Does the Prediabetic Cyclist Need to Worry?

Part 1: Why endurance training increases glucose.

At first, when I ran across middle-aged, but otherwise fit avid cyclists with high blood glucose, I chalked it up to coincidence. By the third, I began to wonder if it was indeed a coincidence. What follows is my research into the special case of hyperglycemia, higher than normal glucose levels, when it takes place in runners and cyclists.

A couple of studies have revealed that an unusual proportion of athletes have hyperglycemic, prediabetic range, blood sugar levels.

This group of physically active, slim individuals do not fit the widely held notion of the prediabetic - the paunchy couch potato. Can endurance exercise raise blood sugars? To look into this question, consider data coming from an offshoot of diabetic monitoring technology.

In 2002, Dr. Kratz published a study of marathon runners whose average age was 49. Almost 60% or 22 out of 37 runners sampled from a Boston Marathon related event demonstrated a blood glucose level which fell outside of the normal reference range generally accepted as 70–110 mg/dL. [Kratz]

Another study from Austria of older endurance athletes in their sixties found 47% qualified for either prediabetes (22 out of 47) or diabetes (1 out of 47). Taken as a group, these exercising senior athletes had a higher percentage with hyperglycemia, compared to a heavier, age-matched control group. [Haslacher]

In another 2011 study, nine competitive American cyclists, age averaging 30, had a group average fasting blood sugar of 110mg/dL, well above the ADA’s fasting blood sugar cutoff of 100 mg/dL. [Roberts]

Continuous glucose monitors (CGM) were invented to take the guesswork out of insulin dosing for diabetics. These implanted glucose sampling devices provide a continuous blood glucose reading which can be faithfully and periodically electronically recorded. When round-the-clock, CGM technology was used to monitor nondiabetic, competitive young cyclists, researchers unveiled surprisingly high glucoses.

In a study from New Zealand, ten subelite riders with an average age of 29 wore continuous glucose monitors. Four were discovered to be regularly hyperglycemic. These four spent more than 70% of their 24-hour day above 110 mg/dL. Even after excluding the 2-hour high glucose period after eating, these individuals were found to be continuously higher than normal. The fasting blood sugar of three of the athletes fell squarely into the ADA’s prediabetic range. [Thomas]

Almost half experienced previously undiagnosed high blood sugar levels. Among endurance athletes, hyperglycemia seems not uncommon, perhaps starting as early as the third decade of life. Let’s see how historically the glucose cutoff’s for prediabetes came about.

The World Health Organization (WHO) hasn’t see eye-to-eye with the American Diabetes Association (ADA) for decades. In 1979, the National Institute of Health (NIH) sponsored the National Diabetes Data Group which formally created prediabetes as a diagnostic category. Prediabetes was meant to identify those at high risk for developing future Type 2 Diabetes (T2DM).

Eighteen years later, in 1997, the American Diabetes Association refined the prediabetic criteria, creating a subcategory within prediabetes called “impaired fasting glucose”, (IFG). IFG identified as prediabetes with a high fasting blood sugar (FBS) instead of a longer test.

By simplifying prediabetes to a bucket category between 110–125mg/dl, (6.1–7.8mmol), the new screening protocol conserved lab resources. Instead of performing the more time-consuming (2 to 3 hour) and expensive oral glucose tolerance test (GTT), a single FBS as conceived, could more easily stand in as a test that could identify those at risk for later developing T2DM. The WHO signed on to this 110 mg (6.1 mmol/dL) prediabetic cutoff threshold in 1999, two years later.

The Glucose Tolerance Test (GTT) can be thought of as a two-part test for diabetes. It begins as a Fasting Blood Sugar (FBS) test. The first blood draw, the FBS takes place after an overnight fast. The following step requires quickly drinking a sugar-loaded, 75 grams of rapidly-absorbed glucose. This high glycemic load stresses the metabolism, principally the pancreas. By drawing blood at the first and more importantly at the second hour mark, the body’s ability to control the rise in glucose can be assessed. While the GTT continues to be the gold standard for T2DM diagnosis, the ADA only uses the second hour’s glucose value (>200 mg/dL) for diagnosing diabetes.

Later in 2003, the ADA lowered their fasting blood glucose diagnostic threshold for prediabetes from 110 mg/dL to 100 mg/dL. Uncompromisingly, the WHO has steadfastly kept to the original 110 mg/dL cutoff, maintaining to this day that the change is not scientifically justified. That 10 mg/dL difference makes a huge difference in the number of people labeled as prediabetic.

The lower ADA FBS threshold of 100 mg/dL results in many more people falling into the prediabetes category. While capturing more prediabetics, the lower threshold trades off potentially misidentifying a group not at risk for diabetes, argues WHO scientists.

Who is right? Let’s circle back to exercise’s effect on the FBS.

While improvements in metabolism result from exercise, a decreased glucose is not ordained. All diabetics can lower their blood glucose when exercising. Overweight prediabetics can lower their blood sugar by exercising. However others, even the slim do not predictably lower glucose with exercise.

When a group of essentially sedentary people becomes active — some will surprisingly increase their blood sugar. In other words, when even a non-obese, sedentary person starts to regularly exercise, there stands a good chance that their fasting blood glucose might rise.

575 sedentary Australian adults were encouraged to walk or engage in light exercise. After 40 days some predictably decreased their fasting glucose, yet others increased their fasting blood glucose value. The two higher and lower glucose camps, converged upon 101mg/dL. [Norton]

Greater stamina is a reliable expectation sticking through any aerobic exercise. Greater stamina requires a sustained blood glucose level so blood glucose levels fall prior to fatigue.

Hardworking muscles draw glucose from the bloodstream. If laboring muscles draw off a lion’s share of glucose, blood glucose levels drop and the brain feels shortchanged of glucose. Like a grid drawing too much power, a glucose brown-out occurs, threatening a system-wide blackout if the offending power hogs are not curtailed.

A fuel-starved brain will abdicate ruling the body. Before blackout, most will reduce their energy consumption, decelerating muscles to draw less power. In the case of a runner or cyclist, they will involuntarily slow down or come to a stop. In this way, the body can prevent an accident through moderation.

Loss of consciousness is averted through this central control mechanism. Whereas walking or low intensity exercise is fat burning, higher intensity exercise is limited by the amount of glucose stored locally and circulating in the bloodstream.

A tally of the entirety of glucose in our five liters of blood and yields a mere one teaspoon of sugar. That four grams will last between a minute or two at the highest levels of muscle exertion. No wonder adapting to prolonged, hard exercise demands system-wide metabolic upgrades.

To draw an analogy between these upgrades to an electrical grid, exercise adaptations can be thought of as a package of more numerous, beefier copper cables, more powerful and alternative energy generation sources, higher efficiency motors and local UPS battery back-ups.

Like a UPS backup system automatically kicking in for a computer during a power outage, energy is locally stored adjacent to muscle. Locally stored energy comes in the form of glycogen (the storage form of glucose) and fat tucked alongside conditioned muscle fibers. This muscle-localized, glycogen storage is what provides increased stamina and most of the sourced energy when huffing and puffing.

Nine previously sedentary, normal weight, and otherwise healthy men aged between the ages of 19 and 33 years old rode a stationary bike six days a week at 75%VO2 peak, (about 80% of their maximum heart rate) finishing out the last ten minutes of an hour’s session with their best effort.

After nine weeks, the men tripled their ability to put glucose into the bloodstream, and increased the amount of muscle glycogen stored in their legs (+62%), explaining greater stamina and enhanced power. [Bergman 2000]

Available power generation increases with coordination of sources elsewhere too. The trained body has an enhanced ability to release glucose from stored liver glycogen into the bloodstream. Power also comes from an enhanced ability to summon fats from stores under the skin into circulation. Some circulating fat is destined for the muscle to directly burn.

The liver also captures and coverts circulating fat into glucose during exercise and for a surprising period afterwards. For up to ten hours after an exhausting glucose-depleting exercise session, the glycogen in the liver, muscles as well as brain needs to be replenished. So even in recovery phase, the liver is working. An athlete’s liver has twice the glucose replenishment ability compared to a non-athlete’s.

Dr. Björntorp compared fifteen well-trained Swedish men in their mid-fifties to sedentary men living in the same city. The active group had been physically active since youth, 2–3 times per week, competing in cross-country running and skiing. Many had not strayed from their high school era weight. The glucose tolerance results of the well-trained men was better than the controls’. Interestingly, the well-trained men had higher, not lower FBS values.

Toward these ends, there are enhancements to the liver enzyme machinery of endurance-trained athletes. A superfluity of bloodstream glucose assures that glucose output can meet future needs.

As long as the total glucose output matches or can exceed the needs of the muscles, the brain cannot complain. Perhaps it’s no wonder why intense exercise can evoke a primal sense of unease!

A non-diabetic person exercising at a low, constant intensity, such as walking, easily maintains an even glucose level, because their energy needs can essentially be met by fat. This fat does not need to be converted into glucose as long as the intensity remains low.

Burning fat requires oxygen. When oxygen becomes the limiting factor, the respiratory rate quickens. Uncomfortably faster breathing signals that the body needs to switch over to a more oxygen-sparing fuel - glucose. An athlete’s metabolism can delay switching over.

Even at the glucose-fat transition zone, a difference in glucose metabolism becomes apparent. If that person isn’t a conditioned athlete, their blood glucose will be sustained initially, but flags in short order. The red trend line in the diagram below shows a flagging glucose level for a minimally conditioned person who is pushing the limits of their endurance.

Notice that the red glucose line doesn’t increase but falters, despite attempts to recover.

Compare the red with the blue line of the blood glucose level from a trained endurance athlete. Training causes overcompensation in glucose. Overabundance is preferable to any shortfall. Rather than a dropping, the blue line blood glucose levels shoot up in response to exercise. An endurance athlete’s blood glucose will continue to rise after the untrained has dropped below the pre-exercise starting point. This unfaltering ability to sustain glucose levels equates to stamina.

(Continue reading Part 2: Exercise Hormonal Changes Which Raise Glucose)

Cornell University. Author of “The FIRST Program: exercise guide for diabetes and prediabetes” at Follow me or contact: