Baixe Neural Influences on Sprint Running: Training Adaptations and Acute Responses e outras Manuais, Projetos, Pesquisas em PDF para Fisioterapia, somente na Docsity! Neural Influences on Sprint Running Training Adaptations and Acute Responses Angus Ross, Michael Leveritt and Stephan Riek School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 409 1. Muscle Activation and Recruitment Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411 1.1 Technique Differences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411 1.2 Electromyographic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412 1.3 Fibre Type Recruitment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412 2. Speed and Degree of Muscle Activation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413 2.1 Nerve Conduction Velocity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413 2.2 Motoneuron Excitability and Reflex Adaptation . . . . . . . . . . . . . . . . . . . . . . . . . . 414 2.2.1 Stretch and Hoffman Reflex in Relaxed Muscle: Effect of Sprint Exercise . . . . . . . . 415 2.2.2 Reflex Potentiation by Contraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416 2.2.3 Reflex Influence on Gait: Implications for Sprinting . . . . . . . . . . . . . . . . . . . . . 417 3. Neural Fatigue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418 3.1 Acute Neural Fatigue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418 3.2 Long Lasting Neural Fatigue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421 4. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421 Abstract Performance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthro- pometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint perfor- mance. Speed of impulse transmission along the motor axon may also have im- plications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint perfor- mance. An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest H- reflex has been reported to be lower in athletes trained for explosive events com- pared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sen- REVIEW ARTICLE Sports Med 2001; 31 (6): 409-4250112-1642/01/0006-0409/$22.00/0 © Adis International Limited. All rights reserved. sitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indic- ative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint- trained athletes. Fatigue of neural origin both during and following sprint exercise has impli- cations with respect to optimising training frequency and volume. Research sug- gests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage. Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance. Sprint exercise for the purposes of this review, is defined as rapid, unpaced cyclic running of 15 seconds or less in duration at maximum intensity throughout. Single bouts of activity are sufficiently separated in time to allow full recovery between repetitions. Examples of such activity in the sport- ing arena include the 60 and 100m sprints in track and field and the push-start in bobsleigh. As shown in figure 1 sprint running performance is the product of stride rate (SR) and stride length (SL) with numerous components influencing this apparently simple formula. Performance in sprint exercise has traditionally been thought to be largely dependent on genetic factors, with only relatively small improvements occurring with training.[1] Mus- cle fibre type has been purported to be one of the principal factors underlying sprint performance,[2] with enzymatic adaptations and hypertrophy of prime movers thought to be largely responsible for post- training improvements in performance. However, re- cent evidence suggests that enzymatic adaptations or changes in the muscle contractile proteins are not al- ways associated with significant improvements in sprint performance.[3,4] Clearly other mechanisms of adaptation are required and this likely includes neu- ral improvements. Evidence from resistance train- ing literature suggests that significant neural adap- tation can occur after training involving repeated bouts of brief, intense exercise.[5-7] Given the highly complex nature of sprint running it may well be that neural adaptations occur over a much longer period of time than has been observed in resistance training literature. As illustrated in figure 1 most of the factors affecting both SL and SR may be influ- enced by the nervous system. The ability of the nerv- ous system to fully or appropriately activate skeletal muscle therefore bears closer examination. Maximal intensity sprint exercise necessitates ex- tremely high levels of neural activation.[8-11] Direct evidence as to whether the level of activation is al- tered through sprint training is uncertain as no train- ing studies have as yet been conducted. Measurable neurological parameters such as nerve conduction velocity (NCV), maximum electromyogram (EMG), motor unit recruitment strategy and Hoffman reflex (H-reflex), however, have been shown to alter in response to physical training programmes.[6,12-17] Cross-sectional differences in these variables are also evident between sprint, untrained and endurance- trained groups.[16-19] While it is likely that neural adaptations to sprint exercise occur, whether they have a causal influence on the improvements in sprint performance is at present unclear. Potential mechanisms for neurally influenced im- provements in sprint performance include: changes in temporal sequencing of muscle activation for 410 Ross et al.  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) 2. Speed and Degree of Muscle Activation The degree of muscle activation [as measured by integrated EMG (IEMG)] is known to increase with increasing running speed.[24,25,31,32] Indeed, in well-trained athletes, muscle activation and SR may continue to increase at supra-maximal speeds.[33] However, during some maximal voluntary exer- cise not all individuals are able to fully activate their muscles.[34,35] Potentially, task-specific train- ing may allow greater activation in a given activity. Indeed, some resistance training research would appear to validate this theory[5-7] with an increase in the IEMG accompanying a marked increase in strength, particularly during the initial stages of training. However, as with the examination of tem- poral changes in muscle activity, the complexity and explosive nature of sprint exercise means there are difficulties with accurately recording IEMG from the active musculature. Slight changes in electrode position or skin preparation from one session to another make it impossible to compare directly the amplitude of muscle activation using IEMG. To com- pare amplitude across sessions it must be normal- ised, typically by the maximum evoked potential (M-wave) obtained within each session, as has been used elsewhere.[36] These techniques have yet to be used with sprint exercise as the large number of muscles used in sprinting make it difficult to perform studies of this nature. Despite the paucity of research directly ex- amining changes in muscle activation, both cross- sectional and longitudinal studies[15,17,37-41] inves- tigating sprint exercise have examined changes in other neural measures such as NCV and reflex meas- ures which may be indicative of adaptations that allow increased neural stimulus to muscle. 2.1 Nerve Conduction Velocity NCV is a measure of the speed an impulse can be transmitted along a motoneuron and is strongly related to muscle contraction time.[42,43] A rapid NCV is also indicative of a short refractory pe- riod.[44,45] In turn, the decreased refractory period may allow for greater impulse frequency, thereby increasing muscle activation levels. While, NCV has been examined in a number of cross-sectional studies of different athletic popula- tions,[17,37-41] no clear trend in its relation to perfor- mance has emerged. Some studies suggest strength and power athletes have faster NCV than endurance athletes,[17,39] while others report sprinters and jump- ers have slower NCV than other groups.[17,41] Other researchers have shown that trained individuals have faster NCV than untrained individuals.[37,38] It has also been reported that no differences were evident between power and endurance groups.[40] Clearly the literature to date has left this point unresolved. Often studies use slightly different methods, and failure to correct for temperature, diurnal variation or age may account for some of the variation. Fur- thermore, the double stimulation technique used in these studies relies on supra-maximal stimulation at 2 sites along a nerve. The difference in transmis- sion time to the recording site allows calculation of conduction velocity (CV). This technique, how- ever, determines the CV of only the fastest con- ducting fibres.[46] An alternative method, termed the ‘collision technique’, determines a range of CVs from the fastest to slowest fibres for a motor nerve, by stimulating submaximally at the distal site and maximally at the proximal site.[46] Determining the potential for changes in the slower conducting fi- bres toward the speeds of the faster fibres may be more informative than examining only the fastest conducting axons of the motor nerve, which may already be at a maximal level. Examination of the range of NCVs may also yield a more consistent pattern in the results. To date, the collision tech- nique has not been used for NCV assessment in a sprint-related study. The only longitudinal study to examine changes in NCV has reported that NCV increases in response to 14 weeks of repeated 10-second cycle sprints training at 48-hour intervals.[15] No change in max- imal IEMG was observed; however, IEMG was mea- sured only in an isometric contraction. Given the specificity of performance and neural adaptations to training[47] this particular test may be insensitive Neural Influences on Sprint Running 413  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) to changes in the degree of muscle activation dur- ing the sprint exercise. Thus, it is not possible to determine the relationship between NCV changes and changes in muscle activation in response to sprint training from the results from Sleivert and associates.[15] Frequency and volume of training may also af- fect NCV. Research suggests that muscle adapta- tion and more specifically myosin heavy chain shift may vary dependent on the frequency of sprint train- ing.[48] Similarly, neural adaptation may be related to training frequency. Some animal studies using a high daily volume of high intensity (but not sprint) exercise have reported a decrease in both axon di- ameter and myelination.[49,50] However, other stud- ies have reported an increase in axon diameter in response to exercise stress.[51,52] It appears there may be a similar frequency threshold as observed in muscle adaptations beyond which exercise stress may negatively affect axon diameter, myelination and, therefore, NCV. Given the lack of data relating to sprint training and NCV, it is not currently pos- sible to speculate what such a frequency might be, other than to suggest it would be greater than the 48-hourly protocol of Sleivert and associates.[15] In summary, NCV would appear to differ be- tween both individuals and different athletic popu- lations although a lack of consistent methodology has made the results difficult to interpret. Further research using the collision technique to assess the range of NCVs across different fibres within an indi- vidual may give greater information with respect to adaptations with training. Despite the numerous studies examining NCV, its implications for im- proving performance would appear to be negligible as interindividual differences appear to have lim- ited functional significance. Furthermore, recent re- search suggests that the relationship between NCV and muscle CV is limited,[53] perhaps a further in- dicator of the lack of functional relevance of NCV. However, in theory, changes in NCV may be indic- ative of adaptations in the nerve structure such as increased axon diameter and myelination. In turn, these adaptations may decrease the refractory pe- riod of the nerve, which would allow increased im- pulse frequency and potentially increased muscle activation. 2.2 Motoneuron Excitability and Reflex Adaptation Motoneuron excitability for the purposes of this review describes how readily the motoneuron pool is activated with respect to a given input. An in- crease in motoneuron excitability leads to a more powerful muscle contraction.[14,54] Therefore, for sprint athletes an increase in motoneuron excitabil- ity would be advantageous with regard to perfor- mance. Motoneuron excitability is commonly assessed using the H-reflex. The H-reflex is often regarded as a monosynaptic reflex response analogous to the tendon reflex though it is elicited by electrical stim- ulation of the peripheral nerve. In addition to stim- ulating motoneuron axons, electrical stimulation of the peripheral nerve also activates Ia afferents from muscle spindles. The Ia afferents synapse on to the motoneurons at the spinal cord level to bring about, after a brief delay, a second EMG response, which is known as the H-reflex. Examination of the rela- tive size of the H-reflex may provide information with respect to motoneuron excitability. Interpreta- tion of the H-reflex is complicated because the gain of the reflex can be modulated via changes in mus- cle spindle sensitivity through the fusimotor sys- tem or via presynaptic inhibition of the Ia affer- ents.[55] Since sprint running is the basis of this review, discussion will focus on the stretch/tendon and/or H-reflexes of the leg, and, in particular, in the tri- ceps surae muscle group where most research has been focused. While the 2 reflexes (tendon and Hoff- man) do differ, their responses to interventions are generally reported to be similar though not identi- cal.[56] The major difference is that the H-reflex is less sensitive to changes in γ-activity[57] because the muscle spindle is bypassed during direct nerve stimulation. The H-reflex has a further methodolog- ical advantage in that it is easier to test compared with a tendon reflex, particularly during high inten- sity ballistic activity. 414 Ross et al.  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) Despite the substantial body of literature exam- ining both the H-reflex and the stretch reflex, the function of these reflexes remains somewhat un- clear. With respect to the physiologically signifi- cant stretch reflex, its proposed functions during gait include compensation for ground irregulari- ties,[55] force production at the end of the stance phase[8,58] and control of muscle stiffness rather than length.[59] Its role in compensation for pertur- bations during stance appear limited. 2.2.1 Stretch and Hoffman Reflex in Relaxed Muscle: Effect of Sprint Exercise In contrast, to what may be anticipated with re- gard to Motoneuron excitability, that is, more ex- citability equals better performance, cross-sectional studies using athletes trained for explosive or an- aerobic events (sprinters and volleyball players) have reported decreased resting H-reflexes in both soleus and gastrocnemius muscles relative to en- durance or aerobically trained athletes.[16,60,61] The authors cited either a genetic- or training-induced decreased synaptic strength of Ia excitatory inter- mediate motoneurons in both soleus and gastroc- nemius motoneuron pools of trained individuals as a possible explanation. An alternative suggestion based on previous research is that the slower fibres within muscle contribute more to the H-reflex re- sponse.[28,62] On this basis, it was suggested that the decreased H-reflex in the explosively trained ath- letes might be related to a slow to fast transforma- tion of motor units.[16,63] Indeed, Almeida-Silveira and associates[63] found both decreased slow twitch fibre percentage and decreased H-reflex amplitude as a result of a plyometric training intervention. However, contraction time is found to decrease with increasing size and force of the H-reflex[62] which would suggest that units other than slow may also be recruited. Nevertheless, an abundance of high threshold motor units may require a certain level of background EMG, or potentiation, for the reflex response to induce contraction. The decreased resting and contraction potenti- ated reflexes of sprint athletes may substantiate such claims.[16,41,60] Furthermore, animal studies also sug- gest that a decrease in H-reflex following a condi- tioning period may be a result of an increase in firing threshold.[64] The use of invasive implanted stimulation and recording electrodes in the Carp and Wolpaw study[64] and resulting high quality data, adds further merit to their results. H-reflex disappears or is unable to be recorded at high stimulation intensities because of collisions between antidromic and orthodromic reflex volleys in the Ia afferent. In addition, the antidromic firing of the motor fibres renders the motoneurons refrac- tory to reflex input.[65] This may limit its applica- tion in the assessment of resting H-reflex of fast twitch units. A further possible explanation for de- creased H-reflex in anaerobically trained muscle may relate to changes in the descending influence as a result of long term training. Elite ballet dancers have negligible reflex activity in the triceps surae muscle group.[66,67] Nielsen and Kagamihara[68] sug- gested that the increased chronic co-contraction of muscles in the lower limb during ballet training (and subsequent presynaptic inhibition) may lead to an enduring decrease in synaptic transmission. The ‘toe-up’ or dorsi flexed ankle emphasis in cur- rent sprint training[69] results in similar amounts of co-contraction of tibialis anterior with the triceps surae muscle group. This provides a possible ex- planation as to the decreased resting H-reflex ob- served in sprint athletes which is an alternative to the slow to fast transformation of motor units pro- posed by Casabona et al.[16] Importantly, resting tendon tap reflexes also ap- pear to differ between sprint and endurance groups. Koceja and Kamen[70] reported a greater reflex in elite sprint athletes than in elite endurance athletes. Similarly, Kamen and associates[71] also reported that weight lifters have a shorter reflex latency for the patella tendon tap reflex. However, there was no difference between Achilles tendon tap reflex between the power and endurance groups. In con- trast, and perhaps more closely related to the pre- vailing H-reflex literature, Kyröläinen and Komi[72] reported diminished tendon tap reflexes in 3 out of the 4 muscles tested in power athletes versus en- durance athletes. The differences in these results are somewhat difficult to explain, although details Neural Influences on Sprint Running 415  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) It is likely that a stiffer system would have positive implications for running, such as, increased rate of force development at contact, resulting in decreased contact time and higher peak force. Therefore, re- flex control of the stiffness of the tendo-muscular system has important implications for sprint per- formance. Some factors influencing stiffness regu- lation via reflex loops include: • Pre-activity and co-contraction also strongly in- fluence the stiffness of the system by resisting undue joint perturbations on contact, as well as influencing the reflex gain on the active muscles (see point iii). • Training. As suggested in the force production section, long term training may have an affect on the gain of the resultant afferent feedback from the muscle spindles. Furthermore, if the inhibitory force feedback component via the Golgi tendon organs could be simultaneously decreased, a further increase in muscle stiffness would result.[89] (iii) Spinal level control of gait. As mentioned in section 2.2.2, reflex gain is influenced by the type of muscle action. During sprint exercise it is likely that the type of muscle action regulates changes in excitability. Control of excitability in this manner may help regulate the contribution of an individual muscle to an action. For example, in the triceps surae muscle group evidence suggests that during the contact phase of sprint running the gastrocne- mius muscle has an isometric muscle action, whereas the soleus is initially contracting eccentrically.[94] H-reflex changes during initial ground contact would appear to reflect this with gastrocnemius showing a potentiated reflex and soleus being inhibited.[95-97] This control of excitability, to some extent, may in- fluence the organisation and output of individual muscles during sprinting. A further process for control at this level is reciprocal inhibition. Co-contraction of agonist- antagonist muscle groups appears to affect the re- flex activity of co-agonist muscles somewhat dif- ferently. For example, co-contraction of tibialis anterior and the triceps surae induces a decrease in soleus H-reflex but no change in gastrocnemius H-reflex.[68] Finally, it has also been suggested that movement commands are processed by stretch reflex mechanisms which improve linearity of re- sponse, hence improving control of stiffness and smoothness of action during gait.[59] This damping function prevents oscillation and jerkiness of move- ment. In summary, reflexes appear to have numerous effects on gait. Although control of reflexes is influ- enced by descending input, adaptations to training are not yet fully understood. However, the available evidence suggests that reflexes do aid in damping undesirable oscillations in movement and do affect muscle stiffness, both of which are positively re- lated to sprinting speed. Furthermore, sprint train- ing may enhance muscle spindle sensitivity, which appears to enhance the stretch reflex, making an increased contribution to force production, also ben- eficial for sprint performance. Finally, it appears the mode of contraction of individual muscles also affects their reflex excitability, a factor that may allow for regulatory control of gait at a spinal level. 3. Neural Fatigue Neural fatigue is potentially a limiting factor during and for a period of time following maximal sprint exercise. Fatigue of central or neural origin has been defined as an involuntary reduction in vol- untary activation.[98] The actual site of neural fa- tigue is often difficult to establish, although there are a number of possibilities including supra-spinal failure, segmental afferent inhibition, depression of motor neuron excitability and loss of excitation at branch points. Fatigue at the neuromuscular junc- tion may also prevent full muscle activation in sprint exercise. In this review, acute neural fatigue refers to fatigue of neural origin during or immediately after exercise, and long lasting neural fatigue refers to ongoing fatigue (minutes to days later) which may have implications with respect to training fre- quency and adaptation. 3.1 Acute Neural Fatigue In a typical 100m running event fatigue will be manifested in a slight decline in speed towards the 418 Ross et al.  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) later stages of the race. As shown in figure 2, typ- ically this will be evident via a slight decrease in SR as an athlete fatigues. Part of the cause for the declining SR may be of neural origin. As suggested in figure 1, changes in technique, altered recruit- ment and changes in firing rate are all components with neural influence that can affect SR. Fatigue of neural origin occurs in maximal in- tensity exercise within a few seconds of maximal exertion.[99,100] Much of the work in this area has been laboratory based using either animals and dis- section techniques, or using electrical stimulation, EMG and nerve blocking techniques – allowing as- sessment of single motor units in humans.[99] The results from this research indicate that acute neural fatigue is evident, particularly in fast twitch motor units with short contraction times and high axonal CV. Similarly, rate of tension development is affected by neural fatigue.[101] Miller and associates[101] re- ported that rapid voluntary isometric contractions of adductor pollicus and tibialis anterior muscles slowed significantly within the first minute of ex- ercise. In contrast, electrically evoked contractions became more rapid (twitch stimulation) or did not change (tetanic stimulation). However, slow twitch motor neurones responded continuously to pro- longed voluntary drive at rates sufficient for full fusion.[99] So while slow motor neurones and the units they activate may be continuously activated, the use of these motor units may be limited in sprint exercise. The mechanisms for this slow twitch ver- sus fast twitch discrepancy are uncertain, although in a prolonged contraction there is a general de- crease in the efficiency of the central drive, which primarily affects motor units with high (force) thresh- olds, that is, fast twitch. There may also be a selec- tive increase in the threshold of such units. Some high threshold units fire mainly phasically in pro- longed contractions compared with low threshold units which, once recruited, continue to fire as long as their critical tension is maintained.[99] At a whole muscle level during progressive fa- tigue contraction-relaxation slows, which reduces the need for high activation.[102] Therefore, to main- tain optimal force output activation rates should decrease over time. As suggested above, individual motor units display rate reduction profiles tailored to their contractile and fatigue properties. How- ever, recovery from decreasing activation levels is rapid with individuals able to momentarily decrease tension and then making a maximal acceleration to reach electrically evoked tension levels. The likely heavy recruitment of fast twitch fibres in sprint- ing[103] may result in a substantial degree of acute 0 0 10 20 30 40 50 60 70 80 90 100 110 1 2 3 4 5 6 0 2 4 6 8 10 12 14 Distance (m) S R a nd S L S pe ed ( m /s ec ) SL (m) SR (s/sec) Speed (m/sec) Fig. 2. Variation of speed stride rate (SR) and stride length (SL) during the course of an elite 100m sprint performance (average data from male finalists of the 1991 World Championships 100m final).[21] Neural Influences on Sprint Running 419  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) neural type fatigue obvious via decreased activa- tion particularly during the latter part of a 100m sprint. The site of neural fatigue is somewhat uncertain and a number of mechanisms may contribute to fatigue. However, a relatively recent technique, trans- cranial magnetic stimulation, allows direct stimu- lation to the motor cortex. During sustained isometric MVCs transcranial magnetic stimulation produces an increase in twitch force within 15 seconds of beginning the MVC.[100] This indicates a less than optimal output from the motor cortex, which leads to less than maximal activation of the skeletal mus- cle.[100] Whether similar effects occur in maximal but more complex ballistic tasks such as sprinting is uncertain, although not an unreasonable propo- sition. This suggests that towards the end of a sim- ilarly maximal 15-second sprint, output from the motor cortex may be less than optimal and poten- tially performance limiting. The inability to maintain maximal activation over 10- to 15-second periods has not been overlooked by leading coaches. Indeed, a maximum velocity drill termed ‘ins and outs’ uses alternating phases of maximal and marginally submaximal velocity running as a means of improving the top-end speed of an athlete.[69,104] For example, following a pe- riod of acceleration an athlete sprints at maximal SR and intensity for 10 to 20m (‘in’ phase) fol- lowed by an ‘out’ phase of 5 to 20m of marginally less than maximal intensity, in an effort to allow the nervous system to recharge. Potentially this may en- able the high (force) threshold units to be re-accessed in the subsequent ‘in’ phase. This may be repeated 2 to 3 times so race length distances can be covered. This method purportedly allows athletes to run at absolute maximal neural intensity for the ‘in’ phases rather than being unable to maintain the maximal activation once fatigued from the acceleration phase. Indeed, race models similar to the above are used by some coaches to optimise performance. In applied sprint literature it has been reported that EMG activity in the skeletal musculature in- creases with increasing running speeds.[31-33] There- fore, maximal intensity speed training is probably the most stressful type of running on the nervous system. Studies using EMG in high intensity run- ning of longer than the 15-second definition of this review (200 and 400m events) showed an increase in muscle activation during fatigue,[105] indicating that peripheral rather than central mechanisms are causing athletes to slow down. The submaximal intensity pacing strategy employed by athletes in these events allows for the increase in activation. In contrast, sprinting as defined for the purposes of this study (in this case the 100m), showed decreased muscle activation by between 4.9 and 8.7% after the accelerative phase of the race, possibly because of fatigue at the neuromuscular junction and/or a decreased firing rate.[105] Again, the drop out of high (force) threshold units such as the IIb fibres may be a further reason for the decrease in activa- tion, with the declining activation an attempt to optimise output and minimise fatigue. Fatigue dis- tal to the neuromuscular junction is also an obvious cause of the decreased activation. The sub-elite in- dividuals used by Mero and Peltola,[105] decreased velocity after attaining maximal speed to a greater extent than the decrease in maximal EMG, giving a further indication of the magnitude of fatigue dis- tal to the neuromuscular junction. Such data are yet to be collected on elite individuals. A final possible cause of acute neural fatigue is a decrease in reflex sensitivity. As suggested in sec- tion 2.2, the stretch reflexes appear to contribute to propulsive force output during running.[8] Adecrease in reflex sensitivity has been observed as a result of large volumes of traumatic SSC exercise, al- though this is yet to be examined during sprint exercise.[106,107] However, by-products from max- imal intensity exercise such as lactate are known to act on group III and IV muscle afferents, which may inhibit reflex pathways, potentially limiting the SSC contribution to propulsion as lactate reaches a certain level.[108,109] Furthermore, even relatively small changes in reflex sensitivity may diminish the quality of sprint performance. 420 Ross et al.  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) 32. Kyröläinen H, Komi PV, Belli A. Changes in muscle activity patterns and kinetics with increasing running speed. J Strength Condition Res 1999; 13 (4): 400-6 33. Mero A, Komi PV. Force-, EMG-, and elasticity-velocity rela- tionships at submaximal and supramaximal running speeds in sprinters. Eur J Appl Physiol Occup Physiol 1986; 55: 553-61 34. Suter E, Herzog W, Huber A. Extent of motor unit activation in the quadriceps muscles of healthy subjects. Muscle Nerve 1996; 19: 1046-8 35. Lloyd AR, Gandevia SC, Hales JP. Muscle performance, vol- untary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syn- drome. Brain 1991; 114: 85-98 36. Keen DA, Yue GH, Enoka RM. Training-related enhancement in the control of motor output in elderly humans. J Appl Phys- iol 1994; 77 (6): 2648-58 37. Hoyle RJ, Holt LE. Comparison of athletes and non-athletes on selected neuromuscular tests. Aust J Sport Sci 1983; 3 (1): 13-8 38. Lastovka M. The conduction velocity of the peripheral motor nerves and physical training. Act Nerv Super 1969; 11 (4): 308 39. Lehnert VK, Weber J. Untersuchen der motorische veneleit- geschwindigkeit (NLG) des nervus ulnaris an sport. Med Sport 1975; 15: 10-4 40. Sleivert GG, Backus RD, Wenger HA. Neuromuscular differ- ences between volleyball players, middle distance runners and untrained controls. Int J Sports Med 1995; 16 (5): 390-8 41. Upton ARM, Radford PF. Motoneurone excitability in elite sprinters. In: Komi PV, editor. Biomechanics. V-A. Baltimore (MA): University Park Press, 1975: 82-7 42. Appelberg B, Émonet-Dénand F. Motor units of the first super- ficial lumbrical muscle of the cat. J Neurophysiol 1967; 30: 154-60 43. Kupa EJ, Roy SH, Kandarian SC, et al. Effects of muscle fibre type and size on EMG median frequency and conduction ve- locity. J Appl Physiol 1995; 79 (1): 23-32 44. Borg J. Axonal refractory period of single short toe extensor motor units in man. J Neurol Neurosurg Psychiatry 1980; 43 (10): 917-24 45. Moyano HF, Molina JC. Axonal projections and conduction properties of olfactory peduncle neuron’s in the rat. Exp Brain Res 1980; 39 (3): 241-8 46. Arasaki K, Ijima M, Nakanishi T. Normal maximal and minimal motor nerve velocities in adults determined by a collision method. Muscle Nerve 1991; 14: 647-53 47. Kitai TA, Sale DG. Specificity of joint angle in isometric train- ing. Eur J Appl Physiol Occup Physiol 1989; 58: 744-8 48. Esbjornsson M, Hellsten-Westing Y, Sjodin B, et al. Muscle fibre type changes with sprint training: effect of training pat- tern. Acta Physiol Scand 1993; 149: 245-6 49. Andersson Y, Edstrom J. Motor hyper-activity resulting in di- ameter decrease of peripheral nerves. Acta Physiol Scand 1957; 39: 240-5 50. Roy RR, Gilliam TB, Taylor JF, et al. Activity-induced morpho- logic changes in rat soleus nerve. Exp Neurol 1983; 80: 622-32 51. Edds MV Jr. Hypertrophy of nerve fibres to functionally over- loaded muscles. J Comp Neurol 1950; 93: 259-75 52. Wedeles CHA. The effects of increasing the functional load of muscle on the composition of its motor nerve [abstract]. J Anat 1949; 83: 57 53. Okajima Y, Toikawa H, Hanayama K, et al. Relationship be- tween nerve and muscle fiber conduction velocities of the same motor units in man. Neurosci Lett 1998; 253: 65-7 54. Güllich A, Schmidtbleicher D. MVC-induced short-term poten- tiation of explosive force. N Stud Athletics 1996; 11 (4): 67-81 55. Dietz V. Human neuronal control of automatic functional move- ments: interaction between central programs and afferent in- put. Physiol Rev 1992; 72 (1): 33-69 56. Voight M, Dyhre-Poulsen P, Simonsen EB. Modulation of short latency stretch reflexes during human hopping. Acta Physiol Scand, 1998; 163: 181-94 57. Burke D. Mechanisms underlying the tendon jerk and H-reflex. In: Delwaide PJ, Young RR, editors. Clinical neurophysiol- ogy in spasticity. Amsterdam: Elsevier, 1985: 55-62 58. Dietz V. Contribution of spinal stretch reflexes to the activity of leg muscles in running. In: Taylor A, Prochazka A, editors. Muscle receptors and movement. London: MacMillan, 1981: 339-46 59. Nichols TR, Houk JC. Improvement in linearity and regulation of stiffness that results from actions of the stretch reflex. J Neurophysiol 1976; 39: 119-42 60. Rochcongar P, Dassonville J, Le Bars R. Modification of the Hoffman reflex in function of athletic training. Eur J Appl Physiol Occup Physiol 1979; 40: 165-70 61. Maffiuletti NA, Martin A, Babault N, et al. Electrical and me- chanical Hmax-Mmax ratio in power- and endurance-trained athletes. J Appl Physiol 2001; 90: 3-9 62. Buchthal F, Schmalbruch H. Contraction times of twitches evoked by H-reflexes. Acta Physiol Scand 1970; 80: 378-82 63. Almeida-Silveira M, Pérot C, Goubel F. Neuromuscular adap- tations in rats trained by muscle stretch shortening. Eur J Appl Physiol Occup Physiol 1996; 72: 261-6 64. Carp JS, Wolpaw JR. Motoneuron plasticity underlying oper- antly conditioned decrease in primate H-reflex. J Neuro- physiol 1994; 72 (1): 431-42 65. Rothwell JC. Control of human voluntary movement. 2nd ed. London: Chapman and Hall, 1995 66. Goode DJ, Van Hoven J. Loss of patellar and achilles tendon reflexes in classical ballet dancers [letter]. Arch Neurol 1982; 39 (5): 323 67. Nielsen J, Crone C, Hultborn H. H-reflexes are smaller in danc- ers from Royal Danish Ballet then in well-trained athletes. Eur J Appl Physiol Occup Physiol 1993; 66: 116-21 68. Nielsen J, Kagamihara Y. The regulation of presynaptic inhibi- tion during co-contraction of antagonistic muscles in man. J Physiol 1993; 464: 575-93 69. Seagrave L. Introduction to sprinting. N Stud Athletics 1996; 11 (2-3): 93-113 70. Koceja DM, Kamen G. Conditioned patella tendon reflexes in sprint and endurance trained athletes. Med Sci Sports Exerc 1988; 20 (2): 172-7 71. Kamen G, Kroll W, Zigon ST. Exercise effects upon reflex time components in weight lifters and distance runners. Med Sci Sports Exerc 1981; 13 (3): 198-204 72. Kyröläinen H, Komi PV. Neuromuscular performance of the lower limbs during voluntary and reflex activity in power and endurance trained athletes. Eur J Appl Physiol Occup Physiol 1994; 69: 223-39 73. Evatt ML, Wolf SL, Segal RL. Modification of human spinal stretch reflexes: preliminary studies. Neurosci Lett 1989; 105: 350-5 74. Wolf SL, Segal RL, Hetner ND, et al. Contralateral and long latency effects of human biceps brachii stretch reflex condi- tioning. Exp Brain Res 1995; 107: 96-102 Neural Influences on Sprint Running 423  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) 75. Butler AJ, Yue G, Darling WG. Variations in soleus H-reflexes as a function of plantarflexion torque in man. Brain Res 1993; 632: 95-104 76. Verrier MC. Alterations in H-reflex by variations in baseline EMG excitability. Electroencephalogr Clin Neurophysiol 1985; 60: 492-9 77. Meunier S, Peirrot-Deseilligny E. Gating of the afferent reflex volley of the monosynaptic stretch reflex during movement in man. J Physiol 1989; 419: 753-63 78. Stein RB, Hunter IW, LaFontaine SR, et al. Analysis of short- latency reflexes in human elbow flexor muscles. J Neuro- physiol 1995; 71 (5): 1900-11 79. Gollhofer A, Schöpp A, Rapp W, et al. Changes in reflex excit- ability following isometric contraction in humans. Eur J Appl Physiol Occup Physiol 1998; 77 (1-2): 89-97 80. Trimble MH, Harp SS. Postexercise potentiation of the H-reflex in humans. Med Sci Sports Exerc 1998; 30 (6): 933-41 81. Hamada T, Sale DG, MacDougall JD. Postactivation potentia- tion in endurance trained male athletes. Med Sci Sports Exerc 2000; 32 (3): 403-11 82. Costill DL, Daniels J, Evans W, et al. Skeletal muscle enzymes and fiber composition in male and female track athletes. J Appl Physiol 1976; 40: 149-54 83. Romanò C, Scheippati M. Reflex excitability of human soleus motoneurons during voluntary or lengthening contractions. J Physiol 1987; 390: 271-84 84. Funase K, Imanaka K, Nishihira Y, et al. Threshold of the soleus muscle H-reflex is less sensitive to the change in excitability of the motoneuron pool during plantarflexion or dorsiflexion in humans. Eur J Appl Physiol Occup Physiol 1994; 69: 21-5 85. Nakazawa K, Yano H, Satoh H, et al. Differences in stretch reflex responses of elbow flexor muscles during shortening, lengthening and isometric contractions. Eur J Appl Physiol Occup Physiol 1998; 77: 395-500 86. Zehr EP, Stein RB. What functions do reflexes serve during human locomotion? Prog Neurobiol 1999; 58: 185-205 87. Gottlieb GL, Agarwal GC, Jaeger RJ. Response to sudden tor- ques about the ankle in man. IV a functional role of α-γ link- age. J Neurophysiol 1981; 46 (1): 179-90 88. Komi PV. Training of muscle strength and power: interaction of neuromotoric, hypertrophic and mechanical factors. Int J Sports Med, 1986; 7 Suppl.: 10 89. Komi PV. Stretch shortening cycle. In: Komi PV, editor. Strength and power and sport. London: Blackwell Science Ltd, 1992: 169-79 90. Voight M, Chelli F, Frigo C. Changes in the excitability of soleus muscle short latency stretch reflexes during human hopping after 4 weeks of hopping training. Acta Physiol Scand 1988; 163: 181-94 91. Hoffer JA, Andreassen S. Regulation of soleus muscle stiffness in premamillary cats: intrinsic and reflex components. J Neu- rophysiol 1981; 45: 267-85 92. Locatelli E. The importance of anaerobic glycolysis and stiff- ness in the sprints (60, 100, 200 metres). N Stud Athletics 1996; 11 (2-3): 121-5 93. Chelly SM, Denis C. Leg power and hopping stiffness: relation- ship with sprint running performance. Med Sci Sports Exerc 2001; 33 (2): 326-333 94. Simonsen EB, Thomsen L, Klausen K. Activity of mono- and biarticular leg muscles during sprint running. Eur J Appl Physiol Occup Physiol 1985; 54: 524-32 95. Moritani T, Oddsson L, Thorstensson A. Differences in modu- lation of the gastrocnemius and soleus H-reflexes during hop- ping in man. Acta Physiol Scand 1990; 138: 575-6 96. Capaday C, Stein RB. Difference in the amplitude of the human soleus H-reflex during walking and running. J Physiol 1987; 392: 513-22 97. Edamura M, Yang JF, Stein RB. Factors that determine the mag- nitude and time course of human H-reflexes in locomotion. J Neurosci 1991; 11 (2): 420-7 98. Gandevia SC, Allen GM, McKenzie DK. Central fatigue: criti- cal issues, quantification and practical implications. In: Gan- devia SC, Enoka RM, McComas AJ, et al., editors. Fatigue: neural and muscular mechanisms. New York (NY): Plenum, 1995: 495-514 99. Grimby L, Hannerz J, Borg J, et al. Firing properties of single human motor units on maintained maximal voluntary effort. In: Porter R, Whelan J, editors. Human muscle fatigue: phys- iological mechanisms. London: Pitman Medical, 1981: 157- 77 (Ciba Foundation symposium 82) 100. Gandevia SC, Allen GM, Butler JE, et al. Supraspinal factors in human muscle fatigue: evidence for suboptimal output from the motor cortex. J Physiol 1996; 490 (2): 529-36 101. Miller RG, Moussavi RS, Green AT, et al. The fatigue of rapid repetitive movements. Neurology 1993; 43 (4): 755-61 102. Windhorst U, Boorman G. Overview: potential role of segmen- tal motor circuitry in muscle fatigue. Adv Exp Med Biol 1995; 384: 241-58 103. Schlicht W, Naretz W, Witt D, et al. Ammonia and lactate: dif- ferential information on monitoring training load in sprint events. Int J Sports Med 1990; 11 Suppl. 2: S85-S90 104. McFarlane B. Speed . . . a basic and advanced technical model. Track Tech 1994 126: 4016-20 105. Mero A, Peltola E. Neural activation fatigued and non-fatigued conditions of short and long sprint running. Biol Sport 1989; 6 (1): 43-58 106. Horita T, Komi PV, Nicol C, et al. Stretch shortening cycle fatigue: interactions among joint stiffness, reflex and muscle mechanical performance in the drop jump. Eur J Appl Physiol Occup Physiol 1996; 73: 393-403 107. Avela J, Kyröläinen H, Komi PV, et al. Reduced reflex sensitiv- ity persists several days after long lasting stretch shortening exercise. J Appl Physiol 1999; 86 (4): 1292-300 108. Sinoway LI, Hill JM, Pickar JG, et al. Effects of contraction and lactic acid discharge on group III muscle afferents in cats. J Neurophysiol 1993; 69: 1053-9 109. Mense S. Nervous outflow from skeletal muscle following chemical noxious stimuli. J Physiol 1977; 267: 75-88 110. Francis C, Coplon J. Speed trap: inside the biggest scandal in Olympic history. London: Grafton Books, Collins, 1991 111. Penfold L, Jenkins D. Training for speed. In: Reaburn P, Jenkins D, editors. Training speed and endurance. St Leonards (NSW): Allen and Unwin, 1996: 24-41 112. Harridge SD, White MJ. A comparison of voluntary and elec- trically evoked isokinetic plantar flexion torque in males. Eur J Appl Physiol Occup Physiol 1993; 66: 343-8 113. Gandevia SC, Herbet R, Leeper JB. Voluntary activation of hu- man elbow flexor muscles during maximal concentric con- tractions. J Physiol 1998; 512: 595-602 114. James C, Sacco P, Jones DA. Loss of power during fatigue of human leg muscles. J Physiol 1995; 484: 237-46 115. Kroon GW, Naeije M. Recovery following exhaustive dynamic exercise in the human biceps muscle. Eur J Appl Physiol Oc- cup Physiol 1988; 58: 228-32 116. Kroon GW, Naeije M. Recovery of the human biceps electro- myogram after heavy eccentric, concentric or isometric exer- cise. Eur J Appl Physiol Occup Physiol 1991; 63: 444-8 424 Ross et al.  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6) 117. Friden J, Seger J, Ekblom B. Sublethal muscle fibre injuries after high-tension anaerobic exercise. Eur J Appl Physiol Oc- cup Physiol 1988; 57: 360-8 118. Bigland-Ritchie BR, Dawson NJ, Johansson RS, et al. Reflex origin for the slowing of motoneuron rates in fatiguing human voluntary contractions. J Physiol 1986; 379: 451-9 119. Saxton JM, Clarkson PM, James R, et al. Neuromuscular dys- function following eccentric exercise. Med Sci Sports Exerc 1995; 27 (8): 1185-93 120. Buchthal F, Schmalbruch H. Contraction times and fiber types in intact muscle. Acta Physiol Scand 1970; 79: 435-52 121. Bottinelli R, Pellegrino MA, Canepari M, et al. Specific contri- butions of various muscle fibre types to human muscle per- formance: an in vitro study. J Electroencephalogr Kinesiol 1999; 9: 87-95 Correspondence and offprints: Angus Ross, School of Hu- man Movement Studies, University of Queensland, Bris- bane, QLD 4072, Australia. E-mail: angur@hms.uq.edu.au Neural Influences on Sprint Running 425  Adis International Limited. All rights reserved. Sports Med 2001; 31 (6)