Case Study: Alteration in Run Performance and Aerobic Power in a Runner With Type 1 Diabetes

B.R. is a 58-year-old university professor who was diagnosed with type 1 diabetes at age 12. He has been physically active throughout life and was an athlete in high school and college, although not as a distance runner. He began distance running is his mid-20s and has continued since. He has completed one marathon, and more than 100 races ranging from 800 m to 10 km.

His running mileage has gradually dropped over the years, but he has been highly consistent in running at least 5 days/week for a similar duration per session as in earlier years, but at a slower pace. The amount of running has averaged about 50 km/week in his 30s to 35 km/week in recent years.

His training regimen has included intense training at or above his laboratory-measured or estimated lactate threshold (LT) two or three times weekly for about 9 months each year. LT represents the velocity of running at which blood lactate concentration falls within 2.5–4 mmol/l. It is a fairly strenuous level of exertion used to condition athletes for competition. For the remaining 3 months, he has run for a similar distance or mileage each week, mostly at a pace well below LT. He has competed consistently in races throughout most of these years, averaging about five races per year.

B.R.’s medical history is free of problems other than diabetes. Recent ophthalmic examination has revealed no evidence of retinopathy. Kidney function is normal with a normal creatinine clearance and absent mircoalbuminuria, and blood pressure is typically < 120/80 mmHg. His lipoprotein profile is normal, with 15-year averages of 195 mg/dl for total cholesterol, 64 mg/dl for HDL cholesterol, 105 mg/dl for LDL cholesterol, and 78 mg/dl for triglycerides. However, he was placed on a statin in 1999 because his LDL values (139 and 145 mg/dl) for a patient with type 1 diabetes indicated increased risk for coronary artery disease. Since that time, LDL has averaged 97 mg/dl.

Doppler examination at age 52 revealed a normal ankle/brachial index, indicating absence of peripheral artery disease (PAD). Low ankle pressure from PAD reduces blood flow to the leg. An index below 0.90 is accepted as a criterion for diagnosis of PAD.10 The index for B.R. was 1.56 and 1.44 for the right and left legs, respectively.

B.R. presently uses lispro rapid-acting insulin before meals and snacks and glargine once daily to cover basal metabolic needs. His BG is monitored six times daily. BG control, as demonstrated by hemoglobin A_1c (A1C) results, has been good: mean A1C over a 21-year period of 6.18% ± 0.65, with a range of 5.1–7.2. This mean value meets the ADA recommendation of < 7.0%.12 

A1C testing was performed in the same physician’s office, but it is unknown whether the methodology was standardized. The A1C results should therefore be viewed with this limitation in mind. No A1C data were available before 1988.

The subject’s most recent laboratory results were as follows:

• A1C: 5.8%

• Lipid panel:

     ✓ Total cholesterol: 192 mg/dl

     ✓ HDL cholesterol: 64 mg/dl

     ✓ Total cholesterol/HDL ratio: 3.0

     ✓ LDL cholesterol: 112 mg/dl

     ✓ Triglycerides: 75 mg/dl

• Blood pressure: 122/74 mmHg

Peak VO₂ was assessed periodically from age 35 to age 58 in a university exercise physiology laboratory. All tests were performed on a treadmill using a SensorMedics metabolic cart. The cart was calibrated before each test per specifications of the manufacturer. Calibration included using a gas of known concentration, volume, and temperature.

The protocol consisted of walking for 3 minutes at 3 mph and then running for 3 minutes at 6 mph. The protocol then progressed in 1-mph stages, each lasting 2 minutes until a self-selected speed was reached. This speed was 10 mph when the subject was younger, and thereafter speeds of 9 mph and, finally, 8 mph were used as the subject aged. Once the selected speed was reached, treadmill grade was increased 2% each minute until volitional exhaustion occurred.

B.R. reached respiratory exchange ratio levels > 1.05 with relative VO₂ plateauing (< 150 ml/minute) for all but one of the tests. Heart rate was also within 10 bpm of the age-estimated maximum. These are criteria used to judge if a maximal effort is achieved during graded exercise testing. His body weight was consistent through the years of testing, varying from 164.0 to 171.6 lb, with a current weight of 169 lb. Consequently, the effect of body weight on peak VO₂ values was small.

Running performance was based on data from track meets and local road races in which distances were certified. The distances reported here are limited to 800 m, 3 mile, and 10 km races because he competed at these distances with the greatest frequency over the time of study. The validity of making comparisons across time was facilitated because he ran many races at the same selected sites on an annual basis. Consequently, characteristics of terrain, such as elevation changes, were constant.

Seasonal variation in peak VO₂ associated with training was minimized because he chose to be assessed in the years he was tested at times during his training cycle when he felt he was near or at a performance peak. However, environmental conditions during the races and training status from year to year obviously varied.

Figure 1 displays the change in peak VO₂ from age 35 to age 58 years. A peak value of 58 ml/kg/minute occurred at age 43. Except for this one year, all other values are fairly constant through age 48. Year-by-year variability in this period appears to be largely dependent on the subject’s training status. For example, the highest value at age 43 is probably explained by his training at this time, which was characterized by relatively high mileage for him, (i.e., > 30 miles/week and intense training two or three times weekly). Intense training consisted of interval training at a pace at or above the velocity at peak VO₂. Peak VO₂ at age 58 declined to 46 ml/kg/minute, a 14.8% decrement from age 35.

Running performance across time declined at each distance as expected (Figures 2,Figure 3–4). Performance in the 800 m, which was run competitively only four times during these years, dropped from a best of 138 seconds at age 33 to 170 seconds at age 55. This represents a deterioration of 23% or ∼ 1% per year. At the 3 mile distance, best performance waned from 18.6 minutes at age 35 to 23.5 minutes at age 58, a drop of ∼ 26.3% or 1.1% per year. In the 10 km event, run time increased 24.8% or 1.5% per year from a best at age 40 of 40.3 minutes to 50.3 minutes at age 57. Performance decline at these three distances was thus similar.

The values for peak VO₂ are modest in terms of endurance performance. B.R.’s highest value of 58 ml/kg/minute demonstrates good aerobic fitness, but falls well below values typical of younger competitive endurance athletes, who often surpass 70 ml/kg/minute at the elite level. In comparing his peak VO₂ values with normative data for the general population based on American College of Sports Medicine (ACSM) standards,11 all of them equal or surpass a percentile rank (PR) of 90. His peak value of 58 ml/kg/minute at age 43 well exceeds the ACSM standard of 48 ml/kg/minute for the 90th PR. It is noteworthy that, even at age 58, he surpassed this standard. His value of 46 ml/kg/minute at age 58 is equivalent to a PR of ∼ 65 for men aged 20–29 years. Consequently, the presence of diabetes did not prevent maintaining a relatively good standard of aerobic fitness throughout the 23-year period for which data were available.

A similar finding in runners with type 1 diabetes has been observed elsewhere.9 In runners with diabetes but no cardiovascular autonomic neuropathy, peak VO₂ was equivalent to runners matched for age and physical activity level without diabetes. However, in those with cardiovascular neuropathy and, consequently, a slower maximal heart rate, peak VO₂ was markedly lower. Thus, it appears that capacity to elevate heart rate and hence cardiac output is critical to maintaining VO₂ max.

The subject in the present study was able to maintain a maximal heart rate as evidenced by a peak rate of 175 bpm at age 58. This value is well within the age-estimated maximum using the “220 – age” criterion (220 – 58 = 162).

The decrement in peak VO₂ associated with age is about 10% per decade or 1% per year in sedentary people, and about half that value in physically active people.13 The subject maintained a peak value of 50 ml/kg/minute or higher until age 48. By age 58, that value had fallen 14.8% to 46 ml/kg/minute. Over 23 years, the decrement in peak VO₂ averaged 0.6% per year. This decline with age is typical of recreational runners. Therefore, B.R.’s overall rate of decline in peak VO₂ as well as the accelerated rate after age 50 appear typical of physically active people.

The decrements in run performance (indicated by time to run specific distances) are similar to those reported in master runners, for whom a 13% decay per decade has been observed in men and a 19% decay per decade for women.14 In a cross-sectional study of elite rowers, the decline in power on a rowing ergometer was about 0.9% per year in men and about 1.2% per year in women. The rate of decline accelerated after age 50.15 The decrements and performance times of the subject are similar to those reported in a recent longitudinal study of master athlete runners.16 B.R.’s performance decrement thus seems typical of master runners in general.

In a cross-sectional study of highly trained women distance runners aged 23– 56 years, part of the decline in 10 km performance was attributed to reduced training volume and velocity.13 The subject’s running mileage declined from ∼ 50 km/week (> 30 miles) in his 30s and 40s to ∼ 35 km/week (∼ 21 miles) in recent years. Consequently, part of his decreased performance may have resulted from reduced training volume.

It is possible that the subject’s weight training in these years assisted in maintaining peak VO₂ as well as running performance up to age 48 because loss of skeletal muscle is a major determinant in age-related reduction in aerobic power.16,17 In master athletes running 22 miles/week, the loss of fat-free weight from age 52 to 62 averaged 0.2 kg/year.18 This training mileage is similar to the subject’s in recent years. However, he trained with weights very consistently twice weekly throughout the period of study. Booth et al.19 have reported accelerated loss of skeletal muscle after age 50 preferentially in type II fibers, as well as reduced number of motor neurons and motor units. The subject’s performance data do not appear to demonstrate this pattern of accelerated drop in performance and aerobic power characteristic after age 50.

Long-standing type 1 diabetes of more than 15 years inhibits normal capillarization associated with training. However, mitochondrial enzyme activity and oxidative capacity of skeletal muscle after endurance training is normal.20 Capillarization and mitochondrial enzyme activity were not assessed in this subject. However, because his peak VO₂ was well above average at age 58 and because the decrement in running performance is typical of master runners, it is likely that reduction in capillarization was either minimized by tight BG control and training or compensated by other factors, such as muscle strength and running economy.

The absence of diabetes-related pathology in this subject after living with type 1 diabetes for 46 years is encouraging for others with this disease. However, the results of this case study cannot distinguish between the effects of tight BG control and exercise as to the absence of diabetes-related pathology. B.R.’s average A1C of 6.18% is just above the normal range. This level of tight BG management undoubtedly explains part of the protection he has experienced. However, before his initiation of self-monitoring of BG at about age 37, his level of control in the previous years would not likely have been as tight. The presence of complications is known to vary in patients with similar patterns of BG control, and the subject may possess some degree of genetic protection from elevations in BG. Possibly some protective effect was provided from his chronic exercise program.

The data suggest that with sustained effort to monitor and maintain normal BG levels, participation in vigorous physical activity may be maintained for many years in people with type 1 diabetes. Furthermore, the deterioration in athletic performance with aging may be no different than that of aging runners who do not have type 1 diabetes. To the author’s knowledge, the longitudinal effects of aging on both athletic performance and aerobic power in people with longstanding type 1 diabetes have not been reported previously in the literature.

The ability to maintain normal patterns of physical activity appears to have allowed the subject to experience a normal decline in aerobic power and physical performance. His interest in maintaining athletic performance seemingly has been a strong motivating force in his training as well as diabetes management program. The underlying motivational factors that sustain behavior conducive to health is a topic worthy of further investigation in the general population as well as in those with chronic disease such as diabetes.