117Diabetes Spectrum Volume 17, Number 2, 2004

Case Study: Alteration in Run Performance andAerobic Power in a Runner With Type 1 DiabetesKris Berg, EdD

The purpose of this case study was tocompare the decrement in distancerunning performance and peak VO2over ~25 years in a runner with type1 diabetes with those of runners whodo not have diabetes. A 58-year-oldman was diagnosed with type 1 dia-betes at age 12. His blood glucose(BG) management has been tightlycontrolled, with glycated hemoglobinvalues averaging just above normal(mean: 6.18%; normal: 4.0–6.0%)for over a 21-year period. His declinein running performance at three dis-tances (800 m, 3 miles, and 10 km),as well as his decrement in relativeoxygen uptake (VO2) peak were com-pared to active runners not havingtype 1 diabetes.

All distances run were certified,and his peak VO2 was assessed in thesame laboratory 12 times over a 23-year period. Values for peak VO2 in

all 12 tests across time were at orabove the 90th percentile rank in age-matched people without diabetes. Therate of decline in peak VO2 averaged0.6% per year. The decrement in runperformance per year ranged from 1.0to 1.5% at the three distances. Thesevalues are typical of competitive run-ners over age 30 who do not havetype 1 diabetes.

These results suggest that with vig-orous effort to monitor and maintainnormal BG levels, a good level of aer-obic fitness may be maintained forseveral decades in people with type 1diabetes. Also, the decline in runningperformance with age appears typicalof runners not having type 1 diabetes.Consequently, no apparent limitationto peak VO2 or running performanceseems to have occurred over severaldecades because of the presence oftype 1 diabetes.

Diabetes is associated with many seri-ous health problems including cardio-vascular disease, neuropathy, kidneydisease, and blindness. Recent datafrom the Centers for Disease Controland Prevention indicate that it is thesixth leading cause of death in theUnited States1 and the leading causeof adult-onset blindness, amputation,and end-stage renal failure.2These complications stem from theinability to effectively control bloodglucose (BG). For example, results ofthe Diabetes Control and Complica-tions Trial3 demonstrated that BG lev-els of patients under tight manage-ment administering insulin and moni-toring BG several times daily resultedin mean BG levels 40% above thenormal range. Furthermore, the morethan 1,400 patients with type 1 dia-betes in this multicenter interventiontrial were seen regularly by a dietitian,diabetes educator, and other health

specialists. Although this idealizedmanagement program improved BGcontrol and reduced the incidence ofspecific diabetes-related sequelaebetween 30 and 70%, it failed toachieve normal BG levels.Consequently, even under tight BGmanagement, people with type 1 dia-betes experience periodic hyper-glycemia, and most experience one ormore diabetes-related pathologies.These findings suggest reduced exer-cise capacity as a consequence oflongstanding type 1 diabetes.Management of type 1 diabetes cur-rently focuses on achieving BG levelsthat are as close to normal as possiblewhile minimizing exposure to frequentand severe hypoglycemia. Exerciseappears to reduce mortality andmacrovascular disease in people withtype 1 diabetes,1,4,5 although its bene-fits in BG management are equivocal.6

The American Diabetes Association

Address correspondence and requestsfor reprints to Kris Berg, EdD, Schoolof HPER, University of Nebraska atOmaha, Omaha, NE 68182.

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Abstract

118Diabetes Spectrum Volume 17, Number 2, 2004

(ADA) recommends regular physicalactivity for people with type 1 diabetesfor overall health benefits.6 However,it is unknown whether the combina-tion of chronic exercise and tight BGmanagement allows exercise toleranceto be maintained at a normal level lon-gitudinally.

Exercise training studies in thosewith type 1 diabetes are typically ofshort durations, lasting about12–16 weeks.7,8 Consequently, lon-gitudinal data are sparse.9 It wouldbe interesting to know if long-termaerobic training affords somedegree of protection from theeffects of glycosylation characteris-tic of the disease. Glycosylation ofcollagen in the heart and lungs andcardiovascular autonomic neuropa-thy leading to a lower exercise heartrate9 are mechanisms offered toexplain the limited exercise toler-ance in diabetes.

The present case study providesinsight regarding the impact ofchronic exercise and tight BG man-agement on physical performanceand a biological marker, peak VO2,over several decades in a person withtype 1 diabetes. The study describesan individual with a 46-year historyof type 1 diabetes who regularlycompeted in distance running eventsfor 25 years and whose peak VO2was assessed 12 times in that period.

To the author’s knowledge, phys-ical performance and laboratory-assessed peak VO2 in a person withtype 1 diabetes have not previouslybeen documented longitudinally norcompared with others who do nothave type 1 diabetes. Furthermore,detailed written records of physicalactivity (e.g., daily running mileageand intensity) were maintained overthis duration. Consequently, thesecomparisons provide insight as tothe effects of long-term type 1 dia-betes imposed on aging in thesevariables.

The purpose of this case study,then, was to compare the decrementin distance running performance andpeak VO2 in a runner with type 1 dia-betes with that of runners who do nothave this disease. It was hypothesizedthat the subject would demonstrate agreater decline in both peak VO2 andrunning performance across time thannormal because of the effects of tissueglycosylation.

Case PresentationB.R. is a 58-year-old university profes-sor who was diagnosed with type 1diabetes at age 12. He has been physi-cally active throughout life and wasan athlete in high school and college,although not as a distance runner. Hebegan distance running is his mid-20sand has continued since. He has com-pleted one marathon, and more than100 races ranging from 800 m to 10km.

His running mileage has graduallydropped over the years, but he hasbeen highly consistent in running atleast 5 days/week for a similar durationper session as in earlier years, but at aslower pace. The amount of runninghas averaged about 50 km/week in his30s to 35 km/week in recent years.

His training regimen has includedintense training at or above his labo-ratory-measured or estimated lactatethreshold (LT) two or three timesweekly for about 9 months each year.LT represents the velocity of runningat which blood lactate concentrationfalls within 2.5–4 mmol/l. It is a fairlystrenuous level of exertion used tocondition athletes for competition.For the remaining 3 months, he hasrun for a similar distance or mileageeach week, mostly at a pace wellbelow LT. He has competed consis-tently in races throughout most ofthese years, averaging about five racesper year.

B.R.’s medical history is free ofproblems other than diabetes. Recentophthalmic examination has revealedno evidence of retinopathy. Kidneyfunction is normal with a normal cre-atinine clearance and absent mircoal-buminuria, and blood pressure is typi-cally < 120/80 mmHg. His lipoproteinprofile is normal, with 15-year aver-ages of 195 mg/dl for total choles-terol, 64 mg/dl for HDL cholesterol,105 mg/dl for LDL cholesterol, and78 mg/dl for triglycerides. However,he was placed on a statin in 1999because his LDL values (139 and 145mg/dl) for a patient with type 1 dia-betes indicated increased risk for coro-nary artery disease. Since that time,LDL has averaged 97 mg/dl.

Doppler examination at age 52revealed a normal ankle/brachialindex, indicating absence of peripher-al artery disease (PAD). Low anklepressure from PAD reduces bloodflow to the leg. An index below 0.90

is accepted as a criterion for diagnosisof PAD.10 The index for B.R. was1.56 and 1.44 for the right and leftlegs, respectively.

B.R. presently uses lispro rapid-acting insulin before meals and snacksand glargine once daily to cover basalmetabolic needs. His BG is monitoredsix times daily. BG control, as demon-strated by hemoglobin A1c (A1C)results, has been good: mean A1Cover a 21-year period of 6.18% �0.65, with a range of 5.1–7.2. Thismean value meets the ADA recom-mendation of < 7.0%.12

A1C testing was performed in thesame physician’s office, but it isunknown whether the methodologywas standardized. The A1C resultsshould therefore be viewed with thislimitation in mind. No A1C data wereavailable before 1988.

The subject’s most recent laborato-ry 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

DiscussionPeak VO2 was assessed periodicallyfrom age 35 to age 58 in a universityexercise physiology laboratory. Alltests were performed on a treadmillusing a SensorMedics metabolic cart.The cart was calibrated before eachtest per specifications of the manufac-turer. Calibration included using a gasof known concentration, volume, andtemperature.

The protocol consisted of walkingfor 3 minutes at 3 mph and then run-ning for 3 minutes at 6 mph. The pro-tocol then progressed in 1-mph stages,each lasting 2 minutes until a self-selected speed was reached. Thisspeed was 10 mph when the subjectwas younger, and thereafter speeds of9 mph and, finally, 8 mph were usedas the subject aged. Once the selectedspeed was reached, treadmill gradewas increased 2% each minute untilvolitional exhaustion occurred.

B.R. reached respiratory exchangeratio levels > 1.05 with relative VO2plateauing (< 150 ml/minute) for allbut one of the tests. Heart rate wasalso within 10 bpm of the age-

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119Diabetes Spectrum Volume 17, Number 2, 2004

estimated maximum. These are crite-ria used to judge if a maximal effort isachieved during graded exercise test-ing. His body weight was consistentthrough the years of testing, varyingfrom 164.0 to 171.6 lb, with a currentweight of 169 lb. Consequently, theeffect of body weight on peak VO2values was small.

Running performance was basedon data from track meets and localroad races in which distances werecertified. The distances reported hereare limited to 800 m, 3 mile, and 10km races because he competed atthese distances with the greatest fre-quency over the time of study. Thevalidity of making comparisons acrosstime was facilitated because he ranmany races at the same selected siteson an annual basis. Consequently,characteristics of terrain, such as ele-vation changes, were constant.

Seasonal variation in peak VO2associated with training was mini-mized because he chose to be assessedin the years he was tested at timesduring his training cycle when he felthe was near or at a performance peak.However, environmental conditionsduring the races and training statusfrom year to year obviously varied.

Figure 1 displays the change inpeak VO2 from age 35 to age 58years. A peak value of 58ml/kg/minute occurred at age 43.Except for this one year, all other val-ues are fairly constant through age48. Year-by-year variability in thisperiod appears to be largely depen-dent on the subject’s training status.For example, the highest value at age

43 is probably explained by his train-ing at this time, which was character-ized by relatively high mileage forhim, (i.e., > 30 miles/week and intensetraining two or three times weekly).Intense training consisted of intervaltraining at a pace at or above thevelocity at peak VO2. Peak VO2 atage 58 declined to 46 ml/kg/minute, a14.8% decrement from age 35.

Running performance across timedeclined at each distance as expected(Figures 2–4). Performance in the 800m, which was run competitively onlyfour times during these years, droppedfrom a best of 138 seconds at age 33 to170 seconds at age 55. This representsa deterioration of 23% or ~ 1% peryear. At the 3 mile distance, best per-formance waned from 18.6 minutes atage 35 to 23.5 minutes at age 58, adrop of ~ 26.3% or 1.1% per year. Inthe 10 km event, run time increased24.8% or 1.5% per year from a best atage 40 of 40.3 minutes to 50.3 minutesat age 57. Performance decline at thesethree distances was thus similar.

The values for peak VO2 are mod-est in terms of endurance perfor-mance. B.R.’s highest value of 58ml/kg/minute demonstrates good aer-obic fitness, but falls well below val-ues typical of younger competitiveendurance athletes, who often surpass70 ml/kg/minute at the elite level. Incomparing his peak VO2 values withnormative data for the general popu-lation based on American College ofSports Medicine (ACSM) standards,11

all of them equal or surpass a per-centile rank (PR) of 90. His peakvalue of 58 ml/kg/minute at age 43

well exceeds the ACSM standard of48 ml/kg/minute for the 90th PR. It isnoteworthy that, even at age 58, hesurpassed this standard. His value of46 ml/kg/minute at age 58 is equiva-lent to a PR of ~ 65 for men aged20–29 years. Consequently, the pres-ence of diabetes did not prevent main-taining a relatively good standard ofaerobic fitness throughout the 23-yearperiod for which data were available.

A similar finding in runners withtype 1 diabetes has been observedelsewhere.9 In runners with diabetesbut no cardiovascular autonomic neu-ropathy, peak VO2 was equivalent torunners matched for age and physicalactivity level without diabetes.However, in those with cardiovascu-lar neuropathy and, consequently, aslower maximal heart rate, peak VO2was markedly lower. Thus, it appearsthat capacity to elevate heart rate andhence cardiac output is critical tomaintaining VO2 max.

The subject in the present studywas able to maintain a maximal heartrate as evidenced by a peak rate of175 bpm at age 58. This value is wellwithin the age-estimated maximumusing the “220 – age” criterion (220 –58 = 162).

The decrement in peak VO2 associ-ated with age is about 10% perdecade or 1% per year in sedentarypeople, and about half that value inphysically active people.13 The subjectmaintained a peak value of 50ml/kg/minute or higher until age 48.By age 58, that value had fallen14.8% to 46 ml/kg/minute. Over 23years, the decrement in peak VO2averaged 0.6% per year. This declinewith age is typical of recreational run-ners. Therefore, B.R.’s overall rate ofdecline in peak VO2 as well as theaccelerated rate after age 50 appeartypical of physically active people.

The decrements in run performance(indicated by time to run specific dis-tances) are similar to those reported inmaster runners, for whom a 13%decay per decade has been observed inmen and a 19% decay per decade forwomen.14 In a cross-sectional study ofelite rowers, the decline in power on arowing ergometer was about 0.9%per year in men and about 1.2% peryear in women. The rate of declineaccelerated after age 50.15 The decre-ments and performance times of thesubject are similar to those reported ina recent longitudinal study of master

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Figure 1. Decrement in peak VO2 with age.

120Diabetes Spectrum Volume 17, Number 2, 2004

athlete runners.16 B.R.’s performancedecrement thus seems typical of mas-ter runners in general.

In a cross-sectional study of highlytrained women distance runners aged23– 56 years, part of the decline in 10km performance was attributed toreduced training volume and veloci-ty.13 The subject’s running mileagedeclined from ~ 50 km/week (> 30miles) in his 30s and 40s to ~ 35km/week (~ 21 miles) in recent years.Consequently, part of his decreasedperformance may have resulted fromreduced training volume.

It is possible that the subject’sweight training in these years assistedin maintaining peak VO2 as well asrunning performance up to age 48because loss of skeletal muscle is amajor determinant in age-relatedreduction in aerobic power.16,17 Inmaster athletes running 22miles/week, the loss of fat-free weightfrom age 52 to 62 averaged 0.2kg/year.18 This training mileage is sim-ilar to the subject’s in recent years.However, he trained with weightsvery consistently twice weeklythroughout the period of study. Boothet al.19 have reported accelerated lossof skeletal muscle after age 50 prefer-entially in type II fibers, as well asreduced number of motor neuronsand motor units. The subject’s perfor-mance data do not appear to demon-strate this pattern of accelerated dropin performance and aerobic powercharacteristic after age 50.

Long-standing type 1 diabetes ofmore than 15 years inhibits normalcapillarization associated with train-ing. However, mitochondrial enzymeactivity and oxidative capacity ofskeletal muscle after endurance train-ing is normal.20 Capillarization andmitochondrial enzyme activity werenot assessed in this subject. However,because his peak VO2 was well aboveaverage at age 58 and because thedecrement in running performance istypical of master runners, it is likelythat reduction in capillarization waseither minimized by tight BG controland training or compensated by otherfactors, such as muscle strength andrunning economy.

The absence of diabetes-relatedpathology in this subject after livingwith type 1 diabetes for 46 years isencouraging for others with this dis-ease. However, the results of this case

Feature Article/Alteration in Run Performance

Figure 2. Decrement in 800 m run times with age.

Figure 3. Decrement in 3 mile run times with age.

Figure 4. Decrement in 10 km run times with age.

121Diabetes Spectrum Volume 17, Number 2, 2004

study cannot distinguish between theeffects of tight BG control and exerciseas to the absence of diabetes-relatedpathology. B.R.’s average A1C of6.18% is just above the normal range.This level of tight BG managementundoubtedly explains part of the pro-tection he has experienced. However,before his initiation of self-monitoringof BG at about age 37, his level ofcontrol in the previous years wouldnot likely have been as tight. The pres-ence of complications is known tovary in patients with similar patternsof BG control, and the subject maypossess some degree of genetic protec-tion from elevations in BG. Possiblysome protective effect was providedfrom his chronic exercise program.

The data suggest that with sus-tained effort to monitor and maintainnormal BG levels, participation invigorous physical activity may bemaintained for many years in peoplewith type 1 diabetes. Furthermore,the deterioration in athletic perfor-mance with aging may be no differentthan that of aging runners who donot have type 1 diabetes. To theauthor’s knowledge, the longitudinaleffects of aging on both athletic per-formance and aerobic power in peo-ple with longstanding type 1 diabeteshave not been reported previously inthe literature.

The ability to maintain normal pat-terns of physical activity appears tohave allowed the subject to experiencea normal decline in aerobic power andphysical performance. His interest inmaintaining athletic performanceseemingly has been a strong motivat-ing force in his training as well as dia-betes management program. The

underlying motivational factors thatsustain behavior conducive to healthis a topic worthy of further investiga-tion in the general population as wellas in those with chronic disease suchas diabetes.

References1http://cdc.gov/diabetes/pubs/estimates. AccessedMarch 27, 2004.

2Herman W, Eastman R, Songer T, Dasbach E:The cost-effectiveness of intensive therapy fordiabetes mellitus. Endocrinol Metab Clin NorthAm 26:679–695, 19973The DCCT Research Group: The effect of inten-sive treatment of diabetes on the developmentand progression of long-term complications indiabetes mellitus. New Engl J Med 14:977–986,1993

4LaPorte R, Dorman J, Tajima N: Pittsburghinsulin-dependent diabetes mellitus morbidityand mortality study: physical activity and diabet-ic complications. Pediatr 78:1027–1033, 19865Moy C, Songer T, LaPorte R, Dorman J, KriskaA, Orchard T, Becker T Drash A: Insulin-depen-dent diabetes mellitus, physical activity, anddeath. Am J Epidemiol 137:74–81, 1993

6American Diabetes Association: Physical activi-ty/exercise and diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S58–S62, 2004

7Mosher PE, Nash MS, Perry AC, LaPerriere AR,Goldberg RB: Aerobic circuit exercise training:effect on adolescents with well-controlled insulin-dependent diabetes mellitus. Arch Phys MedRehabil 79:652–657, 1998

8Laaksonen DE, Atalay M, Niskanen LK,Mustonen J, Sen CK, Lakka TA, Uusitupa MIJ:Aerobic exercise and the lipid profile in type 1diabetic men: a randomized controlled trial. MedSci Sports Exerc 32:1541–1548, 2000

9Veves A, Saouaf R, Donaghue V, Mullooly CA,Kistler JA, Giurini JM, Horton ES, Fielding RA:Aerobic exercise capacity remains normal despiteimpaired endothelial function in the micro- andmacrocirculation of physically active IDDM

patients. Diabetes 46:1846–1852, 1997

10Gardner A: Exercise training for patients withperipheral artery disease. Phys Sportsmed29:25–35, 2001

11American College of Sports Medicine: ACSM’sGuidelines for Exercise Testing and Prescription6th ed. Philadelphia, Pa., Lippincott, Williams,and Wilkins, 2000, p. 77

12American Diabetes Association: Standards ofmedical care in diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S15–S35, 2004

13Evans S, Davy K, Stevenson E, Seals D:Physiological determinants of 10-km perfor-mance in highly trained female runners of differ-ent ages. J Appl Physiol 78:1931–1941, 1995

14Masters age records for 1991. Pasadena, Calif.,National Masters News, February 15, 1990, p.1–6

15Seiler K, Spirduso W, Martin J: Gender differ-ences in rowing performance and power withaging. Med Sci Sports Exerc 30:121–127, 1998

16Hawkins S, Marcell T, Jaque V, Wiswell R: Alongitudinal assessment of change in VO2 maxand maximal heart rate in master athletes. MedSci Sports Exerc 33:1744–1750, 2001

17Fleg J, Lakatta E: Role of muscle loss in theage-associated reduction in VO2 max. J ApplPhysiol 65:1147–1151, 1988

18Jackson A, Beard E, Wier L, Ross R, StutevilleJ, Blair S: Changes in aerobic power of men ages25–70 yr. Med Sci Sports Exerc 27:113–120,1995

19Booth F, Weeden S, Tseng B: Effect of aging onhuman skeletal muscle and motor function. MedSci Sports Exerc 26:556–560, 1994

20Wallberg-Henriksson H: Exercise and diabetesmellitus. Exerc Sport Sci Rev 20:339–368, 1992

Kris E. Berg, EdD, is a professor inthe School of Health, PhysicalEducation, and Recreation and direc-tor of the Exercise PhysiologyLaboratory at the University ofNebraska at Omaha.

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