrong, right? We have a lot of athletes now that actually carry that trait. Sinus bradycardia, we'll talk about some of the physiological adaptations you need to know for endurance exercise. Idiopathic scoliosis, and finally, diastolic heart murmur. And the way I like to think about this is diastolic heart murmurs in general really require further evaluation. And you can see here the differences between early and mid-diastole and some of the cardiac lesions that are associated. So I mentioned earlier cardiac screening. This is something we really need to be familiar with, and in particular, we need to be familiar with the current guidelines in this country, because they are different in different parts of the world. And I think that's where it sometimes gets confusing. And what I'll try to do in the next few minutes is explain the basis for why there are different recommendations. So ultimately, what is our real goal? It's to prevent sudden cardiac death, okay? We know that the American Heart Association, as well as the European Society of Cardiology, they both recommend screening. Fair enough. High school and college athletes before participation are probably our top priority, though the age to best screen and the frequency of screening is still unknown. And I'll elaborate on that with some of our genetic disorders. Because if you take, for example, hypertrophic cardiomyopathy, we know that one in 500 of us carries the gene. The question really becomes, when is that gene expressed and to what degree is it expressed? And that's where I think we're starting to struggle with this idea of genetic testing. As I mentioned earlier, for sake of repetition, because you're going to see this, what's really mandated in this country is the 14 element screening. And Barry Marin's another big name in the area. If anybody's interested in reading more about these topics, Barry's one of the thought leaders. So as I mentioned earlier, what really drives our thinking in this country, at least, in terms of the pre-participation evaluation? What should we be doing to detect, to screen, if you will, for risk for sudden cardiac death and some of these disorders we'll talk about? This slide probably needs to be updated as well, truthfully, and I think the data are coming out here soon. This was published about a decade ago in Circulation. And this just looks at the causes of sudden cardiac death in the U.S., and what I would draw your attention to is we use the age of 35 as a cutoff, right? So if you're over 35, the most common thing is related to vascular disease. It's under 35, it's those college athletes or high school athletes where we're talking about some of the particular problems we'll address here shortly. Pros and cons of screening, I think this is a nice way for you to think about how we really think about decision-making for evaluation. Ben Levine is a well-known person in this area and gave a very eloquent lecture about five years ago at the Advanced Team Physician course. And as you can see here, here are some of the pros and cons for and against screening. And again, if you think about screening and all the things that we talk about, not only in sport medicine, but in medicine in general, it's a very difficult topic, as we all know. And we all certainly live through the era of, for example, smokers and doing yearly chest X-rays. And what we found was that was a lousy screening test, right? Because by the time you detected it on chest X-ray, it was too late. Now we're in the era of recommending that maybe CT scans for high-risk individuals such as smokers would be the way to go. So screening is a very contentious topic, and I just want to draw this to your attention today. So let's move this forward and get more specific for things that you'll see on the test. What are the current best practices? First of all, at least on this side of the pond, if you will, which is in the U.S. and in Canada, as well as the U.K., is still the pre-participation evaluation. And that's the 14-point American Heart Association. There are simply no requirements in place yet that mandate an EKG or an echo. And then you may ask yourself, well, why is it that the Italians, they recommend for any athlete over the age of 10 that they must be cleared, or prior to clearance, they must have a resting EKG as well as an echocardiogram. And we'll get into that more in a second here. We know that 80% of athletes who die from sudden cardiac death, they're asymptomatic with a normal exam. That's the whole point behind saying, what else can we do to screen for these problems? Well, so here's some very specific data, as you can see here. We see that EKG actually, and again, this is in this country at least, it does add some value, but it also has a high false positive rate, right? When we talk about the psychological aspects of screening, we need to be very careful. Aaron Baggish, who I think some of you know up at Harvard, is doing some very nice work in this area now that he's about to publish in the next six months or so, looking at the EKG and its, quote-unquote, cost effectiveness in athletes. And finally, as you know, there's some EKG changes, and these are things you'll need to know in a couple of slides here. This is just things you have to commit to memory for the exam. Another name I draw your attention to is Sharma, Sanjay Sharma from Great Britain is doing some really interesting work now showing that the EKG in the African-American athlete, some of the things that we historically thought were risk factors for hypertrophic cardiomyopathy when you look at an EKG, they're actually normal variants. So we haven't even been able to, we haven't even begun to address that issue in terms of race, for example, and what's the effect on EKGs. This is a slide you need to commit to memory, okay? You need to know that the physiological changes that occur with exercise, particularly cardiovascular endurance exercise, the underlying physiology is what? That there's an increase in vagal tone, and then you can see the subsequent changes on EKG that often are misinterpreted as problems, right? So sinus bradycardia, first degree AV block, incomplete right bundle branch block, early repolarization and isolated QRS voltage changes. Moving to the right side of the slide, these are the warning signs that tip us to perhaps doing further screening. We're about to finish a study at the University of Miami. It's really quite interesting. It's a study I got involved with late when I started last fall, but it turns out about 7 to 9% of our athletes over the last decade have come in with incomplete right bundle branch block, and we're not exactly sure what that means, but stay tuned because it's clearly a normal variant. So let's talk about the problems that we need to know about in that under 35-year-old, right? Why is it we'd want to screen? And the one that draws most of our attention, of course, is the so-called hypertrophic obstructive cardiomyopathy or HOCM. As I mentioned earlier, its incidence is about 1 in 500, so that means there could be, not quite in this room, of course, but if we took a room double this size, one of us would actually carry the gene. It is homosomal dominant. Again, the real, I think, I don't want to say elephant on the wall, but the real challenge right now is to when do we start screening if we know that, in fact, 1 in 500 carry it? Because the real problem is what you need to know is who's going to express it and to what degree, right? That's really what's going to drive our screening. Again, physical exam can be normal for test-taking purposes. It's that systolic ejection murmur that increases with any type of Valsalva maneuver. So we always recommend, of course, examining athletes sitting, standing, and then squatting to perhaps detect the so-called HOCM murmur. And then finally, and this shows up on the exam as well, what's the arrhythmia, if you will, that, and this applies for most of these problems we're going to talk about, and it's ventricular tachycardia leading to ventricular fibrillation. Okay, so again, a couple more thoughts on HOCM because this is something you're going to see. Again, EKG findings are variable, right? So that's why people are saying that EKG isn't going to be enough. ECHO is usually diagnostic, although MRI and genetic studies are quickly becoming the gold standard. Here's what we need to know for test-taking purposes, right? An implantable defibrillator, and that defibrillator does not allow them to participate in sports, right? Don't be fooled by that on the exam. And I mentioned earlier the Bethesda guidelines, so you're going to see this whole idea about 1A sports, right? So these are the low-risk sports, if you will. So low cardiovascular demand and low strength demand. Here's another condition that does come up on the exam, even though it's fairly rare, and that's comedial cortis. So what is that? Well, it's a result of a blunt, non-penetrating chest trauma. These individuals end up in ventricular fibrillation if the blow to the chest, if you will, is delivered at a certain part of the cardiac cycle. Sports where we see it not too surprising are sports such as ice hockey, lacrosse, and baseball. Prevention is an interesting point, and there's a couple of tricky questions here. For test-taking purposes, equipment does not reduce the incidence of this problem, okay? So we talk about that wearing proper equipment, but in reality, it does not. What is known, if you look on the left-hand side here, and these are fairly recent data published last year, as you can see, the survival rate has gone up. And why is that? Because we have defibrillators on the sideline, right? So don't be fooled on the exam. It's got nothing to do with equipment. It's the fact that this continues to occur, but we have the means to resuscitate these individuals quickly, and that, of course, is the ultimate goal. Myocarditis, this comes up. I think I've seen it once or twice in my career, so maybe it has seen me and I haven't seen it. In any event, you can see some of the ideologies here. They're the typical viral causes that we think about. Don't forget, of course, other things such as drugs and toxic agents. These athletes tend to present with shortness of breath, chest pain, fever. It's often preceded by a flu-like illness, right? That's the tip-off. The EKG is actually fairly diagnostic. You see these diffuse ST and T-wave changes across the precordium. Diagnosis is achieved by myocardial biopsy, and for test-taking purposes, we use this magical six months, and I'm not sure why the evidence is so, but that's what you'll see on the examination in terms of returning them to sport. This I would predict you're going to see, and that is the so-called arrhythmogenic right ventricular cardiomyopathy or dysplasia. And why is that? Well, first of all, as I mentioned earlier, this is what's really driving some of the fundamental differences between screening here in this country and screening, for example, in Italy. And that's because, as you can see, in the Italian population, at least, particularly in the Mediterranean side, up to 22% of people actually carry this gene. So it's the genetics of it, if you will, that actually drive our screening, which certainly makes sense. What's interesting here is this is starting to emerge, if you will. We're seeing more cases of this in this country. Now, whether that's a genetic drift phenomena, people moving from Italy, for example, we don't know. But this is something I would predict you're going to see. So what does it involve? It involves the fatty infiltration, if you will, of the myocardium. You can see the EKG changes here. The most specific one is the so-called epsilon wave, which you can see at the bottom here is a representative EKG, where you've got the NOT gene, if you will, following the QRST wave complex. So for test-taking purposes, it's the so-called epsilon wave, which is most sensitive and specific for this condition. Again, it's autosomal dominant, right? So again, now we have a second condition in addition to HOCUM that's autosomal dominant. For test-taking purposes, again, we restrict from all but 1A sports, and you can see here some of the other associated treatment modalities. Long QT is something they like to ask about as well. So what is that? Well, we get these so-called genetic variants, right, in the sodium and potassium channels. The incidence looks to be about 1 in 2,000. These numbers here I don't think you'll necessarily need to know, but there is a difference, as you can see, with the corrected QT interval between males and females. Interestingly, again, it's ventricular fibrillation, as I mentioned, right? That's the end result for any of these structural problems that lead to sudden cardiac death. Something you want to be aware of, if you haven't been before, and that is some of the medications, and of course, we don't use some of these anymore, for example, Seldane, but the macrolides, for example, they can actually increase the QT interval as well as H2 blockers. So some of the medications that we frequently use, particularly in our young athletes, such as the macrolides, such as azithromycin, can actually prolong the QT interval. Second is to use beta blockers to control their heart rate. Interesting point here is a Mayo Clinic study, which was published three years ago now, where they went back and looked at 353 cases, 130 of them with a long QT syndrome actually chose to participate in sports, and there was only one adverse event. So I just throw that out there. It's not going to be on the test, but just so you're aware, I think there's still some challenges to decision-making whether or not these athletes continue to participate in high-risk sports. Another condition to be aware of, of course, is Marfan's, and as you know, this is a connective tissue disorder affecting the proximal aorta. It's also autosomal dominant. Some of the manifestations, as you can see here, the skeletal manifestations, the cardiac and the ocular manifestations, for test-taking purposes, it's the high arch palate that's the most sensitive and specific musculoskeletal finding. We tend to think about the arm span, but it's actually the high arch palate which is the most sensitive and specific, so that may turn up as well. EKG can be normal, but you may see left atrial enlargement. If you think back to the slide I showed you about normal changes, if you will, or reasonable changes associated with exercise and pathological changes on the EKG, left atrial enlargement is something that should get your attention. We tend to recommend yearly echoes for these people. Why is that? So we can monitor the size of the aortic root. They use beta blockers, and again, you see the common theme, which is no contact sports, and the level of activity is based upon the size of the root. So this is a condition, Marfan's, where they need to be followed very closely with yearly echoes to look at that aortic root. Okay, so let's move right along here with a couple of questions. We have a 19-year-old basketball player who is seen at the PPE, denies any cardiac symptoms, has an evaluation at his high school, and he's told he has, quote-unquote, hokum. Which of the following is true about this condition? 90% of the time, EKG is normal. It's the leading cause of death in athletes greater than 35 years of age. He can be cleared to participate if a defibrillator is placed. He cannot be cleared to participate in basketball. He can participate in moderate-intensity exercise if he takes medication and has an implantable defibrillator. So what are we driving at here? We mentioned this earlier, right? Placement of a defibrillator alone does not allow or entitle these athletes to participate in particularly the high-risk contact sports. So this athlete, we would recommend disqualification. Mother of a 12-year-old baseball player is heard about another young boy dying after being struck by a baseball in the chest. So what is true about this condition? So we're driving at here, what, comedial cortis, right? So it produces fatal inflammation, including pericarditis, damages the heart valves, leading to heart failure, occurs when the chest is impacted at a vulnerable period in the cardiac cycle, can be prevented with available chest protectors if worn correctly, and is usually related to underlying congenital heart problem. So we talked about this earlier, right? This is not a condition that can necessarily, at least the current data, don't support that it can be prevented, if you will, by wearing chest protectors. So it really comes down to that answer C, which is where it occurs in the cardiac cycle. They'll try to fool you here and say that, you know, chest protectors will reduce the incidence of this problem. That's not the case. Okay, let's shift gears a little bit. We're still in the cardiac pulmonary area, and we want to talk a little bit about exercise-induced bronchoconstriction. So what's the differential diagnosis of this condition? Well, first of all, we still have to think about cardiac problems, right? So this is the so-called non-cardiac asthma. So we still need to think about cardiac problems such as arrhythmias, hocum, and anonymous coronary arteries, vocal cord dysfunction, and we'll spend a minute or two talking about the differences between EIB and VCD. GERD is another big one that comes up, right, particularly in younger people. If they've got reflux and you put them on a proton pump inhibitor, that will often control their symptoms. And then finally, some of these congenital abnormalities such as tracheomalacia and vascular ring. So what is EIB? Well, it certainly is much more common than we think, right? And here's the key. Cough, wheeze, shortness of breath, or chest tightness that occurs after exercise, right? So these athletes actually become symptomatic after exercise or more symptomatic after exercise. And by definition, as we know, asthma is a reversible condition, right? So these athletes tend to be more symptomatic after exercise, but it's reversible. Some of the pathophysiology, as you know, including bronchial smooth muscle constriction, airway inflammation, cytokine release, and mucus production. For test-taking purposes, it's a drop in the FEV1 greater than 10%, right? So the forced expiratory volume. And the way I was taught 30 years ago, asthma is a condition of expiration, right? So if I have asthma, that means I can take a deep breath normally, but I can't exhale properly because of that airway collapse. That's why we use flow volume loops, right? So asthmatics, number one, they have a problem more with expiration, and they're symptomatic at night as opposed to vocal cord dysfunction, and we'll talk more about this. These are the athletes that have problems with inspiration, taking a breath in. So it's a real easy practical way, I say easy, a relatively easy practical way to distinguish those two problems. Some of the newer tests that we're using, the UVH as well as the mannitol, I don't think you'll necessarily see that. Just be aware that we use those as well. So what are some of the signs and symptoms? I mentioned earlier, it's probably more common than we think, right? It sees us and we don't see it, so to speak. Obviously, the common ones are things such as cough, shortness of breath, chest tightness, wheeze, and of course, our athletes don't necessarily want to tell us that, right? However, we can see things such as poor performance, avoidance of activity, and symptoms in specific environments. The key here, again, is particularly in folks who have mild EIB, their examination is going to be normal unless they're truly symptomatic. And a real important point here is that objective confirmation is really essential, right? That's the standard of care now. When I started, we used to put a lot of athletes on albuterol, for example, if they came in with a cough, and if they got better, we assumed that they had EIB. That's no longer the standard of care. You really want to document it with pulmonary function testing. Treatment, as we mentioned, goes back to the pathophysiology, and this is still gold standard, right? Which is to use our short-acting bronchodilators such as albuterol. It does work. Two to four puffs 15 minutes before exercise provides up to four hours relief. I think a lot of our athletes, particularly in the colder environment sports, maybe ice hockey or skiing, they'll tend to say they need to use it within one to two hours. So whether that's true or not, but that's what they do. We do some of the... We carry on if the short-acting beta agonists don't work completely to start looking at some of the longer-acting beta agonists, but remember that they can stunt growth, right? So we need to be very careful there. I think as a team physician, for any of us in this audience, if it gets beyond that short-acting beta stimulant, we probably want to get some help from our pulmonary colleagues, if you will. Chromelin, sodium, and leukotriene modifiers are still being used. They are permitted by WADA. Here's a real important point, right? If we put athletes on steroids, we need the appropriate documentation, and that gets back to, again, pulmonary function testing. And then some of the practical points that we talked about earlier in terms of avoiding triggers and so on. And finally, don't forget carbon monoxide poisoning. This is something that has come up even within the last six months. I'm aware of a situation that occurred up at University of Wisconsin where there was mild elevated levels of CO in the rink, and fortunately, people were smart enough to recognize that. I mentioned earlier vocal cord dysfunction, right? So this is a real key kind of differentiating point. So we mentioned earlier the difference between VCD, if you will, and EIB is what? VCD, vocal cord dysfunction, these athletes are symptomatic with inspiration, and you'll see them. We had one recently who would actually start running on the track, and she would start clutching her throat, saying, I can't take a deep breath in. That's not asthma, right? Asthma is a disease of expiration, as we all know. There's some debate, but it looks like these conditions actually can coexist frequently. In other words, athletes can have both vocal cord dysfunction and EIB. The way I like to tell our fellows is these are the, quote unquote, asthmatics that come in and they're on four or five medications, and they're still symptomatic. So you really need to think about vocal cord dysfunction. How do we make the diagnosis? Well, flow volume loops can be helpful, but not particularly sensitive here. In this particular case, you want to get ahold of your ENT colleagues and have them look at the vocal cords to see if they're appropriately abducting with inspiration or not. And then how do we treat it? Interestingly, in this condition, it's very successful if it's treated with a speech therapist so they learn the proper breathing techniques. Many would add that you should add an H2 blocker as well, because a lot of them have some concomitant reflux. Just a quick picture to show you here to sort of ingrain this idea that with normal inspiration, the vocal cords will abduct. And on the right-hand side, as you can see here, these vocal cords aren't, quote unquote, abducting or opening. And you can imagine, again, that's why these individuals have problems with inspiration as opposed to asthma, which is expiration. A couple of questions here. First one is a 30-year-old swimmer reports coughing, chest tightness, and shortness of breath after completing a 100-meter freestyle event. What should be the next step in evaluation? And just to move us along here, it's going to be answer C, pulmonary function testing, right? So these are the athletes. In the old days, as I said, we used to put them on albuterol, and if they got better, we sort of empirically made the diagnosis. That's no longer the standard of care. Previous athlete does not have PFTs consistent with asthma. So he doesn't have that 10% drop in his FEV1 or her FEV1. During the next episode, we talked about this, right? You are present and you notice that she is clutching her throat and is inspiratory stridor. So this is VCD or vocal cord dysfunction. And how do we treat it? We're going to look at answer C, okay? So vocal cord dysfunction and asthma, know the differences and know the treatment. All right, let's shift gears a little bit here now and keep moving. We're going to talk a little bit about heat, cold, and altitude. Just a brief event. This comes up as well, which is the mass participation event, right? And what are the responsibilities for any of us here as team physicians or medical directors? So I always like to think about this as you have to plan this as a disaster, right? And there certainly have been examples over the years where even in events like a marathon that's run in Minnesota, when it's only 60 degrees, you can actually see heat stroke. So we need to be ready, right? Here's something that comes up all the time. What's your responsibility as a medical director? And quite simply, it's the health and safety of your participants, making decisions, and being the spokesman. So that comes up as well. A few things here just to kind of keep in mind. One thing I would draw your attention to here is the importance of a rectal thermometer, right? If we want to start making a diagnosis of heat stroke, for example, we want a rectal temperature. So not the most fun thing to do, but it's important that we've got one available. What's our differential diagnosis of the collapsed athlete? Well, obviously cardiac arrest, exertional heat stroke, which we'll talk about in a couple of minutes here. Hypoendotremia, this is coming up more and more, and we'll deal with this in short order, as well as some of the temperature problems. One condition to think about here is the so-called exercise-associated collapse. They like to ask you about this, okay? It is a diagnosis of exclusion, but these are the athletes, they don't collapse on the course, they collapse at the end of the race, right? So this is your high school 400-meter runner who runs a record time. He or she stops at the end of the event, and then they collapse. What's going on? What's the physiology? Well, we tell people to keep moving, right, so that their venous system helps to return blood to the central circulation. So these are the athletes that collapse at the end of an event, and how do we treat it? It's a very benign condition, right? It'll scare you when you first see it, but that's how I like to distinguish true medical emergencies. Those are the ones that occur out on the course, if you will, whereas if you collapse at the end of an event, it's likely to be something like exercise-associated collapse. Physiological adaptations to heat, okay? For test-taking purposes, it takes about two weeks in order to see reasonable changes. You need to know some of the underlying physiology here as to what happens when you adapt to heat. You have a decrease in your heart rate, increased plasma volume, earlier sweating, increased sweat volume and skin distribution, and finally, decreased sodium sweat losses. They're all pretty straightforward sort of physiological principles, but nevertheless, you need to be aware for test-taking purposes. Let's talk a little bit about thermoregulation. First of all, what is it that occurs? Well, these are our big athletes. They have a lot of muscle, right? And this is the exercising muscle produces heat, right? So the blood is shunted to the periphery in order for us to dissipate that heat, if you will, and that's in the form of evaporation. They like to ask you about this, what's the main form of heat dissipation during exercise, and that's evaporation, as you can see. In fact, about 85% of the associated heat loss with heavy exercise. Another thing they like to ask you for some reason is, what's the average amount of sweat that a person loses? So for that 70-kilogram athlete, it's one to two liters per hour. Real key point here is that children are at greater risk for heat-related problems, and why is that? It's because they have a smaller surface area to body mass ratio and lower sweat rate, okay? So they don't have the ability to undergo those evaporative losses, if you will. The risks for heat illness. When do we see heat problems? Fortunately, now, hopefully, we are definitely out of the peak from an epidemiology standpoint, which is the first couple days of football practice in the summer, right? 85 to 90% of the cases that we see are in those first couple of days. Whether it's deconditioning, overtraining, or whatnot, that's when they occur. So hopefully we're out of that part of the year, if you will. It's the so-called double sessions, and as we know, there's been some mandated changes at the NCAA level, as well as the professional level, in terms of trying to reduce the incidence of that problem, and hopefully that's occurring. For test-taking purposes, we look at the wet globe bulb temperature, right? That's how we make decisions whether or not events should be held. So for example, if it's a marathon, right, we look at the wet bulb globe temperature. If it's greater than 28 degrees centigrade, that's the number they like to ask you. You want to shut the event down. So by definition, exertional heat stroke, this is something we need to know, right? So that's a rectal temperature greater than 40 degrees centigrade. Symptoms are often nonspecific early, right? Anybody who's run one of these extended events has probably experienced a lot of these problems. For test-taking purposes, it's CNS changes, okay? That's how we distinguish exertional, say, heat intolerance from exertional heat stroke. Now admittedly, some of these are fairly subjective, right? But for test-taking purposes, if you see an athlete as having CNS changes, confusion, and so on, that's when you need to think about heat stroke. Another important point, seizure is not common, okay? Seizure is not common in exertional heat stroke. In fact, the way I like to think about it is, if it's a short-duration seizure, think cardiac arrest. If it's a longer-duration seizure, that's the so-called hyponatremia that we'll talk about. So by and large, exertional heat stroke does not present with seizure. And of course, what's the treatment here? What's the first-line treatment? Get these folks into an ice tub, right? Okay. Let's talk a little bit about hyponatremia. I mentioned that earlier. So these are the athletes. First of all, remember that thirst is not a good indication of overall hydration status, all right? Exertional hyponatremia occurs when the sodium losses through sweating are not replaced. You can see some of the changes that occur here. I think for test-taking purposes, what you want to think about is, who are the athletes who are at highest risk? Well, these are the slow runners, for example, okay? So somebody who's been out on the marathon course for three hours versus somebody who's been out on the course for five hours. The other thing is, and we have a study here we're going to publish here soon looking at the Ironman. We've got 20 years of data now, and showing that the folks who got into trouble at the Ironman out in Kona, they actually gained body weight during the event. So imagine being out on that course for 12 to 15 hours, and you actually gain body weight, right? So one of the things that we've been able to mandate at the Kona Ironman is, everybody must be weighed within two hours of the event, of the beginning of the event. And as I said, we're going to publish a paper on that soon. So again, for test-taking purposes, these are the slow runners, and they actually increase body weight. Basically, they're taking in too much fluid. Okay, sickle cell trait. We talked a little bit at the beginning of this lecture. I just want to tie this in briefly here to this whole area of heat, if you will. And as you can see, it's a fairly common problem, right? Need to know the difference between trait and disease. When do these athletes get into problems? Again, much like heat stroke, which is early on in those first couple days, here it's in the first couple minutes, two to three minutes of all-out exertion. Some of the problems that increase a risk of this condition, if you will, or having problems with this condition, are obviously heat, dehydration, altitude, and asthma. We now know at the NCAA level, at least, that informed consent screening is mandated. And finally, prevention and education are key. Shift gears a little bit here and talk now about hypothermia. So we talked a little bit about hyperthermia. Now we want to talk about hypothermia. So what is that? By definition, it's a core body temperature, rectal temperature, less than 95 degrees Fahrenheit or 35 degrees Centigrade. So again, let's think about the pathophysiology. What's going on here? So heart rate, respiratory rate, and cardiac output all decrease. We see these athletes coming in, they're shivering, they're clumsy, apathetic, slurred speech. In other words, they've got some CNS changes. And then, of course, we need to distinguish between mild and moderate to severe hypothermia. Another key point here is that shivering stops at less than 90 degrees Fahrenheit and the myocardium becomes very irritable. So in terms of management of anybody with hypothermia, you want to think about the definition, which is less than 95 degrees core temperature. But at 90 degrees Fahrenheit, that's when things start to get interesting in terms of management, as we'll see here. So by definition, if the core temperature is over 90 degrees Fahrenheit, remember I said 90 degrees is your cutoff here, that's the so-called mild hypothermia. And this treatment here is pretty straightforward. Obviously, we want to get them out of their environment, if you will. We want to get their clothes off, you know, the wet clothing, for example. And these folks do very well, okay? They by and large do very well if you just give them oral warm fluids as a first line of treatment. So we don't need IVs or anything necessarily more invasive. It's when you get into the so-called moderate to severe hypothermia that things change here. This is when we start looking at, again, so by definition, we're now below 90 degrees Fahrenheit, and we can see what's going on here, right, in terms of treatment. So we're looking at IV fluids, for example. Remember, back to physiology 101, right? As we start to warm these people up, what's going to happen? They're going to vasodilate, so you need to watch their blood pressure. So aggressive fluid resuscitation is really the key here to people who are in that sort of moderate to severe hypothermia. And you can see here some of the recommendations in terms of CPR, again, because of the irritable myocardium, and then finally, transportation. Moving along, the continuum of hypothermia, if you will, is skin injury, so you need to know the difference between frostnip and frostbite. When we talk about frostnip, it's superficial vasoconstriction without tissue freezing, okay? These individuals present with burning, which is followed by numbness. They have gray or pale skin on the face and extremities, the exposed areas, if you will. The deeper tissues are normal. That's what distinguishes this from frostbite. And the treatment here is direct heat, but remember, you don't want to actually aggressively start to rubber, mechanically stimulate the tissue, because you can cause a lot of damage. Frostbite is a different beast altogether, right? And so frostbite, by definition, we now have tissue damage. They like to ask this as well as, you know, when do you make decisions about when to, example, operate on these individuals? And you need to wait a minimum of six weeks before you make a decision, because often the tissues below are a lot more damaged than you think. So you need a minimum of six weeks. Very different clinical presentation, as you can see from this little picture on the right-hand side here. And these are the people, they come in with blisters, for example, right? They can be yellowish, and if it's severe, they've got red-purple fluids. So these people are obviously a lot, this is a much more severe condition. No blisters at all, that's when you get into gangrene, as you know. And then finally, the initial treatment, as we can see, and these individuals need to be shipped off to the hospital as soon as possible. So in terms of environment, other conditions we need to talk about, the first one is going to be high-altitude illness, if you will. And why does that occur? Well, this is, these are the individuals that rapidly ascend up to altitude, all right? At increasing altitude, we know that there's a decreased barometric pressure as well as partial pressure of oxygen. Symptoms early on for some of the milder conditions, as you can see, include headache, nausea, anorexia, insomnia, and fatigue. So these are the sort of mild cases, if you will, usually mild and self-limited, rest and analgesics. But for test-taking purposes, any individual you suspect altitude problems, the treatment of choice is what? You need to have them descend, okay? So that's the real key point here. Some other things that we talk about, not a lot of high evidence for acetazolamide, but some would recommend that as prophylaxis. It does decrease the risk, but it does not decrease the risk altogether. So again, for test-taking purposes, how do we prevent this from occurring? It's number one, by far and away, is slow ascent. We can have some acclimatization changes and obviously avoiding some of the offending agents. That's in distinction to severe altitude problems, okay? So an individual who's got some mild symptoms, some nausea, maybe loss of appetite, that by far and away is a very benign condition, and once they return down to, out of altitude, they do quite fine. The other two conditions you need to be aware of are very different, okay? The first one is the so-called HAPE, and that's high-altitude pulmonary edema. So these individuals, this is a very different clinical presentation, right? They have dyspnea at rest, they can have hypoxemia, they're cyanotic, and they can have, quote-unquote, non-cardiogenic pulmonary edema. These people are sick. And that's similar to high-altitude cerebral edema. These are individuals who, as you can see, have significant central nervous system changes. These are both life-threatening, and these people need to get down right away, placed on high oxygen, and for the so-called HAPE, steroids are used as well, okay? So for test-taking purposes, we need to know the difference in the spectrum of conditions that can occur at altitude. Let's do a couple of questions here. The first one is, which of the following is true for exercising in the heat? Equal risk for heat illness as adults exercising in the heat. We talked about this earlier, right? Children are clearly at higher risk. They acclimatize to heat faster. Well, probably not if they're at increased risk. They have a higher sweating capacity than adults and can dissipate heat. It's the opposite, right? They have a lower sweating capacity. They have a smaller surface area-to-body mass ratio, and finally, should be encouraged to use sports drinks rather than water for rehydration. And so the answer is D, right? This is a really important concept here. Because of that smaller surface area-to-body mass ratio, they don't have the same abilities to sustain evaporative heat losses, which is our major way to control central temperature. You're covering a marathon in Phoenix. It's a sunny, warm day. Thirty-eight-year-old female athlete collapses at the finish line. She's unconscious but breathing with a good pulse, warm to touch and not sweating. What should be the immediate management here? I'll let you think about this one for a second. This athlete collapses at the finish line but is unconscious. IV dantrolene, measure oral temperature, give oral Tylenol or other antipyretics, encourage cool liquids, immerse in ice water bath. And so the answer is E, right? What's the real key to this question here? It's the fact that this athlete is not sweating, right? So what does that tell us? That means it's probably something to do with hyperthermia, the fact that this individual cannot. So these are the athletes. Two things that always scare me at the Ironman. One is somebody who's stopped sweating, and number two, the so-called salty sweaters, right? Those are the people who are at risk. And you can see it on their singlets. They've got a big white line going around sort of their chest wall outlining their anatomy. Those are the people where you want to suspect hyponatremia. Turns out very few are actually truly salt losers, if you will, but that's how you'll recognize it clinically. Asked about the prevention of altitude sickness. What do you recommend is the best way to avoid symptoms? We talked about this earlier, right? Slow ascent, premedicating with scopolamine, proper nutrition, optimal physical condition, and appropriate clothing. Take-home message here is what? We need to truly practice slow ascent, if you will. Different approach to the same problem we talked about a couple slides ago. During a marathon in August, some participants bring one of their friends to the medical tent. It's his first marathon, and he finished in four and a half hours. He stumbled a little bit and appeared somewhat confused at the finish line. They encouraged him to drink, and he subsequently consumed four liters of water. So where are we going with this question? We have a lot of problems here, don't we? So this is the athlete that's been out on the course for a while, okay? We can argue about four or five hours or whatnot, but still certainly not in that sort of truly elite area, less than, say, three, three and a half hours. So that's your first tip-off. The second thing is that you've got some central nervous system changes. And then finally, what? Is that he's consumed four liters of, quote-unquote, free water. So we are driving at here the so-called hyponatremia. The treatment I glossed over that, and I apologize if you suspect hyponatremia or you confirm that on the spot, is what? You want to give 100 mils of 3% saline. The problem is everybody talks about central pontine myelinitis, but it has never been proven to occur. So for test-taking purposes, the treatment is 100 mils of 3% saline. It's something we always have at the Ironman out in Kona. I think we've used it once in the four times I've been out there. So hopefully we won't have to use it this fall as well. All right. So we're going to shift gears now and get into some of the nutrition, to nutritional aspects of what you want to be thinking about. So to start us off here, the mainstay of what, of exercise is what? It's going to be glucose and free fatty acids, okay? So we start with glucose and carbohydrates. We shift to free fatty acids. If we get into proteins, we're probably in trouble, right? So if we start breaking down proteins during exercise, that's when we get into trouble. So it's the muscle and liver glycogen that are our primary storage agents for carbohydrate, adipose tissue for free fatty acids. Couple numbers to keep in mind. They do like to ask these, what are basic energy requirements? As you can see, for males, it's a pretty broad spectrum. Obviously, it would depend upon their size as well as their particular sport. One point they really like to ask is carbohydrate needs, okay? So it's the predominant fuel beyond about 65% of your VO2 max, and it's about two-thirds of your daily intake. So I like to tell folks exactly that. About two-thirds of your daily intake should be carbohydrates, okay? Protein. Again, these are numbers you need to know, particularly what are the specific requirements for the difference between a strength-trained athlete and an endurance athlete, okay? And you can see the ones here. So first of all, it's about 10 to 15% of your total energy intake. For strength-trained athletes, it's 1.6 to 1.8 grams per kilogram. For endurance athletes, it's a bit less. And why is that important? Because there's a lot of speculation out there, right? If I take in more protein, I'm going to be a better athlete, if you will. And that's just not the case. In fact, it's been clearly shown that there's really minimal to no benefit above two grams per kilogram of body weight. And then finally, fat requirements should be approximately 20 to 35% of total caloric requirements. A lot of numbers there that you need to know some of them. I like this slide because what does it tell us? Well, carbohydrates work. And here are some of the mechanisms. And again, this is something you need to be aware of. So why do carbohydrates improve our performance? Well, first of all, they prevent that fall in blood glucose, right? So you can maintain muscle carbohydrate oxidation and brain glucose supply. Real important point, carbohydrates have been shown to reduce the perception of fatigue. That's been shown in multiple studies. And then finally, you can actually increase your time to fatigue and total work. So you need to know the mechanisms behind why we recommend carbohydrates, particularly as a pre-competition supplement. So speaking of pre-competition and recovery, let's talk a little bit about pre-competition, if you will. So why do we like carbohydrates? Well, we like to enhance muscle glycogen stores, and we also don't forget hydration. The number they like to ask about is three to four hours before an event, right? So you want a high carbohydrate, moderate protein, low fat diet, a meal, if you will, three to four hours before the competition. They like to ask that. What about recovery? Same thing, okay? So intake of protein, as you can see, one to one and a half grams per kilogram after exercise. Some multiple studies now showing that if you add protein as a complement, that these athletes will do even better. And of course, as we all know, chocolate milk works just as well as any of the nutritional supplements that are available and cost a whole lot. Again, as I mentioned, carbohydrates and protein, they do provide some advantage, and I've seen a question on that as well. And obviously, don't forget hydration. So we hate these double negative questions. I know Dr. Borchers will be up here soon, and we always talk about this with our primary care fellows, that you won't see these sort of double negative ones. So I'm going to throw one at you anyways, and that is, which of the following is not true about protein intake in athletes? Number one, protein is the last fuel source used for exercise. Well, it is. We talked about that, right? It's the carbohydrates, free fatty acids, and finally, protein. Strengthening the athletes have greater protein requirements than endurance athletes. That is true, right? But again, remember, nothing over two grams has been shown to be effective. Number three, carbohydrate and protein should be ingested together immediately after muscle damaging workouts. Chocolate milk is as effective as protein, bottom line, you bet. Most athletes that participate in strength sports need protein supplements, and finally, protein should account for 15% of the total intake. And the answer is D, right? And again, these are the numbers that you need to commit to memory, the differences between strength-trained athletes and endurance-trained athletes in terms of nutritional supplementation and the order at which we metabolize our body parts, if you will, for exercise. Shift gears here, let's talk briefly about iron deficiency anemia. So where do we tend to see this? Well, typically, it's in the female athlete, although we've seen it recently in male athletes as well. It tends to occur in the endurance athlete, as we're probably aware. So there's your high-risk group that we talk about screening for. Vegetarians, they also like to keep in mind they can be deficient particularly in vitamin B12 and vitamin D. I've seen that show up in the exam as well. So think about vegetarians. Yes, they're at risk for iron deficiency anemia, but also B12 and vitamin D are important. How do we typically screen for that? And this is probably something that needs a little bit of work as well in terms of high-level evidence. Nevertheless, we talk about screening with a ferritin and a hemoglobin, debatable, but some would recommend that if your ferritin is less than 30, that that's the level at which we supplement. I think we all know that we have athletes with a level of 40 or 50, and they still want to take iron. But for test-taking purposes, we screen with ferritin and hemoglobin. Ferritin under 30 is where you consider supplementation. And they like to ask you about the treatment, and that's typically 100 milligrams a day of elemental iron for at least three months, take it on an empty stomach, ferrous gluconate or sulfate are two reasonable forms. All right. Still with me? We've got eight minutes to go here. So let's talk a little bit about menstrual dysfunction in athletes. You do need to know the differences between primary amenorrhea and secondary amenorrhea. That's something they like to ask, so please commit that to memory. Here's a topic that really has become important, I think, in terms of how we manage athletes with menstrual dysfunction, and that is this so-called energy drain hypothesis, right? So this is really key, that any of these problems that we see in these, whether it's an endurance athlete or whatnot, if they've got menstrual dysfunction, if they've got problems with bone mass, it's really the first line is to talk about the so-called energy drain hypothesis. And what happens here is they get a disruption in their luteinizing hormone release. Now, amenorrheic and oligomenorrheic are both associated with low estrogen. That's another important point. So let's talk about bone loss. What do we do? The effects of low estrogen on bone mineral density, they're not reversible. So that does raise the question, when should we be screening these individuals? Athletes with normal menstrual function can have up to 20% higher bone mineral density in the lumbar spine. Don't forget, of course, that probably makes some sense if you've got an athlete that's loading his or her lumbar spine. There's a couple of recent papers out looking at the wrist in, say, an endurance athlete. So they look at the lumbar spine, and their bone looks great. They look at their wrist, and they have osteopenia or osteoporosis. So something to think about is how we screen these athletes. We do need to know when's that maximal time of bone accretion, and that's from early adolescence until the mid-20s. Now, a key point here is, what do we do in terms of returning menses without medications? So this is really key. This gets back to the energy drain hypothesis. So the first thing we talk about is increasing their caloric intake, decreasing their caloric output, and then assessing their risks for bone problems. And notice, as I said here, medications is a last resort, right? When I started 30 years ago, we used to put all of these people on estrogen, and it turned out that was probably the wrong thing to do. So we needed to focus more on energy, if you will, and energy balance. I mentioned earlier the peak period of bone accretion, so numbers you need to know here, right? Calcium is effective in the pre-pubital child. Numbers you need to commit to memory. Calcium supplementation, 1,200 to 1,500 milligrams a day, and vitamin D, 800 international units. They will expect you to know this. Patients who do have menstrual dysfunction and or eating disorder, what is it that we can talk about? Well, first of all, estrogen prevents further bone loss, but it doesn't add bone mass, okay? Cannot emphasize that enough. You'll see that on the exam. It prevents bone loss. It does not add bone. So when do we think about it? From a practical standpoint, I like to think about oral contraceptives, if they've had no menses for six months, and they have a history of a stress fracture. But again, correct that energy imbalance first. Nasal calcitonin, we mentioned. It doesn't work. And of course, the bisphosphonates and the contraindication under 18 years of age. So bottom line, correct their energy imbalance first, and then think about estrogen, and don't forget calcium and vitamin D. Anorexia nervosa, what do you really need to know here? You just need to know the definition, okay? So it's a refusal to maintain body weight at or above the minimally expected normal body weight for age and height. For me, it's easier to say that weight loss leading to body weight less than 85% of expected. So that's really the take-home message here. Obviously, the treatment, as we know, is very difficult and involves a multidisciplinary approach. The so-called triad, you need to be aware of what that is, right? That's your disordered eating, amenorrhea, and abnormal bone loss. So that's a definition of the triad. Again, I mentioned earlier this whole concept of energy availability, right? So in the old days, we started firing medications at these people, but really, it's that energy balance that you need to address first. We know that with menstrual dysfunction, there's a decreased release of GnRH, and that leads to a decrease in luteinizing hormones. So that's the physiological mechanism behind this. And again, we talked earlier about some of the treatment methods. Exercise and pregnancy, you need to know, and I'll try to hit these highlights here and we'll finish up in a minute or two. So really, it's the ACSM and CDC guidelines. 80% of women during pregnancy who exercise will develop, if you will, some form of a diastasis recti. The physiological changes that occur with pregnancy, in the interest of time, I won't get into, but you do need to commit those to memory, because that drives our recommendations. For some reason, they'd like you to know the difference, what are the absolute contraindications to exercise, and what are the relative contraindications. The questions that I have seen, for example, relate more to the absolute contraindications. So if you can just commit these points to memory, I think you'll be okay. I mentioned the relative contraindications as well. The one that I think tends to fool people is severe anemia. You tend to think that's an absolute contraindication. It's just a relative contraindication. Which of the following is true about exercise in pregnancy? Should we gradually increase in intensity during the second or third trimester? Probably not, right? It should not involve weight training because of detrimental effects on blood flow. Hopefully we disbanded that about four or five decades ago. It is safe to weight train. We increase maternal cardiac output and uterine blood flow. That probably makes some sense. Maximal oxygen consumption at term is greater than in the non-pregnant female because of increased body weight. We have increased maternal blood volume and increased resting heart rate. And that's the answer. Okay? So that gets back to the physiology of what occurs with pregnancy. Most likely cause of fatigue and decreased exercise capacity in a female athlete. We probably should add in there female endurance athlete. Iron deficiency anemia, lack of conditioning, hypothyroidism, mono and amenorrhea. And the answer is iron deficiency anemia. Okay? There's a great paper that just came out of the University of Wisconsin, Alison Brooks just published. She went back and looked at the last 10 years, at least at the University of Wisconsin. And really she couldn't make a case for some of the screening methods we have. So I don't think you'll see that on the test. But we may be spending a whole lot of money screening these athletes for conditions that may or may not be occurring. 33-year-old female runner has increased her running regimen for an upcoming marathon. She's had only three menstrual periods in the last six months. Her pregnancy test is negative. That's always going to be on, right? If you have menstrual dysfunction, don't forget about checking the pregnancy test. What is the most likely ideology? So this gets back to the physiology of what is associated with exercise associated amenorrhea. Increased testosterone, increased LH, decreased GRH, or increased prolactin. And the answer is C. So we need to know a little bit about the physiology of what occurs with pregnancy. I think we have one more question here, folks. 19-year-old female athlete with secondary amenorrhea for six months and no prior history of stress fracture or concomitant eating disorder, which the following is not appropriate. Increase in daily nutritional intake. We talked about that, right? You always want to start with increasing their energy and correcting their energy imbalance. Evaluating for pregnancy and other tests. You bet. Until proven otherwise, that individual is pregnant, right? Evaluate her caloric intake, both quality and quantity. Ensure appropriate calcium and vitamin D. We talked about that as being the mainstay of treatment. Initiating bisphosphonates to increase bone mineral density or continue with regular exercise. And of course, the answer is bisphosphonates, right? They're contraindicated under age 18. And really, that's sort of a last-ditch effort when you've got an athlete who continues to be at risk and has had stress fractures as well. I think I have 60 seconds to spare, so again, it's been a pleasure. And I'll try to be around most of the day and answer any questions you have. So thanks very much for your time and attention.

athlete health

athlete performance

pre-participation evaluation

hypertrophic obstructive cardiomyopathy

exercise-induced bronchoconstriction

heat illness

exertional heat stroke

altitude sickness

iron deficiency anemia