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This study compares the initial outcomes of minimally invasive techniques for single-event multi-level surgery with conventional single-event multi-level surgery. The minimally invasive techniques included derotation osteotomies using closed corticotomy and fixation with titanium elastic nails and percutaneous lengthening of muscles where possible. A prospective cohort study of two matched groups was undertaken. Ten children with diplegic cerebral palsy with a mean age of ten years six months (7.11 to 13.9) had multi-level minimally invasive surgery and were matched for ambulatory level and compared with ten children with a mean age of 11 years four months (7.9 to 14.4) who had conventional single-event multi-level surgery. Gait kinematics, the Gillette Gait Index, isometric muscle strength and gross motor function were assessed before and 12 months after operation.The minimally invasive group had significantly reduced operation time and blood loss with a significantly improved time to mobilisation. There were no complications intra-operatively or during hospitalisation in either group. There was significant improvement in gait kinematics and the Gillette Gait Index in both groups with no difference between them. There was a trend to improved muscle strength in the multi-level group. There was no significant difference in gross motor function between the groups.We consider that minimally invasive single-event multi-level surgery can be achieved safely and effectively with significant advantages over conventional techniques in children with diplegic cerebral palsy.

Surface electromyography (EMG) and torque were measured from knee flexors and extensors in 12 control subjects (CS) aged 25-59 years (10 female) and bilaterally in 12 stroke subjects (SS) aged 27-75 years (four female) with hemiparesis and mild clinical spasticity. They performed isometric and isokinetic maximal voluntary contractions (MVC) and also isokinetic passive movements at angular velocities from 30 to 300°/s. The time taken to walk 10 m was documented. Greater torque was recorded during passive extension in the paretic legs when compared with both non-paretic and control limbs (p<0·01). No EMG activity was measured in any subject. Isometric MVC torque of both muscles in the paretic leg was less (p < 0·01) than both the non-paretic and control limbs. The SS generated relatively less torque bilaterally at the lower velocities than CS. Not all SS reached the higher velocities and none of the paretic limbs achieved 300°/s during flexion. Gait speed correlated with maximal paretic knee extension velocity (p < 0·001). The extent of co-contraction during MVCs was generally low or absent and similar in all three groups. These results suggest a mechanical rather than reflex cause for the restraint detected clinically. Low force generation by the paretic agonists appeared to be the major cause of reduced torque, rather than antagonist opposition.

Eccentric exercise causes release of muscle creatine kinase (CK) 3–4 days after exercise. Racial variation in basal serum CK has been reported but the reasons for this are unknown. We studied 30 subjects of different ethnic origin (Caucasian, Afro-Caribbean, Asian) before and after eccentric exercise. Basal serum CK was significantly higher in the Afro-Caribbean group (201 ± 134IU/L, median ± SD) compared to Caucasians (81 ± 57 IU/L). The Asian group had intermediate CK values (144 ± 93 IU/L).The intra-individual range of peak post-exercise CK values obtained was very wide (95–30 200 IU/L) with little difference in median CK between the Afro-Caribbean (8450 ± 9020 IU/L) and Caucasian groups (7600 ± 8800 IU/L). The median value for the Asian group was lower (594 ± 5410 IU/L). A sub-group of 15 individuals undertook a second bout of exercise 2 weeks later and all subjects demonstrated a training effect resulting in a marked attenuation of enzyme efflux. The variation in CK between the ethnic groups was not related to measurements of muscle strength or body mass, although the torque: body mass ratio followed the same order as the basal CK, i.e. the Afro-Caribbeans had the highest values. These results highlight the importance of considering ethnic origin and previous exercise history when interpreting serum CK assay results.

1. The influence of three mechanical factors, force, muscle length and passive lengthening, on long‐lasting changes in voluntary force generation, the force:frequency relationship and the development of tenderness has been studied in healthy human skeletal muscle. The elbow flexors were used in all studies. The effect of muscle length was also investigated in the quadriceps and adductor pollicis muscles. Eighty maximal voluntary contractions (MVCs) were performed: one contraction, lasting approximately 2 s, every 15 s. The MVC and force:frequency relationships were measured before and immediately after the exercise and, together with an assessment of tenderness, at 24 h intervals thereafter. 2. In a series of experiments designed to investigate the effects of force, eccentric (lengthening) contractions were found to cause greater fatique and delayed‐onset muscle pain than either isometric or concentric (shortening) contractions. There were, however, no substantial differences between the effects of isometric and concentric contractions. Changes in MVC took 24‐48 h to return to normal while the low‐frequency fatigue required 3‐4 days to recover. 3. Passive lengthening with a comparable number of movements over the full range had no effect on the force generation of the muscle, nor did it cause any muscle pain. 4. In the series of experiments designed to investigate the effects of length, isometric MVCs were performed at either short or long length and the muscles subsequently tested at an intermediate length. The contractions at long length resulted in greater low‐frequency fatigue and pain, despite the fact that they generated less force than those at the short length. 5. The results demonstrate that there is no simple relationship between the force generated during exercise and the development of long‐lasting muscle fatigue and pain. Furthermore, there is a length‐dependent component in the generation of low‐frequency fatigue and muscle pain.

1. The relationship between intracellular metabolites and the generation of force during fatigue has been examined in the first dorsal interosseous muscle of the hand. With the arm made ischaemic, the muscle was fatigued by three bouts of maximal voluntary contraction, leaving approximately three minutes ischaemic rest between contractions. During one series of experiments intracellular phosphorus metabolites were measured by nuclear magnetic resonance during the intervals between the fatiguing contractions: in the second series contractile properties were tested with brief electrical stimulation during the rest intervals. 2. The relationships between loss of force and change in metabolite concentrations obtained with four normal subjects were compared with those from one subject with myophosphorylase deficiency (MPD) who could not utilize muscle glycogen and therefore produced no hydrogen ion from glycolysis during exercise. 3. For both the MPD and normal subjects the relationship between relative force loss and inorganic phosphate (Pi) concentration was curvilinear, force changing little in the early stages of the contraction when the intracellular Pi was accumulating rapidly but falling faster when the Pi was above 25 mM and increasing relatively slowly. 4. In the normal subjects intracellular pH fell from a mean of 7.03 +/‐ 0.01 (mean +/‐ S.E. of mean, n = 19) in the fresh muscle to 6.51 +/‐ 0.02 at the end of the fatiguing exercise; force, as a percentage of the initial value, fell in proportion to the increase in H+ concentration. In the MPD subject pH did not change and force loss was therefore independent of H+ accumulation. In the normal subjects the force of the fatiguing muscle showed an approximately linear relationship with the concentration of the monobasic form of inorganic phosphate. However, the MPD subject showed a quite different relationship, with force loss being much greater for a given concentration of monobasic phosphate. This result indicates that monobasic phosphate is not a unique determinant of force loss in fatigued muscle. 5. During the first 60 s of recovery in the normal subjects, pH remained low while force recovered, indicating a mechanism of force loss that was independent of H+ accumulation. However, the recovery of force was not complete, so that for comparable phosphocreatine contents the recovering, more acid, muscle generated less force than the muscle that was being fatigued. It was estimated that H(+)‐dependent and independent mechanisms contributed roughly equally to the observed force loss. The relationship between force and the concentration of monobasic phosphate differed in fatiguing and recovering muscle.

1. The metabolic costs and physiological consequences of shortening contractions of a human muscle working in situ have been compared with those of the muscle maintaining a continuous isometric contraction and when performing repeated brief isometric contractions. 2. After a total of 10 s stimulation, the shortening and intermittent brief isometric protocols had very similar effects, causing a 30% loss of force and a threefold increase in the half‐time of relaxation. This was in contrast to the continuous isometric contraction protocol where there was less than 10% loss of force or slowing of relaxation. 3. The ATP cost over the first 5 s of the continuous isometric protocol was 27 mmol (l intracellular water)‐1 while for the shortening and repeated brief isometric protocols the costs were 48 and 46 mmol (l intracellular water)‐1, respectively. 4. The results show that shortening and repeated brief isometric contractions are considerably more energetically demanding, and hence more fatiguing, than sustained isometric contractions.

1. The relationship between joint damage, quadriceps weakness and arthrogenic muscle inhibition was investigated in eight patients who had sustained extensive traumatic knee injury. Isometric and isokinetic quadriceps and hamstring voluntary strength, and quadriceps arthrogenic muscle inhibition during isometric contractions, were measured before and after 4 weeks (approximately 100 h) of intensive rehabilitation. 2. Compared with the uninjured leg, before rehabilitation the injured leg had larger amounts of quadriceps arthrogenic muscle inhibition (P < 0.025), quadriceps (P < 0.0001) and hamstring (P < 0.0001) weakness and severe functional joint instability. There was a negative correlation between the amount of arthrogenic muscle inhibition and quadriceps voluntary contraction force (P < 0.025). 3. After rehabilitation in the injured leg there were small hamstring strength increases (P < 0.05–0.025), but no overall significant quadricep strength increase. Arthrogenic muscle inhibition was statistically unchanged. Severe functional joint instability was still reported by all patients. 4. Previous studies have shown that minimal joint damage evokes relatively less arthrogenic muscle inhibition that does not impede rehabilitation. These data indicate that greater joint damage is associated with greater arthrogenic muscle inhibition, quadriceps weakness and joint instability. Furthermore, intensive rehabilitation had little affect on either quadriceps arthrogenic muscle inhibition or atrophy.

The effects of eccentric exercise have been examined in human calf and biceps muscles. Release of muscle creatine kinase and uptake of technetium pyrophosphate have been followed for up to 20 days after the exercise and the results are related to the morphological changes seen in needle biopsy samples. The response to exercise was variable, all subjects developing pain and tenderness in the exercised muscles after 1‐2 days and this was followed, in most subjects, by a large increase in plasma creatine kinase 4‐6 days after the exercise. This was paralleled by an increased uptake of technetium pyrophosphate into the exercised muscle. Biopsies of the affected muscles showed little or no change in the first 7 days after the exercise but later degenerating fibres were seen, as well as infiltration by mononuclear cells and eventually, by 20 days, signs of regeneration. Very extensive changes were seen in the calf muscle of one subject; changes in the biceps were qualitatively similar but not so severe. In the severely affected calf muscle type II fibres were preferentially damaged. Mononuclear cell infiltration both between and within degenerating fibres was maximal well after the time of peak plasma creatine kinase and it is likely that in eccentrically exercised muscle infiltrating mononuclear cells act to scavenge cellular debris rather than to cause damage to the muscle.

1. Skeletal muscle strength, contractile properties and radiological composition have been studied in seven morbidly obese adults (six female) before and 1 year after gastroplasty operations. The mean body weight fell from 138.3 kg (sd 25.2) to 99.7 kg (sd 23.0) (P < 0.001). 2. The strength and contractile properties (force/frequency, relaxation rate and fatiguability) of both the adductor pollicis and quadriceps muscles were unaffected by the weight loss. 3. Computerized axial tomography scans obtained 1 year after surgery showed that the quadriceps contained an abnormally high proportion of fat. The mean fat content was 10.8% (range 3.0–30.1%) compared with 1.6% (range 0–5%) for normal muscle. Two individuals were scanned before and after surgery and the fat content of their quadriceps fell from 12.6% and 6.9% to 3.1% and 3.0%, respectively. 4. It is concluded that in obese individuals large amounts of weight can be lost, from both subcutaneous and intramuscular fat stores, without compromising either the strength or contractile properties of skeletal muscles. These results do not support the claim that skeletal muscle contractility is a sensitive indicator of changes in nutritional status.

We have studied the occurrence of skeletal muscle uptake of 99mtechnetium pyrophosphate (Tc-PYP), creatine kinase (CK) release and muscle pain in normal subjects after exercise. Five subjects stepped on and off a high bench in such a way that one leg stepped up and the other down. Pain only developed in the muscles used for descending: quadriceps, adductors and gluteal muscles of one leg and the calf muscle of the other. A large rise in plasma CK occurred in four subjects but no increased Tc-PYP muscle uptake was seen in the quadriceps. In the four subjects with high CK effluxes, increased isotope uptake was seen in the thigh adductors used when stepping down; in the two subjects with the largest CK effluxes there was extensive uptake into the gluteal muscles. Muscle pain preceded and was not well correlated with either the magnitude of the enzyme release or the amount and distribution of increased muscle isotope uptake. We conclude that delayed onset muscle pain, the cause of which remains unknown, is a poor indicator of muscle damage as indicated by circulating muscle enzymes and muscle isotope uptake. Tc-PYP uptake by skeletal muscle can provide useful information about the localisation and time course of muscle damage.

Exercise can cause muscle pain for a number of reasons. Usually the pain is experienced during the exercise and recovers rapidly afterwards. There is one type of muscle pain that has a very different and characteristic time course. In this situation the exercise itself, and the immediate post-exercise period are painfree. The pain is not felt for about eight hours and is maximal 1 or 2 days later. Delayed onset muscle pain occurs after unaccustomed, high force contractions and is particularly associated with eccentric contractions. The concensus of opinion is that the pain is caused by some form of damage, but the mechanism for the pain is not known. This review summarises the literature on the consequences of eccentric contractions and relates them to delayed onset muscle pain. There is clear evidence of damage to the muscle fibres themselves, their membranes and, at a later stage, mononuclear cell infiltration, but all these have very different time courses and none are the same as the pain. Intramuscular pressures are raised in some, but not all, painful compartments and even when raised follow a different time course to the pain. Anti-inflammatory agents do not affect the pain, but due to the incomplete understanding of the action of these drugs, the role of inflammation in delayed onset muscle pain is uncertain.

1. Normal subjects performed a step test in which the quadriceps of one leg contracted concentrically while the contralateral muscle contracted eccentrically. 2. Maximal voluntary force and the force:frequency relationship were altered bilaterally as a result of the exercise, the changes being greater in the muscle which had contracted eccentrically. Recovery occurred over 24 h. 3. Electromyographic studies using three sites on each muscle showed an increase in electrical activation during the exercise only in the muscle which was contracting eccentrically. Recovery followed a time course similar to that of the contractile properties. 4. Pain and tenderness developed only in the muscle which had contracted eccentrically. Pain was first noted approximately 8 h after exercise and was maximal at approximately 48 h after exercise, at which time force generation and electrical activation had returned to pre-exercise values. 5. Eccentric contractions cause more profound changes in some aspects of muscle function than concentric contractions. These changes cannot be explained in simple metabolic terms, and it is suggested that they are the result of mechanical trauma caused by the high tension generated in relatively few active fibres during eccentric contractions.

Intermittent High Intensity Exercise: Preparation, Stresses and Damage Limitation, D.A.D. Macleod, R.J. Maughan, C. Williams, C.R. Madeley, J.C.M. Sharp and R.W. Nutton (eds), E. & F.N. Spon, London, 1993. xiii + 605 pp., £39.95 (hb), ISBN 0419 17860 0Sports Without Pressure, E. Margenau, Gardner Press, New York, 1990. vii + 160 pp., £7.95 (pb), ISBN 0 89876 165 4The Sporting Body, M. Cross, N. Gibbs and J. Gray, McGraw-Hill, Sydney, 1991. xvi + 184 pp., £25.00 (pb), ISBN 0 07 452830 0Clinical Sports Medicine, P. Brunkner and K. Khan, McGraw-Hill, Sydney, 1993. xxi + 697 pp., £99.00 (hb), ISBN 0 07 452852 1Swimming into the 21st Century, C.M. Colwin, Leisure Press, Champaign, IL, 1992. xvi + 255 pp., £20.50 (hb), ISBN 0 88011 436 3Drugs in Competitive Athletics, J.R. Shipe and J. Savory (eds), Blackwell Scientific, Oxford, 1991. v + 139 pp., £18.50 (hb), ISBN 0 632 03181 6A Collection of European Sports Science Translations: Parts I, II and III, J. Jarver (ed.), South Australian Sports Institute, Adelaide, 1990. 262 pp., A$59.95 (pb), ISBN 0 7308 1674 5Anabolic Steroids in Sport and Exercise, C.E. Yesalis (ed.), Human Kinetics, Champaign, IL, 1993. xi + 325 pp., £26.50 (hb), ISBN 0 87322 401 9Children and Sport: Fitness, Injuries and Diet, V. Grisogono, John Murray, London, 1991. xi + 244 pp., £18.95 (hb), ISBN 0 7195 4908 6Isokinetic Exercise and Assessment, D.H. Perrin, Human Kinetics, Champaign, IL, 1993. x+212 pp., £18.50 (hb), ISBN 0 87322 464 7Applied Sociology of Sport, A. Yiannakis and S.L. Greendorfer, Human Kinetics, Champaign, IL, 1992. viii + 288 pp., £21.50 (hb), ISBN 0 87322 320 9Weight Training for Sports: Based on the Revolutionary Matrix Principle, R. Laura and K. Dutton, Partridge Press, London, 1993. 296 pp., price unknown (pb), ISBN 185 225 206 5Flexibility, P. McNaught-Davis, Partridge Press, London, 1991. xiii + 146 pp., £14.99 (hb), ISBN 185 225 109 3Muscles, Masses and Motion: The Physiology of Normality, Hypotonicity, Spasticity and Rigidity, E.G. Walsh, Blackwell Scientific, Oxford, 1992. xi + 220 pp., £32.00 (hb), ISBN 0 9012 97 5Facilitated Stretching, R.E. Mcatee, Human Kinetics, Champaign, IL, 1993. xi + 108 pp., £11.50 (pb), ISBN 0 87322 420 5ACSM's Guidelines for the Team Physician, R.C. Cantu and L.J. Micheli (eds), Lea and Febiger, Philadelphia, PA, 1991. xv+323 pp., £17.50 (pb), ISBN 0 8121 1370 5Cycling Physiology and Health, E. Burke, Vitesse Press, Brattleboro, Vermont, 1992. xi + 234 pp., price unknown (pb), ISBN 0 941950 25 5Observations on the Soviet/Canadian Transpolar Ski Treek, R. Shepherd and A Rodes (eds), Karger, Basel, 1992. x+190 pp., £85.30 (hb), ISBN 0 8055 5410 9Physical Activity, Fitness, and Health: Consensus Statement, C. Bouchard, RJ. Shephard and T. Stephens, Human Kinetics, Champaign, IL, 1993. xv + 102 pp., £14.50 (pb), ISBN 0 87322 470 1New Dimensions in Aerobic Fitness, B.J. Sharkey, Human Kinetics, Champaign, IL, 1991. vi +106 pp., £10.95 (pb), ISBN 0 87322 326 8

1. The effect of muscle length on the development of muscle pain and fatigue has been studied. 2. Eight normal young adults performed maximal eccentric contractions of the elbow flexors. The muscles of one arm were exercised at short length, and the contralateral muscle at long length. Each contraction lasted approximately 1 s, and was repeated once every 10 s for 30 min. 3. Muscle strength and frequency-force characteristics were measured from isometric contractions before, immediately after and at 24 h intervals for the next 4 days. Muscle tenderness was assessed daily. 4. The muscle strength was reduced by approximately 10% by exercise at short length, and by 30% by exercise at long length. 5. The 20:100 ratio (force generated by stimulation at 20 Hz/force generated at 100 Hz) fell by 30% after exercise at short length and had recovered after 24 h. Exercise at long length reduced this ratio by 65% and the muscles had not fully recovered 4 days later. 6. Muscle pain developed after both exercise regimens, but was slightly worse after that at long length. 7. It is concluded that there is a length-dependent component in the development of pain and fatigue after eccentric exercise, which had previously been thought to be caused solely by high force generation.