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Diagnosis: What caused this racer’s crippling fatigue?

Editor’s Note: “Diagnosis” is a new monthly column found in the print issue of  VeloNews. It is a collaboration between the editors of VeloNews and the University of Colorado Sports Medicine and Performance Center. The anecdotes found in “Diagnosis” come from actual patients, and the names of these patients have been changed. 

 

Overtraining is becoming all too common as endurance athletes push themselves to their limits. The consequences can be significant.

 

An elite cyclist—we’ll call him Racer X—arrived at the University of Colorado Sports Medicine and Performance Center laboratory complaining of serious fatigue. Racer X regularly placed inside the top-10 at the beginning of the season. By mid-season, he was struggling to even finish a race. His coach increased his training intensity in an effort to improve his form. Racer X’s training volume ranged from 22 to 28 hours per week.

His coach had heard that restricting carbohydrate intake and slightly increasing fat intake a few days a week might help Racer X with energy consumption. Racer X restricted carbohydrates two to three days a week coinciding with his long rides or high-intensity workouts. Additionally, Racer X wanted to lose five pounds, so he then decreased carbohydrates even further. Surprisingly, he gained three pounds after restricting carbohydrates.

Racer X’s power output decreased. His heart rate did not rise in proportion to his high-intensity workouts; on easier (zone 2) training days, he needed to increase his effort substantially to achieve the prescribed heart rate. Feeling frustrated, Racer X consulted the Performance Center and its director of sports performance Iñigo San Millán.

Tests

Millán conducted a battery of tests, including comprehensive blood analysis, physiological and metabolic testing, as well as skeletal muscle glycogen assessment and a nutrition evaluation.

Blood analysis revealed decreased red blood cell and hemoglobin levels, with normal ferritin levels, significant muscle damage, decreased testosterone levels, and increased cortisol levels. In addition, tests showed elevated levels of thyroid stimulating hormone (TSH) and C-reactive protein (CRP).

Other tests showed that Racer X’s maximal power output had dropped to 315 watts (4.5 W/kg) from 350 watts (5.0 W/kg) before the season. His lactate clearance capacity significantly worsened. As an example, at 250 watts Racer X’s blood lactate concentration was 2.6mmol/L in the winter and at mid-season 5.3mmol/L. His maximal lactate was 6.8mmol/L versus 10.7mmol/L in the winter. Finally, his maximal heart rate was 173bpm; before the season it had been 187bpm.

Racer X’s fuel efficiency had dropped. His carbohydrate oxidation (how much fuel he burned) was lower than in the winter, while his fat oxidation was higher. So, at 250 watts Racer X was burning 0.45 grams/minute versus 0.30 grams/minute before the season.

His body composition showed a three-pound decrease in muscle mass and a six-pound increase in body fat.

His diet comprised a carbohydrate intake of approximately 1 g/kg/ day (grams per kilogram per day) on his easy days and 2 g/kg/day on his hard and long days.

Non-invasive glycogen assessment (via MuscleSound, which we detailed in “Diagnosis” in May 2017) revealed a very low glycogen content. His preseason Muscle Energy Score (MES) was 72 (out of 100) and during his visit it was 15, confirming his diet was poor in carbohydrate given his workload.

Conclusion

Racer X presented a typical, though severe, case of overtraining. He also had anemia (low red blood cell count) and a catabolic situation caused by excessive training, poor nutrition, and poor recovery. Long story short: Racer X was doing more harm than good with his training.

Racer X’s red blood cell capacity had decreased by approximately 15 percent due to the reduced quantity of red blood cells (RBCs) and hemoglobin production. (Every day our body destroys some 200 billion RBCs and needs to replace them. If the body enters a catabolic state, the ability to regenerate enough RBCs is impaired, leading to anemia.) His ferritin levels (iron stored in the body) were normal, indicating his anemia was not caused by iron deficiency.

The detection of several muscle enzymes in the blood indicated that Racer X had developed muscle micro-tears. This was likely due to the combination of low glycogen content from carbohydrate restriction and high intensity training.

Around 95-97 percent of energy during exercise comes from fats or carbohydrate and a small percentage (~3-5 percent) from protein. During high intensity exercise, energy cannot be synthesized fast enough from fat, so muscles rely exclusively on carbohydrate from glycogen stores. When these stores are low, protein contribution can increase up to 20 percent. The problem is that most of this protein comes from skeletal muscle, so muscles start “eating themselves to feed themselves,” as Millán describes it.

This elicits the catabolic situation and muscle damage seen in Racer X. Damage was confirmed by elevated levels of cortisol, a stress hormone that is involved in muscle catabolism and the main mediator of it. The catabolic situation also explains the decrease in muscle mass compared to preseason. These two factors were mainly responsible for Racer X’s decreased power output and significant increase in blood lactate. His muscles became weaker and, thus, could not contract as powerfully. Metabolically they were working harder for a comparable power output.

New research shows that muscle damage impacts glycogen synthesis and storage. Scientists don’t know why; one hypothesis compares it to trying to “grab” water with your hands. Racer X’s decreased capacity to store glycogen, on top of the low carbohydrate diet, meant he had less fuel to power his workouts. Furthermore, the muscle damage, along with the slight increase in fat consumption, may also explain Racer X’s increase in body fat. This is because when glycogen levels are full, carbohydrate cannot be stored and it is converted to fat.

The slight increase in C-reactive protein (CRP) indicated the presence of inflammation, likely due to muscle damage.

“In our laboratory we see chronic muscle damage in many endurance athletes,” San Millán says. “Therefore we see chronic low-grade inflammation, which from the study of other diseases has been correlated with atherosclerosis and cardiovascular disease.”

Racer X also had low levels of thyroid stimulating hormone (TSH), which is produced in the pituitary gland and stimulates the thyroid. Thee disorder hypothyroidism (low thyroid hormone production) is becoming more prevalent within the endurance community; usually it impacts obese people with co-morbidities. It is very rare to see this condition in lean, healthy athletes without any family history. The athletes who are diagnosed with hypothyroidism are often prescribed thyroid replacement medication.

“Unfortunately, in our center we see about one athlete each week who has been ‘wrongly’ diagnosed with hypothyroidism, when in fact he or she was quite overtrained,” San Millán says. “The problem here is that when an athlete has been on thyroid medication for several years, TSH function shuts down from the pituitary gland. That athlete needs to be on thyroid medication for the rest of his or her life. In most cases it was never needed in the first place as there was not hypothyroidism but significant overtraining.”

Intervention

San Millán explained the disorder to Racer X. He told the athlete to thoroughly rest for two weeks, after which he could resume training for two weeks for approximately 1.5 hours per day without any intensity. He told Racer X to pay close attention to his heart rate, noting if it rose easily, and listen to his body and sensations. He taught Racer X about nutrition, telling him to normalize his carbohydrates to 4g/ kg/day (~280g) every day for the following month, then increase this amount to 6-8g/kg/day (~480-560g) once he resumed normal training and for any long, hard training days.

Results

One month later, San Millán performed another blood analysis, physiological test, and muscle glycogen scan. All the parameters in Racer X’s blood analyses returned to normal. Anemia was corrected and there was no sign of catabolism. His hormonal profile was completely normal.

Racer X’s glycogen scan was completely normal, with an MES of 80. Finally, his body composition improved. He lost five pounds of fat and regained the three pounds of muscle mass he had lost.

His physiological and metabolic tests showed very similar results to what he obtained in the winter. His maximal power output was the same as in the winter. His lactate clearance capacity improved significantly, although it remained slightly lower than in the winter. His fat oxidation was lower than what it was in midseason and also slightly lower than what it was in the winter. His carbohydrate oxidation was slightly higher than what it was in the winter. Every week he felt better with no signs of fatigue or overtraining. After a four-week training block, he resumed racing after being on the sidelines for over two months. By the end of the season he was very competitive, finishing with multiple top- 10s, two thirds, and his first victory of the season.

Takeaway

The case of Racer X is not an isolated one. What he and his coach learned was to always listen to science-based information when monitoring performance. They also learned to stick to a training program that emphasized building a robust base, increasing intensity and duration properly, and allowing ample recovery time. Another important lesson was nutrition, and to ignore fashionable diets. Finally, Racer X learned to listen to his body for signals of overtraining or fatigue.

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