Monthly Archives: May 2007

TV And Blood Sugar Control In Children With Type 1 Diabetes

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Just a “heads up” about a medical study that will likely make a big spash nationally. I read in my local newspaper (the Columbia Tribune) this afternoon that researchers at the University of Oslo found a direct relationship between the number of hours of TV watched per day and the average blood glucose level in children with type 1 diabetes. The study is to be published in the June issue of the journal Diabetes Care. The results are not a big surprise but I will be very interested in analyzing the report when I can get my hands on it and then writing about it.

What does TV have to do with blood sugar control?

In people with diabetes, many factors affect the blood sugar level but in general it is a tug-of-war of sorts between factors that use up sugar in the blood and those that increase the sugar level (let’s use the term “glucose” instead of “sugar,” since it’s really the molecule glucose we are talking about when when use the word “sugar” when referring to the “blood sugar level’). Anyway, eating food will increase the blood glucose level as will insufficient insulin which allows the liver to release stored glucose into the blood. It’s not so simple; there are other things that will tend to increase the blood glucose level including stress (hormones such as cortisol and adrenaline (epinephrine) raise the blood glucose level) but these factors all do it through effects on the liver’s glucose stores.

Factors that tend to lower the blood glucose level include the hormone insulin, through decreases in the liver’s release of stored glucose and increases in tissue use of glucose, and through exercise, which can stimulate glucose uptake by muscles even independent of insulin.

So, sitting around and watching TV means less exercise and it may mean more munchies, both of which would tend to result in higher blood glucose levels.

Is this information of any relevance to people who do not have type 1 diabetes?

For people who do not have type 1 diabetes, this report is a reminder that sitting around watching TV for hours and hours might not be such a good idea- what we see as higher blood glucose levels in people with type 1 diabetes will likely be seen as weight increases in people who do not have diabetes (in people with type 1 diabetes, high blood glucose levels usually mean high urine glucose levels and thus loss in calories, limiting weight gain if the high blood glucose levels are due to excessive caloric intake). Is there anything much worth watching on TV anyway?

More On Avandia

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Just to keep you up on the latest news; there was a long article in the New York Times today written by Stephanie Saul and Gatrdiner Harris, entitled “Years Ago, Agency Was Warned of a Drug’s Risks,” (Section C, page 1). The gist of the article was that several years ago the FDA was warned by at least one physician, Dr. John Buse, that rosiglitazone (Avandia) might pose cardiovascular risks for patients with diabetes. Dr. Buse is soon to be the president of the American Diabetes Association. It is interesting that he has done studies for Eli Lilly on a competing drug, Actos. I like Dr. Buse but deep down might there be some bias or conflict of interest in his current criticisms? Maybe not?
Enter the cool-headed British

Most interesting to me was an editorial published yesterday on-line in the distinguished British medical journal, The Lancet. The editorial (I couldn’t find out who wrote the piece), which appeared in my e-mail today courtesy of the Lawson Wilkins Pediatric Endocrine Society, summarized the Avandia “press” over the past 2 days. The author, like me, was surprised at the incredible uproar over the Nissen paper in the New England Journal of Medicine (see my last entry for the details) and the FDA warnings.
The Lancet editorial pleaded for calm and reason; there were already considerable data showing increased cardiovascular risks for patients with type 2 diabetes who took Avandia. The author suggested we might wait until more data are available from large prospective studies that might allow us to sort things out better (just to remind you, the paper by Nissen and colleagues was a meta-analysis of ALREADY PUBLISHED data. Oh, what are the British to think of us?

What does the Avandia story tell us?

Clearly, the way we in American medicine and our patients get information about drugs and other therapies that are commonly used needs rethinking. The Avandia “the sky is falling” story should be embarrassing to us all. Pharmaceutical companies, physicians, the medical journals, and the FDA need to do a much better job in sorting out the risks and benefits of this or that therapy; every treatment, drug or otherwise, has a risk/benefit ratio- sometimes the risks are unknown, but it’s worth knowing that.

I believe most physicians who prescribe this or that drug are very shaky regarding the risk side of things; if physicians do not know the risks of the drugs they prescribe, patients will not get the chance to “weigh in” on whether the recommended therapies are right for them. All physicians, including yours truly, are guilty of not always sharing enough information with patients about a recommended therapy, even if we do know the risks involved. I wonder how many physicians who have prescribed Avandia were even aware of the data suggesting increased risks of heart disease? Don’t get me wrong, even if a drug or other therapeutic approach has risks, it may be well worth the risk for the potential benefits, and that may be the case with Avandia. Who knows?

Avandia (Rosiglitazone Maleate): New Hazard or Hoax?

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I have been nothing short of astonished about the hype over the New England Journal of Medicine (NEJM) article published yesterday (actually published on-line prior to it’s scheduled hard-copy release on June 14) on the possible dangers of a widely-used drug for people with type 2 diabetes. In summary, the article, written by Stephen Nissen and colleagues at the Cleveland Clinic, reviewed 44 previously published reports on the use of Avandia and concluded there was a 43% increased risk (relative risk 1.4) of heart attack in people taking the drug compared to those taking placebo or a different diabetes drug. Thus, here we have a meta-analysis- a study that combines the results of actual clinical studies and analyses the data as if they came from a single large study. This is a well-established statistical tool but one with many pitfalls.

How this all unfolded

First, those of us who subscribe to the NEJM, received an e-mail on May 21 with the article. Apparently, the press release was not to take place until after the stock market closed on the 21st. But, earlier in the day of May 21, the report was released by several news services and chaos ensued. The maker of the drug, GlaxoSmithKline had a 7% drop in their stock by the close of the market on the 21st. They, of course, issued a statement defending the drug’s safety. The FDA issued an “alert,” warning patients taking the drug to check with their doctors.

There is more!

In an article today in the New York Times, the interesting course of events and the economic impact of the NEJM report are detailed nicely. The article, written by Stephanie Saul made the front page of the business section and was entitled “Heart Risk Seen in Drug For Diabetes.” The new report summarized the NEJM report and the economics of diabetes drugs (big bucks). In addition, Ms. Saul tells us that as far back as last August, the FDA had data showing increased risk of heart disease in patients taking the drug.

Why so much excitment over this study?

I am amazed at the hype over this report and it does not say much good about the news media, the FDA, medical journals, and doctors. This morning, the news of the dangers of Avandia were everywhere- I just couldn’t hide from it: I even heard about it on CNN when I was waiting to pick up my car (a hybrid) which was getting an oil change.

This is not the way for important medical information to be disseminated. First, I would question how important the news is. Remember, all of the studies that the Nissen article had already been published and those of us “in the field” already knew there were concerns about the cardiocascular side effects of Avandia. The increased risks of heart failure with the drug and with other “glitazones” is well known already. Even worse, along with the Nissen article, there was an editorial and an editor comment that the results should be considered preliminary and interpreted with caution. Give me a break- the NEJM rushes this report to publication, hypes it big time, and asks us to interpret the results with caution. Don’t get me wrong, I LOVE the NEJM and have subscribed to it since 1965, but this was done poorly.

I almost forgot- what should people with diabetes do?

First, I wouldn’t start any patients on Avandia or any of the other glitazones at this time. There are many other drugs (those manufacturers are smiling today). In fact, most of my colleagues who are “expert” in the management in patients with type 2 diabetes, rarely if ever use the glitazones because of their known side effects: I find the vast majority of physicians who prescribe the glitazones and the newer drugs for the treatment of type 2 diabetes, are primary care physicians who learned about these drugs at a drug-company sponsored lecture or from their drug company rep, who provided samples (forgive me if I generalize to excess).

Where do we get our medical information?

One last thing- I am concerned that, increasingly, we (health-care professionals and the lay public) get most of our medical information from the media- TV ads and news reports. The news reports are of particular concern to me. I would be willing to bet that 90% of medical news reported in the media (including the New York Times) comes from only a few out of thousands of medical journals- The Journal of the American Medical Assoication, the NEJM, and Nature. Is it marketing by these journals or is it that the science/medical news journalists rely most heavily on these few journals? I don’t know, but it’s not healthy for any of us.

A Pound of Treatment: Is it Better than an Ounce of Prevention?

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Yesterday, I received a telephone call from the mother of a young man who will turn 19 years old in about 10 days. The boy, who we will call Rick, has type 1 diabetes mellitus, diagnosed when he was about 10 years old. For a number of reasons, he has not done particularly well with his diabetes over the years, including many missed clinic appointments. Regardless, he is a pleasant, personable, and intelligent young man. He will graduate from high school in about 3 weeks. He wants to attend college but he has made no plans so far and does not know what he wants to study. I should add that he has had some drug problems and has just gotten out of a rehabilitation center.

Why did Rick’s mother call me?

Rick’s mother told me that Rick is now very focused on doing better with his diabetes and wants to see me in the next week or so, before his Medicaid coverage runs out (in my state, Missouri, Medicaid coverage for children is terminated on their 19th birthday). Rick lives with his mother. The parents are divorced and the father plays no role in Rick’s life, including financially. Rick’s mother has a full-time job, but no health insurance. So, in about 2 weeks, Rick will have no Medicaid coverage for his diabetes. So, what are his options?

First, he could try to get health insurance through one of the insurance carriers licensed in our state (e.g., Blue Cross/Blue Shield, United Health Care). That won’t work since he has a “pre-existing condition,” and is not eligible. He could get coverage through the state “high risk insurance pool,” a way for people like Rick to get health insurance. That won’t work given the cost which is about $800/month for a high deductible plan; neither Rick nor is mother have the resources to afford such a plan. I could lay out lots of other possible solutions, but I can assure you that none will work for Rick.

What if Rick had serious diabetes complications?

Quite a few years ago, I wrote an editorial to a medical article about the high prevalence and high costs of kidney failure in patients with diabetes. My editorial was entitled (as you might guess), “Is a pound of treatment better than an ounce of prevention?” As I recall, the results of the landmark Diabetes Control and Complications Trial, or “DCCT,” had just been published. The DCCT showed that diabetes complications (including kidney disease) could be prevented if the diabetes is well-controlled (we’ll come back to the DCCT in future entries). Anyway, in my editorial I tried to make the case for promoting excellent diabetes care “up front” to prevent the costly complications.

Rick’s dilemma

So, in about 10 days, Rick will have no means to pay for his costly diabetes supplies, let alone clinic visits and laboratory studies. I’ll do the math for you- the cost for his basic diabetes care is dramatically less than if he should develop serious diabetes complications, which he surely will unless he works to do well with his diabetes. But, Rick won’t even have the means to do well. Great system we have!

What am I going to do about this situation?

In a few days, I will see Rick in my clinic. I will try to help him develop strategies that will get his diabetes on track. I will encourage him to keep in close contact with me by telephone or e-mail over the next 1-2 months. I have looked into a free health clinic where Rick could go and even get some of his medications for free. He will need to apply; to qualify his mother’s income will need to be below a certain level- it will be a close call. The next available appointent is in about a month.
He could look for a job with health insurance- typically jobs with large companies that have health insurance for all employees without exclusions for “pre-existing conditions,” governmental agencies, hospitals, etc. He may have trouble given his drug history, but maybe not. I think full-time college is out for the moment, if he wants to do well with the diabetes (some colleges offer heatlh insurance to full-time students at very reasonable rates but one must have pre-existing insurance to qualify. Bummer.

The crazy thing is that if Rick has serious complications now, such that he has serious “functional limitations,” he could get coverage and an income to boot through the U.S. Supplemental Security Income program (SSI). Of course, if we just wait a few years, that will be a good option for Rick.

What am I trying to say?

What I have tried to explain is that our health-care system is not very good at facilitating optimal medical care for people with certain chronic medical conditions, such as diabetes who cannot obtain affordable health insurance. The end result is often dramatically greater costs (borne by all citizens with health insurance) to treat disease complications than would have been required to carry out high quality basic care of the condition. Diabetes is a great example since we know that all of the complications of this disorder are preventable.

Is “Fighting” Obesity a Lost Cause?

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Gina Kolata, an excellent science reporter from the New York Times, has been getting quite a bit of attention lately- an appearance on Comedy Central, a review of her new book, “Rethinking Thin,” in the New York Times Book Review section (May 6, 2007), and her own article in yesterday’s New York Times (“Genes take Charge and Diets Fall By the Wayside,” page D1).

The Kolata message

Ms. Kolata’s basic thesis is that we are fat and that we cannot do much about it because the causes are mostly genetic. She cites various well-known studies that demonstrate the strong genetic effects on obesity. She seems to be telling us that we can try to diet but we are probably doomed to failure because genes rule.

Is the Kolata message correct?

I (as did the book reviewer, Emily Bazelon) think Ms. Kolata, who writes very well, is off the mark. She is correct in identifying some of the data supporting strong genetic effects on body weight. What she basically ignores is the large body of data showing an enormous upsurge in obesity over the past 50 years or so; from the plethora of news reports in the past few years and warnings from the U.S. Government, one would think the epidemic has occurred entirely in the past 5-10 years). The obesity epidemic cannot be “blamed” on genetics alone; many studies have documented the environmental factors- cheap food, larger portion sizes, decreased activity levels, etc. Ms. Kolata acknowledges these phenomena but hardly considers them important enough to consider dealing with given the power of the genes.

I believe we can have an impact on the environmental factors, and while success in this area will still leave us with plenty of obesity to go around, we can have major successes in decreasing the prevalence of obesity. Of course, we individually and as a society will need to come to grips with our passion for large portion sizes and extraordinary inactivity.

What Is Diabetes Mellitus?

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In my last entry (May 4, 2007), I discussed the diagnosis of diabetes and prediabetes. I completely forgot to first explain what diabetes is. Diabetes mellitus, or “sugar” diabetes to distinguish it from another type diabetes, diabetes insipidus, is really a group of disorders that have 3 things in common. First, all types of diabetes have insulin deficiency. Insulin is a hormone protein produced by the beta cells of the pancreas. Insulin is an amazing hormone with many actions, but simply put, it helps control the blood glucose level. In fact, as far as I know, it is the only hormone that directly lowers the blood glucose level (sometime in the future, we will discuss the many hormones that raise the blood glucose level).

What causes insulin deficiency?

There are many causes of insulin deficiency. The easiest to understand is the type of insulin deficiency because the beta cells are decreased in number or totally missing from the pancreas as in type 1 diabetes (T1DM). Type 1 diabetes is the type of diabetes that is most often diagnosed in childhood- it used to be called juvenile-onset diabetes. In most instances T1DM is a genetic disorder caused by autoimmune destruction of the beta cells. About 10% of diabetes in the U.S. is classified as T1DM.

Another kind of insulin deficiency is what I would call “relative deficiency.” This means that the beta cells are producing insulin but the person is resistant to the insulin- it just doesn’t work well. This is typically present in people who have type 2 diabetes (T2DM), the most common form of diabetes in the U.S. This form of diabetes is also inherited but in most instances requires that the person be overweight (all overweight people are somewhat resistant to insulin). It is all a bit complicated, but in most instances of type 2 diabetes there are several factors involved including insulin resistance, impaired insulin release from the pancreas in response to high blood glucose levels, and some element of actual deficiency. Anyway, the end result is not enough insulin to prevent high blood glucose levels or hyperglycemia, the second feature in all forms of diabetes.

Hyperglycemia

It is not enough to have insulin deficiency (either actual deficiency, resistance to insulin action, or both) to call it diabetes. The end result must be hyperglycemia, the hallmark of diabetes. In my last entry I discussed the specific blood glucose levels that define a diagnosis of diabetes.

The third feature

The last component of all types of diabetes is a tendency to develop serious complications. Most people know something about these problems- eye disease, called retinopathy, kidney disease, called nephropathy, and nerve disease, called neuropathy. Together these three “opathies” account for much of the misery associated with diabetes and are often called “microvascular” complications even though they do not all affect the microvasculature (don’t ask me to explain that). The microvascular complications are to be distinguished from the “macrovasular” complications of diabetes, peripheral vascular disease, stroke, and heart disease.

Diabetes mellitus as a syndrome

In summary, diabetes is a group of distinct disorders that share 3 things in common- insulin deficiency, hyperglycemia as a result, and high risks for developing medical complications. There are many different types of diabetes but probably 99% are either T1DM or T2DM. Maybe sometime in the future we will discuss the other 1%. We will definitely come back to further discussions about T1DM and T2DM.

What is Prediabetes?

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In today’s New York Times, there is an interesting article in the “Styles” section, front page. The article is entitled ” A Healthy Mix of Rest and Motion,” written by Peter Jaret. In the article, Mr. Jaret discusses the physical fitness benefits of interval training, the technique of alternating fast (very vigorous) and slow (one’s usual energy expenditure for the activity) energy expenditure as a way of improving physical fitness. Those of us who are or were “serious” athletes know only too well about interval training. Until I read this article, I had not really appreciated how effective interval training is in boosting physical fitness. It works well with many activities including walking, running, cycling, rowing, swimming, etc. For me, and I suspect for many, interval training is a “love-hate” relationship; you know it’s good for you but it’s such hard work.

What does interval training have to do with “prediabetes?”

The paragraph above really has nothing to do with prediabetes except that in the article, the author wrote the following: “weight watchers, prediabetics, and those who simply want to increase their fitness all stand to gain,” referring to the technique of interval training. I would be willing to bet that most of the people who read the article do not have any idea what prediabetes is. I’m here to help.

Prediabetes is an old term in the diabetes field but which has been “reinvented” recently. It used to mean a more-or-less theoretical state in which a person was at genetic risk for developing diabetes mellitus or “sugar diabetes” (to distinguish it from diabetes insipidus, a condition related to water balance) but had normal blood sugar levels. More recently, the term is used to define a group of people who are at increased risk for developing diabetes based on specific blood sugar levels, which are above normal but not high enough to allow one to definitively diagnose diabetes. Are you with me so far?

Definitions

Diabetes is defined by certain blood sugar levels, either in the “fasting state,” which usually means with no caloric intake for the previous 12 hours, or after a standard sugar water drink called a glucose tolerance test. Technically speaking what is measured is the “plasma glucose level” even though many people talk about the “blood sugar level.” Anyway, for a variety of reasons, some scientifically sound and some more politically sound, a person is said to have diabetes if either the fasting plasma glucose is 126 mg/dl or greater on two occasions, or the value two hours after 75 grams of oral glucose is 200 mg.dl or greater. The diagnosis can also be made if a “casual” plasma glucose value (this means testing without regard to interval since the previous meal) is 200 mg/dl or greater with typical symptoms of diabetes- excessive thirst, excessive urination, etc.  There are a number of conditions that need to be met before the diagnosis can be made, such as the person must be well-nourished, not acutely ill, etc. Also, a definitive diagnosis cannot be made using the little portable blood glucose meters that we see advertised on TV; the test must be carried out in a laboratory with actual measurement of the plasma glucose level.

Impaired fasting plasma glucose, impaired glucose tolerance, and prediabetes

This brings us to “prediabetes” states. Diabetes experts define impaired fasting plasma glucose (IFG) as fasting plasma glucose of 100-125 mg/dl; impaired glucose tolerance (IGT) is defined as fasting plasma glucose <126 mg/dl but 2-hour plasma glucose after a glucose tolerance test of 140-199 mg/dl. Finally, prediabetes is defined as either IFG, IGT, or both. Recent studies show that people who have prediabetes are at great risk to develop diabetes within a few years. As it turns out, things are not quite so simple. For example, if the fasting plasma glucose is 100-109 mg/dl, the risk for progression to diabetes from IFG is rather low- much higher if the fasting plasma glucose is in the range 110-125 mg/dl.

So?

THe reason it is important to understand these definitions is that recent studies have shown that treating patients with prediabetes can slow progression to diabetes. Thus the very recent American Diabetes Association’s Consensus Statement entitled ” Impaired Fasting Glucose and Impaired Glucose Tolerance” (Diabetes Care 30:753-759) in which it is recommended to treat all people who have either IFG, IGT, or both.  Depending on a number of factors, the treatment would be lifestyle modification and moderate intensity phycical activity (defined as roughly 30 minutes/day) or the above and medications. All of this is to decrease the risk for progression from prediabetes to the real thing, diabetes.

So?

These are bold recommendations that if followed by all medical practitioners would lead to an astonishing increase in testing for IFG and IGT. What I find so amazing is that despite these recommendations, the American Diabetes Association (ADA) and many of the experts who wrote the Consensus Statement discussed above are ambivalent about testing for prediabetes. To quote the recently published ADA’s Clinical Practice Recommendations 2007 (Diabetes Care 30 (suppl 1.):S1-S104, 2007) for diabetes screening: “Screening to detect prediabetes (IGF or IGT) should be considered in individuals >45 yeares of age, particularly in those with a BMI >25 kg/mXm.” They go on to say that screening should be considered in people <45 years of age who are overweight if they have other risk factors for diabetes. How seriously should we take a recommendation of "should be considered."? On the one hand the "experts" tell us we should be treated for prediabetes but our doctors should only "consider" testing us for it. Does any of this make sense to you?

What should we do?

Given that about 60% of people in the U.S. are overweight and that we have a diabetes epidemic, we should (not should consider) begin testing on a regular basis (e.g., every 1-2 years) for prediabetes or diabetes in all adults who are overweight. It is the only logical thing to do based on the available scientific information. Why are the “experts” so afraid to speak up? I’m not sure but I suspect there are powerful health-care industry lobbyists who do not feel insurers can cope with the expense of making so many diagnoses of prediabetes and diabetes and then having to treat the patients? Of course, they need not worry; our health-care system is so disorganized that we couldn’t possibly find a way to actually carry out the testing and provide the proper treatment. Am I being unfair? I don’t think so.

Obesity Watch: Information on Portion Sizes

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In earlier entries about obesity, I discussed some of the research on the psychology of portion sizes- bigger plates mean bigger portions eaten, etc. I hope you remembered. In case you didn’t, today in the New York Times, David Leonhardt wrote an article that made the front page of the Business section (don’t ask me why the article is in the Business section?). The author discussed Brian Wansink and his book, “Mindless Eating” which was published last year. Professor Wansink has done much of the interesting research on the psychology of eating as it relates to portion sizes. The article is a good review of the subject.

The gist of Professor Wansink’s “message” is that people make decisions about eating and drinking, i.e., how much to eat and drink, not based on appetite, but rather, on various cues such as the size of the plate, the bowl, or the glass. The data are rather compelling.

Do the professor’s data help explain the obesity epidemic?

Professor Wansink’s studies and similar studies by others leave me wondering one thing. If we do eat more at time-point A than our appetite centers compell us to do, is the appetite center smart enough to “recommend” less intake at time-point B, resulting in no net increase in caloric consumption over and above what the appetite center has “calculated” we need overall? Given the steady increase in obesity in the U.S., I suspect the appetite center is not capable of such fancy adjustments, but I’d like to see some data on the subject.

Anyway, I intend to read Professor Wansink’s book and I hope many others will also do so. Let me know what you think.

Heart Rate Monitoring With Exercise: Is It Useful?

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Background

Recently, my son John, who lives in the San Francisco Bay area and is an avid bicycle rider, asked me if I could explain to him something about the technique of heart rate monitoring with exercise. Apparently, many of his friends hold to the theory that a work-out is not worth doing unless one can monitoir his heart rate to be certain the activity is being performed optimally. John told me he was completely baffled about the subject. As a good father, I told him I would do what I could to allay his anxiety about the quality of his bicycle rides.

First- the short answer

I reminded John that I had discussed heart rate monitoring in an earlier entry about using an exercise bicycle. I suggested that for most people it was quite sufficient to first calculate their maximum heart rate (220 minus age in years) and aim for a heart rate of 60-70% of the calculated maximum to assure a ride that would contribute to cardiovascular fitness. John, who is quite serious about his level of cardiovascular fitness, told me he had read the entry but really wanted quite a bit more information.

More information than almost anyone needs about heart rate monitoring

First, I need to say something that may upset many serious exercisers. It is fine to carry out heart rate monitoring during exercise (unless one falls off his bicycle or the treadmill while checking the pulse), but for most people it is not very important. For all but elite athletes and those in cardiac rehabilitation, very little heart rate monitoring is necessary. Now that I’ve offended lots of people, including manufacturers of heart rate monitoring equipment, I need to defend my audacious statement.

Heart rate monitoring is used during exercise as a measure of work rate and oxygen uptake, which are really what we want to know but which can only be assessed properly in a laboratory. So, heart rate (HR) is a surrogate measure of energy expenditure. Its main virtue is that it is easy to measure. HR does increase linearly with work rate and oxygen consumption but the HR response to exercise depends on many factors including age, body position during exercise, level of fitness, environmental factors (e.g., air temperature, relative humidity, altitude), whether or not heart disease is present, medications, blood volume, and on and on.

What happens to the heart rate with training?

At rest, energy expenditure is very low (1-2 kcal/minute) with the skeletal muscles contributing very little, about 20%. With exercise, things change drastically. Energy expenditure can increase 10-30X, mostly for the muscles. For this to happen, the muscles need more oxygen which can only occur if the heart gets more blood to the muscles. The heart has a limited bag of tricks for increasing blood flow to muscles. For one, it can shunt blood from certain parts of the body, i.e., the gut, to the muscle. The heart can also increase its rate, resulting in more blood, hence more oxygen, to the muscles per unit time.

With training, the heart can also enlarge, allowing more blood to be ejected per beat (the amount of blood ejected per beat is called the stroke volume or SV). This is very important since the heart needs more oxygen during exercise just like the rest of the muscles. The blood vessels that supply the heart muscle with oxygen are called the coronary arteries. These arteries fill only during diastole, the resting phase of the heart. The more rapid the heart rate, the shorter and shorter the diastolic phase and the less time for the heart to feed itself. The trained heart with its greater SV can pump as much blood as the untrained heart but at a much lower heart rate, thereby increasing the supply of oxygen to the heart muscle. Pretty nifty, huh? In addition, the trained heart has decreased oxygen demand at rest and during exercise.
Resting heart rate

As you would suspect based on the fact that the conditioned heart is larger and thus ejects more blood per unit time, the resting heart rate is lower in people who are fit. The “normal” heart rate is about 65-75 beats/minute; the highly conditioned athlete can have a heart rate as low as 40 beats/minute and still deliver as much oxygen as the body needs in the resting state. If the resting heart rate is consistently less than 60 beats/minute, that suggests reasonable cardiovascular fitness assuming the low heart rate is not due to some disease of the heart or some medication (my son’s was 48 beats/minute).

Aging

With increasing age, the heart changes: the maximal heart rate decreases, the maximal SV decreases, and as you would expect, the maximal cardiac output (measured as the amount of blood pumped/minute) decreases- in a 65 year old the cardiac output is 10-30% less than in a 30 year old. The maximal SV also decreases with age.

Recommendations

We could go on and on and discuss many other aspects of cariovascular fitness. We didn’t even get into “METS” or metabolic equivalents which are a measure of the metabolic cost of activity. Put in another way, a MET is an estimate of the intensity of an activity looking at a ratio of the working metabloic rate to the resting rate.  One MET is equivalent to a certain amount of oxygen uptake (3.5 mL/kg/min, if you are interested).  Studies have determined how many METs are used in various activities.  For example, using a stationary bicycle with very light effort uses 3 METs while vigorous effort uses 10.5 METs.  walking the dog uses 3 METs and walking at a 4 mile per hour pace (considered a brisk pace) uses 5 METs.  Maybe we’ll come back to METs sometime?

For those of you who are not aiming for a gold medal at the next olympics, I would relax a bit about quantifying your cardiovascular effort with each exercise session. I would calculate maximum heart rate and try to sustain at least 60-70% of that for at least 20-30 minutes. If at that level of physical activity you barely raise a drop of sweat, maybe you need to rethink your maximal heart rate. Remember, the 220 minus age in years for maximum heart rate is just a rough guideline. Also, it is important to keep track of your resting heart rate- after 2-3 months of fitness training, it should be under 60 beats/minute. One other thing- if after exercising 30-60 minutes at 60-70% of your calculated maximum heart rate your heart rate is still quite a bit over your usual resting heart rate (e.g., greater than 100 beats/minute) 30 minutes out, you may have overdone it or you may be a bit dehydrated.

Summary

Well, maybe I was a bit brash in denegrating the use of heart rate monitoring with exercise. Maybe I should have said, heart rate monitoring can be useful but don’t go crazy with it? One other thing- I never did discuss how to monitor heart rate. As I discussed in my exercise bicycle entry, checking the radial pulse is the easiest and cheapest way- the index and third finger of one hand placed on the wrist of the opposite hand thumb side. You’ll find the radial artery pumping away. If you count for 10 seconds and multiply that by 6 you have a heart rate; the longer you count, the more accurate the estimate of the heart rate. I think expensive fancy monitors are just fine but very optional (if these gadgets are fun to use and increase the pleasure in the exercise, they are probably worth the cost even if they do not directly do much to improve cardiovascular fitness).

Resources

For those who want to explore the subject of cardiovascular/fitness training in depth, I recommend the American College of Sports Medicine (ASCM) Resource Manual For Guidelines For Exercise Testing And Prescription, Fifth Edition, Lippincott Williams & Wilkins, 2006. This is “the bible” for exercise testing and is both comprehensive and readable (and expensive- $59.00). You can access the ACM at www.acsm.org.