pathophysiology of exercise in the sick child

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01959131/86/1 803-0276$2.00/0MEDICINE AND SCIENCE IN SPORTS AND EXERCISECopyright


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PATHOPHYSIOLOGY OF EXERCISE IN THE SICK CHILD

Aortic StenosisCardiomyopathyDetrainingHypohydralion . severePulmonary Stenos isTetralogy of FallotVent. Septal Defect

AnemiaAsthma severeCystic FibrosisHemoglobinopathiesObesity extremeAlghttoLeft ShuntScoliosis severe

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Figure 1-Maximal aerobic power ('VO .... in pediatricdisease. Listed are diseases that affect a specific component of the Fick equation. Reproduced with permission from Bar-Or (4).

{3 blockersCong. Compl. Heart Block DetrainingMalnutrition severeMuscle AtrophyMuscle DystrophySpina Bllida23 DPG Deficiency

in pulmonary stenosis (41, 56) and tetralogy of Fallot(14, 46, 48, 54), cannot sufficiently raise his strokevolume (SV) during exercise. The degree of such deficiency is proportional to the degree of valvular stenosis,as shown in Figure 2. In the presence of an interventricular shunt, as in ventricular septal defect (58) ortetralogy of Fallot (11, 25, 54), some of the ejectedblood goes through the shunt rather than "forward" tothe aorta or the pulmonary artery. The result is asomewhat diminished effective SV. The degree of reduction in maximal aerobic power in ventricular septaldefect depends on the extent of the shunt and on thepresence or absence of pulmonary hypertension. Theresult is that patients with this lesion may have maximalaerobic power that ranges from normal to very low (24,34). A low SV will result also from a reduction invenous return, as in hypohydration, or from low contractility of the myocardium, as in cardiomyopathy ( 1)or in detraining. There are very few data available aboutthe hemodynamic response to exercise of children withthese conditions.

Low maximal heart rate. A low maximal cardiacoutput can also result from an inability to reach theage-appropriate maximal HR. A low maximal HR, asa primary deficiency, occurs very seldom in children.One documented example is congenital complete heart block (CCHB), in which resting, submaximal, and maximal ventricular HR lag behind the atrial HR (Fig. 3)(32, 38, 43, 53, 65, 67, 72). An above normal SVpartially compensates for the low ventricular HR at restand during submaximal exercise (25, 53, 65) but, evenso, cardiac output is usually low in such patients (65,72). The child with CCHB may compensate for a lowcardiac output by an increase in peripheral 02 extraction and therefore in Ca02- Cv02 (65). This is usefulin submaximal exercise, but there are no data whichshow that maximal Ca02 - Cv02 is high in these

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Figure 2-Stroke index at rest and during moderate supine exerciseas a function of cross-sectional area of the pulmonary valve in 64patients (adapted from Ref. 56). Values for healthy children are takenfrom Cumming (23). Mean + 1 SD.patients. Due to the wide range of maximal HR andcompensatory hemodynamic changes in this disease,the maximal aerobic power in CCHB ranges fromnormal to extremely low (32, 37, 43, 67, 69).Some medications are known to lower HR. An example are the ,B-blockers. The administration of 10 mgpropranolol induced a reduction of up to 30 beat/minin maximal HR ofhealthy 11-yr-old girls and boys (66).

Low arterial 02 content. Insufficient oxygenation ofthe blood can result from a respiratory, circulatory, orhematological deficiency. The two most common pediatric respiratory conditions that may be accompaniedby low Ca02 during exercise are severe bronchialasthma and cystic fibrosis. While most children withasthma have a normal Pa02, those who respond toexercise with marked bronchoconstriction may have asubnormal arterial 0 2 pressure and mild 0 2 desaturation (47). In cystic fibrosis both anatomical and "physiological" dead space may be high (18, 31, 33). Furthermore, lung diffusion in these patients may notsufficiently rise during exercise (33, 74). The end resultis a disruption in gas exchange and 02 desaturation,


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278

Figure 3-Ventricular and atrial heart rate in congenitalcomplete heart block at rest, submaximal, and maximalexercise. Individual values of 7- to 15-yr-old patients. Datafrom Thoren et al. (67). Reproduced with permission fromBar-Or (4).

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especially during maximal exercise (18, 2 I) . A hyperbolic relationship has been described between peakaerobic power and the degree of 02 desaturation (21 ).Severe obesity (28, 73), advanced kyphoscoliosis (10,12, 59), and weakness of the respiratory muscles (e.g.,in muscular dystrophy) are sometimes accompanied bysubnormal alveolar ventilation and a ventilation-perfusion abnormality which may result in 02 desaturationduring intense exercise.A right-to-left shunt, as in tetralogy of Fallot, maycause 02 desaturation, cyanosis, and a reduction inmaximal aerobic power (32, 63, 64).Anemia, of any origin, will result in a reduced 0 2-carrying capacity. One means of compensation is anincrease in HR and in cardiac output. While such amechanism is adequate at rest and at low intensities ofexercise, it may not be sufficient at intense activitieswhen cardiac output has reached its maximum. As aresult, children with anemia have low maximal aerobicpower and exercise tolerance, in proportion to theseverity of the anemia (20, 57, 68, 71 ). As shown inFigure 4, the maximal 0 2 uptake of a child with 150g.l- 1 hemoglobin concentration and a maximal cardiacoutput of 121 min- 1 is about 1.8 1min-1, as comparedwith only 0.55 lmin- 1 in a child with the same maximal cardiac output but with 50 g.l-1 hemoglobin concentration. If maximal 02 uptake of an anemic child islower than that expected, one should look for additionalpathophysiological factors. Some anemias result fromhemoglobinopathies, such as in sickle-cell disease or inthalassemia. Maximal aerobic power in sickle cell dis-

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ease (2) and in sickle-cell trait (29) may be lower thanexpected from the hemoglobin concentration (61 ).High mixed-venous 02 content. Whenever 02 ex-traction from the exercising muscle is deficient or whenthe blood flow to the exercising muscle is low, mixedvenous 02 content will be high, and maximal aerobicpower will be low. This may occur when the skeletalmuscles are atrophied, as in spina bifida, other causesof paraplegia, poliomyelitis, spinal muscular atrophy,crippling arthritis, other causes of disuse atrophy, or inextreme malnutrition. It may also take place when themuscles are dystrophic, as in Duchenne muscular dystrophy. High mixed-venous 0 2 content may also resultfrom reduced activity of the oxidative enzymes, as indetraining, or when 0 2 release from the hemoglobin isreduced, as in 2,3-diphosphoglycerate deficiency. Sofar, no data are available on the mixed-venous 02content during maximal exercise in children with theabove diseases.

HIGH SUBMAXIMAL 0 2 COSTInability to sustain a certain task may result from ahigh metabolic cost of performing this task. In somediseases this is manifested by a high metabolic cost

during walking or running, but it can also occur duringarm cranking, during propelling of a wheelchair, orwhile performing other movements. Conditions inwhich 02 uptake during a standardized walking orcycling task has been found to be above normal include


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PATHOPHYSIOLOGY OF EXERCISE IN THE SICK CHILD3.0

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cerebral palsy (7, 8, 51, 55), the use of leg prosthesisfollowing amputation (3, 55), advanced scoliosis (49},other neuromuscular diseases (17, 35), and markedobesity (26, 27). In obesity, the high metabolic cost ofventilation (28, may also contribute to an overallhigh submaximal 0 2 uptake:Figure 5 is an example showing the high metaboliccost of cycling in cerebral palsy. It is apparent that,even if all three groups of subjects had a similar maximal aerobic power, a child with muscle spasticity wouldbe working at a much higher percentage of his maximalaerobic power than a healthy one.

LOW MUSCLE STRENGTHWhile for healthy children most play and sportsactivities do hot require the use of maximal muscleforce, children with neuromuscular disease are oftenlimited in their activities by their low muscle strength.This occurs in such conditions as juvenile rheumatoidarthritis (often accompanied by contractures and muscle atrophy), cerebral palsy of the spastic type, musculardystrophies, spinal muscular atrophy, or limb paresis.A documented example is that of children withDuchenne muscular dystrophy (30, 39, 60). Such children first lose the strength of their proximal limb muscles and, later on, that of the distal ones. By the age of7-8 yr the strength of most muscles is below the 5th

percentile of healthy children (39). Such a progressivestrength loss is the main reason for the eventual inabilityof these patients to walk. More studies are needed onthe "natural history" of strength loss in other pediatricneuromuscular diseases.

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Figure 4 ~ M a x i m a l 02 uptake as a function of bloodhemoglobin concentration and maximal cardiac output(Qnwc). Regression lines were constructed based on thefollowing assumptions: I g hemoglobin carries 1.36 ml 0 2;arterial hemoglobin is 90% saturated at maximal exercise;0 2 extraction at maximal exercise is 80% of arterial 0 2content. Reproduced with permission from Bar-Or (4).

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280been tested to evaluate their peak power output andmuscle endurance (mean power output) in the 30-scycling or arm cranking Wingate anaerobic test (e.g. ,4). Diseases that have been evaluated so far includeDuchenne muscular dystrophy, Becker's muscular dystrophy, spastic and athetotic cerebral palsy, and disuseatrophy. Both the peak power and mean power outputseem to be distinctly subnormal in these conditions (4,6).Figure 6 is a case in point, comparing the meanpower output of patients with cerebral palsy or withDuchenne muscular dystrophy to norms derived forhealthy controls. Whether expressed in absolute powerunits or corrected for body weight (as in Fig. 6) theperformance of most of these patients is 2 to 4 standarddeviations below the expected mean. Particularly affected are those boys with Duchenne muscular dystrophy. To determine whether such low values reflect ageneral deficiency in fitness (i.e., in both aerobic and

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Figure 6-Anaerobic performance in pediatric neuromuscular disease.Eleven boys with cerebral palsy (e ) and three with Duchenne muscular dystrophy (.t.) performed the Wingate anaerobic leg cycling test.Norms for nonathletic healthy boys arc from Bar-Or (4). Data fromthe author's laboratory.REFERENCES

I. ALPERT, B.S., K. R. Bi.ooM, C. J. NEWTII, and P. M. OLLEY.Hemodynamic responses to supine exercise in children with leftsided cardiac disease. Am. J. Cardiol. 45:1025-1031, 1980.2. ALI'ERT, B.S., P. A. GILMAN, W. B. STRONG, M. F. ELLISON, M.D. MILLER, J. MCFARLANE, and T. HAYASIIIDERA. Hemodynamic and ECG responses to exercise in children with sickle cellanemia. Am . J. Dis. Child. 135 :362-366, 1981.3. BARD, G. and H. J. RALTSON. Measurement of energy expenditure during ambulation, with special reference to evaluation of

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE

anaerobic performance) or a specific deficiency in anaerobic performance, a "metabolic index" was calculated for each child. This index is the. ratio of peakanaerobic power to peak aerobic power, the latter beingdetermined in a progressive, continuous protocol ofsome 6 to 10 min duration. This index in healthychildren is about 2.5, and it often exceeds 3.0. Preliminary data for children with advanced neuromusculardisease suggest that their metabolic index seldom exceeds 2.0 (6). The implication is that, even though suchpatients have a low maximal aerobic power, their anaerobic power is even more affected.The only other attempt to assess the local muscleendurance of patients with muscular dystrophy wasreported by Hosking et al. (39). The authors measuredthe time that these children could hold their head orlegs at 45 from the floor while lying supine. Theperformance of the patients was markedly lower thanthat of heaithy controls. More information is neededon the anaerobic characteristics of children with neuromuscular disease. It is of particular importance tofind out whether this component of fitness is trainablein such children.In conclusion, this paper has attempted to analyzesome specific pathophysiological factors that limit theexercising ability of sick children. Although each component of physical fitness has been discussed separately,it is seldom that a single pathophysiological factor limitsthe exercise capability of the sick child. In obesity, forexample, pulmonary, metabolic, thermoregulatory, andmechanical deficiencies can all interact (28). Someconditions may be just one manifestation of a morecomplex disease. Anemia, for example, may accompany other nutritional and metabolic diseases which,in themselves, may limit the activity and exercise capacity of the child. This can occur in chronic renalfailure which, due to multiple metabolic aberrations,interferes with appetite, growth, and fitness (68).Much more research is needed to further understandthe specific processes that limit the exercise capacity ofsick children, the way these processes interact, the longrange response of the organism, and the ways in whichsurgery or other modes of therapy can modify them.Knowledge of such pathophysiological processes mayincrease the repertoire and sophistication of exercisetesting in pediatric laboratories. It may also serve as abasis for more rational exercise intervention programs.

assistivc devices. Arch. Pllys. Med. Rehab. 40:415-420, 1959.4. BAR-OR, 0. Pediatric Sports Medicine For the Practitioner: fromPhysiologic Principles to Clinical Applications. New York: Springer Verlag, 1983, pp. 1-37 6.5. BAn-On, 0. Exercise in pediatric assessment and diagnosis.Scand. J. Sports Sci. 7:35-39, 1985.6. BAR-OR, 0 . Exercise performance of the sick child. In: Child andSport, J. Borms (Ed .). Champaign, IL: Hurn an Kinetics, in press,1986.


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PATHOPHYSIOLOGY OF EXERCISE IN THE SICK CHILD7. BAR-OR, 0. , 0. INBAR, and R. SPIRA. Physiological effects of asports rehabilitation program on cerebral palsied and post-poliomyelitic adolescents. Med. Sci. Sports 8:157-161, 1976.8. BERG, K. and J . BJURE. Methods for evaluation of the physicalworking capacity of school children with cerebral palsy. ActaPaediat. Scand. (Supp/.) 204:15-26, 1970.9. BERGMAN, A. B. and S. 1. STAMM. The morbidity of cardiacnondisease in school children. N. Engl. J. Med. 276:1008-1013,

1967.10. BERGOFSKY, E. H., G. M. TURINO, and A. P. FISHMAN. Cardiorespiratory failure in kyphoscoliosis. Medicin e38:263-317, 1959.II . BJARKE, B. Oxygen uptake and cardiac output during submaximal and maximal exercise in adult subjects with totally correctedtetralogyofFallot.ActaMed. Scand. 197:177-186, 1975.12 . BJURE, J., Q. GRIM BY, and A. NACHEMSON. The effect of physicaltraining in girls with idiopathic scoliosis. Acta Orthop. Scand.

40:325-333, 1969.13. BRADFIELD, R. B., J. PAULOS, and L. GROSSMAN. Energy expenditure and heart rate of obese high school girls. Am. J. Clin. Nlllr .24:1482-1488, 1971.14. BRISTOW, J. D., F. E. KLOSTER, M. H. LEES, V. D. MENASHE, H.E. GRISWOLD, and A. STARR. Serial cardiac catheterization andexercise hemodynamics after correction of tetralogy of Fallot.Circulation 41: 1057-1066, 1970.15. BULLEN, B. A., R. B. REED, and J. MAYER. Physical activity ofobese and nonobese adolescent girls appraised by motion picturesampling. Am. J. Clin. Nlllr. 14:211-223, 1964.16. CAMPBELL, M. Congenital complete heart block. Br. Heart. J.5:15-18, 1943.17. CARROLL, J . E., J. M. HAGBERG, G. H. BROOKE, and J. B.SHUMATE . Bicycle ergometry and gas exchange measurements inneuromuscular diseases. Arch Neural. 36:457-461, 1979.18. CERNY, F. J., T. P. PULLANO, and G. J. A. CROPP. Cardiorespiratory adaptations to exercise in cystic fibrosis. Am. Rev . Respir.Dis. 126:217-220, 1982.19. CORBIN, C. B. and P. PLETCHER. Diet and physical activitypatterns of obese and nonobese elementary school children. Res.Q. Exerc. Sport 39 :922-928 , 1968.

20. COVITZ, W., C. EUBIG , I. C. BALFOUR, R. JERATH, B.S. ALPERT,W. B. STRONG, and R. H. DURANT (technical assistance, B. G.Hadden). Exercise-induced cardiac dysfunction in sickle cell anemia. Am. J. Cardia/. 51:570-575, 1983.21. CROPP,G . J., T. P. PULLANO,F.J . CERNY, and I. T. NATHANSON.Exercise tolerance and cardiorespiratory adjustments at peakwork capacity in cystic fibrosis. Am . Rev . Respir. Dis. 126:211-216, 1982.22. CuETo, L. and J. H. MOLLER. Haemodynamics of exercise inchildren with isolated aortic valvular disease. Br. Heart J. 35:93-98, 1973.23 . CUMMING, G. R. Hemodynamics of supine bicycle exercise in"normal" children. Am. Heart J. 93:617-622, 1977.24. CUMMING, G. Maximal exercise capacity of children with heartdefects. Am. J. Cardia/. 42:613-619 , 1978.25 . CUMMING, G. Ma ximal supine exercise hemodynamics after openheart surgery for Fallot tetralogy. Br. Heart J. 41 :683-691, 1979.26. DAVIES, C. T. M. , S. GODFREY, M. LIGHT, A. J. SARGEANT, andE. ZEIDJFARD. Cardiopulmonary responses to exercise in obesegirls and young women. J. App/. Physiol. 38:373-376, 1975.27 . DEMPSEY, J. A., W. REDDAN , B. BULKE, and J. RANKIN . Workcapacity determinants and physiologic cost of weight-supportedwork in obesity. J. App/. Physio/. 2 1: 1815-1820, 1966.28. FAREBROTJJER, M. J. B. Respiratory function and cardiorespiratory response to exercise in obesity: a review article. Br. J. Dis.Ches/73:211-229, 1979.29. FLOOD, N. L., B.S. ALPERT, W. B. STRONG, J . R. BLAIR, J. B.WALPERT, and A. L. LEVY. Exercise in children with sickle celltrait (Abstract). Med. Sci. Sports Exerc. 14:123, 1982.30. FOWLER, W. M. , JR . and G. W. GARDNER. Quantitative strengthmeasurements in muscular dystrophy. Arch. Phys. Med. Rehab.48:629-644, 1967.31. GERMANN, K., D. ORENSTEIN, and J. HOROWITZ . Changes inoxygenation during exercise in cystic fibrosis (Abstract). Med.Sci. Sports Exerc. 12 :105, 1980.32 . GoDFREY, S. Exercise Testing in Children:Applications in Health

281and Disease. Philadelphia: W. B. Saunders, 1974, pp. 1-168.33. GoDFREY, S. and M. MEARNS. Pulmonary function and responseto exercise in cystic fibrosis. Arch. Dis. Child. 46: 144-151, 1971.34. GOLDBERG, S. J., F. MENDES, and R. HURWITZ. Maximal exercisecapability of children as a function of specific cardiac defects.Am. J. Cardia/. 23:349-353, 1969.35. GORDON, E. E. Energy cost of activity in health and disease.AMA Arch . Int. Med. 101:702-713, 1958.

36. GRAFF-LONNEVIG, V. Cardiorespiratory function, aerobic capacity and effect ofphysical activity in asthmatic boys (M. D. Thesis).Stockholm: Karolinska Institute, 1978.37. HANNE-PAPARO, N., Y . DRORY, and J. J. KELLERMANN. Complete heart block and physical performance. Int . J. Sports Med.3:9-13, 1983.38. HOLMGREN , A., P. KARLBERG, and B. PERNOW. Circulatoryadaptation at rest and during muscular work in patients withcomplete heart block. Acta Med. Scand. 164:119-130, 1959.39. HOSKING, G. P., U. S. BHAT, V. DUBOWITZ, and R. H. T.EDWARDS. Measurements of muscle strength and performancein children with normal and diseased muscle. Arch. Dis. Child.51:957-963, 1976.40. HossACK, K. F. and G. H. NEILSON. Exercise testing in congenitalaortic stenosis. Aust. N.Z. J. Med. 9:169-173, 1979.41. HownT, G. Hemodynamic effects of exercise in pulmonarystenosis. Br. Heart J. 28:152-160, 1966.42. HYDE, J . S. and C. L. SWARTS, Effect of an exercise program onthe perennially asthmatic child. Am. J. Dis. Child. 116:383-396,1968.43. IKKOS, D. and J. S. HANSON. Response to exercise in congenitalcomplete atrioventricular block. Circulation 22:583-590, 1960.44. JACKSON, R. L. and H. G. KELLY. A study of physical activity injuvenile diabetic patients. J. Pediatr. 33:155-166, 1948.45. JOHNSON, M. L., B. S. BURKE, and J. MAYER. Relative importance of inactivity and overeating in the energy balance of obesehigh school girls. Am. J. Clin. Nutr. 4:37-44, 1956.46. JORANSEN, J. A., R. V. LUCAS, JR., and J. H. MOLLER. Postoperative haemodynamics in tetralogy of Fallot. A study of 132children. Br. Heart J. 41:33-39, 1979.47. KATZ, R. M. , S.C. SIEGEL, and G. S. RACHELEFSKY . Blood gasin exercise-induced bronchospasm: a review. Pediatrics (Suppl.)56:880-882, 1975.48. LAMBERT, J., R. J. FERGUSON, A. GERVAIS, and G. GILBERT.Exercise capacity, residual abnormalities and activity habits following total correction for tetralogy ofFallot. Cardiology 66: 120-131, 1980.49. LINDH, M. Energy expenditure during walking in patients withscoliosis. The effect ofsurgical correction. Spine 3: 122-134, 1978.50 . LUDVIGSSON, J. Physical exercise in relation to degree of metabolic control in juvenile diabetics. Acta Paediatr. Scand. (Suppl.)283:45-49, 1980.51. LUNDBERG , A. Mechanical efficiency in bicycle ergometer workof young adults with cerebral palsy . Dev . Med. Child. Neural.17 :434-439 , 1975.52. LUNDBERG , A. Oxygen consumption in relation to work load instudents with cerebral palsy. J. Appl. Physio/. 40:873-875, 1976.53. MocELLJN, R. and C. BASTANIER. Functional studies in childrenand adolescents with congenital complete heart block (in German). Z. Kardiol. 66:298-302, 1977.54. MOCELLIN, R., C. BASTANIER, W. HOFACKER, and K. BOHL

MEYER. Exercise performance in children and adolescents aftersurgical repair of tetralogy of Fallot. Eur. J. Cardia/. 4:367-374 ,1976.55. MoLBECH, S. Energy cost in level walking in subjects with anabnormal gait. In: Physical Activity in Health and Disease, K.Evang and K. L. Andersen (Eds .). Oslo: Universitets Forlaget,1966, p. 146.56. MOLLER, J. H., S. RAO, and R. V. LUCAS. Exercise hemodynamics of pulmonary valvular stenosis (study of 64 children).Circulation46:1018-1026, 1972.57. PARSONS, C. G. and F. H. WRIGHT. Circulatory function in theanemias of children. I. Effect of anemia on exercise toleranceand vital capacity. Am. J. Dis . Child. 57:15-28 , 1939.58 . PETER, C. A., K. BOWYER, and R. H. JONES. Radionuclideanalysis of right and left ventricular response to exercise in


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282patients with atrial and ventricular septal defects. Am. Heart J.105:428-435, 1983.59. SHNEERSON, J. M. The cardiorespiratory response to exercise inthoracic scoliosis. Thorax 33:457-463, I978.60. SQCKOLOV, R., B. IRWIN, R. H. DRESSENDORFER, and E. M.BEMAUER. Exercise perforrn.ance in 6- to I !-year-old boys withDuchenne muscular dystrophy. Arch. Pliys. Med. Rehab. 58:I95 -201, 1977.61. SPROULE, B. J., E. R. HALDEN, and W. F. MILLER. A study ofcardiopulmonary alterations i11 patients with sickle cell diseaseand its variants. J. Clin. Invest. 37:486-495, 1958.62. STERKY, G. Physical work capacity in diabetic school-children.Acta Paediatr. 52:1-10, 1963.63. STRIEDER, D. J., K. AZIZ, A. G. ZAVER, and K. E. FELLOWS.Exercise tolerance after repair of tetralogy ofFallot. Ann. Thorac.Surg. 19:397-405, 1975.64. TAYLOR, M. R. H. The response to exercise of chilqren withcongenital heart disease. Ph.D. Thesis, University of London,1972.65. TAYLOR, M. R. H. and S. GoDFREY. Exercise studies in congenitalheart block. Br. Heart J. 34:930-935, 1972.66. THOREN, C. Effects of ,8-adrenergic blockade on heart rate andblood lactate in children during maximal and submaximal exercise. Acta. Pm!diatr. Scand. (Suppl.) I77: 123-125, 1967.

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE67. THOREN, C., P. HERIN, and J. VAVRA. Studies of submaximaland maximal exercise in congenital complete heart block. ActaPaediatr. Belg. (Suppl.) 28:132-143, 1974.68. ULMER, H. E., H. GRIENER, H. W. SCHULER, and K. SCHARER.Cardiovascular impairment and physical working capacity inchildren with chronic renal failure. Acta Paediatr. Scand. 67:43-48, 1978.69. VARTIA, A. and I. VALIMAKI. The effect of some chronic cardiacarrhythmias on the physical working capacity of children. ActaPaediatr, Scand. 5 ~ : 5 5 5 - 5 5 6 , 1969.70. VERMA, S. and J. S. HYDE. Physical education programs andexercise-induced asthma. Clin. Pediatr. 15:697-699, 1976.7I. VITERI, F. E. and B. TOR UN. Anaemia and physical workingcapacity. Clin. Haematol. 3:699-626, 1974.72. WATSON, G., D. FREED, and J. STRIEDER. Cardiac output duringexercise in children with idiopathic complete heart block. In:Frontiers of Activity and Child Health, H. Lavallee and R. J.Shephard (E

pathophysiology of exercise in the sick child

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