VOLUME 6 • NUMBER 1 • JULY 1999 The South African Journal of Sports Medicine The official publication of the South African Sports Medicine Association R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) AHEAD IN COX-2 SELECTIVITY WITH A 3 j/EAK TKACKRECOKD. i i ii ii I ■ O N C E - D A I L Y w O e / e Inflammatory pain relief and mobility in any body's language. Boehrinaer ^oplicant details: Ingelheim Pharmaceuticals (Ptyi Ltd. Co. Beg No 6&/O8610/O7 "™“ J | r l(_ _ | h Q i r | t 407 Pine Avenue. Randburg; Tel (011) 886-1075; Fax epartment o f Paediatric Surgery University o f Natal Medical School rivate Bag 7 ongella 4013 pi: 031 - 260 4227 j x : 031 - 260 4572 -mail: hadley@med.und.ac.za ly the recognition o f entrapments, injuries and congen­ ital abnormalities has increased awareness o f stenoses in young active individuals. Raised compartment pres­ sures and compartment syndromes occur in a myriad o f clinical situations and awareness is essential for diag­ n o s i s . 1'4 -7 -9 1 2 . ^ , 1 7 - 2 0 ,2 2 ,2 5 - 2 7 ,2 9 No practitioner can afford to be unaware o f the concepts involved. Pathophysiology Arterial stenosis Any lesion occupying space in a vessel will alter the dynamics o f blood flowing past the lesion. The energy wasted in turbulent flow causes a loss in potential ener­ gy that is measured as a fall in blood pressure distal to the stenotic lesion. This reduction in blood pressure results in a reduction in the pressure at the arteriolar end o f the capillary bed and therefore relative hypo­ perfusion o f the exercising muscle distal to the stenosis.24 During exercise there is an increased demand for oxygen that is normally met by increased muscle blood flow. I f this cannot be achieved because there is a prob­ lem with inflow, then claudication may result. Further, as muscle volume increases during exercise and is con­ tained within a relatively inelastic osseofascial com ­ partment, there is a tendency for the compartment pressure to rise. The relationship between inflow pres­ sure and tissue pressure is critical in determining the adequacy o f tissue perfusion and cellular oxygenation. Compartment syndrome Matsen16 has defined a compartment syndrome as damage to the cells caused by increased tissue pres­ sure within a compartment, resulting in loss o f func­ tion. We do not want to wait for loss o f function before recognising and treating changes in tissue pressure, and it is our aim to diagnose an increasing compart­ ment pressure and institute treatment before a com ­ partment syndrome occurs.14 Increased tissue pressure in itself is not diagnostic o f inadequate cell nutrition, rather it is tissue pressure relative to the inflow pres­ sure that is crucial.828 Inflow pressure to a muscle group can b e low, even in the presence o f systemic hypertension, i f there is a lesion in the axial artery that causes a loss o f pressure. aORTS MEDICINE JULY 1999 3 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) mailto:hadley@med.und.ac.za Muscle nutrient blood flow and the effects of stenosis and raised intracompartment pressure Any fluid, including blood, wall only flow along an energy gradient. To all intents and purposes this means a pressure gradient. Although there are some situations where blood will move against an apparent pressure gradient (for example, when standing the blood pressure in the foot will be higher than the pres­ sure in the aorta), the kinetic and potential energy of the blood is sufficient to overcome this.24 Therefore for the purposes o f this discussion, in order for blood to circulate throughout the body there must be a gradual fall in blood pressure from the left ventricle, through the capillary beds and the venous system, to the right ventricle. The left ventricular pressure is reflected in the systolic blood pressure. The diastolic pressure reflects the peripheral resistance. It is convenient to think in terms o f the mean arterial pressure (MAP), which is an expression o f the effective pressure generat­ ed by pulsatile flow. It is calculated as the diastolic pressure plus one-third o f the pulse pressure. Blood pressure is affected by the stroke volume, i.e. the amount o f blood that must b e moved, and the peripheral vascular resistance against which the blood must b e pumped. As peripheral vascular resistance increases, the blood pressure must increase to main­ tain the same flow. I f the blood pressure cannot be increased then flow must fall. At a micro-circulatory level the same principles hold. The driving force, or inflow' pressure to the cap­ illary bed, must b e lower than the systemic blood pres­ sure, but is derived from it. Regional inflow pressure may b e reduced by a systemic hypotension or by the presence o f a proximal stenotic lesion. The resistance to flow at this level is determined by the calibre and length o f the capillaries and the pressure gradient across the capillary b ed .24 As capillaries are a single cell thick and have little inherent strength, their diam­ eter is governed by the tissue pressure around them.2 In addition to these factors the function o f the capillary is to allow nutrients, including oxygen, to diffuse into the cells. For this to occur, Starling’s hypothesis sug­ gests that fluid leaves the arterial end o f the capillary and fluid is returned at the venous end. This is again, like all fluid shifts, a pressure-depen­ dent process, with the driving forces being the arterio­ lar capillary pressure and the osmotic pressure o f the interstitial fluid, and the opposing forces being the tis­ sue pressure and the oncotic pressure that tends to keep fluid within the vessel.24 Anything that disturbs this balance wall interfere with cell nutrition. Therefore reducing the perfusion pres­ sure by either lowering arteriolar pressure or increasing venular pressure, will tend to reduce flow. Increasing the tissue pressure or lowering capillary pressure wall therefore secondarily affect oxygen delivery'. Increasing tissue pressure will also tend to cause collapse o f the vessel, a tendency that is minimised by a reflex increase in venous pressure.3 While keeping the vessel open this also has the effect o f reducing the pressure gradient and thereby reducing flow". Obviously this will b e maximal in situations where there is no flow. No flowr will occur when the pressure gradient is reduced to zero. In fact flow' ceases before this when the pressure difference is so low that the thickness o f the blood becom es an important factor. The rheologi- cal features o f blood are affected by many factors, including cell count and protein content, and in many clinical situations reducing the haem atocrit will improve oxygen delivery' to the tissues by improving the flow'.24 Any tendency to an increase in tissue pressure is usually accommodated by' increase in volume o f the tis­ sue, or swelling. Compromise o f capillary blood flow' only occurs in those anatomical areas w'here swelling is not possible, or can only occur to a limited extent. A prime example is the intracranial haematoma that in the adult cannot be accommodated by increasing the volume o f the skull, so pressure in the head rises. Similarly, any increase in pressure within an osseo-fas- cial compartment cannot b e accommodated by increas­ ing the volume o f the compartment, consequently compartmental pressure will rise. In fact within any fascial space there is potential for a harmful increase in pressure, and the importance o f micro-compartments, such as within the epineurium, should not be forgot­ ten.23 As the microcirculatory pressures are much low'er than pressures in the axial vessels, it is possible, in fact usual, to have normal axial artery pulses despite com ­ plete cessation o f flow in the capillary b eds.13 This is an important concept — the muscles o f a leg may b e gan­ grenous in the presence o f arterial pulses. Time is also an important parameter. The tolerance o f tissue to ischaemia is varied, wdth neuronal tissue being most sensitive.2,5 In clinical practice, therefore, early' signs o f ischaemia are often neuronal, such as paraesthesia or anaesthesia. In summary, the pressure gradient across a capillary' b e d is small, much less than mean arterial pressure, but derived from it. I f the system ic pressure is low'- ered, then the pressure gradient across the capillary bed wi 11 be low'ered. Capillary blood flow will stop w'hen tissue pressure exceeds or comes close to arteri­ olar inflow' pressure. At this stage the axial artery puls­ es wall still be clearly palpable. When capillary blood flow' stops, cell death will ensue within a short time period that is dependent on the type o f tissue involved, but w'hich is shortest in neural tissue. Management Management can b e aimed at either elevating the per­ fusion pressure by resuscitating the individual, or at reducing the tissue pressure by' decompression o f the compartment, or both. Definitive management o f an arterial lesion by resection, bypass or disobliteration may be necessary for ultimate resolution o f the prob­ lem. 4 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) Assessment may be clinically difficult. Particularly troublesome are children in whom it is difficult to elic­ it clinical signs or in whom co-operation is a problem. In patients with spinal injuries, be they traumatic or iatrogenic injuries such as those resulting from epidur­ al anaesthesia, signs may be difficult to elicit. When the limb is encased in plaster, examination may be lim ­ ited.21 For these reasons invasive compartment pres­ sure monitoring is advised; the techniques and indices for intervention wi 11 be discussed by other authors. Management is usually described in terms o f surgi­ cal decompression, but a lot can be done while waiting for surgery, which may occasionally obviate the need for an operation. This has been aptly described as ‘first aid for hypoxic cells’ . All circumferential dress­ ings should be removed, the limb should be kept at heart height as elevation decreases the arterial perfu­ sion pressure, the patient should be resuscitated with crystalloid to restore volume and reduce haematocrit, and maximum oxygenation should be assured.13 1 Compartment pressure can b e measured serially dur­ ing these manoeuvres and compared with MAP We believe that in children fasciotomy should b e consid­ ered when compartmental pressure reaches MAP - 3 0 mmHg, and in adults when it reaches diastolic - 20 mm H g.14 Time is o f the essence and such patients should be regarded as true surgical emergencies. R e f e r e n c e s 1. Anglen J. Baiiovetz J. Compartment syndrome in the well leg resulting from fracture-table positioning. Clin Orthon 1994- 301- 239-42. 2. Ashton H. The effect o f increased tissue pressure on blood flow Clin Orthop 1975; 113: 15-26. 3. Belcaro G, Vasdekis S, Nicolaides AN. Evaluation o f skin blood flow and venoarteriolar response in patients with diabetes and periph­ eral vascular disease by laser Doppler flowmeti-v. Anqioloqu 1989- 4 0 :95 3 -7 . ' 4. Block IT, Dobo S, Kirton OC. Compartment syndrome in the criti­ cally injured following massive resuscitation: case reports J Trauma 1995; 39: 787-91. 5. Brotman S, Browner BD, Cox EF. MAS trousers improperly applied ) causing a compartment syndrome in 1 owcr -cxtre mi tv trauma. J Trauma 1982; 22: 598-9. 6. Brown RL, Greenhalgh DG, Kagan RJ, Warden GD. 'Hie adequacy of limb escharotomies-fasciotoinies after referral to a maior bum ecnter. J Trauma 1994; 37: 916-20. 7. Handler EG. Superficial compartment syndrome o f the foot after infiltration o f intravenous fluid. Arch Phils Med Rehabil 1990- 71(1): 58-9. 8. Ileppenstall RB, Sapega A A, lzant T, Fallon R, Shenton D, Park YS, Chance B. Compartment syndrome: a quantitative study o f high- energy phosphorus compounds using 31P-magnetic resonimce spec­ troscopy. J Trauma 1989; 29: 1113-9. 9. Janzing II, Broos I! Ronmcas E Compartment syndrome as com ­ plication of skin traction, in children with femoral fractures A cta Chir Belg 1996; 96(3):135-7. 10. Manoli A 2nd, Fakhouri A, J, Weber TG. Concurrent compartment syndromes o f the foot and leg. Foot Ankle Int 1993; 14: 339-442. 11. Mars M. Hand’s up? A preliminary' study on the effect o f post-oper­ ative hand elevation. J Hand Surg 1988; 13B: 430-3. 12. Mars M, Brock-Utnc JG. The effect o f tourniquet release on intra- compartmcntal pressure in the bandaged and unbandaged limb J Hand Surg |Br] 1991; 16: 318-22. 13. Mars M, Hadley GE Raised mtracompartmental pressure and com ­ partment syndromes. Injury 1998; 29: 403-11. 14. Mars M, Hadley GE Raised compartmental pressure in children: a basis for management. Injury 1998; 29(3):183-5. 15. Mars M. tladlcy GP, Aitehison JM. Direct mtracompartmental pres­ sure measurement in the management o f snakebites in children S Afr Med J 1991; 80: 227-8. 16. Matsen FA 3rd. Compartmental syndrome. An unified concept Clin Orlhop 1975; 113: 8-14. 17. Minkowitz B, Busch MT. Supracondylar humerus fractures. Current trends £uid controversies (Review). Orthop Clin North Am 1994- 25- 581-94. 18. Naito M, Ogata K. Acute volar compartment syndrome during skele­ tal traction in distal radius fracture. A case report. Clin Orthon 1989; 241: 234-7. 19. Perry MO, Thaler ER, Shires GT. Management o f arterial injuries Ann Surg .1971; 173: 403-8. 20. Pinltowski J I ,, Weiner DS. Complications in proximal tibial osteotomies in children with presentation o f technique. J Pediatr Orthop 1995; 15: 307-12. 2 1 -Price C, Ribciro J, Kinnebrew T. Compartment syndromes associ­ ated with postoperative epidural analgesia. A case repoit. J Bone Joint Surg Am 1996; 78: 597-9. 22. Qvist .1, Pcterfreiuid RA, Perlmutter GS. Transient compartment syndrome o f the forearm after attempted radial artcrv cannulation A neslh Analg 1996; 83(1): 183-5. 23. Rydevik B, Lundborg G, Bagge U. Effects o f graded compression on intrancural bloodflow. J Hand Surg 1981; 6(1): 3-12. 24. Sumner' DS. Essential haemodynamic principles. In: Rutherford RB, ed. Vascular Surgery. 4th ed. Philadelphia: WB Saunders 1995:18-44. 25. Sundararuj GD, Mani K Management ofVolkmann’s ischaemic con­ tracture o f the upper limb. J Hand Surg [Br.l 1985; 10: 401-3. 26. Sutin KM, Longaker MT, Wahiander S, Kasabian AK, Capau EM, Acute biceps compartment syndrome associated with the use o f a noninvasive blood pressure monitor. Anesth Analg 1996; 83: .1345-6. 27. Tomctta P 3rd, Templeman D. Compartment syndrome associated with tibial fracture. In: American Academy o f Orthopaedic Surgeons, ed. Instr Course Lect 1997; 46: 303-8. 28. Whitesides TE, Haney TC, jMorimoto Iv, Harada 11. Tissue pressure measurements as a determinant for the need o f fasciotomv. Clin Orlhop 1975; 113: 43-51. 29- Wright R, Reynolds SL, i\acli islicim B. Compartment svnclromc secondary to prolonged mtraosseous infusion. Pediatr Emern Care 1994; 10: 157-9. □ SPORTS MEDICINE JULY 1999 5 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) A quantification o f competition-induced increase in heart rate during 10, 21 and 4-2 km races ORIGINAL RESEARCH ARTICLE WM Tucker (BSc (Med) (Hons) Exercise Science) TD Noakes (MB ChB, MD, FACSM) MI Lambert (PhD) M R C /U C T B io e n e r g e t ic s o f E x e r c is e R e s e a r c h U nit, D e p a r tm e n t o f P h y siolog y , U n iv e rs ity o l C a p e lo\vn M e d ic a l S c h o o l, S p o r ts S c ie n c e In stitu te o f S o u th A fr ic a Abstract Objective. Our previous study has shown that, at any running speed, heart rates (HRs) are higher during competition than during training. The aim o f this study was to determine whether this com- petition-induced increase in H R (HRjjfi) was affect­ ed by race intensity or perceived effort (luring the race. Design. Male runners training at least 60 km /wk underwent a maximal oxygen consum ption ( V U test 4 days before a 10 km (N = 6), 21 lan (N = 6) or 42 km (N = 5) race. Two days before the race, subjects underwent a track test to determme the relationship between running speed and H R under non-competitive conditions (r = 0.98 ± 0.01). Results. The average H R during the 10, 21 and 42 km races were 163 + 13, 166 ± 10 and 156 ± 6 beats/m in respectively, representing 90 ± 5, 93 ± 4 and 84 ± 4% o f laboratory-derived maximum H R (H R ,„J (P > 0.05). The subjects ran the 10, 21, and 42 km races at 74 ± 5, 75 ± 4 and 64 ± 7% o f peak treadmill running speed. The TlR(nn for the 10, 21 and 42 km races were 20 + 7, 15 + 7 and 19 ± 13 beats/m in respectively. The subjects’ perception o f fatigue measured after the track test and after each race were not different. Conclusions. HRs during competition are higher than HRs at the same speed in a non-competitive situation. This HRtllfT is independent o f racing speed and cannot be explained by the perceived fatigue measured immediately after the race. In conclusion, HR measured during competitive exercise is not an accurate measure o f exercise intensity. CORRESPONDENCE: Ml Lambert MRC/UCT Bioenergetics o f Exercise Research Unit Sports Science Institute o f South Africa PO Box 115 Newlands 7725 Tel: 021 - 686 7330 Fax: 021 - 686 7530 E-mail: mlambert@sports.uct.ac.za Introduction In a previous study it was found that runners’ heart rates (HRs) in 10 and 21 1cm competitive races were higher than their H Rs at similar running speeds d in ­ ing training (HR^n)-14 This study raised two issues. Firstly, H R monitors are used widely by athletes during competition. Many o f these athletes measure their FIRs during competi­ tion in order to select an appropriate exercise intensity for that event. But the athlete will run slower than expected during a race should a racing target H R be calculated on a H R determined during training. Indeed, this very effect and its negative consequences on competitive athletes has already been documented in the lay press." Secondly, several factors including work load,1 time o f day,11 state o f fitness,4 dehydration,7 plasma vol­ um e,12 duration o f exercise6 and temperature” 10 may affect H R during exercise. However the mechanism causing the HR,UI1 is not known. Nor has the extent o f the HR,,a-,- been quantified. A b etter understanding o f this phenomenon has practical application for com pet­ itive athletes and will contribute to a better under­ standing o f the physiological mechanisms that affect H R during competition. Accordingly, the aims o f this study w e r e to deter­ mine the ITR,liir in runners in competitive races over v a r y i n g race distances and to determine whether this increase in competition HR was affected by race inten­ sity or perceived effort before and during the race. Methods Subjects The study was approved by the Ethics and Research Committee o f the University7 o f Cape Town. Eight long­ distance runners who were training at least 60 km /w k were recruited for each o f 3 races (10 km, 21 km and 42 km). Informed consent was obtained from all sub­ jects once the testing protocols had been explained. Study design Subjects were familiarised with all testing equipment • in the orientation phase o f this stud}’. Thereafter 4 days before the race each subject underwent a maxi­ mum running test on a treadmill during which maxi­ 6 SPORTS MEDICINE JUEY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) mailto:mlambert@sports.uct.ac.za mum oxygen consumption (V 02max) and maximum HR (HRm,,,) were determined. Two days before the race subjects ran on an indoor track to determine their HWrunning speed relationship in non-competitive cir­ cumstances. All laboratory and field tests were con­ ducted between 5:30 and 8:00 a.m. to coincide approximately with the time o f day during which the races were to be held. During each race runners wore H R monitors (Vantage XL, Polar Electro Oy, Kempele, Finland) that recorded HRs continuously and split times for each kilometre. These data were then retrieved from the H R receiver after the race via an interface to a com ­ puter (Polar Electro Oy, Kempele, Finland). Following each laboratory field test and race the perceived level o f fatigue o f each subject was also evaluated. Treadmill test After a 5-minute warm-up, subjects started running on the treadmill at 12 k m /h. The treadmill speed was increased by 0.5 k m /h every 30 seconds. The test was terminated when the subject was unable to maintain the speed o f the treadmill belt. Each subject breathed through a rubber mask that covered his nose and mouth. The expired air was directed to 0 2 and C 0 2 analysers (OxyconSigma, Mijnhart, Netherlands) for the measurement o f oxygen consumption (V 02), carbon dioxide production (C 0 2) and respiratory exchange ratio (RER). The highest V 0 2 measured during the test was recorded as the V 0 2max. The equipment was calibrated before each test with a Hans Rudolph 3 litre syringe and a standard gas o f known concentration. H R was recorded throughout the test using a Vantage XL H R monitor. Track test After a standard warm-up, subjects ran 1 000 m at a submaximal pace on an indoor tartan track. The start­ ing pace was calculated to be 10 s/km slower than the subject’s current 5 km racing pace. Each subject kept his running speed constant by pacing him self with a researcher who blew-a whistle at regular intervals coin­ ciding with the time the subject should have been at respective 100 m marks on the track. After a rest period o f 2 minutes, the subject ran another 1 000 m, this time 10 seconds faster. This pattern was repeated until the subjects were unable to maintain the required running pace. The subjects usually completed 5 or 6 km before the onset o f fatigue. After the test each sub­ je ct s average H R for the last 60 seconds o f each kilo­ metre, and the average running speed for each kilometre, were calculated. Then the line o f best fit between HR and running speed was calculated using a linear regression analysis. The ambient temperature during the test was between 19 and SOX. Race Subjects wore H R monitors while competing in 10, 21 or 42 km races. Subjects were instructed to record the time splits for each kilometre by pressing the appro- piiate button on the H R monitor receiver. The H R was recorded every 5 seconds during the 10 and 21 km races and every 15 seconds for the 42 km race. The average H R and average running speed were calculat­ ed for each kilometre during the race. The temperature for the duration o f the 10 km race was 19°C, between 16 and 19°C for the 21 km race and 20 °C at the end o f the 42 km race. Measure of fatigue The subject’s perception o f fatigue was evaluated after each indoor running test and race according to the Rose/N oakes running fatigue scale (0 = sluggish, exhausted, unable to run — 10 = best ever).8 Body composition Subject’s percentage body fat was predicted using the Dumin and Womersley anthropometric technique.3 Statistics Descriptive statistics are presented as the mean ± the standard deviation (mean ± SD). A line o f best fit was calculated between HR and running speed in the field test. The Pearson’s correlation coefficient was calculat­ ed between these variables. The equation established for the relationship between H R and running speed for each subject was used to calculate his predicted HR based on the racing running speed. The difference between the subject’s H R measured in the race and the HR predicted from the regression equation was deter­ mined using a paired t-test. A Spearman’s ranked test was used to determine relationships between the fatigue scores and HR(|ifi. Statistical significance was accepted when P < 0.05. Results HR data were available for 6 subjects for the 10 and 21 km races and for 5 subjects for the 42 km race. The other subjects had poor FIR recordings during the races as a result o f malfunctioning H R monitors, and were excluded from further analysis. General characteristics and laboratory data o f the subjects participating in each race are shown in Table I. The relationship between H R and running speed determined in the field test under non-competitive TABLE I. General characteristics and laboratory data o f subjects participating in the 10, 21 and 42 km races (values expressed as mean ± SD) Variables 10 k m 21 kin 4 2 kmll (jV = 6 ) CV= 5 ) Age (years) 3 6 .8 ± 4 .8 3 6.0 ± 4.3 3 6.2 ± 4 .9 M ass (kg) 7 5.8 ± 13.9 7 5 .5 ± 13.0 6 9 .0 ± 12.9 Stature (cm ) 1 7 7 .8 ± 9 .6 17 8 .7 ± 9 .5 17 2 .4 ± 8.0 P er ce n t fat 14.5 ± 4 .4 1 5 .9 ± 4 .6 1 2 .9 ± 4 . 0 v o a (m l O V k g /m in ) 5 3 .6 ± 8.1 5 3 .7 ± 8.1 5 3 .8 ± 10.5 HRfUax (b e a ts /m in )) 182 ± 8 181 ± 10 181 ± 7 IT R S (k m /h ) 18.8 ± 1.3 1 8 .4 ± 1.3 18.9 ± 1.7 RER 1.05 + 0.05 1.05 ± 0.05 1.09 ± 0.06 F I R S - p ea k treadm ill running sp e e d ; R E R = respira tory exchange ratio. SPORTS MEDICINE JULY 1999 7 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) conditions was r = 0.98 ± 0.01. (mean ± SD). The average running times for the 10, 21 and 42 km races were 43:25 ± 5:15, 92:48 ± 7:51 and 212:03 ± 24:55 (min:s). The subjects’ personal best times for the 10, 21 and 42 km were 40:31 ± 4:21; 89:42 ± 10:6 and 190:27 ± 33:43 min:s respectively. Therefore, dur­ ing the 10, 21, and 42 km races in this study the sub­ jects ran 7, 3 and 10% slower than their personal best times for the same distances. The average HRs mea­ sured during all three races, and the average HRs pre­ dicted at the same running speeds on the basis o f measurements taken during the indoor testing, are shown in Table II. TABLE I I . Average measured and predicted HRs for the subjects in the 10, 21 and 42 km races (values expressed as mean ± SD) Variables 10km 2 1 k m 4 2 km ( N = 6 ) (AT = 6 ) ( N = 5) Average m easu red H R (b e a ts/m in ) 16 3 ± 13 1 66 ± 10 156 ± 6 P redicted H R (bea ts/m iii) 1 4 3 ± 22* 151 ± 13* 137 ± 17* 11R:; | {1 leal s in in) 20 ± 7 15 ± 7 19 ± 13 % H R,llix 90 ± 5 9 3 ± 4 8 6 ± 4 % PTRS 74 ± 5 * 75 ± 4 * 6 4 ± 7 * P < 0 .0 3 p r e d ic te d H R v . average m easu red H R in 10, 21, ’ P < 0 .0 1 %PTRS 10 k in v. % PTRS 4 2 kin. ' P < 0 .0 5 %FTRS SI k in v. %PTRS 42 km . PTRS - p ea k trea d m ill running sp eed . and 4 2 km raees. The HRs measured and predicted for each subject in the 10, 21 and 42 km races are shown in Figs 1, 2 and 3 respectively. The HRs measured during the races 150 100 5 0 0 200 150 (1 ) (2 ) T v ^ 'sv ^ s' S y A >v. ............................... (3) 7 14 21 28 3 5 42 km (4) (5), 7 14 21 2 8 3 5 42 km F ig. 1. H e a r ts r a te s o f th e s u b je c ts ( N = 6 ) m e a su red d uring th e 1 0 km r a c e a r e sh o w n a s 0 . E a c h s u b je c t ’s h e a r t r a te p r e ­ d ic te d fr o m th e s a m e ru nn in g s p e e d in n o n -co m p etitiv e con di- to n s is s h o w n as O • F ig. 2 . H e a r t s r a te s o f th e s u b je c ts ( N = 6 ) m e a su red d uring th e 2 1 km r a c e a r e sh o w n as # . E a c h s u b je c t ’s h e a r t r a te p r e ­ d ic te d fr o m th e s a m e ru n n in g s p e e d in n o n -co m p etitiv e con d i- to n s is sh o w n a s O ■ F ig. 3. H e a r ts r a te s o f th e s u b je c ts ( N = 6 ) m e a su red d uring th e 4 2 km r a c e a r e sh o w n a s 0 . E a c h s u b je c t's h e a r t r a te p r e ­ d ic te d fr o m th e s a m e ru n n in g s p e e d in n o n -co m p etitiv e con di- to n s is sh o w n a s (J • were consistently higher than the HRs predicted from the running speeds during the races in all the subjects (P < 0.03).' The fatigue scores, according to the Rose/Noakes scale, after the races and track test are shown in Table III. There was no difference in these fatigue scores measured after the track test or after each race. The 8 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) Discussion TABLE III. Fatigue scores according to the Rose/N oakes scale after the track test and each race (values expressed as mean ± SD) Variables Race Track test 10 k m (N = 6) 6 .2 ± 1.7 7 .2 ± 1.7 21 km (N = 6) 6 .8 ± 2.5 6 .7 ± 2.5 4 2 km GV = 5) 7.0 + 1.7 6 .0 ± 2.5 level o f fatigue after each race, as measured by this questionnaire, did not explain IIR li(r (r = 0.01, P = 0.96). The magnitude o f IIRuir was not explained by the subjects’ V 0 2max (r = 0.44, P = 0.08), perception o f fatigue after the race (r = -0 .0 2 , P = 0.93), running speed during the race (r = 0.17, P = 0.51), or running s intensity' (%MR,II1LX) during the race (r = -0 .0 1 , P = 0.97). The graph o f racing speed versus %HRIllax and racing speed versus TLRtlin are shown in Fig. 4. There were weak relationships between the laborat ory measures o f peak treadmill running speed (PTRS) and HR|lfr (r = 0.51 and P = 0.04), and H R nax achieved during the treadmill test and H R ^ (r = 0.64, P = 0.006). 100 95 X CO (z 90 i 85 80 0 0 30 r 25 j- c E 20 ; w *30) q 15 : ~o CL 10 rI • 10 km O 21 km A 42 km 200 250 Racing speed (m/min) 300 Fig. 4. G ra p h s o f ra cin g s p e e d (m / m in ) v. %>I1 R,„,Lr a n d I I K diir (b e a ts / m in ) d uring 1 0 ( N = 6 ) , 2 1 ( N = 6 ) a n d 4 2 km ( N = 5 ) ra ces. The major finding o f this study was that H R measured during races o f varying distances was consistently higher than the H R elicited at similar running speeds in non-competitive situations. This finding supports an earlier study done in this laboratory.14 The mechanism for the HR(Hfr is not known and cannot b e ascribed to the perception o f effort as the fatigue scores were sim­ ilar after the non-competitive field test and after the races. The next important finding was that the running intensity, as predicted as a %HRmax, was not different between the 10, 21 and 42 km races (Table II) although there was a significant difference in the sub­ jects’ running speed (expressed as a percentage o f PTRS) (Table II). This suggests that under competitive racing conditions the H R expressed as a percentage o f H R na.x, is not an accurate marker o f exercise intensity. This is in contrast to a non-competitive situation where HR as a measure o f exercise intensity accurately reflects increases in running speed (r = 0.98). It should b e noted that the subjects ran 3 - 10% below their best times for the various race distances in this study. It is therefore tempting to conclude that the results could even underestimate the real extent o f ITR,ii(T in elite athletes. Had the subjects been racing with the intention o f trying to better their personal best times, then it is possible that the HR,]nr could have been greater. The regulation o f H R during exercise is complex913 and it is beyond the scope o f this study to explain the mechanism causing IIR(lin. It can, however, be con­ cluded that the HRs during competition are higher than the HRs at the same running speed in non-com- petitive situations. In addition, this H R liff cannot be accounted for by the subjects’ perception o f fatigue measured after the race or running speed or running intensity during the race (Fig. 4). Although there were weak relationships between the laboratory measures o f PTRS and IIR(Un (r = 0.51) and HR,llax achieved during the treadmill test and HR,nn (r = 0.64), these relation­ ships lacked the power needed to predict accurately HR|ifr from laboratory measurements conducted before the race. In summary, H R measured during competitive exer­ cise is not an accurate measure o f exercise intensity'. The study was supported by Polar Electro Oy, Kempele, Finland, the Medical Research Council of South Africa and the Nellie Atkinson and Harry Crossley Research Funds of the University of Cape Town. R e f e r e n c e s 1. Arts FJP, Kuipers H. The relation between power output, oxygen uptake and heart rate in male athletes. Int J Sports Med 1994; 15: 228-31. 2. Claremont AD, Nagel F, Reddan WD, Brooks GA. Comparison of metabolic, temperature, heart rate and ventilatory responses to exercise at extreme ambient temperature (0 and 35°C). Med Sci SporLs Exerc 1975; 7: 150-4. continued on p a g e 1 9 SPORTS MEDICINE JULY 1999 9 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) ORIGINAL RESEARCH ARTICLE Improved time-trial performance after tapering in well-trained cyclists A Bosch’ (BSc, MA, PhD) A Thomas2 (BA, BSc (Med)(Hons) Sports Science) TD Noakes8 (MB ChB, MD, FACSM) 'L ib e r ty L ife C h a ir o f E x e r c is e a n d S p o r ts S c ie n c e a n d M R C /U C T B io e n e r g e tic s o f E x e r c is e R e s e a r c h U nit, D e p a r tm e n t o f P h y siolog y , U n iv e rs ity o f C a p e T ow n M e d ic a l S c h o o l “ 3M R C /U C T B io e n e r g e tic s o f E x e r c is e R e s e a r c h U n it, D e p a r tm e n t o f P h y siolog y , U n iv e rs ity o f C a p e Tow n M e d ic a l S c h o o l Abstract Objective. The purpose o f this study was to deter­ mine whether cycling performance improved dur­ ing a 14-day taper, the tim e course o f any improvement, and the possible physiological rea­ sons for any change in performance. Design. Twenty trained male cyclists (> 250 km /wk) were randomly assigned either to a control group that continued training as usual, or to a reduced-training (tapering) group. Groups were further randomly subdivided and then pair- m atched into a time-trial group (5 controls and 5 experimental subjects) who completed four 20 km time-trials on days 0, 4, 8 and 14 o f the tapering programme, or a laboratory test group that per­ formed a variety o f laboratory tests instead o f the time-trials. On the same days the remaining sub­ jects participated in ’ a laboratory-based trial in which maximum oxygen consumption, peak power output (PPO) and peak post-exercise blood lactate concentrations, anaerobic power and resting mus­ cle glycogen concentrations were measured. Setting. Trials were conducted in an exercise labo­ ratory and at a cycling track. Interventions. Experimental subjects reduced their training frequency to 66% and their weekly training duration to 60% o f normal. Training intensity in both experimental and control groups was main­ tained. Main outcome measure(s). Performance would be improved after tapering in both time trial and lab- CORRESPONDENCE: Professor TD Noakes MRC/UCT Bioenergetics o f Exercise Research Unit Sports Science Institute o f South Africa Boundary .Road Newlands 7700 Tel: 021 - 686 7330 Fax: 021 - 686 7530 E-mail: TDNOAKES@SPORTS.UCT.AC.ZA oratory subjects, with the physiological parameters measured in the latter group providing a physio­ logical explanation for the improved performance. Results. Time-trial performance became slower in the control subjects from day 0 (28.3 ± 0.3 min) to day 14 (29.3 ± 0.2 min), but became significantly faster (P < 0.05) in the reduced training (taper) group from day 0 to day 8 (29.5 - 28.7 ± 0.8 min) and from day 8 to day 14 (28.7 - 28.5 min). Similarly, PPO increased significantly with reduced training from day 0 (382 ± 32 Watts (W)) to day 14 (404 ± 34 W; P < 0.05), but did not change in the control group. No other measured physiological variable changed significantly. Conclusions. Similar to previous reports, these data demonstrate that a 14-day period o f reduced train­ ing can improve exercise performance, both in field tests and in laboratory tests, in cyclists who habit­ ually train 250 km or more per week. Eight to 14' days o f reduced training were required for time- trial performance to be optimal. However, the mechanism for this effect was not identified by the measured physiological variables. Introductioii Athletes frequently reduce their training load imm edi­ ately before major competition or after a competitive season in order to allow recovery from the fatigue asso­ ciated with racing and heavy daily training.710 Recent findings show that a number o f physiological and performance adaptations can be maintained even when training volume and frequency are reduced,91013 provided that the usual exercise intensity is main­ tained.9 However, many athletes fear that any reduc­ tion in training volume for more than a few days will inevitably lead to a dramatic fall in fitness and impaired racing performance. Studies o f reduced training have been done on run­ ners,1011 swimmers*0 and cyclists.14 The aim o f the pre­ sent study was to determine the effect o f a period o f reduced training on the exercise performance o f cyclists using both a field and laboratory test to evalu­ ate performance changes and provide possible physio­ 10 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) mailto:TDNOAKES@SPORTS.UCT.AC.ZA logical mechanisms that might explain the findings. These tests included measures o f neuromuscular mechanisms in addition to conventional measures o f aerobic and oxygen independent ‘ fitness’ . It was hypothesised that whatever mechanisms may be responsible for improvement in performance after tapering would apply equally whether the cyclist was endeavouring to improve performance in the laboratory or on the track. Materials and methods Twenty well-trained male cyclists volunteered to par­ ticipate in this study, which was approved by the Research and Ethics Committee o f the Faculty of Medicine o f the University o f Cape Town Medical School. All signed informed consent and were free to withdraw from the trial at any time. Entrance to the study was limited to cyclists who had consistently trained more than 250 km /w k throughout the year for at least the last year. This included racing and inter­ val training. Before the study subjects were asked to record a 2-week training schedule in order to deter­ mine their training volumes, frequencies and intensi­ ties. Typically, training consisted o f one training session o f approximately 100 km on the weekend, with five other training sessions o f approximately 60-minute duration during the week. Most training was done at moderate intensity (based on subject heart rate and rating o f perceived exertion), with approximately one ride per week o f high intensity. Subjects were randomly assigned to control and experimental groups. Control subjects continued their usual training programme, whereas the experimental subjects followed a 14-day taper regimen during which training frequency was reduced to 66% and training duration to 60% o f their normal training schedules. However previously documented training intensity was maintained throughout the study. Training was reduced in a single step rather than a graded reduc­ tion. Whereas it has been suggested that a graded reduction m aybe advantageous over a step reduction,12 this applies to swimmers, not runners. Runners may need a greater reduction in training than is suggested in the studies cited by Houmard and Johns.12 The con­ trol and experimental (reduced-training) groups were then further subdivided into laboratory and field groups, and then pair-matched. On the day before a test each subject performed a training session stan­ dardised according to previous training documented in his training log book. After familiarisation with the procedures, cyclists in the two field groups performed four 20 km time-trials on an outdoor cycle track on days 0, 4, 8 and 14 o f the study. Time-trials were conducted individually to pre­ vent drafting. The control subjects were used to control for the influence o f environmental factors, especially differences in wind speed and temperature. Matched subjects from both the control and experimental groups performed the time-trial on the same day and at the same time o f day to avoid any diurnal variation in performance measures, on the subject’s own bike, and wearing the same type o f clothing. Subjects in the laboratory group were tested on days 0, 4, 8 and 14 for a number o f physiological parame­ ters, described subsequently. Before the start o f the performance trials all sub­ jects were weighed and their per cent body fat was cal­ culated from biceps, triceps, subscapular and supra-iliac skinfold measurements using a skinfold caliper (Holtan Ltd., Crymych, UK) according to the equations o f Dumin and Wormersly6 as described by Brozek et al." Subjects in the laboratory trial reported to the labo­ ratory on days 0, 4, 8 and 14 for the performance o f a Wingate Anaerobic Test (WT) on a mechanically-braked Monark 818 cycle ergometer (Varberg, Sweden) that was calibrated by means o f a weighted torque balance attached to the crank. The ergometer was modified with toe straps, adjustable racing handlebars and sad­ dle, and interfaced with an Apple HE microcomputer. The same seat height was used for each individual dur­ ing each test. Sample periods o f 0.5 seconds enabled calculation o f peak power (WT-PP), taken as the high­ est average power for any 5-second period during the test and the mean power (MP) that was sustained throughout the test. After a 5-minute warm up at a load and speed select­ ed by the cyclist, subjects began pedalling at minimal resistance and gradually increased the cadence to 115 - 120 rev/min. When this cadence was attained, the full load (0.075 kp/kg body weight) was applied by an investigator and the computer programme was activat­ ed.7 Subjects were instructed to remain seated and were verbally encouraged to maintain maximal pedal rates throughout the test, i.e. to perform ‘all out’ from the start. Blood lactate concentrations were deter­ mined spectrophotometrically from venous blood (1 ml samples) drawn immediately on completion o f the Wingate test and then at 1-minute intervals for 5 min­ utes via a cannula placed in an antecubital forearm vein before testing commenced. After a 10-minute rest period, testing was conducted for determination o f maximum isometric tension, max­ imum speed o f contraction (Vmax) and total work done on the same Monark bicycle ergometer as for the Wingate test. From rest, with the pedal 10° above the horizontal, a countdown o f 3 seconds was given to the subject who subsequently pedalled as quickly as possi­ ble for 5 seconds at randomly chosen resistance set­ tings o f 3 kp (29.4 N), 5 kp (49 N), 2 kp (19.6 N), 7 kp (6 8 .6 .N), 4 kp (39.2 N) and 6 kp (58.8 N).15 Rest periods o f at least 2 minutes were allowed between each exercise bout. The theoretical power output at zero load (Po) was calculated from the zero point o f the graph o f power output versus resistance, Vmax from a graph o f velocity versus resistance and total work done from the area under the power/resistance graph. After another 30-minute rest period, subjects per­ formed maximal progressive exercise to exhaustion on an electrom echanically braked cycle ergometer SPORTS MEDICINE JULY 1999 11 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) (Excalibur, Lode, Groningen, the Netherlands). For measurement o f peak power output (PPO) and maximum oxygen consum ption (V 0 2max), air was inspired from a Hans Rudolph 2 700 one-way valve (Hans Rudolph Inc., Kansas City, Kansas, USA) con­ nected to a Mijnhardt dry gas meter. A nose clip pre­ vented nasal breathing. Expired air was passed through a 15 1 baffled mixing chamber from which con­ tinuous sampling occurred by Ametek N-22M oxygen and CD-3A carbon dioxide gas analysers (Thermox Instruments, Pittsburgh,. PA). Before each test, the gas meter was calibrated with a Hans Rudolph 3 1 s y r i n g e and the analysers were calibrated with air and a 4% CO.,: 1 6 % 02:80% N2 mixture. The cumulative value for each minute o f the test for ventilation (Vi), oxygen con­ sumption (VOs), carbon dioxide production (VC02), and respiratory exchange ratio (RER) were printed "out at the end o f the test using standard formulae for calcu­ lations. Subjects first pedalled at a workload o f 3.33 Watts (W )/kg for 6 minutes, during which time submaximal V 0 2 was measured. Blood was drawn from a forearm vein through a stopcock for subsequent measurement o f blood lactate concentrations. Ratings o f perceived exertion (RPL) were recorded at regular intervals dur­ ing the exercise bout using the 1 - 10 point Borg scale. Heart rate was recorded on a Lohmeier M607 Monitor (Munich, West Germany). On completion o f the sub- maximal test, the workload was increased by 50 W for 150 seconds. Thereafter the workload was increased by 25 W every 150 seconds until the subject voluntari­ ly terminated the test. Venous blood was again drawn immediately via the indwelling cannula on completion o f the test and then at 1-minute intervals for 5 minutes for subsequent determination o f blood lactate concen­ trations. Peak workload was calculated using the formula: Peak workload (W) = final workload (W) +(t/150 x 25),7 where t is time in seconds o f the final workload com ­ pleted. This battery o f tests could lead to fatigue, with one test possibly affecting a subsequent test. However, this was consistent each time that testing was done and would affect all subjects. Post-exercise muscle samples were obtained at the end o f the trial from the right vastus lateralis o f each cyclist, using the needle-biopsy technique as described by Bergstrom.1 The sample was immediately frozen in liquid nitrogen and stored at -8 0 °C for subsequent determination o f muscle glycogen content according to the method o f Lowry and Passonneau.13 Statistical analyses Statistical significances o f changes over time and between groups were assessed by means o f a two-way analysis o f variance (ANOVA) for repeated measures. When a significant F-ratio (P < 0.05) was found, a Scheffe test was used for p ost hoc analysis. Where necessary, between-group differences were measured with a Student’s unpaired M.est. A value o f P < 0.05 was regarded as significant. TABLE I. Physical characteristics before a reduced training protocol Laboratory groups Field groups R educed- R educed- training C ontrol training C ontrol group group grou p group A ge (yrs) 22.6 21.2 26.0 21.3 ± 2.6 ± 1.2 ± 2.9 ± 0 .4 M ass Ckg) 75.2 74.7 73.9 71.2 ± 5 . 4 ± 4 . 3 ± 2 . 3 ' ± 2.7 B ody fat con ten t % 9.9 10.5 11.6 10.8 ± 0 . 8 ± 0 . 8 ± 1.1 ± 1.0 Peak pow er output (W ) 382.8 37 4 .6 _ _ ± 32.3 • ± 19.1 M axim um oxygen consum ption (l/m in ) 4.5 4.7 . _ ± 0 . 2 ± 0 . 2 Values are m eans ± S D ( X = 5 in each sub-group). Results Subjects’ physical characteristics are shown in Table I. Subjects in the laboratory group had high V 02nlax values (4.6 ± 0.2 l/min; mean ± SD) and reached high PPO (394 ± 27 W). Subjects in the time-trial group did not do V 0 2max or PPO tests as the only point o f interest was whether their time-trial performance improved or not. There were no significant differences in age, mass or per cent body fat between the laboratory and field groups or in V 0 2max and PPO in the control and reduced-training subjects in the laboratory group. Changes in 20 km time-trial performance in the field group are shown in Fig. 1. Performance for both control and reduced-training (taper) groups were con­ stant for days 0 and 4 o f the trial. Thereafter perfor­ mance in the control group was significantly impaired on days 8 and 14, whereas performance in the reduced training group improved significantly by day 14. Similarly, PPO measured during the V 0 2max test (VOa-PPO) increased steadily in the reduced training 30 25 □ Control D Reduced training I I I J 14 Time (days) F ig. I. T w en ty km tim e-tria l p e r fo r m a n c e (m i n ) in c y c lis ts in co n tr o l a n d red u ce d -tra in in g g r o u p s on d a y s 0, 4. 8, a n d 1 4 . T im e-trial p e r fo r m a n c e im p r o v e d s ig n ifica n tly in th e red u ced - tra in in g g r o u p on d a y 1 4 b u t w a s im p a ired on d a y s 8 a n d 1 4 in th e c o n tr o l g r o u p . V alues a r e m e a n s ± S D . * S ig n ifica n t ( P < 0 . 0 5 ) im p r o v e m e n t fro m d a y 0. 12 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) Q Control □ Reduced training 450 L T I 350 : 0 | 300 1 CO. Costill DL, King DS, Thomas R, Hargreaves M. Effects o f reduced anting on muscular power in swimmers. Physician and Sportsmedicine 198ob; 13: 94-101. 6. Dumin JVGA, Wonnersly J. Body fat assessed from the total bodv density and its estimation from skinfold thickness: measurements on 481 men and women aged from 16-73 years. Br J Nutr 1974; 32: 7. Hawley JA, Noakes TD. Peak power output predicts maximal oxygen uptake and performance time in trained cyclists. Ear J Appl Physiol 1992; Go: 79-83. 8. Hickson RC, Roscnkoctter MA. Reduced training frequencies and uicreased aerobic power. Med Sci Sports Exerc l y o l ; ±o: 13-o. 9. Hickson RC, Foster C, Pollock ML, Galassi TM, Rich S. Reduced training intensities and loss o f aerobic power, endurance, and car­ diac growdi. J Appl Physiol 1985; 58: 493-9. 10. Houmard JA, Costill DL, Mitchell JB, Park SH, Fink WJ, Bums JM. Testosterone, cortisol, and creatine kinase levels in male dis­ tance runners during reduced training. Int J Sports Med 1990a; 11: 11. Houmard JA Costill DL, Mitchell JB, Park SII, Hickner RC Roemmich JA. Reduced training maintains performance in dis­ tance runners. Int J Sports Med 1990b; 11: 46-52. 12 Houmard JA, Johns RA. Effects o f taper on swim performance (Review). Sports Med 1994; 17: 224-32. 13. Lowry- OH Passoimcau JV A Flexible System o f Enzymatic Analysis. New York: Academic Publishers, 1972. 14. Martin DT, Scifres JC, Zimmerman SD, Wilkinson JG. Effects of mterval tu n in g and a taper oil cycling performance and isokinetic leg strengdi. Int J Sports Med 1994; 15: 485-91. 15. Nadeau M, Cuerrier J-l! Brassard A. The bicycle ergometer for 1983- 8-P4 l 6r teStillg' Canadian Journal Applied o f Sports Science 16' m!TPr }\ B’ ^ !IC° ougaJ1 J ° . Cipriano N, Sutton JR, Tamopolsky MÂ Coates G. Physiological effects o f tapering in liighlv trained athletes. J Appl Physiol 1993; 72(2): 706-11. ' g 22 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) POSITION STATEMENT Position Statement: Diabetes Mellitus and Exercise International Sports Medicine Federation (FIM S) The following Statement was approved by the FIMS Executive Committee, 26 October 1996 Introduction Diabetes mellitus is a common metabolic disease char- •icterized by insulin insufficiency resulting in impaired ability to transport glucose across the cell membrane for its subsequent oxidation. Also, muscle and liver glycogen re synthesis, triglyceride synthesis in adipose cells, inhibition o f their breakdown (antilipolytic effect), as well as protein synthesis and storage (ana­ bolic effects) are being impaired. Insulin insufficiency thus leads to metabolic disturbances leading to such common symptoms as fatigue, weakness, weight loss, hunger, overeating, polyuria, and signs o f glycosuria, and ketosis. Though being clinically silent for many years, dia­ betes mellitus often leads to serious pathological com ­ plications o f various organ systems (eyes, kidneys, peripheral nerves, coronary and peripheral arteries) which may substantially impair quality o f life and reduce life expectancy. There are two distinct forms o f diabetes, termed insulin dependent diabetes mellitus (IDDM) and non insulin dependent diabetes mellitus (NIDDM). IDDM is an auto-immune disease hi which the body attacks and ultimately destroys insulin producing pan­ creatic beta-cells. In addition to a genetic component, evidence supports a viral infection triggering an auto­ immune process either due to similarities with beta cell protein or sensitization to destructed beta-cells. The key pathogenetic factor o f NIDDM is relative insufficiency o f insulin due to insulin resistance and/or defective insulin secretion. Insulin resistance is often ■ associated with hypertension, lipid disturbances, and obesity. Apart from genetic dispositions, diet and obe­ sity, animal experiments as well as epidemiological data suggest that a lack o f physical activity may also contribute to a relative deficiency o f insulin. Diabetes may be precipitated by, or a similar syn­ drome brought about by endocrine disorders (e.g., hypercorticosteroidism, acromegaly, hyperthyroidism, pheochroniocytoma), drugs (e.g., glucocorticoids, thy­ roid hormones, contraceptives, thiazides), and pancre­ atic or liver disease. Rationale for exercise in prevention and therapy Due to an insulin-like effect on muscle contraction (an increase o f membrane permeability to glucose) exercise has a potential to increase insulin sensitivity, lower blood glucose and increase its utilization. Improved glu­ cose tolerance positively influences the glycemic profile that can be detected by lower concentration o f glycosy- ated hemoglobin. A better glycemic profile may post­ pone and reduce the risk o f late complication. Since this effect is rather short-lived, regular frequent exer­ cise sessions are needed to maintain such a benefit. Also reducing body fat due to the increased energy expended and its effect on the basal metabolic rate may indirectly but significantly decrease insulin resis­ tance. In addition to obesity, exercise has the potential to favourably alter other risk factors o f cardiovascular dis­ ease, namely elevated blood lipids and hypertension. In this way an already increased risk o f coronary heart disease (3 times higher than general population) may be reduced. Last but not least, exercise may reduce psychologi­ cal stress, positively influence a feeling o f well being, and improve quality o f life. Exercise guidelines Clearance by a knowledgeable physician is recom­ m ended prior to the initiation o f an exercise program. In addition to a general assessment, screening should include an exercise stress test to detect latent cardio­ vascular disease. Requisites include an absence o f ketoacidosis and glycemia under 300 mg %. When late complications are evident., such as hypertension or renal impairment, the risks and benefits should care­ fully be considered. During the initial stages o f an exercise program, close medical supervision which includes blood glu­ cose monitoring is strongly recommended in order to adjust diet and medication (insulin or PAD doses) to the exercise altered metabolic situation. Modes of exercise Aerobic activities carried out at moderate intensity such as brisk walking, cycling, jogging, running, or cross country skiing are preferred m odes o f exercise. Since the majority o f diabetics are obese, non weight bearing exercise like cycling and swimming may pose less stress on the locomotor system and contribute to better compliance. General daily activities o f a habitu­ al nature are encouraged in addition to the exercise sessions. In the past, resistance exercise has not been recom­ mended because o f the potential for a dangerous increase in blood pressure, especially in those with vas­ cular complications. Recent findings indicate that appropriate forms o f resistance exercise are safe and may potentiate the positive effects o f aerobic exercise. A circuit training approach aimed at all major muscle groups is recommended. The resistance should allow 10 to 12 comfortable repetitions. SPORTS MEDICINE JULY 1999 23 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) Intensity o f exercise T h e exercise intensity should be between 50 and 70% ° f V 0 2max- H igher intensities excessively activate the sym pathoadrenal system with subsequent increase o f glycemia. With caution, heart rate can be used as an indicator o f intensity, bi patients with autonom ic neu­ ropathy, heart rate may not accurately reflect exercise intensity. As an alternative, perceived exertion o f METs (m etabolic equivalents) should be used for the exercise prescription. Duration of exercise Exercise sessions between 20 and 60 minutes are recom m ended. Less than 20 minutes yields litd e car­ diovascular benefit, longer exercise tends to increase the risk o f hypoglycemia. Frequency of exercise Daily exercise is suggested because such an approach enables easier insulin adjustment and d iet planning. A more realistic and practical goal may be 4 to 6 sessions a week. Practical remarks • Patients should be educated about the effects and potential risks o f exercise, namely hypoglycemia. • The participants should wear identification indicat­ ing their diabetic condition and should exercise with a know ledgeable partner in case o f hypo­ glycem ia including loss o f consciousness. • When possible exercise should b e p erform ed at the sam e convenient time with sim ilar intensity and duration. • Because o f the pro insulin effect o f exercise, insulin d epend ent dia betics should reduce insulin d oses by 20% or adequately increase food intake upon initiat­ ing an exercise program. • To avoid hypoglycem ia a small carbohydrate snack should be eaten 3 0 minutes prior to exercise. During more prolonged activity a 10 g carbohydrate snack (fruit, fruit ju ice, or soft drink) should be ingested for each 30 m inutes o f exercise. • Pay careful attention to the feet ol the exercising diabetic patient. Loss o f sensation due to neuropa­ thy a n d /o r im paired peripheral circulation increas­ es the risk o f injuries. G ood footwear and careful foot hygiene are essential to avoid injuries like ca l­ luses, corns and blisters that may lead to serious com plications. • Warm up and cool down periods should be an inte­ gral part o f an exercise program. SUGGESTED READING C hish olm D.I. D iabetes m cUilus. In: B loom field J . I'rickcr PA, Fitcli KB. (ed s). Textbook o f Science and Medicine in Sports. Blackwell S cience I.id., Oxford, pp. 560. 1992. W allbcrg-H cnriksson II. E xercise and diabetes m ellitus. Exer Sport Rev. 20, 33 9-36 8, 1992. S ciin ck lcr SH, R udcrm an MB. Exercise and M D D M . D iabetes Care 13, 78 5-789, 1990. T h is statem ent was prepared for the FIMS Scientific C om m ission by A ssoc. Prof. Dusan Hamar, MD, PhD, R esearch Institute o f Sports Sciences, Bratislava, Slovakia. [N ote: T h is statement may be reproduced and disU-ibutcd with the sole requirem ent that it be id cn liiicd clearly as a Position Statement o f (lie LntcmaUonal Federation o f Sports M cdiciiic.J 24 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) IOC OLYMPIC PRIZE i ; m k ) a i : i » m (g) PARKE DAVIS IOC Olympic Prize b y Beiino M Nigg THE IDEA OF THE IOC OLYM PIC PRIZE M ovem ent nncl m obility are am ong the m ost precious aspects o f human life. Imagine a person who cannot move! A person who cannot play g o lf with M en d s, cannot go for a hike with family or friends, or cannot visit the next-door neighbours for a chat. Mobility' and movem ent arc extrem ely important for the quality o f life o f humans. W ithout the ability' to move, life can be v e r y difficult. Movement is important in all situations of life, from ch ild h ood to old age to high perform ance atliletics. Mobility and movement are equally important for children, adolescents, athletes and the elderly. A young child learns to move and engraves movement patterns into the motor control system. If these pat­ terns are correct, early degenerative disease such as osteoarthritis may be avoided. Adolescent girls and boys strengthen their muscles, bones, ligaments and tendons by providing the neces­ sary stimuli during movement, exercise and sport. Bone formation in girls, for instance, is maximal during this time and a ‘bone bank’ may be established due to appropriate sport activities, reducing the risk o f osteo­ porosis. Athletes expose their bodies to high and repetitive loading situations. This loading may cause damage to the body. However damage can be avoided if training and equipment are well controlled. Elderly people want to enjoy their retirement age by being physically active, playing games, and spending time with their grandchildren. To d o so, they need to be m obile. Consequently, understanding the factors influencing m obility and m ovem ent and the resultant loading o f the hiunan body is important. Scicntific research studying m ovem ent, exercise and sport can contribute substantially to the im proved understanding o f m obili­ ty and movement. With the increased life expectancy o f humans, such research is growing in importance. T h e activities o f the International O lym pic Com m ittee (IOC) centre around all aspects o f m ove­ ment, exercise and sport. The IOC is interested in high perform ance sport, physical activities for children, a d o ­ lescents, adults and the elderly, exercise and sport in developing countries, his ton ' o f exercise and sport, health and w ell-being due to physical activity and sport, and many other facets o f movem ent, exercise and sport. The IOC M edical Com m ission was and is often in the lim elight because o f athlete doping cases. However, the IOC M edical C om m ission has many other less well- known activities. T hanks to the initiative of its Chairman, Prince .Alexandre de M erode, the IOC Medical Com m ission has many groups that con cen ­ trate on th e p ositive aspects o f movem ent, exer­ cise and sport. Li 1987, one such group, the S u b com m ission for B io ­ m echanics and Physiology, w anted to som eh ow ac- laiowledge the importance o f science related to m ove­ ment, exercise and sport. The d iscussions o f the Subcom m ission for B iom e­ ch a n ics and Physiology Prince Alexandre de Merode, resulted in two major pro- Chairman o f the je c t p rop osa ls. First, to IOC Medical Commission esta b lish an IOC W orld Congress for sciences related to movement, exercise, and sport; and second, to establish a highly prestigious prize for science related to m ovem ent, exercise and sport, namely the IOC OLYMPIC PRIZE. U nder the le a d e rs h ip and g u id a n ce o f Prince Alexandre de M erode, chairman o f the IOC M edical Com m ission, selected m em bers o f this Subcom m ission went to work to develop the two ideas. Dr Charles Dillm an p rovid ed le a d e rs h ip for the IOC W orld C ongress and acts as scientific chair o f all IOC World Congresses. Dr Benno M Nigg provided leadership for the IOC Olympic Prize and acts as the chair o f the Selection C om m ittee for the IOC Olympic Prize. T h e first IOC World Congress was organised by Dr Charles Dillman in 1989 in C olorado Springs. The developm ent o f the IOC Olympic Prize took longer to arrange, since a sponsor had to b e found. The initial contact with Parke-Davis, a Warner-Lambert division, S P O R T S M E D IC IN E J U L Y 1 9 9 9 2 5 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) was established in 1992 following unsuccessful initial contacts and discussions with several other world- leading companies. After several meetings between representatives o f Parke-Davis (Mr Wayne Dickerson) and the IOC M edical Com mission (Drs Patrick Schamasch, Richard Nelson, Charles Dillman, and Benno M Nigg), an agreement between Parke-Da\is (Lodewijk de Vink, president and COO o f Warner- Lambert) and the IOC Medical Commission (Prince Alexandre de Merode) was signed and announced dur­ ing the 1994 Olympic Winter Games in Lilfehammer. Currently, Parke-Davis is the exclusive sponsor o f the IOC Olympic Prize and all other functions o f the IOC Medical Commission which relate to movement, exer­ cise and sport sciences (MESS). The IOC Olympic Prize is awarded each Olympic Game year. The IOC Olympic Prize is an exciting development for the field o f sciences related to movement, exercise and sport (MESS) and for anyone who loves and sup­ ports mobility and longevity. THE IOC OLYMPIC PRIZE The IOC Olympic Prize honours important findings resulting from outstanding basic an d /or applied research related to human movement, exercise and/or sport. These findings must represent a significant inno­ vation, contribute to the betterment o f humankind, and have significant impact upon science, health and/or society. The IOC Olympic Prize con­ sists o f • a gold medal • a diploma o f excellence • a cash award o f SUS 500 000 The IOC Olympic Prize is awarded for work in four areas o f science: medical, biological, physical, and psy­ chological. Examples o f research to be considered include: (a) the understanding o f the healthy develop­ ment o f the human body and its main components, (b) the effect o f exercise on health, wellness and qual­ ity o f life, (c) the prevention o f injuries in movement, exercise and sport, and (d) the improvement and optim isation o f physical perform ance through enhanced understanding of the functioning o f the human body in all age groups. The winner is announced during a banquet in New' York approximately 6 to 8 weeks before the start o f the Olympic Summer or Winter Games. The gold medal is awarded during the Opening Ceremony o f the IOC Session before the Games. EFFECTS OF THE IOC OLYMPIC PRIZE The IOC Olympic Prize was initially (for 1996 and 1998) USg 250 000, but will be USg 500 000 for the year 2000. This substantial sum, the public announce­ ment o f the winner, and the award ceremony have sub­ stantial influence on the development of sciences dealing with movement, exercise and sport. Specifically, the IOC Olympic Prize: • improves the recognition for research on movement, exercise and sport • attracts established scientists to study these impor­ tant questions. • attracts brilliant young scientists into the study of movement and mobility. THE FIRST WINNERS The first prize, the 1996 IOC Olympic Prize, was awarded to: Dr J erem y N Morris and Dr Ralph S Paffenbarger Jr for their pioneering studies demonstrating how' exer­ cise reduces the risk o f heart disease. The research findings of Drs Morris and Paffenbarger changed the practice o f medicine and inspired the fitness revolu­ tion. The ground-breaking work o f these two leading epidemiologists has brought respect to research in the area o f health and fitness and inspired additional stud­ ies that have contributed enormously to establishing the relationship between physical activity and a reduc­ tion in the incidence o f coronary heart disease. Dr Morris was the first epidemiologist to offer scien­ tific support for the (at that time revolutionary) hypothesis that regular physical activity reduces the risk o f coronary' heart disease. Dr Paffenbarger was the first to study risk factors and life habits o f male graduates o f the University o f 1 Pennsylvania and Harvard University. He found that physical activity is a relevant factor in reducing the risk o f hypertension, non-insulin-dependent diabetes, some forms o f cancer, and premature death in general. The winners of the first IOC Olympic Prize, Drs Morris (left) and Paffenbarger (middle), with the winner of the second lOC-Olymplc Prize, Dr Woo (right). /o C o i y ^ c 2 6 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) The second prize, the 1998 IOC Olympic Prize, was awarded to: Savio LY Woo, PhD for his pioneering contributions to the understanding o f the properties o f connective tissues, the effects of exercise on tissue properties, and the possibilities for repair o f injured tissues. His work had a significant effect on basic research in this area as well as on the medical treatment o f ligament injuries, injuries that occur frequently in physical activities. A large number of individuals benefited directly from his research. A more detailed description o f the research work of these prize winners will be presented in one o f the next publications on the IOC Olympic Prize. T I M E T A B L E FOR TI1E IOC OLYM PIC PRIZE 2000 1 • December 1998 Meeting: Selection Committee in Lausanne. Finalising the format for nominations for the 2000 Prize. • March to Jime 1999 Information on nomination procedure published in scientific journals and newsletters. • September 1, 1999 Deadline for submission o f nomination packages to the headquarters o f the IOC Medical Conunission in Lausanne, Switzerland. • A u g u s t 2 0 0 0 Announcement o f winner during a special IOC Olympic Prize Function in New York. • September 2000 Medal Ceremony during the Opening Ceremony of the IOC Session in Sydnev, Australia. A D D IT IO N A L IN F O R M A T IO N Additional information concerning the IOC Olympic Prize can be found at the IOC Olympic Prize web site http://www.olympic.org/FAM ILY/ioc/medical/ olyprize l_e.html The Parke-Davis IOC Olympic Prize web site http://www.parke-davis.com/version_4/iocprize.html Further information can be received from: Benno M Nigg, DSc (Nat) Chair: Selection Committee, IOC Olympic Prize: Human Performance Laboratory The University o f Calgary Calgary, Alberta, Canada, T2N 1N4 Fax: 403-284-3553 E-mail: uheinz@ucalgary.ca IOC World Congress on Sport Sciences bv Charles J Dillman In 1988, the IOC M edical C om m ission d ecid ed to develop a series o f World Congresses on the scientific aspects o f sport that would further the growth o f this young scientific field. The First Congress was con d u ct­ ed in C olorado Springs in 1989, with subsequent p ro­ gram m es being organised in Barcelona (2 ) 1991, Atlanta (3) 1995, and M onaco (4) 1997. T he purpose o f the World Congress is to p rorid e a forum for leading scientists to exchange ideas about c i u T e n t research and to dissem inate new information about human perform ance to practitioners who are involved in developing athletes for international and Olympic com petitions. T he field of sport scien ces is segm ented into four subdisciplines, namely m edical, biological, physical and psychological sciences. T he next program m e, the Fifth IOC World Congress for the Science o f Movement, Exercise, and Sport, will be held in Sydney, Australia, from October 31 to November 5 in 1999. FIFTH IOC WORLD CONGRESS KNI>0*KI> B\ © P A R K E - D A V I S FIFTH IOC WORLD CONGRESS FOR THE SCIENCE OF MOVEMENT, EXERCISE, AND SPORT Endowed by Parke-Davis In conjunction with the Australian Conference of Science and Medicine in Sport 31 October - 5 November, 1999 Sydney Convention and Exhibition Centre, Sydney, Australia The IOC World Congress will combine the very best in science and medicine related to move­ ment, exercise and sport with the warmth and hospitality of Sydney — the host city of the 2000 Olympic and Paralympic Games. SPORTS MEDICINE JULY 1999 2 7 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) http://www.olympic.org/FAMILY/ioc/medical/ http://www.parke-davis.com/version_4/iocprize.html mailto:uheinz@ucalgary.ca The International Olympic Committee’s Medical Commission, the Sydney Organising Committee for the Olympic Games, and Sports Medicine Australia invite you to attend this spe­ cial Congress. Under the theme of ‘The Science and Medicine of Skilled Performance: Optimisation, Injury Prevention and Rehabilitation’, the world’s lead­ ing exercise and sport scientists and practitioners wall present their research — theoretical, applied and clinical — in a spectacular setting, namely the Sydney Convention Centre in beautiful Darling Harbour. Further highlights include the Opening Ceremony/Cocktail Party, Congress Dinner, Olympic Venue Tour, Sports Afternoon, and optional tours in and around Sydney. The Congress also offers a unique opportunity for sport and team healthcare professionals to meet representatives of SOCOG’s Medical and Doping Control Programmes to discuss planning for the Sydney 2000 Olympic and Paralympic Games. PROGRAMME HIGHLIGHTS Professor Savio Woo, PhD, from the Muscle Research Centre, University of Pittsburgh and wanner of the prestigious IOC Olympic Prize, wall give the opening presentation at the Congress. Keynote and Invited Speakers Professor Ed Coyle, USA Professor Bente Pedersen, Denmark Professor Cy Frank, Canada Professor Richard Lieber, USA Professor Joachim Mester, Germany Dr Jos de Koning, Netherlands Professor Simon Gandevia, Australia Professor Lew Hardy, UK Symposia Articular cartilage repair Keeping people physically active (1): Motivation through the lifespan Strategies to enhance fatigue resistance Research on muscle mechanics Ethics in sport Women in the Olympic Games Clinical and physiotherapy symposia Workshops Application of muscle mechanics in sport Keeping people physically active (2): Public health programmes Supplements to enhance performance: The evi­ dence? Biomechanics feedback for the elite athlete Workshops in sports medicine, sports physiother­ apy, sports podiatry and sports dietetics. Free Papers Oral, video and poster presentations in the disci­ plines of medical, biological, physical & behav­ ioural sport sciences Parke-Davis Symposium The Cardiovascular Dysmetabolic Syndrome: Diabetes/Insulin Resistance, Hypertension and Hyperlipidaemia taking place on Sunday 31 October will be of particular interest to internists and general practitioners. Important Dates Abstract application forms & abstracts due by 15 May 1999 Early Bird registration closes 30 June 1999 Accommodation Bookings by 17 Sept 1999 Further Information on Congress Congress Secretariat, Sports Medicine Australia PO Box 897 Belconnen ACT 2616 Australia Ph.- +6126251 6944 Fax: +6126253 1489 E-mail: smanat@sma.org.au Visit the official Sydney 2000 Olympic Games web site: http: / / www. Sydney. Olympic. or g / 28 SPORTS MEDICINE JULY 1999 R ep ro du ce d by S ab in et G at ew ay u nd er li ce nc e gr an te d by th e P ub lis he r (d at ed 2 01 2. ) mailto:smanat@sma.org.au