Guest Editorial

An apparent anomaly is that a medical curriculum can With such advances it is perhaps appropriate that the be considered complete even if it pays only passing review section o f the first issue o f our re-launched Jour­ reference to the largest organ in the human body, skele­ nal should focus attention on skeletal muscle and ex­ tal muscle which can com prise up to 25 kg in the aver­ ercise. The aim has been to review various aspects of age male. Skeletal muscle, it would seem, lacks the skeletal muscle function that will be of interest to the romantic charisma of that far more puny (less than different disciplines that comprise the membership of 500g) organ, the heart. Yet the established, indeed re­ the South African Sports Medicine Association. vered specialities of cardiology and cardiac surgery and In the article devoted to the basic sciences, Dr a thriving industry in cardiovascular medicines attest Kathryn Myburgh PhD, who has recently completed her to the far greater importance humans and the medical post-doctoral studies in the muscle research laborato­ profession attach to their hearts. Physiotherapists, neu­ ry o f Dr Roger Cooke in San Francisco, carefully reviews rologists and specialists in physical medicine are the historical development, still less than 50 years old, perhaps the sole medical practitioners for whom dis­ o f the biochemical and structural studies that have laid orders of skeletal muscles are of more than passing in­ the foundation of the modern understanding of how terest. muscles contract. She next discusses the different con­ But if much of medicine has yet to embrace the sig­ tractile properties including force production and resis­ nificance of such a weighty organ, powerful forces at tance to fatigue of the separate muscle fibres and ex­ its fringes will ultimately influence that indifference. In­ plains how the different (iso)forms o f the contractile pro­ deed the single most important factor influencing the teins can explain some of these functional differences Cinderella status of skeletal muscle in the medical cur­ She concludes that training and other interventions riculum has been the growth of the exercise sciences. alter not only muscle fibre size, their mitochondrial en­

) It is perhaps obvious that those who would study the zym e content and their substrate utilization patterns but .

2 human in motion should begin to champion the study also the mix of the different contractile protein isoforms 1

0 of the organ of movement. comprising the different fibres. She wonders whether 2

d But even amongst the exercise scientists there are sporting success might be linked to specific molecular e t still those who are reluctant to believe the importance combinations in the different skeletal muscle fibres. In­ a d o f the skeletal muscles in exercise and sport. So a popu­ deed one must ask whether one specific combination (

r lar view is that exercise performance especially during of skeletal muscle contractile protein isoforms explains e h the success of the sprinters of West African origin and s high intensity exercise of short duration is limited by i l the capacity of the heart to provide an adequate oxy­ another, different combination the exceptional fatigue b u gen supply to the large muscle mass that is activated resistance of the East African distance runners? Clear­ P

e during this type o f exercise. If this is true, the main e f­ ly if we are to honour our continent and its peoples, h t

fect of physical training we are led to believe must be those questions must be tackled and answered by Afri­ y

b to develop so-called “cardiovascular fitness” . Yet there can scientists. Perhaps Dr Myburgh’s article will have

d are solid arguments that question the scientific validi­ served its purpose if it were to encourage one young e t ty of the pioneering studies on which this concept is scientist to chose a career that will address these ques­ n a

r based.1 tions. g Furthermore the factor that best identifies success­

e The dynamic disorders o f skeletal muscle provide an c ful endurance athletes is the ability specifically o f their n intriguing insight into the interface between the basic e c skeletal muscle to resist the development o f fatigue dur­ and the clinical sciences. These extremely rare condi­ i l ing prolonged exercise.2 In these athletes it is their tions which produce symptoms only during exercise are r e

d muscles, not their hearts, that determine their success. of interest to clinicians who must consider them in the n Then perhaps most challenging is the new paradigm differential diagnosis of conditions causing exercise- u

y which suggests that the exercise tolerance of persons related symptoms. For the basic scientist, patients with a with advanced heart disease is limited by an associat­ these conditions provide a unique model for the study w e t ed myopathy (of chronic disease), rather than by the of the biochemical changes causing (premature) fatigue a severely impaired function of their diseased hearts.3 during exercise. The surprising finding is that fatigue G t As a result, exercise training which improves skeletal in patients with M cArdle’s syndrome occurs, as expect­ e n i muscle function, can enhance exercise capacity and re­ ed, without changes in blood lactate levels or blood pH b

a duce exercise-related symptoms even in persons with but, m ore interestingly, without a large reduction in S advanced heart disease, even heart failure.4 muscle ATP concentrations y b d e c u d o r

p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 1 e R GUEST EDITORIAL

One explanation for this finding is that skeletal mus­ misconception in the general sporting population. cle function during exercise is regulated to prevent a Rather DOMS is due to tissue damage from which there reduction in muscle ATP content sufficiently large to is a delayed recovery; damage is especially likely after produce muscle rigor. This postulate holds that under eccentric exercise, a finding well-known to runners in any condition in which the rate o f muscle A TP produc­ the “down” Comrades Marathon. Each step on the long tion is approaching some maximum value, the rate of downhill section from Kloof to the finish in Durban muscle A TP use is reduced by regulatory processes that places a large eccentric load on the runner’s quadriceps reduce the force and frequency o f muscle fibre contrac­ muscles. And the results are very apparent the follow­ tion (thereby reducing the rate o f ATP use). Thus in this ing day. Readers of this article will now be able to give model, fatigue of skeletal muscle during exercise is con­ a detailed scientific explanation to help their runners ceived as a regulatory process which links skeletal mus­ through their post-race misery. cle contractile function to the rate of ATP production Practical information provided by these authros is (perhaps through changes in the levels of metabolites that neither anti-inflammatory medications nor rest of ATP breakdown including Pi and ADP) specifically make any real difference to the rate of recovery from to prevent the development of muscle rigor. DOMS. But training reduces the amount of muscle stiff­ Another interesting finding is that patients with Mc- ness symptoms during a subsequent bout of similar ex­ Ardle’s syndrome exhibit an excessive rise in cardiac ercise. This effect may last for weeks to months. output, muscle blood flow and ventilation during exer­ The wish of the authors is that we have been able cise. This is because of a large fall in peripheral vascu­ to convey some of the excitement and enthusiasm we lar resistance caused by excessive vasodilation in the feel in our studies of skeletal muscle in active persons active skeletal muscles. Metabolic interventions that and the relevance that such studies have for the exer­ reduce muscle ADP and Pi concentrations during exer­ cise sciences and for clinical sports medicine. cise reduce the vasodilation, the skeletal muscle blood Lastly we would hope that, perhaps, we have been flow and ventilation. Interestingly the metabolic disord­ able to convince you that, in exercise and sport, the )

. er common to all forms of muscle disease is that mus­ heart of the matter is skeletal msucle. 2

1 cle ADP and Pi levels rise more rapidly than normal 0

2 during exercise; conversely highly trained muscle is able

d to resist this change until very high intensities of exer­ REFERENCES e t

a cise are reached. 1. Noakes TD. Implications o f exercise for prediction of athletic per­ d formance: A contemporary perspective. Med Sci Sports Exerc 20: ( Hence these studies provide intriguing evidence for

r 319-330, 1988.

e metabolic factors in skeletal muscle that influence the 2. Coetzer P, Noakes TD, Sanders B, Lambert Ml, Bosch Afi, Wig­ h

s cardiovascular and respiratory response to exercise and

i gins T and Dennis SC. Superior fatigue resistance of elite black South l the onset of subjective symptoms of fatigue. b African distance runners. J Appl Physiol 75: 1822-1827, 1993. u In the section dealing with clinical aspects of skele­ 3. Minotti JR, Christoph I, Oka R, Weiner MW, Wells L and Massie P BM. Impaired skeletal muscle function in patients with congestive e tal muscle, Dr Mike Lambert and Professor Steven Den­

h heart failure. Relationship to systemic exercise performance. J Clin t nis review perhaps the most common skeletal muscle Inuest 88: 2077-2082, 1991. y ailment in the exercising population, what is popular b 4. Sulliuan MJ, Higginbotham MB and Cobb FR. Exercise training in

d called muscle stiffness but which now enjoys the more patients with severe left uentricular dysfunction. Circulation 78: e t elaborate official title of Delayed Onset Muscle Sore­ 506-515, 1988. n a ness (DOMS). r g

In this review we learn that DOMS is not due to lac­ e c tate accumulation and retention in the previously ac­ Professor TIM NOAKES n e tive muscles. This is perhaps one of the commonest Guest Editor c i l r e d n u y a w e t a G t e n i b a S y b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 e 2 R THE SOUTH AFRICAN JOURNAL OF SPORTS MEDICINE

VOLUME 1 NUMBER 1 SEPTEMBER 1994

Guest Editor Prof T D Noakes CONTENTS University of Cape Town Editorial Board Dr M P Schwellrtus University of Cape Town Editorial 1 Dr M E Moolla TD Noakes Private Practitioner Durban Dr A Venter Private Practitioner Forthcoming Conferences 5 Bloemfontein Dr P de Jager Private Practitioner Pretoria The Dynamic Disorders of Skeletal Dr J Skouuno Private Practitioner Muscle Metabolism with Special Johannesburg Reference to exercise 6 Dr I Surve Private Practitioner TD Noakes Cape Town Dr P Schwartz Private Practitioner Port Elizabeth Muscle Proteins and the Contractile Prof G Strydom Potchefstroom University Properties of Muscle Fibres 11 Prof R Stretch KH Myburgh University of Fort Hare Mrs J Morton Private Physiotherapist Durban ) Delayed — Onset — Muscle — Soreness 18 .

2 Mr D Rehbock

1 Podiatrist Ml Lambert and SC Dennis 0

2 Johannesburg d e

t International Advisory Board a Lyle J Micheli

d Advances in Sports Equipment (

Associate Clinical Professor of r Technology that enhance performance 21 e Orthopaedic Surgery h s Boston, USA CR Kyle i l Chester R Kyle b

u Research Director, Sports P

Equipment Research Associates e h California, USA Die Effek van ’n Stresweerbaarheidsprogram t Prof HC Wildor Hollmann y

b President des Deutschen op Valskermspringers 30

d SportSrztebundes e D Scheepers en J Potgieter t Koln, West Germany n

a Howard J Green r

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NATIONAL ence Services, Division of University Extension, Univer­ August 22-26, 1994. SOUTHERN AFRICAN NUTRI­ sity of Victoria, PO Box 3030, Victoria BC, Canada V8W TION CONGRESS, ROYAL HOTEL, DURBAN. Focus 3N6. Fax: 604 721 8774. will be on diseases of over and undernutrition and life­ style, the role of nutrition in PHC, nutritions and food August 17-19, 1994. 7TH INTERNATIONAL CON­ policy, the sensory aspects of food and how it relates GRESS ON OBESITY — SATELLITE SYMPOSIUM, to the practice of nutrition and dietetics and the food QUEBEC, CANADA. Contact Exercise and Obesity Sat­ industry, nutrition education and sports nutrition. For ellite, c/-Angelo Tremblay, Physical Activity Sciences La­ further details please contact: Ms Carol Herbert; Con­ boratory, PEPS, University Laval, Ste-Foy, Quebec, Cana­ gress Co-ordinating Committee, PO Box 1209, Durban, da G1K 7P4. Tel: 418 656 7294. Fax: 418 656 3020. 4000. Fax: (031) 304-9652. August 29-03 Sept, 1994. THE CENTENNIAL OLYM­ August, 1994. 40TH SAOA ANNUAL CONGRESS, PIC CONGRESS, PARIS, FRANCE Contact Internation­ PRETORIA. Guest speakers: Dr Allan E Gross, Toronto, al O lym pic Comm ittee, Chateau de Vidy, CH-1007 Canada; Dr R W Bucholz, University o f Texas, USA. Con­ Lausanne, Switzerland. Tel: 41 21 621 6111. Fax- tact: Dr L van Wyk, 404 Muelmed Medical Centre, 577 41 21 621 6216. Pretorius Street, Arcadia, Pretoria, 0083. Tel: (012) 341-7573. September 10-16, 1994. 25TH F1MS WORLD CON­ GRESS OF SPORTS MEDICINE, ATHENS, GREECE. O ctober 3-4, 1994. W ORKSHOP O N COMPUTER- Abstracts should be submitted before January 31, 1994. BASED EXERCISE FOR TEACHING PHYSIOLOGY, For further details contact: Organization Idea, 24 Vou- AND: lis Street, 10563, Athens, Greece. Tel: 32 42 045, 32 42 529. Fax: 32 21 023. O ctober 5-7, 1994. 22ND A N N U A L CONGRESS O N THE PHYSIOLOGICAL SOCIETY OF SOUTHERN September 16-18, 1994. ORTHOPAEDIC MEDICINE. AFRICA, STELLENBOSCH. For further details please AN INTRODUCTORY COURSE ON DIAGNOSIS AND

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y November 27-30, 1994. THE SOUTHERN AFRICA April 5-7, 1995. CO N FER ENC E O N NUTRITION A N D b CARDIAC SOCIETY 19TH BIENNIAL CONGRESS. PHYSICAL ACTIVITY, TO OPTIMIZE PERFORMANCE d e AND WELL-BEING. The Ritz-Carlton, Buckhead, Atlan­ t Education Building, University of Cape Town. Contact: n Mrs Sally Elliott, Postgraduate Medical Centre, UCT ta, Georgia, USA. Contact: Ms Lili C Merritt, Internation­ a r al Life Science Institute, 1126 Sixteenth Street, NW,

g Med School, Observatory, 7925. Tel: (021) 406-6381.

e Fax: (021) 448-6263. Washington, DC 20036, USA. Tel: 202 659 0074. Fax: c

n 202 659 3859. e c i March 22-24, 1995. SIXTH SOUTH AFRICAN SPORTS l

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y (021) 406-6504. Fax: (021) 47-7669. Physical Education, Department of Information, Post- a boks 40, Kringsja, N-0807, Oslo, Norway. w e t a September 14-17, 1995. THE XITH FINA WORLD

G INTERNATIONAL

t SPORTS MEDICINE CONGRESS. Athens Hilton Hotel, e August 10-14, 1994. COM MONW EALTH G AM ES 1994, n Greece. Contact: Public Relations Center, Halen Haly- i b INTERNATIONAL SCIENTIFIC CONGRESS, UNIVER­ vides, foz Michalaropoulou Street, 115-28 Athens, a SITY OF VICTORIA, BC, CANADA. Contact: Common­ S

Greece. Tel: (301) 775 6336 — 777 1056. Fax: (301) y wealth Games International Science Congress, Confer­ 771 1289. □ b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 e 5 R The Dynamic Disorders of Skeletal Muscle Metabolism with special reference to Exercise

TD Noakes MB ChB MD FACSM

Introduction ercise, even when the exercise is of a mild in­ Most of the skeletal muscle disorders encountered in tensity. clinical medicine are of a sufficiently severe nature that Third, the cardiorespiratory response to exer­ they cause such weakness that participation in physical cise is abnormal with an elevated heart rate, activity is not possible. These degenerative or myopathic cardiac output and minute ventilation. disorders cause progressive muscle weakness and Fourth, there may be rhabdomyolysis with atrophy usually leading to death at a relatively young myoglobinuria. If severe, this may lead to acute age. renal failure. However there are a group of skeletal muscle disord­ ers which cause symptoms only during exercise. These Classification are known as the dynamic muscle disorders and are There are four subgroups in this category: compatible with an unaltered life expectancy. They are — Defects of carbohydrate metabolism, the classic form of special interest to sports scientists as the biochemi­ of which is McArdle’s syndrome. cal abnormalities present in these conditions allow in­ — Defects of lipid metabolism. sights into metabolic factors in skeletal muscle which — Defects of mitochondrial function. influence cardiovascular function during exercise, and — Defects of adenine nucleotide metabolism. to sports physicians because these conditions need to be considered in the differential diagnosis of exercise- MCARDLE’S SYNDROME induced syndromes. In addition, the clinical syndromes In this condition which has its onset early in life, either of malignant hyperpyrexia, exercise-induced heatstroke late childhood or early adulthood, the patient has se­ )

. and rhabdomyolysis which acute renal failure are prob­ vere exercise intolerance (M cArdle, 1951). There is the 2

1 ably inter-related and may be caused by one or more onset of muscle pain and contractures during more 0 vigorous exercise. The contractures are electrically si­ 2 of the dynamic disorders of skeletal muscle metabo­

d lism, perhaps as yet undefined. lent unlike nocturnal cramps in which there is increased e t electrical activity. If the exercise is continued, the con­

a This review will emphasize especially the dynamic d tractures may lead to ischaemic damage of the mus­

( skeletal muscle disorders that cause symptoms during r exercise. No attention is paid to the degenerative skele­ cle leading to myoglobinuria with possible renal e h damage. In less severe cases, there may also be mus­

s tal muscle disorders that cause symptoms at rest These i l conditions are well described in conventional medical cle swelling and soreness, followed after exercise by b u texts and are o f no special interest to sports practition­ elevated serum enzyme activities and myoglobinuria, P

on occasion.

e ers. It should be emphasized that the dynamic disord­ h But if the exercise is continued at low intensity, the t ers of skeletal muscle metabolism are exceedingly un­

y common. The intellectual interest they evoke is quite patient experiences a “second wind” in which the pain b out of proportion to their clinical importance. diminishes so that he or she is able to continue exer­ d e

t cising albeit at a relative low exercise intensity. Factors n Clinical presentation that expedite the onset of the second wind include ex­ a r ercising in warm weather and the avoidance of a high g The dynamic disorders of skeletal muscle metabolism

e carbohydrate meal shortly before exercise. Factors that c are characterized by the following features: n aggravate the symptoms are obviously the reverse — e First, there are no sym ptom s at rest. In par­ c i exercising in the cold and eating a high carbohydrate l ticular, muscle weakness, a characteristic feature r of the atrophic and destructive myopathies, is meal shortly before exercise. Carbohydrate ingestion e d absent. causes serum-free fatty acid concentrations to fall there­ n by limiting the availability of this alternate fuel for the u

Second, the diagnostic feature is the early on­ y exercising muscles. Factors which reduce skeletal mus­

a set o f fiatigue — easy fiatigueability — during ex- cle blood flow also delay or prevent the onset of the w e t Liberty Life Chair of Exercise and Sports Science and second wind. a

G M R C /U C T Bioenergetics of Exercise Research Unit The biochemical hallmark of the condition is the t

e Department of Physiology failure of the exercising muscles to produce appropri­ n i University of Cape Town Medical School ate amounts of lactate during vigorous or ischaemic b

a Observatory exercise. McArdle (1951) recognized the similarity be­ S South Africa tween this clinical picture and the developm ent o f con- y b d e c u d o r 6 SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p e R MUSCLE METABOLISM

tractures without lactate production by muscles poi­ reducing equivalents (N ADH and FADH2) will ultimately soned with the glycolytic inhibitor iodoacetate. He con­ limit the rates of oxidative phosphorylation and there­ cluded that patients with this syndrome must be suffer­ fore the V02max. ing from an enzymatic defect in the glycogenolytic or Although whole body V02 is normal at rest in these glycolytic pathways. Indeed, the absence o f one or more patients, at any given workload total body V02 is of the following enzymes have been described in pa­ greater than normal. This is explained by an increased tients with the symptom complex described by McAr- oxygen consumption of the cardiac and respiratory dle: glycogen phosphorylase, glycogen phosphorylase muscles due to an excessive tachycardia and elevation b kinase, phosphofructokinase, phosphoglycerate of systolic blood pressure and a greater than normal kinase, phosphoglycerate mutase and lactate dehydro­ pulmonary ventilation. Respiratory exchange ratios dur­ genase. ing exercise are also abnormally low indicating an in­ All these enzyme defects reduce the ability of the cell creased reliance on fat as the major metabolic fuel for to produce ATP by oxygen-independent pathways. This exercise. is confirmed by the low levels of glycolytic intermedi­ The V 02 max of patients with McArdle’s syndrome is ates and pyruvate measured by muscle biopsy during increased by intravenous glucose or lactate infusions. exercise in these patients (Kono et al 1984; Wahren et Even then, blood lactate concentrations do not increase al 1973). In addition, there is an inability to produce indicating that a major reason for the reduced work ca­ pyruvate at a sufficiently fast rate to fuel oxidative pacity o f these patients is a lack of oxidizable substrate, metabolism (Lewis and Haller, 1986). Patients with especially pyruvate, to fuel the Krebs cycle. This also glycogen phosphorylase deficiency are able to oxidize indicates that blood glucose cannot fully substitute for glucose and free fatty acids for energy whereas those muscle glycogen as an oxidative substrate in short-term with enzyme deficiencies below phosphorylase can ox­ heavy exercise. idize only free fatty acids as interruption of the glyco­ Similarly an elevation of serum-free fatty acid con­ lytic pathway prevents the complete metabolism of glu­ centrations also increases V02 max by the order of cose — > pyruvate — > acetyl CoA for further oxida­ 18-25%. Thus a limitation in the availability of free fat­ tion in the Krebs cycle. Thus whereas the provision of ty acids also contributes to the low V02max of these glucose by infusion will increase the exercise tolerance patients. of patients with a pure phosphorylase deficiency, such Cardiovascular function infusions will have no effect on those with enzyme Patients with McArdle’s syndrome show an hyperkinetic defects in the glycolytic pathway. circulatory response to exercise. This hyperkinetic cir­ )

. The result of this inability to supply adequate sub­

2 culatory response is not due to cardiac or vascular dis­

1 strate to the Krebs cycle for oxidative metabolism is

0 ease; cardiac muscle is spared in M cArdle’s disease be­

2 that, during exercise, there is an abnormally large cause of the presence of cardiac specific glycogen phos­ d decrease in muscle PCr concentrations and muscle pH e phorylase isoenzymes. There is also no evidence for ab­ t a and a large increase in muscle Pi concentrations. normal glycogen phosphorylase activity in vascular d

( When stimulated electrically, the muscles of patients smooth muscle. r with this syndrome also lose their action potentials, pos­ e The elevated cardiac output during submaximal ex­ h

s sibly suggesting that glycolytically-produced ATP may i ercise is believed to result from excessive vasodilata­ l be required for maintaining the excitability of mem­ b tion in the active muscles possibly related to the large u branes especially the sarcolemma and TTubules.

P fell in intramuscular PCr and the excessive rise in Pi

e Disturbances of oxygen transport and cardiac function concentrations This hyperkinetic circulation is partial­ h t

in patients with McArdle’s syndrome ly normalized during the infusion of free fatty acids or y b during exercise when serum-free fatty acid concentra­ Oxygen transport and utilization d tions are elevated This finding links mechanisms regu­ e McArdle’s syndrome had been used as a model to study t lating systemic haemodynamics and local vasodilata­ n the metabolic factors in the active skeletal muscle that a r influence cardiovascular function (Lewis and Haller, tion with the availability of oxidizable substate to the g contracting muscles. Hence it is not only the availabili­ e 1986; Lewis et al 1991). c ty of oxygen that controls peripheral vascular function.

n It is found that the maximum oxygen consumption e c (V02 max) of patients with McArdle’s syndrome is about Glucose infusion simultaneously decreases both the i l 18 ml 0 2 Kg-1 Viin -1 or roughly half that found in nor­ cardiac output and the extent o f the decline in PCr and r e mal patients. The reduced V02max is not due to re­ the rise in Pi concentrations during exercise in these d n duced muscle mass and is thus distinct from the low patients. This indicates that there is probably a recipro­ u VO max observed in patients with primary muscle dis­ cal relationship between skeletal muscle blood flow and y 2 a eases such as muscular dystrophy in which there is cellular ATP/ADP.Pi ratios (the phosphorylation poten­ w e muscle wasting. tial). This suggests that the crucial metabolic conse­ t a The low V02max of patients with McArdle’s syn­ quence o f M cArdle’s disease is an abnormally large de­ G drome has been related to the abnormally slow rate of cline in this ratio in muscle during exercise. t e substrate flux through the Krebs cycle and the electron The exact vasodilator substances acting in McArdle’s n i syndrome are not known but increased concentrations b transport chain. The inability to fuel the Krebs cycle a of lactate and hydrogen ions, or a low arterial P0 2 or

S with pyruvate causes the Krebs cycle to become “run

y down” . Thus the rate of formation of mitochondrial increased PC02 have all been excluded as none is dif­ b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 7 e R MUSCLE METABOLISM

ferent from values measued in normal persons. Thus creased intracellular Pi concentrations which impair the likely vasodilators are phosphate, potassium and muscle contraction and cause fatigue. adenosine, the latter derived from AMP. O f these, intra­ There is also evidence that the rate of ATP turnover muscular phosphate concentrations are known to in­ is reduced during fatigue in McArdle’s patients indicat­ crease steeply in these patients during exercise and ing product inhibition of the rate of ATP hydrolysis This there is also increased potassium release by muscle. mechanism is thought to explain exercise-induced fa­ Either or both could be important vasodilators in this tigue also in healthy persons. disease. Alternatively, these metabolites may stimulate A decline in skeletal muscle excitation shown by a skeletal muscle (Group 111 and IV) afferents which then fall in the muscle action potential is also found in these induce the excessive cardiovascular response during ac­ patients. This could be the result of product inhibition tivity (Lewis et al 1991). of the membrane Na + /K+ ATPase reaction which can In contrast, during static exercise, patients with Mc­ be relieved by the removal of phosphate via glycogenol­ Ardle’s syndrome do not show the expected increase ysis in normal but not in phosphorylase deficient mus­ in muscle sympathetic nerve activity. Thus, in normal cle. muscle this reflex is probably activated by increased Lewis and Haller (1986) conclude that events which rates of glycogenolysis with a fall in muscle pH (Pryor limit ATP synthesis in McArdle’s patients also limit ATP et al 1990). hydrolysis, thereby slowing ATP turnover and prevent­ Patients with McArdle’s syndrome also show an ab­ ing muscle rigor from developing, analogous to the sit­ normal increase in ammonia production by muscle, fur­ uation that develops in normal muscle during exhaus­ ther indicating/increased AMP production with conse­ tive, maximal exercise. quent deamination to ammonia and IMP. Glucose in­ Thus the biochemical basis for fatigue in skeletal fusion also reduces the production of ammonia; thus muscle in both normal and diseased muscle may be a reduction of ammonia production may also be a fac­ quite similar. tor reducing the abnormal cardiac output in these pa­ There are two other interesting features of this con­ tients. dition. First, patients with M cArdle’s syndrom e show a “ventilation turnpoint” during exercise indicating that Biochemical features o f fatigue in McArdle’s syndrome this phenomenon, also known as the “anaerobic thresh­ The outstanding observation in these patients is that old” , has no relationship to lactate production by the despite the limited capacity of phosphorylase deficient muscle to resynthesize ATP, little or no decline in mus­ skeletal muscles. Second, patients with McArdle’s syndrome also show cle ATP concentrations has been observed during a post-exercise oxygen debt (excess post-exercise oxy­ )

. fatigueing exercise in M cArdle’s patients. However there

2 gen consumption — EPOC). Traditional theories have

1 is an abnormally large accumulation of Pi and proba­

0 suggested that the EPOC is due to an excess oxygen

2 bly of ADP and AM P and these could contribute to fa­ consumption required during the post-exercise recov­ d tigue by inhibition of intracellular processes involved e

t ery period to oxidize the lactate produced during the in muscle contraction. Glucose infusion reduces the ex­ a preceding exercise. The presence of this phenomenon d tent to which Pi concentrations rise and increases re­ ( in these patients indicates that this cannot be the cor­ r sistance to fatigue. This indicates a metabolic shift from e rect explanation. h the creatine kinase (Equation 1, below) and myokinase- s i l AMP deaminase coupled reactions (Equation 2, below)

b Lactate transporter defect u in which there is net accumulation of phosphate, to Fishbein (1986) has recently described the first case o f P those of oxidative phosphorylation and glycolysis in e an intriguing and possibly not uncommon muscle dis­ h which both ADP and Pi are used to resynthesize ATP t order in which there is an absence of the lactate trans­

y (Lewis and Haller, 1986). porter in both skeletal muscle and red blood cells. The b lactate transporter is believed to be a membrane pro­ d e t Equation 1 tein that co-transports a lactate anion and a proton ex­ n

a The creatine kinase reaction ternally without a requirement for ATP. The transporter r g ATP -> A D P + Pi is thought to be responsible for 90% of lactate efflux e

c ADP + PCr -> ATP + Cr from these cells. Its activity is sensitive to the pH gra­ n net: PCr -> Pi + Cr e dient across the cell membrane and increases markedly c i

l as the intracellular pH falls (Fishbein, 1986).

Equation 2 r The patient described by Fishbein was a 26 year old e The myokinase-AMP deaminase reaction d 2ATP -> 2ADP + 2Pi military drill instructor who was investigated for chest n

u pain and coincidentally found to have markedly elevat­ 2ADP -> AMP + ATP y ed serum CK activities (up to 13,700 10 — normal up a AMP -> NH3 + IMP w net: ATP -> 2Pi + NH3 + IMP to 20010) on several occasions. Exercise tests revealed e t that the patient showed elevated blood lactate concen­

a Thus the abnormally large rises in intramuscular Pi con­

G centrations during exercise in these patients indicates trations after exercise and was therefore not suffering t from McArdle’s syndrome. However the rate at which e their reliance on the creatine kinase and the myokinase- n i AMP deaminase coupled reactions to regenerate ATP his blood lactate concentrations returned to the normal b resting levels after exercise was profoundly delayed. a (Equations 1 and 2) rather than on oxidative metabo­ S lism. The detrimental result is the accumulation o f in­ Laboratory studies confirmed that the rate of lactate y b d e c u d o r SA JOURNAL OP SPORTS MEDICINE SEPTEMBER 1994 p 8 e R MUSCLE METABOLISM

release from the patient’s red blood cells was also se­ sis when muscle glycogen depletion occurs. Prevention verely abnormal. of complications is therefore through the prescription Whilst the patient had no symptoms directly attri­ of a high carbohydrate diet to maintain muscle and liver butable to this condition, Fishbein suggests that ex­ glycogen concentrations. treme exercise in such patients could lead to rhabdo­ The condition can be diagnosed with muscle biopsy myolysis due to their inability to decrease intracellular which confirms the absence of CPT activity. Lipid-filled acidosis sufficiently rapidly during and after exercise. vacuoles may be shown predominantly in Type 1 fibres; The condition may also explain the frequently unex­ they are especially marked in the form of this condi­ plained finding of chronically elevated serum CK ac­ tion which results from carnitine deficiency (Bye and tivities and attacks of rhabdomyolysis in some appar­ Kan, 1988). ently healthy individuals. DEFECTS OF MITOCHONDRIAL FUNCTION DEFECTS OF LIPID METABOLISM Syndromes associated with excessive lactate formation The classic disorder of lipid metabolism is that due to In these patients there are deficiencies in one or more the absence of the enzyme carnitine palmityltransfer- o f the enzymes o f the electron transport chain; in som e ase (CPT) in skeletal muscle. This enzyme is essential patients no defect has yet been identified. The effect for the transport of long chain fatty acids across the in­ of these abnormalities is to reduce the capacity for ox­ ner mitochondrial membrane for their further metabo­ idative ATP production and therefore to increase reli­ lism by beta-oxidation with the production of acetyl- ance on glycolytic ATP production with increased rates coA which enters the Krebs cycle. To date there have of lactate and pyruvate production and the associated been approximately 25 subjects with this condition severe metabolic acidosis reported in the literature. Two have been females. The The clinical features common to all these conditions inheritance o f the condition is autosomal recessive (An- are extreme exercise intolerance associated with early gelini et al 1981). fatigue, muscle weakness and dyspnoea. The patients A related condition is muscle carnitine deficiency. respond to acute exercise as if they were extremely un­ Carnitine is also essential for the transport of fatty acids fit. Some patients have high resting blood lactate con­ across the mitochondrial membrane. Carnitine is pro­ centrations; however in all, there is a steep increase in duced in the liver and transported to muscle via blood blood lactate concentrations at very low levels of exer­ from where it is actively absorbed. Carnitine deficiency cise. may therefore result from the failure of carnitine syn­ In common with patients with McArdle’s syndrome thesis by the liver or be due to the failure of carnitine

) these patients also show very low V02max values and .

2 uptake by the muscles. Treatment with carnitine helps an abnormal cardiovascular response to mild exercise 1

0 those patients who do not produce carnitine. including a disproportionate cardiac output, tachycardia 2 Muscle CPT exists in two different forms on the in­ and ventilation for the appropriate metabolic rate (Haller d

e ner (CPT-11) and outer (CPT-1) mitochondrial membranes t et al 1989). The m etabolic basis for this is presumably a It is a deficiency of CPT-11 which causes this syndrome

d the same as that in McArdle’s syndrome, that is in­

( (Trevisan et al 1987).

r creased intramuscular Pi concentrations due to an ab­ e Symptoms of CPT deficiency usually begin late in

h normal reliance on the creatine kinase and myokinase- s childhood or in early adulthood. A s in M cArdle’s syn­ i l AMP deaminase coupled reactions to regenerate ATP

b drome, there are no abnormalities at rest but fasting in muscles which have an impaired capacity to produce u may cause serum CK activities to rise markedly (Car­ P

ATP by oxidative metabolism. e roll et al 1979).

h The inheritance of these conditions is unique because t Patients are usually able to perform vigorous exer­

y the mitochondrial DNA, which codes for the 13 protein

b cise without complications and their VOz max values

components of the electron transport chain, is trans­ d and cardiovascular function during exercise are normal e mitted exclusively by the mother (Jones and Round, t (Lewis et al 1991). This finding indicates the importance n 1990). This suggests that the mother may have an in­ a of normal carbohydrate metabolism for maximum exer­ r ordinate influence on the child’s ability to produce ATP g

cise and for the normal cardiovascular response to ex­ e by oxidative pathways (and therefore to become a cham­ c ercise. n pion athlete?). e However muscle tenderness, pain and swelling may c i DEFECTS OF ADENINE NUCLEOTIDE l occur after very prolonged exercise. Cramps may also

r METABOLISM e be a feature o f the condition (Bye and Kan, 1988). More d generalized muscle swelling may occur when exercise Myoadenylate deamine deficiency (MD) n u

follows a bout of prolonged fasting or after a period on The enzyme myoadenylate deaminase (MD) hydrolyzes y

a a low carbohydrate, high fat diet. Muscle pain and swell­ the breakdown of AM P (produced by the myokinase re­ w ing are accompanied by very marked elevations in se­ action) to ammonia and IMP (Equation 2). Absence of e t

a rum enzyme activities and in myoglobinuria. There may this enzyme is one of the commonest of the known

G also be acute renal failure. muscle enzyme defects and exists in two forms — the t e Patients with this condition are dependent on carbo­ primary type which is inherited as a complete gene n i hydrate to provide their energy requirements during ex­ block in an autosomal recessive pattern and the secon­ b a ercise. Thus they bum carbohydrates more rapidly than dary type which results from muscle damage due to S usual during exercise and may develop rhabdomyoly­ other diseases (Fishbein, 1985). y b d e c u d o r

p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 9 e R MUSCLE METABOLISM

The enzyme defect is believed by some to explain Jones DA, Round JM. Skeletal muscle in health and disease. Man­ chester University Press, 1990. cramping and exercise intolerance in some individuals, Kono N, Mineso I, Sumi S, Shimizu T, Kang J, Nonaka K, Tarui S. usually in adult to middle-age (Fishbein, 1985). Larger Metabolic basis of improved exercise tolerance: muscle phosphory­ studies, however, have failed to shown any association lase deficiency after glucagon administration. Neurology 34: between symptoms and this enzyme defect (Mercelis 1471-1476, 1984. Lewis SF, Haller RG. The pathophysiology of McArdle's disease: clues et al 1987). It may be that this is an enzyme defect still to regulation in exercise and fatigue. J App Physiol 61: 391-401, searching for a disease! 1986. Lewis SF, Vora S, Haller RG. Abnormal oxidative metabolism and O- transport in muscle phosphofructokinase deficiency. JAppl Physiol REFERENCES 71: 391-398, 1991. Angelini C, Fneddo L, Banistella P, et al. Carnitine palmityl tranferase McArdle B. Myopathy due to a defect in muscle glycogen breakdown. deficiency: Clinical variability, carrier detection and autosomal reces Clin Sci 10: 13-33, 1951. siue inheritance. Neurology 31: 883-886, 1981. ^ Mercelis R, Martin JJ, de Barsy T, Van den Berghe G. Myoadenylate Bye AME, Kan AE. Cramps following exercise. Aust Paediatr J 24 deaminase deficiency: absence of correlation with exercise intoler­ 258-259, 1988. ance in 452 muscle biopsies. J Neurol 234: 385-389, 1987. Carroll JE, DeVito DC, Brooks MH, Planer GJ, Hagberg JH. Fasting Pryor SL, Lewis SF, Haller RG, et al. Impairment of sympathetic acti­ as a provocative test in neuromuscular disease. Metabolism 28: vation during static exercise in patients with muscle phosphory­ 683-687, 1979. lase deficiency (McArdle's disease). J Clin Invest 85: 1444-1449, Fishbein WN. Lactate transporter defect: A new disease of muscle. 1990. Science 234: 1254-1256, 1986. Trevisan CP, Isaya G and Angelini C. Exercise-induced recurrent myo­ Fishbein WN. Myoadenylate deaminase deficiency: Inherited and ac­ globinuria: defective activity of inner carnitine palmitoyltransferase quired forms. Btochem Med 33: 158-169, 1985. in muscle mitochondria of two patients. Neurology 37: 1184-1188, Haller RG, Lewis SF, Estabrook RW, DiMauro S, Servidei S, Foster DW. 1987. Exercise intolerance, lactic acidosis, and abnormal cardiopulmo­ Wahren J, Felig P, Havel RJ, Jorfeldt L, Pernow B, Saltin B. Amino nary regulation in exercise associated with adult skeletal muscle acid metabolism in McArdle's syndrome. N Engl J Med 288: cytochrome oxidase deficiency. J Clin Invest 84: 155-161, 1989. 774-777, 1973. □ ) . 2 1 0

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d e c u d o r p e 10 SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 R Muscle Proteins and the Contractile Properties of Muscle Fibres

Kathryn H Myburgh PhD

Introduction second proposal for the mechanism of force generation Muscles are machines which provide the power that is by the actomyosin cross-bridge. In the second model, the basis for all vertebrate movement. The mechanical it was proposed that force is generated shortly after at­ properties of an active muscle are dependent on many tachment as the cross-bridge changes to a more sta­ factors such as the shape and size of the whole mus­ ble configuration (see Fig. 1: 3a and 3b). This hypothe­ cle, its fibre type, fibre size and length, and the angle sis requires that the attached cross-bridges exist in two of the fibre-tendon attachment, as well as a variety of or more configurations (see Fig. 1: 1, 3a and 3b) and neural factors including cortical drive and motor unit that the head can rotate from a 90° angle to a 45° an­ recruitment patterns. However, the force originates at gle (Fig. 1: 3a to 3b). Indeed, a 45° orientation of the the molecular level from the interaction of the major cross-bridges had already been shown in electron muscle proteins, actin and myosin, in the presence of micrographs of rigor muscle,9 and there was no rea­ ATP and Ca + + . This review will outline some of the son to believe that the cross-bridge could not rotate major discoveries which led to the theories of the through that orientation during a contractile cycle. mechanism of force production at this level in skeletal muscle, including the roles played by ATP and Ca + + , and the relationship between force and velocity. It will M then discuss factors within a single muscle fibre which influence these contractile properties and which are of particular relevance to exercise scientists.

I. The mechanism of force production Our current understanding of the mechanism of force production is based in large part on 3 discoveries made ) . in the 1950’s At that time the band-like structure of 2

1 muscle was already well described even at the level of 0 2

the sarcomere, but the function of the bands was not d

e known. Two important discoveries linking the structure t a of the sarcomere to its function were (i) that the pattern d (

of the bands is caused by thick and thin filaments1 r e and (ii) that in those bands where the two types of fila­ h s ments overlap, they also interact at regular intervals by A-M i l

b means of bridges.2 The third discovery, which was u made at the same time by two different investigators Figure 1. A schematic representation of ATP hydrolysis, P release o f the products o f ATP hydrolysis and actomyosin e and was published in the same edition of the presti­ h

t interaction during the contractile cycle. Abbreviations: A

gious journal Nature, was that the filaments themselves y = actin; M = myosin; A-M = actomyosin complex; ATP

b do not shorten during contraction. Instead, they appear = adenosine triphosphate; A D P = adenosine diphos­ d to slide between one another so that the amount by e t which they overlap increases during active shortening phate; Pi = inorganic phosphate. Steps: 1 - cross-bridge n a in a contracting muscle.34 These results led to the for­ attachment; 2 = phosphate release; 3a and 3b - con­ r

g figurational changes; 4 = A D P release; 5 = ATP bind­ mulation of the sliding filament theory of cross-bridge e c interaction during muscle contraction.5 Huxley pro­ ing; 6 = cross-bridge detachment; 7 = ATP hydrolysis. n e posed that force was produced by each projection from c i l II. The role of ATP in the cross-bridge t^cle

the myosin thick filament as it attached to the actin fila­ r e ment and that the force was related to the kinetic ener­ While physiologists and physicists were piecing toge­ d

n gy available in the cross-bridge before attachment.5 ther the structural and mechanical data, biochemists u

More than a decade later following many more mechan­ were actively investigating the kinetics of ATP hydroly­ y a ical experiments performed at faster time resolutions sis by an ATPase enzyme which is part of the myosin w molecule. It had already been discovered in 1939 that e and employing very accurate, quick changes in ten­ t

a sion6 or length,7 Huxley and Simmons8 formulated a the major muscle protein complex, actin-myosin, (also G

termed actomyosin), catalysed the hydrolysis of ATP.10 t e MRC/C1CT Bioenergetics o f Exercise Research Unit It was not until 1971 that a scheme was presented by n i (JCT Medical School Lymn and Taylor11 which integrated the steps in the b a Observatory chemical splitting of ATP to ADP and Pi, with a cycli­ S

y 7925 cal attachment and detachment o f actin and myosin. b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 11 e R MUSCLE FIBRES

In short, ATP hydrolysis occurs before myosin attaches ured. The data can be fitted to the Hill equation19 and to actin (Fig. 1: 7), this is followed by attachment and the maximal velocity of shortening (Vmax) is calculated formation of the actomyosin-ADP-Pi complex (Fig. 1: 1). After release of the hydrolysis products, Pi and ADP (Fig. 1: 2 and 4), actin and myosin remain associated (Fig. 1: A-M), probably with the cross-bridge head at an angle o f 45°. Actin and myosin dissociate with the bind­ ing of ATP to myosin (Fig. 1: 5 and 6), and once again, ATP hydrolysis occurs in the detached state (Fig. 1: 7). It only became apparent later that Pi is released in a separate step before the release of A D P12 and that the actomyosin-ADP-Pi complex (Fig. 1: 1) is relatively weak and produces less force than the subsequent strong- binding actomyosin-ADP complex (Fig. 1: 3b).13

III. The role of Ca++ in the cross-bridge cycle Biochemical studies of actomyosin-ATP hydrolysis done in solution have highlighted different properties of the myosin-ATPase enzyme. For example, unlike whole pCa muscle which requires both ATP and Ca++ to contract, a mixture of purified myosin and purified actin can hy­ Figure 2. The characteristic relationship between force drolyse ATP without the presence of Ca++ in the so­ and calcium ion concentration. Abbreviation: pCa = lution.14 This indicated the presence of an additional negative log of calcium concentration in moles e.g. protein, or proteins, that could inhibit the cross-bridge pCa 6 = 70~6M Ca+*. cycle unless calcium was present to remove that inhibi­ tory action. These proteins were identified as tropomyo­ from an extrapolation of the data to 0 load/0 A cha­ sin and the troponin-complex1516 and became known racteristic hyperbolic curve is obtained (see Fig. 3) as regulatory proteins. A very important early discovery showing how the velocity of contraction is maximal which made it possible to define the role of Ca++ on when the load (P) is equal to 0, and slows down as P actual force production in the cross-bridge cycle, was )

. increases until the velocity is 0 at maximal load (Po).

2 the development of the so-called “skinned” fibre. By in­

1 At this point, no shortening occurs and Po is analogous

0 cubating a muscle fibre in a solution containing 50% to maximum isometric force. 2 glycerol, the m em brane is m ade perm eable to ions, d e small molecules and even larger molecules.17 The ini­ t a tiation of contraction in the skinned fibre is no longer d (

dependent on membrane depolarisation, but is under r e control of the investigator, and is achieved by the addi­ h s i tion of calcium to the solution bathing the fibre. It was l b later discovered that the level of force production, meas­ u

P ured by a force transducer to which one end of the ti e skinned fibre is attached, could be varied by varying -O h t

the concentration of free calcium.18 The characteristic y b relationship between force and calcium ion concentra­

d tion (see Fig. 2) shows that force is negligible at pCa e t

n 6 (=10-6 M Ca++) and maximal around pCa 4 (=10~4 a

r M Ca++). The sigmoidal shape of the curve indicates g that few cross-bridges attach initially, but that there is e c a large cooperative action between adjacent myosin- n e Force (P/Po)

c binding sites on actin, so that force increases steeply i l

from approximately pCa 5.5. r e Figure 3. The characteristic relationship between force d

n IV. The force-velocity relationship and velocity of contraction. Abbreviations: P = force; Po u When a skinned fibre is attached to a force transducer = maximum force. y a on one side and a very rapid servo-controlled motor arm w

e on the other, it is possible to vary the tension in the t V. The effect of muscle fibre type on the a fibre by varing the position of the motor arm and hence

G mechanics of contraction the length of the fibre. The shortening velocity can be t e determined at specific fractions of the maximum ten­ V.i The characteristics of the basic fibre types n i The basic characteristics of the contractile cycle de­

b sion by several load clamps in which the tension in the a fibre is released to specified levels of submaximal ten­ scribed above apply to all muscles with the banded sar­ S

y sion and the velocity of tension redevelopment is meas­ com ere structure. But, in 1873 the French physiologist, b d e c u d o r p 12 SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 e R MUSCLE FIBRES Ranvier, noted that red and white skeletal muscles have TABLE I different contractile properties: red muscles contract slowly, while white muscles contract and relax rapid­ Basic Skeletal muscle fibre type classifications ly.21 This apparently simple observation set the stage Skeletal Muscle Fibre Types for numerous physiological, biochemical and histolog­ ical studies which aimed to define the properties of Nomenclature different mucles and muscle fibre types. Type 1 11A IIB In mammals, whole muscles are generally composed slow fast oxidative- fast of various fibre types. This heterogeneity complicates oxidative glycolytic glycolytic research studies, but allows for a great deal of physio­ S O FOG FG logical variation. Fortunately, in smaller mammals such as mice, rats and cats, the soleus is composed almost Characteristics: entirely of red muscle fibres and the extensor digito- Colour red red white rum longus of white fibres. This made it quite simple Twitch slow fast fast for electrophysiological studies to determine clear differ­ ATPase activity low high high ences betweent those muscle groups in the properties lost at pH 9.4-10.4 4.4-4.6 4.4 o f a single twitch contraction and led to general accep­ Glycogen content low tance of the terms slow-twitch and fast-twitch fibres.22 high high At around the same time biochemical studies showed Fatigue resistance high high high that the myosin from fast-twitch fibres hydrolysed ATP Oxidative capacity high high low much faster than did the myosin from slow-twitch mus­ not consistent and range from indicating no significant cle23 and histochemists were able to differentiate be­ difference,32 to higher values in slow-twitch fibres,33 or tween different myosin ATPase types (isozymes) due to higher values in fast-twitch fibres.34 Data from human their differing susceptibility to losing their enzymatic biopsy samples were in agreem ent with the latter find­ activity at different pH’s.24 (See Table 1). Another ap­ ings.35 These discrepancies are most likely due to proach was to differentiate between the fibre types by difficulties in the measurement of the cross-sectional determining either their resistance to fatigue during im­ areas of single fibres. The fibre diameter is not always posed stimulation,25 the number of mitochondria pre­ consistent along the length of a fibre which has been sent and the oxidative enzyme capacity,26’27 or the gly­ attached to a force transducer and a small error in the cogen content28 In these ways it was made possible to m easurement o f diam eter is m agnified in the calcula­ draw up a table of basic fibre type classifications (see tion of cross-sectional area. However, further technical Table 1). advances have reopened this question and it is currently )

. Interestingly, it was found that all the muscle fibres under investigation in several laboratories. 2

1 activated by the same motor unit fit into the same his- Although the issue of maximal force production by 0 tochemically determined classification of fibre type.25 2

different fibre types is not resolved, it is currently ac­ d However, the following question arises: can the contrac­ e cepted that there are most likely no differences between t tile characteristics of each fibre type be ascribed to a a fibre types of healthy muscle and this observation is d combination of the neural activation process and the (

explained by assuming that the number of cross-bridges r metabolic characteristics, or do the contractile proteins e per unit area of muscle is consistent36 and that the h themselves also exert an independent influence? The s force per cross-bridge is the same. A s mentioned in sec­ i l single skinned muscle fibre is the perfect experimen­ b tion 1, cross-bridges can be in either a weak, low force u tal model to answer this question since, as mentioned (actomyosin-ADP-Pi) (see Fig. 1: 1) or a strong, high P before, the activation is controlled by the investigator. e force (actomyosin-ADP) state (see Fig. 1: 3b). The rela­ h The following paragraphs will consider whether fibre t

tive proportion of each state could therefore also in­ y type affects peak isometric force production, velocity

b fluence force production. Recent mechanical data sug­ of contraction and the force-pCa curve irrespective of d gest that during a maximal isometric contraction in a e

t neural control. previously rested muscle, the majority of the cross- n a bridges are in the strong-binding state.37 But when r g

V.ii Contractile properties of the basic fibre types muscle is fatigued and the intracellular Pi concentra­ e c Early experiments on a large range of muscle types and tion is high, m ore cross-bridges are in the weak-binding n e sizes showed that the maximal force was related to the state and force can be reduced by as much as 30%.20 c i l cross-sectional area of the muscle.29 Fibre diameters

Although peak isometric force is apparently similar r e of single muscles fibres can vary up to 10-fold. There­ in both fibre types, the force developed at submaximal d fore, measurements o f force or tension must be correct­ n Ca++ concentrations is different for fast- and slow- u

ed for cross-sectional area, before differences inherent twitch fibres of the rat.33’38 Slow-twitch fibres could y

a in the muscle proteins can be discovered. Early reports produce low levels of force at significantly lower con­ w found that there were no differences in the maximal centrations of Ca++ than fast-twitch fibres. However, a e t

a force (Po) when expressed relative to the cross-sectional steeper slope o f the force-pCa curve in fast-twitch fibres

G area of slow- or fast-twitch muscles30 or fibres dissect­ indicate that once the Ca++ concentration threshold t e ed from purely slow-, or purely fast-twitch muscles31 for force development has been reached the fast-twitch n i (see Fig. 3: both Type 1 and 11 have the same Po). In fibres develop peak force at a faster rate. These obser­ b a skinned fibres the data on maximal values of force per vations can be attributed to differences in the calcium S unit of cross-sectional area in different fibre types are sensitivity of different isoforms of the regulating pro- y b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 13 e R MUSCLE FIBRES two distinct subtypes of fast-twitch fibres named IIAC tein, troponin.38-39 It is interesting to note that the myo­ and 11AB.41 Also, comparisons o f biochemical and sin and troponin isoforms change after complete inac­ tochemical classification has shown that types UA and tivity and weightlessness induced by hind limb susperv UB fibres do not always correspond to the FOG and l-

or Ca++ sensitivity and can therefore be ascribed to have done several elegant experiments w h i c h combmed the contractile proteins themselves. histochemical ATPase staining followed by micro­ dissection of each o f the various fibre types into smal V.iii Further division of fibre type based on contractile pieces which were then analysed biochemically by gel protein subunits . electrophoresis for the presence of different myosin E v e n though the classification of fibre types in Table heavy chain isoforms.44-45 These studies showed that I is not simple, for a number of r e a s o n s there are not there are three different myosin heavy chain isoforms sufficient categories to take into account all the differ which are named type 1, type Haandtype nbsmcethey ences that are now a p p a r e n t betweenmusc^ires correlate with histochemically identified type I, type 11A instance, a type I1C fibre, which can be placed between and type UB fibres. Type IIAB fibres, which ^ ^ c o n ­ type 11A and I1B in characteristics was identified in tinuum of ATPase staining intensities between Type 1IA 1970.24 Within a decade, improvements in histoch and UB, contained both type Ita and type lib myosin ical techniques suggested that there were also another ) . 2 1 0 2 d e t a d ( r e h s i l b u P e h t y b d e t n a r g e c n e c i l r e d n u y a w e t a G t e n i b a S y b d e c u d o r p e R MUSCLE FIBRES heavy chains45 The presence of both types of fast fibre types Based on average values type IIB were the myosin heavy chains has also been shown by several fastest and significantly faster than either type IIX or other groups in rat and human muscle.4647 It has re­ type I1A. The range of Vmax values for type IIA, IIB and cently suggested that the type IIAB fibres can be broken IIX fibres overlapped considerably, and the authors sug­ down into type UAb (containing predominantly type Ila gested that differences in the isoforms of the myosin heavy chains), type IIAB (containing 50-50 type 11a and light chain subunits could be responsible for additional b heavy chains) or type IlaB (containing predominant­ regulation o f the maximal velocity of contraction. In­ ly type lib heavy chains).48 deed, Greaser et al39 had previously shown in rabbit For the exercise scientist an important question plantaris (mixed fibre type composition), that myosin arises at this point: are these more subtle histochemi- light chain composition significantly influenced the cal and biochemical differences really functionally sig­ Vmax of the fast fibres In short, all the slow velocity nificant? fibres contained only slow isoforms of light chain; the fibres in the group with highest velocities contained V.iv Relationships between contractile properties and only fast isoforms of both heavy and light chains; the contractile protein subunits group with intermediate velocities had various combi­ Reiser et al49 tested the relationship between myosin nations of fast and slow isoforms of both heavy and heavy chain composition and maximal shortening velo­ light chains. city in rabbit soleus The majority of the soleus fibres contained only the slow heavy chain isoforms and con­ V.v Contractile protein subunits in human skeletal tracted with a low Vmax. A few fibres which had signi­ muscle ficantly higher Vmax values had differing proportions Another important issue from the point of view of the of slow and fast myosin heavy chain isoforms, and the exercise physiologist, is whether the findings in animal greater the proportion of the fast isofbrm, the higher studies are relevant to human muscle. As noted earlier, the Vmax values obtained. This study did not subdi­ rat muscle contains an extra distinctive fast fibre, name­ vide the fast myosin heavy chain into the Ila and lib iso­ ly the type IIX,34 which is not present in either rabbit forms. However, recently a rat study which combined or human muscle. But histochemical and biochemical mechanical measurements with immunocytochemical studies on human muscle biopsy samples have shown staining with 6 different myosin heavy chain antibodies, heterogeneity within the broad classifications of fibre identified type I, type IIA and type IIB fibres as well as types Biopsies obtained from the vastus lateralis of another fibre type which they named type IIX (see Ta­ healthy men showed that the slow-twitch fibres con­ ble II).34 As expected, type I fibres had significantly tained only slow myosin heavy chains but light chains slower maximal shortening velocity than any of the fast of both the slow and fast isoforms, although the slow ) . 2 1 0 2 d e t a d ( r e h s i l b LEADER u P e h t y

b OF THE d e t n a r g

PACK e c When you need n e c i pain-killing power l r e to get there first. d n u y a w e t a G t e n i b a S y b d e c u d o r p e R myosin heavy chain composition changed from pre­ isoforms predominated (see Table 11).50 Furthermore, dominantly fast to about 25% slow isoforms. The ef­ the histologically classified fast type 11A fibres (shown fects of more dynamic exercise on contractile protein in the rat to have intermediate maximal shortening velo­ isoform composition has not yet been investigated. cities34) contained predominantly a different light chain isoform than did the fast type 11B fibres (as was VII. Implications for sport also found in the rat). These histochemical and bioche­ Variability in athletic potential between individuals can, mical results are also very similar to those found in the at least in part, be traced to heterogeneity of the con study of the rabbit plantaris a muscle of mixed fibre tractile proteins themselves The adaptations of skele­ type.39 Although Wada et al50 did not do mechanical tal muscle to exercise training include more than hyper­ measurements on their human muscle fibres, one trophy, improved resistance to fatigue and changes in would expect that their contractile properties would also enzyme activity and substrate utilisation. It is as yet demonstrate the continuum of shortening velocities unknown exactly how different types and quantities of correlating with the biochemical composition of the training influence the contractile protein composition myosin molecule subunits which was shown in the and to what extent their mechanics can be changed. animal studies. However, these issues provide a challenge to research­ ers in this area.

TABLE II Conclusion Heterogeneity of skeletal muscle typed by The diversity of mammalian skeletal muscle is due in histological methods or by biochemical part to both obvious as well as more subtle molecular analysis of contractile protein composition differences in the contractile proteins These are charac- terisable histochemically and biochemically and there Skeletal Muscle Fibre Divisions is abundant evidence that these differences influence the mechanics of contraction of the individual muscle Slow-twitch: Fast-twitch: fibres It is appropriate to mention again that we have Histological typing: 1, 1C HA, 11AC, 11C, not even considered differences which exist in the ar­ IIAB, 11X* 11B chitecture of the whole muscle or the activation of the Biochemical typing: motor units We have also paid little attention to the — myosin heavy chain 1 Ha, 11AU enzymatic and substrate content of the muscle fibres, (MHC): HaB, 11X*, 11B except as these directly influence their histochemical — myosin light chain mostly: mostly: classification. Nevertheless this paper has described the (MLC): Is, 2s If, 2f, 3f molecular basis of muscle contractile protein hetero­ also: lf-3 f also: Is, 2s geneity and its functional consequences (see Table 111 )

. * rat muscle only ______for summary). Given all these com plexities it is not sur­ 2

1 prising that quantitative differences exist in the mus­ 0

2 cular capacity of athletes particularly elite athletes and

d we suggest that these differences can be traced to the e t VI. Current research issues contractile proteins themselves. In addition, with this a d It is therefore apparent that muscle contractile protein information at hand, it is now possible to investigate (

r composition is even m ore heterogeneous than was pre­ more systematically the adaptation of muscle proteins e h viously believed. The cause of this heterogeneity is to environmental influences such as increased or altered s i l almost certainly a combination of both genetic and en­ exercise training regimens b

u vironmental factors The relative importance of each of P

these mechanisms is a current issue in the field o f skele­ e TABLE III: h tal muscle research, and there is no doubt that interest­ t A summary of mechanical and biochemical y ing information will soon become available. Another is­ b sue currently under investigation is the effect of train­ properties of skeletal muscle fibres d e ing on muscle histology and muscle contractile protein t • Maximal force production is related to cross- n isoforms A recent human study reported the compo­ a sectional area in intact muscle as well as in sin­ r

g sition of a biopsy of the vastus lateralis of a highly

gle fibres in vitro e strength-trained woman.52 In addition to the usual type c • Maximal shortening velocity can be as much as n 1,11A, and UB fibres there was a distinctly different set e 6-fold higher in fast glycolytic fibres compared c i of C-fibres which comprised 15% of the total number l with slow oxidative fibres

r of fibres The biochemical data revealed that even the

e • Myosin is a large m olecule with 6 subunits, all o f

d C-fibres had sub-types (1C, 11C and UAC) which could be which may occur in different isoforms n distinguished by the ratios between the different iso- u

• The myosin heavy chain isofbrm regulates max­ y forms of myosin heavy and light chains which they con­

a imal velocity of contraction tained. The authors suggested that these fibres were w • The myosin light chain isoform is responsible for e t either specifically adapted and existed as a distinct additional regulation of the maximal velocity of a population of fibres in highly trained muscle, or they G

contraction t were in the process of being transformed from fast to e • Myosin isoforms change after inactivity indicat­ n slow fibre types. In a rat study, where the plantaris was i ing that adult muscle fibres adapt to environmen­ b overloaded by surgical removal of the medial gastroc­ a tal influences S

nemius and the soleus Diffee et al52 showed that the y b d e c u d o SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 r p e R MUSCLE FIBRES

References 1. Huxley HE. Electron microscope studies of the organisation of the 30. Close Rl. Properties of motor units in fast and slow skeletal mus­ filaments in striated muscle. Biochimica et Biophysica Acta 1953- cle of the rat. J Physiol 1967; 193: 45-55. 12: 387-394. 31. Sexton AW, Gersten JW. Isometric tension differences in fibers of 2. Huxley HE. The double array of filaments in cross-striated mus­ red and white muscles. Science 1967; 157: 199-202. cle. J Biophys Biochem Cytol 1957; 3: 631-648. 32. Donaldson SKB, Hermansen L. Differential direct effects of H* on 3. Huxley AF, Niedergerke R. Interference microscopy of living mus­ Ca2* -activated tension generation of skinned fibers from the cle fibres. Nature, Lond 1954; 173: 971-973. soleus, cardiac, and adductor magnus muscles of rabbits. Pfluaers 4. Huxley HE, Hanson J. Changes in the cross-striations of muscle Arch 1978; 376: 55-65. during contraction and stretch and their structural interpretation 33. Gardetto PR, Schluter JM, Fitts RH. Contractile function of single Nature, Lond 1954; 173: 973-976. fibers after hindlimb suspension. J Appl Phusiol 1989■ 66 5. Huxley AF. Muscle structure and theories of contraction Prog Bi­ 2739-2749. ophys Chem 1957; 7: 255-318. 34. Bottinelli R, Schiafftno S, Reggiani C. Force-velocity relations and 6. Civan MM, Podolsky RJ. Contraction kinetics of striated muscle myosin heavy chain iso form composition of skinned fibres from fibres following quick changes in load. J Physiol, Lond 1966• 184- rat skeletal muscle. J Physiol, Lond 1991; 437: 655-672. 511-534. 35. Fitts RH, Costill DL, Gardetto PR. Effects of swim exercise train­ 7. Huxley AF, Simmons RM. Mechanical properties for the cross­ ing on human muscle fiber function. J Appl Physiol 1989- 66- bridges of frog striated muscle. J Physiol, Lond 1971; 218:59-60P. 465-4 75. 8. Huxley AF, Simmons RM. Proposed mechanism of force genera­ Fitts RH, McDonald KS, Schluter JM. The determinants of skele­ tion in striated muscle. Nature, Lond 1971; 233: 533-538. tal muscle force and power: their adaptability with changes in ac­ 9. Reedy MK, Holmes KC, Tregear RT. Induced changes in the orien­ tivity pattern. J Biomech 1991; 24(Suppl 1): 111-122. tation of the crossbridges of glycerinated insect flight muscle Na­ 37. Metzger JM, Moss RL. pH modulation of the kinetics o f a ture, Lond 1965; 207: 1276-1280. Ca* * -sensitive cross-bridge state transition in mammalian single 10. Engelhardt WA, Ljubimowa MN. Myosin and adenosinetiiphospha- skeletal muscle fibers. J Physiol, Lond 1990; 428: 7551-7564. tase. Nature 1939; 144: 668-669. 38. Metzger JM, Moss RL. Greater H * ion-induced depression of ten­ 11. Lymn RW, Taylor EW. Mechanism o f adenosine triphosphate hy­ sion and velocity in single skinned fibers of rat fast versus slow drolysis by actomyosin. Biochemistry 1971; 10: 4617-4624. muscles. J Physiol, Lond 1987; 393: 727-742. 12. Eisenberg E, Hill TL. A cross-bridge model of muscle contraction. 39. Greaser ML, Moss RL, Reiser PJ. Variations in contractile proper­ Prog Biophys Mol Biol 1978; 33: 55-82. ties of rabbit single muscle fibres in relation to troponin T isoforms 13. Cooke R, Pate E. The effects of AD P and phosphate on the con­ and myosin light chains. J Physiol 1988; 406: 85-98. traction of muscle fibres. Biophys J 1985; 48: 789-798. 40. Campione M, Ausoni S, Guezennec, Schiafftno S. Myosin and 14. Eisenberg E, Greene L. The relation of muscle biochemistry to mus­ troponin changes in rat soleus muscle after hindlimb suspension cle physiology. Ann Rev Physiol 1980; 42: 293-309. J Appl Physiol 1993; 74(3): 1156-1160. 15. Ebashi S, Kodama A. Interaction of troponin with F-actin in the 41. Ingjer F. Effects of endurance training on muscle fibre ATPase ac­ presence o f tropomyosin. J Biochem Tokyo 1966; 59: 425-426. tivity, capillary supply and mitochondrial content in man. J Phusiol 16. Greaser ML, Gergely J. Reconstitution of troponin activity from 1979; 294: 419-432. three troponin components. J Biol Chem 1971; 246: 4226-4233. 42. Greene HJ. Muscle power: recruitment, metabolism and fatigue. 17. Szent-Gyorgyi A. Free-energy relations and contractions of ac- , In Human Muscle Power (eds. NL Jones, N McCartney and A J

) tomyosin. Biol Bull Woods Hole Mass 1949; 96: 140-161. I ' . McComas). Champaign, Illinois: Human Kinetics, pp 65-79, 1986. 2 18. Heilman DC, Podalsky RJ. Force measurement in skinned mus­

1 43. Cooke R. The mechanism o f muscle contraction. C R C Crit Rev cle fibres. J Physiol Lond 1969; 200: 807-819. / 0 Biochem 1986; 21: 53-118. ^ 2

19. Hill AV. The heat of shortening and the dynamic constants of mus­ 44. Staron SR, Pette D. Correlation osS^^tttXyo^S^^TP^ase ac­ d cle. Proc Royal Soc Lond (B ) 1938; 126: 136-195. e tivity and myosin heavy chain composition in rabbit muscle fibres. t 20. Cooke R, Franks K, Luciani GB, Pate E. The inhibition o f rabbit a Histochemistry 1986; 86: 19-23.

d skeletal muscle contraction by hydrogen ions and phosphate J

( 45. Staron SR, Pette D. The multiplicity of combinations of myosin

Physiol Lond 1987; 395: 77-97. r light chains and heavy chains in histochemically typed single fibies. e 21. Ranvier ML. Proprietes et structures differentes des muscles rouge

h Rabbit tibialis anterior muscle. Biochem J 1987; 243: 695-699.

s et des muscles Wanes, chez les Lapins et chez les Raies. Com- i 46. Danieli-Betto D, Zerbato E, Betto R. Type I, Ila and lib myosin heavy l ptes Rendus des Academie de Sciences 1873; 77: 1030-1034. b chain electrophorectic analysis of rat fibres. Biochem Biophys Res u 22. Close Rl. Dynamic properties of mammalian skeletal muscles Commun 1986; 138: 981-987.

P Physiol Rev 1972; 52: 129-197. 4 7. Biral D, Betto R, Danieli-Betto D, Saluiati G. Myosin heavy chain e f 23. Bamny M. ATPase activity of myosin correlated with speed of mus- h composition of single fibres from normal human muscle. Biochem t cle shortening. J Gen Physiol 1967; 50: 197-218. X V <7 n < T J 1988; 250: 307-308. y 24. Brooke MH, Kaiser KK. Three myosin adenosine triphosphatase b 48. Staron RS. Correlation between myofibrillar ATPase activity and systems: the nature of their pH lability and sulphydryl dependence d myosin heavy chain composition in single human fibers. e J Hlstochem Cytochem 1970; 18: 670-672. t Histochemistry 1991; 96: 21-24.

n 25. Burke RE, Levine EW, Tsairis P, Zajae FE. Physiological types of 49. Reiser PJ, Moss RL, Giulian GG, Greaser ML. Shortening veloci­ a histochemical profiles in motor units of the cat gastrocnemius J r ty in single fibres from adult rabbit soleus muscles is correlated g Physiol Lond 1973; 234: 723-748. with myosin heavy chain composition. J Biol Chem 1985■ 260- e 26. Noyikoff AB, Shin W-J, Drucker J. Mitochondrial localization of c 9077-9080. n oxidative enzymes: staining results with two tetrazolium salts J e 50. Wada M, Katsuta S, Doi T, Funo S. Favourable associations be­

c Biophys Biochem Cytol 1961; 9: 47-61. i tween myosin heavy-chain and light-chain isoforms in human l

27. Peter JB, Barnard RJ, Edgerton VR, Gillespie CA, Stempel KE.

r skeletal muscle. Pflugers Arch 1990; 416(6): 689-693. e Metabolic profiles of three fiber types o f skeletal muscle in guinea 51. Staron RS, H ik id a RS. Histochemical, biochemical and ultrastruc- d Pigs and rabbits. Biochemistry 1972; 11: 2627-2633. n tural analyses of single human muscle fibers, with special refer­

u L’ Ku3etber9 £ Histochemical composition, distribution

ence to the C-fiber population. J Histochem Cytochem 1992- y of fibres and fatigability of single motor units. Anterior tibialis mus- 40(4): 563-568. a jq the rat J Neurol Neurosurg Psychiatry 1968; 31: 424-433. 52. Diffee GM, McCue S, LaRosa A, Herrick RE, Baldwin KM. Inter­ w

e l nOWlt° n <~*<~' Hines HM. The effects ofgrowth and atrophy upon

t actions of various mechanical activity models in regulation of my­ the strength of skeletal muscle. A m J Physiol 1939/40; 128: a osin healvy chain isoform expression. J Appl Phusiol 1993■ 74(5)■ 521-525. G 2517-2522. t e n i b a S y b d e c u d o r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p 17 e R Delayed-Onset-Muscle-Soreness

Ml Lambert and SC Dennis

point is that McArdle's patients, who lack the enzyme Introduction glycogen phosphorylase and are therefore unable to Muscle soreness that occurs during intense exercise is break down glycogen to lactate during exercise, do not most often caused by muscular compression of capil­ show an increase in blood lactate concentrations while laries and hence an inadequate blood flow within the exercising, and yet may still experience severe DOMb. contracting muscle. The resulting accumulation of pro­ (2) Tissue damage theory for DOMS h a m c tons, phosphate ions and nucleotides arising from in­ The more scientifically plausible theory is that DOMS adequate removal of the products o f energy production, is caused by tissue damage. The following observations all stimulate pain receptors in the muscle (Jones and Round 1990). Once the exercise is terminated, this acute support of this theory: (a) Muscles with DOMS have microscopically muscle soreness subsides rapidly. Teleologically, it may identifiable disruptions of myofibrils and be argued that such pain occurs as a “back-up” to the streaming of the Z-lines, a common non­ rapid fatigue that prevents the muscles from becom­ specific finding in many muscular diseases ing irreparably damaged by critically depleting the (Friden, 1984). energy stores that are vital for muscle relaxation. (b) DOMS causes an increased leakage into the Another form of muscle soreness occurs several blood of intramuscular enzymes such as hours after the end of exercise. This condition is charac­ creatine kinase (CK) and lactate dehydroge­ terised by discomfort or pain in skeletal muscle with nase, (LDH) (Clarkson et al, 1992). even modest muscular exertion. The pain is first evi­ (c) DOMS is associated with the excretion of dent several hours after the cessation of exercise, peaks high concentrations of 3-methylhistidine in 24-72 hours later and subsides after 5 to 7 days The the urine which is a non-metabolizable ami­ pain is elicted when the muscle is pressed, contracted no acid found in the actin protein of the mus or stretched. The pain, in contrast to the acute pain that cle thin filaments occurs during exercise, is known as delayed-onset- (d) After exercise causing DOMS there are high muscle-soreness (DOMS). Although DOMS can be concentrations of C-reactive protein in the caused by stretching a muscle and by isometric and blood which indicate tissue damage (Stra- )

. concentric muscle contractions, it occurs most com­

2 chan et al, 1984), and

1 monly after eccentric contractions when muscles are

0 (e) Following a marathon race, runner’s leg mus­

2 used in a breaking motion (Ebberling and Clarkson, cles have intra- and extra cellular oedema d e 1989). with endothelial injury, and dilation and dis­ t a ruption of the T-tubules. There is also focal d Theories of DOMS (

disruption of the mitochondria (Warhol et al r Several theories have been proposed to explain DOMS. e 1985). In a rat experiment Armstrong et al h The two most common theories are the metabolite ac­ s i (1983) showed that monocytes, macro l cumulation theory and the muscle damage theory. b phages, satellite cells and fibroblasts were u (1) Metabolite accumulation theory for DOMS P present in the muscle 1 to 2 days after se­

e Although no longer supported by any scientific evi­ vere exercise which also suggest severe mus­ h t

dence, the metabolite accumulation theory is still often cle damage. Furthermore, Warhol et al (1985) y b used as an explanation for DOMS by m a n y coaches. showed that 12 weeks after a marathon,

d This theory erroneously relates DOMS to the increased many muscle fibres had central nuclei and e t blood and muscle lactate levels that occur during high satellite cells indicating that the previously n a intensity exercise. However, neither muscle nor blood r damaged fibres had regenerated g

lactate concentrations remain elevated for more than e c 15-30 minutes post-exercise and return to pre-exercise n e concentrations within 60 minutes (Oyono-Enguelle et c i l al, 1989). Furthermore, DOMS is more severe after ec­ Why Does Eccentric Exercise Cause DOMS? r

e centric exercise, even though there is less blood lactate The contrast between eccentric and concentric muscle d accumulation with this type of exercise. In addition, se­ n contractions in terms of causing DOMS was shown u

vere DOMS may occur after stretching a muscle, despite

y clearly by Asmussen (1956) in an experiment in which

a the feet that blood lactate levels do not increase. A final subjects raised a weight with one arm, and lowered it w e

t with the other. The subjects claimed that raising the a Address for correspondence weight (concentric contraction) often exhausted the G

Mike Lambert, PhD , t muscle, whereas lowering the weight (eccentric contrac­ e MRC/C1CT Bioenergetics o f Exercise Research Unit,

n tion) felt easier. Nevertheless, the muscles involved in i Department of Physiology, b the eccentric contractions were more painful several a UCT Medical School,

S days later. This can be explained because eccentric mus-

y Observatory 7925 b d e c u d o

r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p 18 e R DOMS

cle contractions lowering a load have less electromyo­ Physiological consequences of DOMS graphic activity (EMG) compared to concentric contrac­ tions raising the same load (Newham et al, 1983). A (a) Accumulation of calcium in the sarcoplasm lower EMG activity indicates that less fibres are recruit­ One to two days after exercise causing muscle damage, ed to move the same weight and so during eccentric the affected muscles shorten, and remain shortened for contractions each fibre undergoes more strain and about 5 days (Jones et al, 1987; Cleak and Eston, 1992) hence is more prone to mechanical disruption (Lieber This excessive contraction at rest is thought to occur and Friden, 1988). as a result of an influx of Ca++ into the sarcoplasm either through the Ca++ channels or through physical disruption of the cell membrane (Cullen and Fulthorpe, Muscle damage and pain during DOMS 1975). It is also possible that the damaged connective Mechanical disruption o f the muscle fibre affects the tissue network is involved in causing the muscle to structural and functional proteins and the connective shorten (Jones et al, 1987). The stiffness and shorten­ tissue network (Lieber and Friden, 1988), causing a de­ ing develop before the delayed pain which suggests that crease in maximal force production (Clarkson and they are not causally related. Tremblay, 1988) which may remain impaired for 3 Continuously higher than normal resting levels of weeks (Newham et al, 1987). Within a few hours there Ca++ in the sarcoplasm are sequestered by the mito­ is a significant elevation in circulating neutrophils chondria. Ca++ uptake into mitochondria occurs at the (Smith et al, 1989) which infiltrate the site of injury expense of ATP production and in extreme cases com­ (Kuipers et al, 1983). The pain in the muscles at this promises the extent to which cytoplasmic Ca++ con­ stage is possibly due to a disruption of the connective centrations can be controlled. Uncontrolled rises in cyto­ tissue and to the damage in the muscle itself (Jones plasmic Ca++ concentrations activate a Ca^-depen­ et al, 1987). v dent proteolytic enzyme which preferentially degrades During exercise which causes DOMS it appears that Z-discs, troponin and tropomyosin. A Ca++-activated the weak or more susceptible fibres are damaged to phosphoiipase also destroys cell and other membranes a greater extent (Newham et al, 1987). If the damaged (Jones and Round, 1990). It is not known whether phos- fibres are not repaired within a day the entire fibre or pholipase activity promotes CK release or whether the a segment o f the fibre degenerates as macrophages in­ release of CK occurs earlier as a result of the mechani­ filtrate and remove the cellular debris. At this stage cal damage. there is an increase in serum prostaglandin E2 (PGE ) (b) Elevated plasma CK activity concentrations (Bansil et al, 1985; Smith, 1991). PGE2 The mechanism causing increased plasma CK activity )

. decreases the threshold of the pain receptors in the

2 is not entirely understood. It appears to be exercise de­ muscle (Smith, 1991). The delayed muscular pain may 1 pendent since downhill running causes plasma CK ac­ 0 in part be due to inflammation that occurs several hours 2

tivity to increase 3-6 hours after the bout, peaking 18-24

d after the activity (Smith, 1991). During this period the

e hours later, whereas local eccentric exercise causes plas­ t size of the damaged muscle may increase by 5-10% a ma CK activity to increase after 48 hours and to peak d (Jones and Round, 1990). Most of this swelling can be (

at about 7 days post-exercise (Clarkson and Tremblay,

r attributed to oedema. This produces a significant in­ e 1988). The delayed appearance of CK activity in the

h crease in intramuscular pressure at rest (Newham and s

i plasma is thought to be due to the slow increase in

l Jones, 1985). Small movements or palpitations may fur­

b membrane permeability (Newham et al, 1987). It has

u ther increase the intramuscular pressure, which pro­

P also been suggested that the delayed CK response vides a stimulus for the pain receptors already sensi­ e might also be due to the diffusion and mixing within h tized by the PGE2. This pain, however, is not reduced t

the lymphatic system that clears the CK from the ex­

y by anti-inflammatory drugs (Donnelly et al, 1988; Jones

b tracellular space (Jones and Round, 1990). and Round, 1990). The potential benefits of the delayed d Because there is large variability in plasma CK ac­ e pain are not clear. Whereas it can be argued that acute t tivity increases following exercise, which is not depen­ n pain has a protective role by preventing further muscle a

r dent on age, fitness or degree of soreness (Noakes contractions that may cause damage, DOMS does not g 1987), elevated blood CK activity cannot be used as a e rail into this category because of its delayed response. c clinical test to quantify the degree of muscle damage, n e c i l

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d SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 o

r 19 p e R DOMS

to a large intra-subject variation and the variation due especially as the time course of the elevation of plas­ to the type of exercise activity. A nti-inflan^atoiy medi­ ma CK activity is dissociated from both painand mus­ cation does not reduce the severity ot DOMS. There is cle function impairment (Newham et al, 1987). no difference in recovery time when subjects have com­ plete rest compared to when they exercise moderately. Training response to DOMS REFERENCES Th e muscles may adapt to DOM S for several w eeks af­ Armstrong RB, RW Ogiluie and JA Schwane. ewrcBe- ter a single bout of eccentric exercise. This is suggested induced injury to rat skeletal muscle. J Appl Physiol. 54. 80-91, by the lower plasma CK activity in response to a subse­ quent exercise bout, even though the pain rating is simi­ Asmussen E. Observations on experimental muscle soreness. Acta lar. There are 3 possibilities to explain this phenome­ Rheum. Scand. 2: 109-116, 1956. Bansil CK, GC Wilson and M H Stone. Role of prostaglandins Eand non (Newham et al, 1987); F2 alpha in exercise-induced delayed muscle soreness. Med Sa (1) there is a change in motor unit recruitment Sports and Exerc. 17:276, 1985. pattern, Clarkson P M and 1 Tremblay. Rapid adaptation to exercise-induced (2) there is som e intrinsic adaptation in the mus­ muscle damage. J Appl Physiol. 65: 1-6, 1988. cle fibre, or Clarkson PM, K Nosaka and B Braun. Muscle function after exercise- induced muscle damage and rapid adaptation. Med Sci Sports and (3) fibres nearing the end of their growth, or a Exerc. 24: 512-520, 1992. small part o f a weakened fibre are destroyed Cleak M J and R G Easton. Muscle soreness, swelling, stiffness and at the first exposure. strength loss after intense eccentric exercise. Br J Sports Med. 26: 267-272, 1992. n t At this stage it seems that the latter 2 points are the Cullen M J and JJ Fulthorpe. Stages in fibre breakdown in Duchenne muscular dystrophy. J Neurol Sci. 24: 179-200, ^ 7 5 . more likely explanations because the EMG pattern does De Vries HA. Quantitative electromyographic investigation of the muscte not change with training, suggesting that muscle re­ spasm theory of muscle pain. A m J Phys Med 45:119-134 1966. cruitment is unaltered. There is also evidence f°r con­ Donnelly AE, K McCormick, RJ Maughan, PH Whiting and PM Clark­ nective tissue involvement in the adaptation to DOMS. son. Effects of a non-steroidal anti-inflammatory drug on delayed onset muscle soreness and indices of damage. Brit J Sports Med One possible explanation may be that the first exposure 22: 35-38, 1988. . . . , . . . to unfamiliar exercise causes mainly muscle tissue dis­ Friden J. Muscle soreness after exercise: implications o f morphologi­ ruption, but that as the muscle becomes trained the cal changes. Int J Sports Med. 5: 57-66, 1984. DOMS is attributed more to connective tissue disrup­ Jones DA, D J Newham, J M Round and SEJ Tolfree. Experimental human muscle damage: morphological changes in relation to other tion. indices of damage. J Physiol. 375: 435-448, 1986. Jones DA, D J Newham and PM Clarkson. Skeletal muscle stiffness Treatment for DOMS and pain following eccentric exercise of the elbow flexors. Pain. 30, ) . Presently the treatment for DOMS can only be pre­

2 233-242, 1987.

1 scribed based on empirical observations. There is de­ Jones DA and JM Round. Skeletal muscle in health and disease. Man­ 0

2 chester Uniuersity Press, 1990.

bate whether to rest completely until the pain subsides Kuipers H, J Drnkker, PM Frederik, P Geurten and GV Kranenburg. d e or whether to continue exercising, albeit at a low in­ Muscle degeneration after exercise in rats. Int J Sports Med. 4: t a tensity. Sherman et al (1984) did not find a difference 45-51, 1983. , , d

( Lieber RL and J Friden. Selective damage o f fast glycolytic muscle

in the recovery rate after a marathon between a group r fibres with eccentric contraction of the rabbit tibialis anterior. Acta e of runners who rested compared to a group who con­ h Physiol Scand. 133: 587-588, 1988. s tinued to train. Also, since both m odes of treatment are i Newham DJ, D A Jones and RHT Edwards. Large delayed plasma crea­ l b commonly practised by sports participants, it can be tine kinase changes after stepping exercise. Muscle Nerve. 6: u assumed that neither method is overtly superior to the 380-385, 1983. . P Newham DJ and DA Jones. Intra-muscular pressure m the painful hu­ e other. h man biceps. Clin Sci. 69: 27P, 1985. t

Although static stretching exercises have been pro­ Newham CJ, D A Jones and PM Clarkson. Repeated high force ec­ y posed as a mode of treatment for DOMS, (De Vries, b centric e x e r c is e : effects on muscle pain and damage. J Appl PhysioL

d 1966) this theory has not been tested adequately. In­ 63: 1381-1386, 1987. e t tuitively it appears that if the muscles are damaged in Noakes TD. Effects of exercise on serum enzyme activities in humans. n a the acute phase of DOMS, then stretching the muscle Sports Med. 4: 245-267, 1987. . u c j r Oyono-Enguelie S, M Gartner, J Marbach, A Heitz, C Ott and H Freund g may be counter-productive. Comparison of arterial and venous blood lactate kinetics after short e c exercise. Int J Sports Med. 10: 16-24, J989. n e Summary Sherman WM, LE Armstrong, TM Murray, F C Hagcrman, DL CostiU, c i R C Stamn, JL Ivy. Effect of a 42.2km footrace and subsequent l Exercise, particularly exercise involving eccentric mus­

r rest or exercise on muscular strength and work capacity. J Appl e cle contractions, causes delayed muscle pain with peak

d Physiol 57: 1668-1673, 1984. soreness occurring about 24 hours after the activity an n Smith LL. Acute inflammation: the underlying mechanism in delayed u

continuing for up to a week. Muscle contractile func­ onset muscle soreness? Med Sci Sports Exerc. 23: 542-551, 1991. y Smith LL, M McCammon, S Smith, M Chamness and K OBnen. White a tion may be impaired for several weeks after the blood cell response to uphill walking and downhillpgging at similar w damage. There is much evidence to show that muscle e

t metabolic loads. Eur J Appl Physiol 58: 833-837, 1989. fibres with delayed-onset-muscle-soreness are damaged. a Stmchan AF, TD Noakes, G Kotzenberg, A E Nel, FC de Beer.C reac­ G

These fibres do, however, repair and becom e more resis­ tive protein concentrations during long-distance running. Bnt Med t e tant to damage in subsequent bouts of exercise. Al­ J 289: 1249-1251, 1984. n i though elevated plasma creatine kinase activity is as­ Warhol MJ, A J Siegel, WJ Evans and LM Silverman. Skeletal b injury and repair in marathon runners after competition. A m J Path a sociated with muscle damage, it cannot be used to

S 118: 331-339, 1985. U quantitatively assess the amount of muscle damage due y b d e c u d o

r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p e R Advances in Sports Equipment Technology that Enhance Performance

Chester R Kyle Ph D

Introduction of this sort on rules committees there will always be Modern equipment has revolutionized many sports, some degree of continual change in sports equipment leading to major improvements in performance, radical This cycle o f change creates problem s o f major pro­ changes in technique, an increase in the sport’s popu­ portions. A new piece of equipment previously unde­ larity or safety, or in som e cases a com plete change in fined within the rules gives an athlete an obvious ad­ the structure of the sport. It is the purpose of this vantage. The sport’s rules committee passes a regula­ presentation to show the importance of equipment tion to control the new innovation. Designers find a technology in modern Olym pic sports and the competi­ loophole in the new regulations and design equipment tive advantage that can be gained by equipment im­ to evade the rule which leads to new revisions and rules provement. This adversarial ballet continues on and on. It can be Whenever there is an athletic competition, there is a distinct disadvantage to a country that does not have an automatic conflict between those who make the con­ the technology to produce its own sports equipment. test rules and those who try to interpret the rules to Such countries must rely upon the open market which their own advantage. In sports that use high technolo­ may be several generations behind. gy, it is even more complex. The rule makers would like However, in general, designing equipment to the very to ensure a fair contest between athletes and not have limit and even beyond the rules has a healthy, stimulat­ their sport degenerate into a competition to see who ing and beneficial effect on sports Without such ac­ can design the best equipment. On the other hand, tivity, for example, skis would still be made o f wood with manufacturers and designers will try to find ways of leather straps and the pleasure of skiing with confidence stretching or interpreting the rules so that equipment and skill would be denied to millions of skiers improvements might give their athletes an “unfair” ad­ vantage. For this reason, athletic governing bodies fre­ High tech sports quently rule against equipment improvement and in ef­ A 1984 report of the CISOC Sports Equipment and ) . fect freeze the sport in a time capsule. An example Technology Committee classifies the Olympic Sports 2

1 is the racing bicycle which remained basically un­ as either High, Medium or Low Technology. See Table 0

2 changed for about 100 years, (it has undergone rapid

d change recently). e In each of the high tech sports the outcome of the t Obviously, a certain amount of standardization in a event depends heavily upon the type of equipment d

( equipment is necessary. Logically a contest should be

used. Equipment design changes can often result in r between athletes and not between equipment designers e major improvements in athletic performance. An aver­ h However, many times there are good reasons for allow­ s

i age athlete could conceivably defeat a world class per­ l ingequipment innovation. Changes will often improve b former by using illegal equipm ent For instance, in arch­ u athletic performance and make a competition safer Bet­

P ery, m odem compound bows and long radius sights are ter equipment can give the athlete a longer competi­ e forbidden since they would radically improve scores h tive life. For exam ple m odern materials in running t

compared to the more traditional bows If equipment y shoes absorb shock and help prevent injury. In com bi­ b designers are seeking to get measurable results they nation with resilient track and field surfaces there is d would do well to concentrate on the high tech sports e t no doubt that they also improve performance. Medium tech sports, depend somewhat on equipment, n

a n the United States sporting goods manufacture and however athletic skill for outweighs equipment technol­ r

g sale is a 30 billion dollar per year business There is ogy. In low tech sports, any equipment is so standar­ e c a great deal of competition among manufacturers to dized that it has almost no influence on the outcome n e ave winning athletes use their equipment and there of the event. Track and field is a sport that spans all c i l ,s a 9reat deal of pressure upon the sports rules com­ three categories

r mittees by the equipment manufacturers to permit in­ e d novation in order to stimulate sales of new equipment EQUIPMENT CHANGES THAT HAVE n u m the huge sporting goods market. There is also pres­ REVOLUTIONIZED SPORTS: TRACK AND FIELD

y sure from the athletes and coaches to permit use o f the The Bole Vault a

w est equipment available. These forces have much the Until the 1950’s, pole vaulters used bamboo poles and e t same effect as lobbying in government. With pressure vaulted into a sawdust pit and the runways were of a

G cinders or dirt. Modern pits are now made of deep ab-

t Adjunct Professor of Mechanical Engineering e sorbant foam and the runways are o f a shock absorbant n ^m om ia State Universitu, Long Beach i synthetic material that gives better traction. It would be b 9539 yy. Old Stage Rd. a inconceivable for a modern vaulter to jump as high as

S Weed, CA 96094 USA 6 metres and land in a sawdust pit without injury. The y b d e c u d o

r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p 21 e R SPORTS EQUIPMENT

TABLE 1 Olympic Sports where equipment technology influences performance High ARCHERY BIATHLON BOBSLEDDING Tech CANOEING / KAYAKING CYCLING LUGE MODERN PENTATHLON ROWING SHOOTING SKIING YACHTING Medium FENCING FIELD HOCKEY ICE HOCKEY Tech FIGURE SKATING ROLLER SKATING SPEEDSKATING TENNIS Low BASEBALL BASKETBALL BOXING Tech DIVING EQUEST1AN GYMNASTICS JUDO FOOTBALL SOFTBALL SWIMMING SYNCHRO. SWIMMING TABLE TENNIS TEAM HANDBALL VOLLEYBALL WATER PO LE WEIGHTLIFTING WRESTLING HIGH, MEDIUM AND TRACK AND FIELD LOW TECH, COMBINED

most spectacular improvement, however, has been in for the previous 18 years At present the record is about the poles. Using a bamboo pole, Cornelius Warmerdam 6.1 meters. held the record for nearly 18 years at 4.72 meters, from The reason composite poles are superior is that ener­ 1942 to 1961. A slight improvement came with the in­ gy may be stored in the pole when it flexes, allowing troduction of steel and aluminium poles in the 1950’s the vaulter to hit the vault box much faster without un­ although they did not improve the record significantly. due shock.2 The pole bends to one side, so that the In the early 1950’s, Herb Jencks, a manufacturer of vaulter may swing straight through. At the top of the fiberglass fishing poles in Southern California made a swing, the stored energy in the pole is returned, cata­ new model deep sea tuna pole for commercial fisher­ pulting the vaulter over the ban Poles are wrapped so men. The pole was about 3 meters long and 3 cm in that they have a soft side and will bend preferentially diameter. Jenck’s son was a 45 kilo Junior High-school in one direction — this side is marked on each pole.

) polevaulter. As a lark, he and some of his friends took Modern poles are made of carbon and glass laminate. .

2 one of the fishing poles, used wooden plugs for pole The pole used by the present World record holder Serge 1

0 tips and tried polevaulting with the tuna pole. They Bubka weighs only 2.6 kg and is 5.25 meters long 2

d promptly bettered their best height by several inches (about .75m shorter than his record height)! Poles are e t compared to the bamboo or steel poles they had been specifically designed for the weight and skill of the a

d using. Jencks began building poles for local high school vaulter. Bubka’s pole is manufactured by Gill Sports o f (

r vaulters and later for all comers as they became more (Jrbana, Illinois. e

h popular. Figure 1 shows what happened to the pole Probably the most famous incident involving a com­ s i l vault record after introduction o f the fiberglass pole. The posite pole was when US Vaulter Bob Seagren had his b

u record went from 4.7 meters to over 5.2 meters in just carbon pole outlawed at the last minute by officials at P

four years, from 1961 to 1965, after remaining stagnant the 1972 Olympics They ruled that the pole had not e h t y b d e t n a r g e c n e c i l r e d n u y a w e t a G t e n i b a Figure 1 WORLD POLE VAULT RECORDS 1900-1984. S y b d e c u d

o SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 r p e R SPORTS EQCJIPMENI

1 S T 2a^ ? : ComP °s*e poles bend and store energy on the upswing, and release t H s e n e Z Z %Theu1^ £ % V op' -fcu*w/»fe<2 g hHu f 5 sPc«fc utf/iouf undue shock. The pole bends to the side to let the vaulter SZSJ T ? ce " * HntucotfZnS fibreglass and carbon poles in 1961, the pole vault record has increased over 1.5 metres. ) . 2 1 0 2

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been on the market for sufficient time to permit every­ a javelin for him that wouldn’t break. Dick made one one to have the chance to purchase one. He was forced of aluminium that was an immediate success Using the to vault with a borrowed pole and won the silver medal new javelins, Bud won the NCAA championship three although he was the World record holder. At present times and the AAU meet several times When he im­ a vaulter m ay use any pole design as long as it is com ­ proved his distance by about 7 meters, the Held javelin mercially available at least six months before the Olym­ attracted international attention. Within a few months, pic gam es Dick Held was designing and building javelins full-time. One unforeseen side-effect of high technology in the He is still in business at O regon Track Equipment, Eu­ polevault is that poles are so expensive (about $300- gene, Oregon and has designed the javelins that have $450 CIS) that their cost eliminates many of the deve­ set most of the recent World records loping countries from competing in the event. A dent The brilliant innovation introduced by Held came or mar in the surface can cause a pole to shatter. Ex­ when he realized that with javelin flight as with any treme care must be taken to protect the pole or a good other flight, aerodynamics was critical. He built his jave­ vaulter can go through several poles in a season. lins to take advantage of aerodynamic lift like a wing The introduction of the foam pit is often overlooked and he streamlined their shape so that they were far when considering pole vault and high jump records. more efficient. Unlike conventional javelins, the Held This m ade it safe for jumpers to fall from great heights javelin barely landed point down if thrown properly. It safely even if they landed incorrectly. Also runway sur­ kept a positive angle of attack during its flight If thrown faces have been specially designed to give the right in a vacuum for maximum distance, a modern javelin spring and traction to match the stride frequency of the would not travel as far, about 18% less than in air. The jumpers Modern shoes give better traction and resili­ Held javelins were termed “unstable” since they did not ence. The combination is a very high-tech system which align themselves with the flight path like an arrow, but permitted the vault record to increase more in 30 years continually changed their angle of attack during flight. than it had in the previous 65 years since the begin­ By 1986, the javelin World record was 104,8 meters, ning of the sport. a distance so far that javelins were sometimes landing The high jump record also increased 15% in the on the track, an obvious danger to the competitors See same time period. Part of this was no doubt due to Figure 3. A new javelin design was mandated by the changes in technique and training, but the major im­ governing body that changed the center o f gravity and provement was due to equipment technology. Aside shape of the javelin so that it would not have as much from improvements in shoes and the take off surface, aerodynam ic lift. Th e World record im m ediately fell to the Fosbury flop would be impossible without the foam 84.7 meters — it has since risen to 90.98 meters, about

) pit. Jumpers could only land a few times in sawdust 15 meters short of the old record. Among other things, .

2 without spending the rest o f their life in a wheel chair. the regulations specify the dimensions and weight dis­ 1

0 tribution of the new javelin and that they must be made 2 The javelin, discus and hammer

d Like the pole vault, the javelin record didn’t change of a single material. Javelins have been ruled illegal e t much during the 1930’s and 1940’s. In the late 40’s, a several times in the past three years for violating these a d rules One recent World record was voided because it

( Stanford javelin thrower, Bud Held, was discouraged at

r the high cost of hollow wooden Swedish javelins The was determined the competitor had used an aluminium e h wooden javelins of the time were very fragile and bad javelin stiffened with composite materials which s i l luck might cause several to break in a week. They were changed the launch and flight characteristics b u also hard or impossible to repair. He asked his brother One recent developm ent in javelin technology is the P Dick Held, an electrical engineer and contractor, to build work of Mont Hubbard of the University of California e h t y 3H3'lOin\ . b

JoH.BOm d e t n a r g e c n e c i l r e d n u y a w e t a G t e n i (900 I9IO 1920 1930 1940 19S0 l%0 1970 1900 1900 b a S

Figure 3 JAVELIN: OLYMPIC WINNING DISTANCES AND WORLD RECORDS. y b d e c u d o r 24 SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p e R SPORTS EQUIPMENT at Davis.345 Using an interactive computer and a high Like the javelin, the discus also has the potential of speed digitized video camera (200 frames per second), flying much further in air than in a vacuum due to its Hubbard has built a device that will measure the launch airfoil shape (about 11% further). W hen the wind blows characteristics of the javelin including velocity, launch from the right direction, the discus throwers are ecstatic angle, angle of attack and angular velocity. Using com­ since a proper wind lifts the discus and carries it further. puter simulation, Hubbard has been able to successfully The stronger the wind the better. Contrary to logic, it is predict the optimum launch conditions that will pro­ a quartering head wind that is best; it corrects the ten­ duce maximum distance. The javelin thrower is able to dency o f the discus to tip over and follow a curved path. instantaneously compare his actual throw with the ideal Figure 4 shows the progress of discus Olympic records throw and to correct technique to achieve longer dis­ Unlike the pole vault and javelin, the shape of the dis­ tances World class javelin throwers can launch the jave­ cus has been fixed rigidly for a long time and distance lin at about 30 meters per second. Hubbard, using wind improvements have mostly been due to better tech­ tunnel data, has shown that at this velocity, the old Held nique and training. This is shown by the uniform rise javelin should be thrown with a 5.9 degree initial angle in the distance versus time curve in Figure 4. One major of attack, a launch angle of about 30 degrees and a change has been made recently; the discus weight has slight negative pitching angular rotation of 9.2 degrees been concentrated almost entirely in the rim, making per second. The maximum distance is very sensitive to the discus more stable in flight and easier to throw at errors in pitch angular velocity (twist). If an error of a higher velocities The body is made of Kevlar or sheet few degrees per second is made, the javelin could fall aluminium, which weighs very little as compared to the 20 meters short even when thrown with the same ve­ rim. This high-tech discus is expensive and is only used locity. In other words, the “lucky” throw was a real fac in competition since it can be easily damaged. tor with the old javelin. A n analysis o f form er World re Even with the hammer, aerodynamics can play a part. cord holder Tom Petranoff showed that his record In the early 1980’s the East Germans manufactured a launch conditions with the old javelin almost identical hollow bronze hammer ball filled with mercury. Since ly matched Hubbard’s predictions. the ball had a smaller diameter, it had less air resistance For the new javelin, the release conditions are quite and flew further. The rules committee solved this pro­ different.6 Although the launch angle is the same at blem by specifying a minimum diameter for the ball, 30 degrees, the ideal pitch rotation is nose upward at thus making the material irrelevant. three degrees per second while the angle of attack is a negative two degrees The new javelin is much less Fast running tracks, tuned tracks and shoes sensitive, so the lucky throw is not such a factor in elite Igor Garrow, a US inventor, has recently obtained a pa­ competition. Probably the next major improvement in tent on a tuned running shoe that he claims will con­

) the javelin will be to increase its stiffness. Vibrations serve 70% of the impact energy now lost when the foot .

2 decrease the efficiency o f the throw. contacts the ground. The shoe utilizes light efficient car­ 1

0 This brings up a point that when new equipment and bon springs in the heel and sole to absorb the shock 2 techniques are introduced, careful analysis by biomech- of impact and later returns the energy when the foot d e t anicists and scientists can help improve performance leaves the ground. In theory this should work, however a the spring would have to be tuned to the stride frequen­ d still further. Close ties between athletes, coaches, train­ ( cy, weight and running technique of each athlete to be r ers and sports scientists has become essential for suc­ e cess. effective without altering the runner’s motion patterns h s i l b u P e h t y b d e t n a r g e c n e c i l r e d n u y a w e t a G t e n i b a S

Figure 4 DISCUS: OLYMPIC W INNING DISTANCES 1900-1990. y b d e c u d o r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994

p 25 e R SPORTS EQUIPMENT

and hindering performance. Several new devices have recently been built in the In 1977, a group o f Harvard scientists were asked to United States. A stationary paired oar rowing Simula help design a new indoor track; in their studies, they tor that displays force and power during a rowing cycle predict that if the compliance (springiness) of the track for both rowers, allows athletes, coaches and trainers were tuned to the runner, that running times should im­ to more accurately gauge training status and ability. prove from 2 to 3% when compared to a hard track At the US Olympic training center, an instrumented surface. In observations of comparative running times swim flume allows swimmers to be video taped in place on the Harvard track and at other tracks, this was for analysis of their technique. A light nylon line fed proven. One of the last real frontiers to be explored in from an instrumented reel, is attached to the swimmer events involving running or jumping, is to theoretical­ and gives instantaneous velocity. Pressure pads on the ly and experimentally design the surface to suit the swimmer’s palms provide a measure of the thrust force event (i.e. the long ju m p triple ju m p pole vault, high per stroke. Biomechanical studies are under way that jump and track running events). Each event and dis­ should identify efficient swimming motions and allow tance would thus use a different surface, and even have swimmers to refine their technique. variations in material at different locations (such as the A new table tennis robot has recently been demon long jump take off area). This of course would be time strated that can fire balls to any point on the table with consuming and expensive, however the results should variable velocities up to 160 kph and with adjustable be worth the effort. spin up to 6 000 RPM. It can be programmed to simu OTHER SPORTS Rowing, Canoeing, Kayaking late the serve and returns of any player from average In 1982 the CIS Olympic Committee created the Elite to an elite World champion. The inventor of the robot. Athlete Program to improve the chances of CIS athletes Waquidi Falicoff of the Logic Handle of Ashland, Ore in the Olympic Games by trying to develop better gon, has improved his standing in US table tennis by equipment, training techniques, coaching and support. 200 places since he started training with the simulator One of the outgrowths of this program was the design It allows a player to practise against World class com o f new rowing shells, canoes and kayaks. Ted Van Dus- petition at any time. Probably the most spectacular of the current simu en, president o f the Composite Engineering Inc. of Con­ cord, Massachusetts who is an Ocean Engineer and a lators is a project of Mont Hubbard of the University former CIS elite rower, has designed and built a fleet of California, Davis. Mont and his students have ob of carbon/Kevlar boats for the US teams.9 tained the digital coordinates of several of the World Cup and Olympic bobsled runs. The coordinates are Using shapes derived from computer models and re­ used as input into a real time computer model of bob )

. fined in tow tank tests, Van Dusen’s field experiments

2 sled dynamics.10

1 and competition results have proven the value of his

0 boats. US rowing, canoe and kayak teams have medaled Using an actual bobsled, they have fitted hydraulic 2 actuators that tilt the sled to simulate motion, allow d in both the 1988 and 1992 Olympics. Besides improved e

t ing the driver to practise sled runs down the track of shape to lower wave and friction drag, Van Dusen has a their choice without leaving the laboratory. They can d developed light weight composite wing-shaped paddles ( follow any arbitrary path they choose. A Silicon Graph r and oars which are more efficient in producing propul­ e ics computer and display monitor allows the driver to h sion. Composite oars and paddles, weigh about half s i steer using the standard bobsled steering linkage and l what traditional wooden ones do. Anoiher of Van Dus­ b pull handles. At the finish, the computer gives both the u en’s innovations is the aerodynamic rigger for rowing

P time and top speed of the run and plots a red line along shells. Instead of a conventional round tubing frame­ e the course showing the path as well as a green line h work, the riggers are airfoil shaped, making them both t showing the fastest run. By repeating the program, the y lighter and stronger than conventional riggers. In addi­ b tion they have a much lower air drag. Although air drag driver can compare each trial with the fastest path and d

e try different strategies to improve the time. The colour

t is only 12 percent of the total drag of a rowing shell, n races are often won by fractions o f seconds and any im­ computer display is amazingly convincing, it includes a r shadowing, a horizon that tilts as the sled travels up and

g provement could be the winning margin. One interest­ down the banks and realistic motion as indicated by e ing sidelight of Van Dusen’s computer studies showed c the texture and shadows speeding by the sled. Since n that for maximum speed, the length and shape of a e

c actual ice time is very expensive, the bobsled simula­ i boat should be matched to the weight of the crew. Van l tor allows the driver to become familiar with a course r Dusen has therefore built special boats for the women’s e before actually making live runs. d teams since their weight is much less than a typical n The object of any simulator is to reproduce reality

u men’s crew.

y accurately enough to make any training experience on a Simulators the simulator as valuable as the real thing. In this age w e of electronics it is a fertile field for development. Prob­ t One rapidly growing field is the design of sports simu­ a lators to give the athlete a chance for a realistic work ably the easiest sport to simulate is cycling. An elec­ G

t out in a laboratory environment. With the advent of fast tronically controlled ergometer can realistically simu­ e

n computers, with crisp graphics displays, athletes are late any course in the world. A powerful fan is required i b able to gauge their performance in real time and thus to provide equivalent cooling for the rider. Performance a

S use bio-feedback to improve. on a cycling ergometer has been shown to correlate well y b d e c u d o r 26 SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 p e R SPORTS EQUIPMENT with actual road or track performance.11 TABLE III Athletic clothing Advantage in running due to a 2% decrease in wind resistance Well designed athletic clothing can improve perfor­ Distance Lead mance in ways that are not always obvious. Dr Susan Time Difference (M etres) Watkins along with her Textiles and Apparels Depart­ (M eters) (Seconds) ment students at Cornell University have designed an 100 0.1 0.01 award winning protective uniform for female hockey 200 0.3 0.03 players.12 Previously women were forced to wear uni­ 400 0.9 0.10 forms made for male players, and the protection was 800 1.3 0.17 dangerously inadequate since nothing fitted properly. 1 500 2.0 0.29 Designed specifically for the female form, the new uni­ 5 000 5.8 0.90 form is lighter, more flexible, the padding remains in 10 000 9.2 1.55 place in competition and the special protective padding Marathon 35.4 6.44 is placed where needed. The lighter, well fitting, and (42 195 m ) more flexible clothing allows the players to accelerate Kyle CR, Athletic Clothing, Scientific American, March 1986, 254: faster and to move with increased fluidity, therefore im­ 3: 104-110. proving their game. The freedom from bruises and in­ jury, assured by the efficient padding, allows the ath­ letes to play with m ore confidence. The same approach hurdles. However in the 4x100m relay, the second US taken by Dr Watkins could be applied to field hockey Team was allowed to race in the preliminaries and failed or any other contact sport where protective clothing is to qualify when one of the runners passed the baton used. Light weight, flexibility and better protection over the line. The team complained that the hood muf­ should be the goals of such a design program. fled the audible commands. However the relay team had In cycling, speed skating, skiing, the bobsled, the not tried the suits before the Olympics. This under­ luge, and even in track and field, clothing is important scores the importance of thoroughly practising with any for another reason — aerodynamic drag. Loose fitting equipment you intend to use before competition. Be­ clothing has a much higher wind resistance at the high cause of the bad experience, the hooded suits have not speeds of these sports. Tight fitting, wrinkle-free suits been used since, however, skin suits are now common that cover the entire body like a second skin have been in track and field. used to substantially lower the wind resistance. Wind Even in swimming, clothing can lower drag. The US ) . tunnel tests indicate that even in running, wind resis­ team has been experimenting with slick full body suits 2

1 tance is significant, see Table 2.1314 The tests in Table for male swimmers. In theory they could have a lower 0

2 2 were performed on a manikin, fixed in a running pos­ drag than human skin.

d ture.15 By changing the clothing or hair fashion, large Another important factor in clothing is heat reflec­ e t differences in wind resistance have been recorded. A a tivity. Larry Bergland of the Cornell John B Pierce Foun­ d

( mathematical model shows that even a 2% reduction dation has shown that reflective clothing improves heat

r in wind resistance can have dramatic results on running

e dissipation from an athlete exercising in direct sunshine, h

s performance, see Table 3. The lead generated by a 2% as compared to bare skin.14 At high noon, the body i l reduction in air drag varies from 0.1 meters in the 100 can absorb as much as 100 watts in radiant energy from b u meter dash to 35 meters in the marathon. the sun. This added heat load must be carried away P In 1987, 1 designed a prototype skin suit for the US

e through sweating, thus adding to dehydration. Reflec­ h Olympic track team that included a hood'to cover up t tive clothing can decrease this water loss, keep the body

y the runners hair. This was worn by Roger Kingdom in cooler and therefore lower the heart rate and increase b

d winning the 1988 Olympic gold medal in the 110 meter endurance. The best clothing Bergland tested had an e t aluminized reflective coating, but lighter colours proved n

a to be better than dark. Bergland highly recommended r g that the New Zealand All-Blacks change their colours. TABLE II e

c Joking aside, in hot climates, special heat reflective

n Clothing wind tunnel tests

e clothing that efficiently wicks moisture away from the c i T Y P E O F CLOTHING Drag (g ) l Change in wind skin can definitely improve performance in endurance

r resistance (% ) events. e d Hair Tests n u N o Hair 1.50 0.0 Cycling y Long Sm ooth Hair 1.52 + 1.5% a Historically, European manufacturers have always pro­ w Short Curly Hair 1.556 + 3.9% e t Medium Wavy Hair 1.56 + 4.2% vided bicycles for the US Cycling teams because Euro­ a pean racing equipment was superior. In 1984, for the

G Clothing Tests

t first time, the US O lym pic Cycling Team used their own e Tight Lycra Track Suit 1.50 0.0

n cycling equipm ent with spectacular results. The last i Medium Track Suit 1.53 + 2.1% b Olympic cycling medal the US had won was a bronze a Large Track Suit 1.57 + 5.1%

S in the road race in 1912. In 1984, they won nine, in­ Tests at California Institute of Technology, C R Kyle, 1986. y cluding two gold medals. b d e c u d o r p SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 e 27 R SPORTS EQUIPMENT

Starting in 1982, under the USOC Elite Athlete Pro­ Record in the 4 000 meter pursuit, winning the event gram, at the request o f Dr Edmund Burke, then Tech­ by several seconds Burrows had been working on com­ nical Director of the (JSCF, I organized a group of 20 posite monocoque bikes since 1982 and neatly took people to design and test cycling equipment The group advantage of the rule revision with brilliant results As included Dr Paul MacCready, Paul Van Valkenburgh, I mentioned in the beginning of this paper, rule changes Don Guichard, Dr Allan Abbott Jack Lambie, Jim Gor­ continually occur, usually as a result of political pres­ don and Bruce Longson. We designed and built a com­ sure of one sort or another. When changes do happen, pletely integrated aerodynamic cycling system includ­ it pays to rapidly take advantage of them as Burrows ing clothing, helmets, shoe covers, disk wheels, an aero did. tubing funny bike, aero shifters, disk sprockets, aero cranks, and clip on pedals The wheel size of the bikes varied with the event In the team pursuit we used two 24 inch wheels so that the teams could draft closer for lower air drag. We performed hundreds of full scale wind REFERENCES tunnel tests at Texas A&M and Cal Tech that verified Advances in Sports Equipment Technology that that our system had a much lower air drag than con­ Enhance Performance ventional racing bicycles The CIS Olympic bike frames 1. Sports Equipment / Technology, Problems and Programs. Report were made by Huffy based on our prototypes The other of The CIS Olympic Committee Sports Equipment and Technolo­ gy Committee, December 5-7, 1984, Colorado Springs, Colora­ equipment was manufactured by our group Our tests do, (ISA, p. 7. showed that the equipment was seconds to minutes 2. Hubbard M. “Dynamics of the. Pole Vault". J. Biomechanics, V13, faster in the Olympic cycling events Experience proved no. 11, 1980, pp 965-976. us right.1718 3. Hubbard M and HJ Rust "Javelin Dynamics with Measured Lift, Drag and Pitching Moment". ASMEJ. Applied Mechanics.' V51, No. 2, pp 406-409, 1984. 4. Hubbard M and HJ Rust “Simulation of Javelin Flight using Ex­ perimental Aerodynamic Data". J. Biomechanics. ' V17, No. 10 pp 769-776, October 1984. 5. Hubbard M. "Optimum Javelin Trajectories". J. Biomechanics.’ V17, No. 10 pp 777-787, October 1984. 6. Hubbard M. "The Flight of the Javelin". In a special adversiting section, "The Technology of Winning", In Scientific American fol­ lowing p. 60. Scientific American, September 1988, p. T20-T21.

) C

. 7. Fmhlich ''Aerodynamic Effects on Discus Flight". Personal com­

2 munication with Cliff Frohlich, University of Texas, Marine Science 1

0 Institute, Galveston, Texas. 2

8. McMahon TA and PR Greene. "Fast Running Tracks". Scientific d American, v239, December 1978, pp 147-157. e t 9. Van Dusen ES. "Racing Shells, Canoes and Kayaks". Same ad­ a

d vertising section as in ref. 6. Scientific American, Sept. 1988, p. ( 76-77. r e 10. Hubbard M, M Kalla y and P RowhanL ‘Three Dimensional Bobsled h s Turning Dynamics". International Journal of Sport Biomechan­ i l Figure 5. Wind tunnel testing o f bicycles lead to the de­ ics. v5, pp 222-237, 1989. b

u velopment o f the time trial funny bike in 1984. The photo 11. Kyle CR and VJ Caiozzo. "Experiments in Human Ergometry as P

shows the Texas A&M wind tunnel, and the bicycle that Applied to the Design of Human Powered Vehicles". International e Journal of Sports Biomechanics. v2, pp 6-19, 1986. h was used to set the World Amateur Hour record (John t

12. Watkins S. “A Protective Uniform for Female Hockey Players". A y Frey USA, 49.946 km; Oct, 10, 1991). Cornell University student team report, winner of the 1992 USOC b Sports Equipment and Technology Committee Student Design d e Since 1984, every important time trial record in the Contest Presented at the SETC Quadrennial Conference Novem­ t n world has been broken using variations of the “funny ber 20-23, 1992, Colorado Springs, Colorado. a r bike” . In 1986 and 1987 Don Guichard and I built a 13. Kyle CR and VJ Caiozzo. "The Effect of Athletic Clothing Aero­ g

dynamics upon Running Speed'. Medicine and Science in Sports e monocoque carbon funny bike for the Dupont Compa­

c and Exercise. vl8, no. 5, 1986, pp509-515. n ny which was intended for use by the CIS team in the 14. Kyle CR. "Athletic Clothing". Scientific American, v. 254, no. 3, e c

i 1988 Olympics It had the lowest air drag o f any bike pp 104-110, 1986. l

15. Kyle CR. "The Wind Resistance of Racing Bicycles, Cyclists and r we ever measured in the wind tunnel. However when e Athletic Clothing. Report to the USOC Sports Equipment and Tech­

d Ed Burke took our plans to the Technical Commission nology Committee. March 10, 1987. n of the UCI, they rejected the bike as illegal and immedi­ u 16. Bergland L, "Evaporative Weight Loss as a Measure of Absorbed

y ately passed a set o f rules restricting tubing size and Radiation in the Human". 8th Conference of Biometeorology and a mandating a triangular frame. This assured that our Du­ Aerobiology, American Meteorological Society, Boston MA, 1987. w

e 17. Kyle CR and ER Burke. "Improving the Racing Bicycle". Mechan­ t pont bike could not be used. We abandoned the project

a ical Engineering. vl09, no.6, pp 35-45, 1984. In 1991 the (JCI unaccountably changed their racing

G 18. Kyle CR. “Wind Tunnel Tests of Aero Bicycles". Cycling Science,

t regulations making monocoque composite bikes legal. v3 no. 3, Sept/Dec 1991, pp 57-61. e

n Mike Burrows of England along with Lotus Ltd, de­

i • These papers are available through the author, Mont Hubbard, b signed and built a bike very similar to ours (but much Mechanical Engineering Department, University of California, Davis, a

S improved) on which Chris Boardman set a new World California 95616, Tel. (916) 752-6450. y b d e c u d o SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 r 28 p e R READERSHIP SURVEY

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d SPECIALITY: e t a d ( r e h s i l b u P e h t y b d e t n a r g e c n e c i l r e d n u y a w e t a G t e n i b a S y b d e c u d o r SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 29 p e R Die Effek van ’n Stresweerbaarheidsprogram op Valskermspringers

Dawie Scheepers en Justus Potgieter

Summary sel van drie tot 1 720 spronge. Hierdie groep is in ’n eksperimentele groep (n=18) en ’n kontrolegroep (n= A stress management programme for skydivers was de­ 18) verdeel. Om praktiese redes is die verdeling gedoen veloped from available literature. A n Experimental group op die basis van klublidmaatskap. Slegs die eksperi­ (n =18) and Control group (n =18) were used to evaluate mentele groep het tussen die twee evaluasiesessies ’n an eight-week programme. Pre- and post-experimental stresweeerbaarheidsprogram gevolg. psychological and physiological data proved the pro­ gramme to be effective according to a variety of criteria. Die stresweerbaarheidsprogram Inleiding Die intervensieprogram het oor ’n periode van agt weke gestrek en word kortliks bespreek. Stres kan ’n beduidende invloed op sportprestasie uit- Tydens die eerste sessie word psigometriese evalue­ oefen en in ’n sportsoort soos valskermspring kan dit ring gedoen. Toetslinge voltooi die IPAT-Angsskaal as- een van die belangrikste sielkundige probleme wees ook ’n biografiese vraelys. Die Sport Competion Anxiety waarmee die deelnemer te doen kry. Talle valskerm­ Test (SCAT) (Martens, 1977) ’n sportspesifieke meetin- springers met goeie potensiaal tree vroeg uit, dikwels strument wat uit 15 stellings bestaan en trek-angs bin- omdat hulle nie geleer het om stres te hanteer nie. Daar ne sportsituasies bepaal, is ook voltooi. Beide groepe is ook valskermspringers wat as gevolg van stres nooit is opgelei om hul harttempo te monitor. Toe hierdie stu- werklik doeltreffend kan konsentreer op hul spronge die uitgevoer is was daar nie tegnologiese middels, soos en formasies nie. byvoorbeeld polshorlosies, geredelik beskikbaar om Fenz en Jones (1972) se navorsing dui daarop dat harttempo op ’n gerieflike en ekonomiese manier te stres wat in vaiskermspring ervaar word, nie net opJos monitor nie. Harttempo is geneem op die oggend van en verdwyn nie, maar deur die springer beheer moet hul sprang, tydens die opstygfase en wanneer die vlieg- ) . word. Fenz (1973) haal enkele studies aan wat daarop 2 tuig sy hoogste hoogte bereik. 1 dui dat die kwessie van streshantering in valskerm­

0 In sessie twee tree die intervensieprogram in werking

2 spring vaag en indirek aangespreek word. Verder wys met ’n bespreking van rasionele emotiewe terapie (RET) d Brewer en Shillinglaw (1992) daarop dat die literatuur e

t (Ellis, 1974). Die grondslag van hierdie benadering is

a wat handel oor sportsielkundige dienste gewoonlik ver- dat sielkundige probleme grootliks die gevolg is van d

( wys na intervensies op ’n individuele basis en dat daar irrasionele denke. Die mens kan homself van baie on- r

e ’n behoefte is aan navorsing oor die geskiktheid van gelukkigheid bevry as hy leer om irrasionele denke te h s sielkundige ondersteuning in groepsverband. Die hui- i elimineer en logies en rasioneel te dink. Die basis van l

b dige ondersoek het in hierdie behoefte probeer vol- hierdie sielkundige intervensie is dus om die valskerm- u doen. Die primere probleem wat hierdie ondersoek aan­

P springer te leer om rasioneel te dink. Die RET-sessies

e gespreek het, was die daarstelling en evaluering van 'n is spesifiek van toepassing op valskermspring gemaak. h t stresweerbaarheidsprogram spesifiek vir 'n groep val­ In hierdie sessie maak die springers ook kennis met y skermspringers, maar wat ook vir ander sportsoorte van b

progressiewe ontspanning. Die tradisionele tegniek

d nut kan wees.

e word effens gewysig om aan te pas by die beknopte t ’n Belangrike faktor by die ontwerp van ’n sielkundige n ruimte binne die vliegtuig. Aan die einde van die ses­ a program is die praktiese toepasbaarheid daarvan op die r sie, asook na afloop van elk van die daaropvolgende g

teikengroep. Die opsteller van so ’n program behoort

e sessies, kry die springers tuiswerkopdragte. c dus benewens sy sielkundige bevoegdheid ook genoeg- Sessie drie word weer eens ingelei met RET. Die in- n e same praktiese ervaring in valskermspring te he. Die c houd van die vorige sessie word hersien waarna die i l hoofnavorser het aan hierdie vereistes voldoen. springers se tuiswerk oor RET en progressiewe ontspan­ r e ning gekontroleer en bespreek word. Irrasionele gedag- d Streekproef n tes wat algemeen voorkom word bespreek. Die sprin­ u

Ses-en-dertig aktiewe valskermspringers in die Weste- gers word daarop gewys dat irrasionele opvattings wat y

a like Provinsie en Boland is by hierdie eksperiment be- emosionele probleme veroorsaak deur vorige ervarings w trek. Die ervaringsvlakke van die springers het gewis- e (kondisionering) maar veral as gevolg van sosiale leer t a Departement Menslike Bewegingskunde ontstaan. Die belangrikste kategorieS waaronder hier­ G die irrasionele gedagtes manifesteer sluit onder ande- t (Jniversiteit van Stellenbosch e re in absolutistiese denke, katastrofering, negatiewe self- n Stellenbosch i b 7600 beoordeling, ongeldige gevolgtrekkings, swart/wit den­ a ke, en “ek-kan-dit-nie-verdra-nie” denke. Die sessie word, S

South Africa y b d e c u d o SA JOURNAL OF SPORTS MEDICINE SEPTEMBER 1994 r 30 p e R STRES

soos die vorige sessie, afgesluit met ’n volledige oefe- kaar verskil het, is daar in die statistiese verwerking van ning van progressiewe ontspanning en ’n RET-tuiswerk- die data ’n ontleding gedoen van die relatiewe verskille opdrag asook ’n opdrag om progressiewe ontspanning tussen die voor- en na-toetse binne die twee groepe. Die met behulp van ’n geskrewe uiteensetting van die pro- mate waarin die veranderlikes binne een groep toe- of sedure daagliks tuis te oefen. afgeneem het, is vergelyk met die hoeveelheid veran- Sessie vier begin met hersiening van vorige werk. dering wat binne die ander groep plaasgevind het. Daar word seker gemaak dat die springers die kriteria Die resultate (sien Tabel 1) dui daarop dat beide die van rasionele opvattings ken en dat almal ’n paar voor- psigometriese en fisiologiese veranderlikes by die ek­ beelde met betrekking tot die ABC-analise van emo- sperimentele groep ’n verbetering getoon het, terwyl die sies neergeskryf het. Die sessie word afgesluit met pro­ kontrolegroep se tellings konstant gebly of sells ver- gressiewe ontspanning, maar sonder die spanningsfa- sleg het. se. Die doel van hierdie ontspanningsprosedure is om die springer m eer suggereerbaar te maak vir die daar- In die geval van die IPAT-veranderlike (angs) het die kon­ opvolgende beeldingsoefening. trolegroep se telling toegeneem terwyl die eksperimen­ In sessie vyf word RET bespreek waarna progressiewe tele groep se telling nie beduidend verander het nie. ontspanning en outosuggestie as ontspanningstegnie- Die toename in die angstelling van die kontrolegroep ke geoefen word. kan nie verklaar word nie, maar het moontlik te make Sessie ses word met RET begin waarna progressiewe met n verhoging in stres in die alledaagse lewe van die ontspanning, outosuggestie-ontspanning en beelding toetslinge. geoefen word. Realistiese beelding van die valskermsp- Die gemiddelde SCAT-telling (kompetisie-angs) van ring in die bepaalde formasies wat gedoen gaan word, die eksperimentele groep het ’n beduidende afname word geoefen. In hierdie stadium word springers gehelp getoon na afloop van die stresweerbaarheidsprogram. om in rasionele terme aan valskermspring te dink son­ Die kontrolegroep se telling, daarenteen, het redelik der om byvoorbeeld te verabsoluteer o f te katastrofeer. konstant gebly. Dit is belangrik dat hulle hierdie prosedures so veel Wat die harttempo betref, het die eksperimentele moontlik oefen aangesien dit is hoe hulle sal moet dink groep beduidende afnames getoon by al drie metings wanneer hulle spring. Die springers word aanbeveel om (oggend van sprang, opstygfase en wanneer die vlieg­ of progressiewe ontspanning, outosuggestie-ontspan- tuig sy hoogste punt bereik het). Die kontrolegroep se ning o f ’n kombinasie van die twee tegnieke te gebruik gemiddelde tellings het konstant gebly, maar in die ge­ wanneer die vliegtuig besig is om tot op hoogte te klim. val van die opstygfase het dit selfs verhoog. Die springer m oet tydens hierdie fase kan ontspan ter- As gevolg van ’n gebrek aan narvorsingspubfikasies wyl hy die sprang wat voorle in detail beeld. hieroor kon hierdie bevindinge ongelukkig nie met an- ) . Sessie sewe word gewy aan ontspanning en beelding. 2 der navorsingsresultate vergelyk word nie. 1 Daarna word die hele proses van rasionele denke her- 0 2

sien in die vorm van ’n lesing en ’n groepbespreking. Subjektiewe evaluering deur proefpersone d e Tydens sessie agt word psigometriese evaluering t Springers is gevra o f hulle steeds deel van die program a (SCAT en IPAT) gedoen asook bepaling van harttem­ sou wou gewees het as hulle vooraf geweet het wat die d ( po. Springers word ook gevra om die afgelope stres- program behels. Van die agtien proefpersone het elf r e weerbaarheidsprogram te evalueer. aangedui dat hulle “beslis” daaraan sou deelgeneem h s i het, terwyl die res (7) aangedui het dat hulle wel aan l Resultate b die program sou deelgeneem het. Verder het ses per- u

P In die voortoets is met die uitsondering van die SCAT- sone aangedui dat die program “beslis nodig” was, ter­ e tellings geen verskille tussen die eksperimentele en wyl nege persone van mening was dit dit “nodig” was. h t kontrolegroep gevind nie. Op grand van die feit dat daar Drie persone was onseker. Sewe toetslinge het aange­ y b wel een veranderlike was waar die twee groepe van me- dui dat hulle "geweldig baie” baat daarby gevind het, d e t n TABE L 1 a r g ’n Vergelyking van Voor- en Natoets-Gemiddeldes e c n Eksperimentele Qroep (n==18) e Kontrolegroep (n= 18) c i Voortoets Natoets t l Voortoets Natoets t r e IPAT 31.28 27.39 1.84 d 26.67 30.89 - 6 .3 1 * * * n SCAT 22.28 19.78 3 .1 0 ** 18.44 18.50 - 0 .0 8 u HARTTEMPO y a O ggend 79.33 76.44 2.82* 80.39 82.00 -1 .7 1 w e Opstyg 96.61 90.56 4 .6 4 *** t 93.00 95.33 -2 .1 7 * a H oog 101.50 96.78 3.1 9 ** 102.11 104.89 - 1 .8 3 G t

e * p < .05 n i ** p < .001 b

a * * * p < .0001 S y b d e c u d o SA SPORTS MEDICINE SEPTEMBER 1994 r JOURNAL OF 31 p e R STRES

tien persone “redelik baie” en een persoon het “gemid- Slot deld” baat gevind. Op grond van die die objektiewe data en subjektiewe Die respondente is versoek om aan te dui by watter beoordeling van die proefpersone kan daar aanvaar aspekte van die program hulle die meeste baat gevind word dat hierdie stresweerbaarheidsprogram suksesvol het. Vyftien persone het aangedui dat die rasioneel was in terme van streshantering vir die groep valskerm­ emotiewe terapie vir hulle die nuttigste was Twee per­ springers. Hoewel dit nie impliseer dat hul prestasies sone het progressiewe ontspanning as die waardevolste noodwendig verbeter het nie, onderstreep dit nogtans aspek beskou. Agt persone het outosuggestie as die die nut van sportsielkundige ondersteuning by die voor- swakste gedeelte van die program geevalueer terwyl se- bereiding van sportlui. we persone beelding as die aspek beskou het waarby hulle die minste gebaat het. Drie persone het aange­ dui dat die progressiewe ontspanning die minste nut gehad het. Die lae waarde wat aan progressiewe ont VERWYSINGS spanning toegeken is, is verrassend aangesien hierdie Brewer BW & Shiiiinglaw R (1992). Evaluation of a psychological skills tegniek in talle programme van hierdie aard buite die training workshop for male intercollegiate Lacrosse players. The Sport sportarena ingesluit word. Psychologist, 6, 139-147. Ellis A (1976). Humanistic psychotherapy. The rational-emotive ap­ Hoewel die response van die toetslinge uiteraard sub- proach. New York: McGraw Hill. jektief is en nie statistics bevestig kan word nie, is dit Fenz WD (1973). Stress and its mastery: Predicting from laboratory nogtans belangrik om na hul subjektiewe ervarings te to real life. Canadian Journal of Behavioral Science, 5, 332-346. kyk. Die meeste proefpersone (10) wat die program ge­ Fenz WD & Jones GB (1972). Individual differences in physiological volg het, het aangedui dat hulle na afloop van die pro arousal and performance in sport parachutists. Psychosomatic Medicine, 34, 1-8. gram stres beter kon kanteer as voor die aanvang van Fenz WD & Jones GB (1974). Cardiac conditioning in reaction time die program. Daarteenoor het die meeste toetslinge (11) task and heart rate control during real life stress. Journal of Psy­ in die kontrolegroep aangedui dat hulle dieselfde ma­ chosomatic Research, 18, 199-203. te van stres as tevore ervaar het. Daar het dus nie ’n Martens R (1977). Sport competition anxiety test Champaign IL: Hu­ verbetering ingetree met betrekking tot hul subjektiewe man Kinetics. Rowel FM & VemerJP (1982). Anxiety and performance relationships vermoe om stres te hanteer nie. Dit impliseer egter nie in first-time parachutists. Journal of Sport Psychology, 4, 184-188. dat hierdie groep persone tekortkominge met betrek Roginska W (1969). A psychological analysis of parachuting. Prezegtad king tot streshantering gehad het nie. Psychologiczy, 18. 33-50. CD ) . 2 1 0 2

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