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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 anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications 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 performance. 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 compared 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 sensitivity 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 indicative 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 implications with respect to optimising training frequency and volume. Research suggests 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.
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Neural Influences on Sprint Running
Tr a i n i n g A d a p t a t i o n s a n d A c u t e R e s p o n s e s
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 200 1; 31 (6): 409-4 25
0112-1642/01/0006-0409/$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 andhypertrophy 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.
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more efficient movement, altered motor unit recruit-
ment strategies (i.e. preferential recruitment of the
fastest motor units), increased NCV, frequency or
degree of muscle innervation and increased ability
to maintain muscle recruitment and rapid firing for
the duration of the sprint activity. The purpose of
this review is to discuss these mechanisms and their
possible influences on performance. Where possi-
ble practical implications of the research will be
discussed.
1. Muscle Activation and
Recruitment Strategy
In a complex movement task such as sprinting,
amultitudeofdifferentmusclesmustbeactivated
at the appropriate times and intensities to maximise
speed. Optimising the timing of agonist and antag-
onist muscle activation may allow for decreased co-
contraction at an appropriate point of contraction
and hence improved movement speed. Measure-
ment of gross changes may be visible in technique
modification seen via biomechanical analysis. Alter-
natively, more direct measurement using electromyo-
graphy enables a detailed assessment of changes as
aresultoftraining.
1.1 Technique Differences
Some differences in running technique have
been observed in elite and non-elite sprint perform-
ers with particular reference to joint angles (nota-
Sprint performance
Acceleration Maximum
speed
Stride length
Range of movement
· Muscle and tendon length
and flexibility
· Joint range
Power (rate of and quantity of
force application)
·
Fibre type/cross sectional area
· Muscle strength
· Contraction speed
· Muscle recruitment
· Muscle, tendon and joint
stiffness/elasticity
Technique
· Direction of force application
throughout stance phase
Fatigue
·
Metabolic, decreased ATP and CP
·
Increased acidosis
· Neural, decreased firing frequency
· Pain tolerance
Anthropometric characteristics
Stride rate
Time on ground and time in air
Muscle contraction/relaxation rate
Power (rate of and quantity of
force application)
·
Fibre type/cross sectional area
· Muscle strength
· Contraction speed
· Muscle recruitment
· Muscle, tendon and joint
stiffness/elasticity
Technique
· Recovery mechanics
· Direction of force application
Fatigue
·
Metabolic, decreased ATP and CP
·
Increased acidosis
· Neural, decreased firing frequency
· Pain tolerance
Anthropometric characteristics
Speed
maintenance
Fig. 1. Components of sprint performance. Components in italics are not neurally influenced. ATP =adenosinetriphosphate;CP =
creatine phosphate.
Neural Influences on Sprint Running 411
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bly hip and knee flexion) and movement velocity
of limb segments in hip extension.[20-22] Some of
the observed differences may be the result of re-
finement of the neural innervation patterns or mo-
tor programmes as a result of the extensive training
histories of the elite performers. Mero and Komi[23]
have provided further evidence of a more devel-
oped and/or efficient motor programme in elite ath-
letes. While no differences were found at unassisted
speeds (aside from the trained being faster than un-
trained), the authors found that when relatively un-
trained individuals were towed to supra-maximal
running velocities they were unable to increase SR
above their normal maximum and responded tothe
increased speed with inefficient increases in SL. In
contrast, well-trained athletes responded to such
stimuli by increasing both SR and SL,[23] perhaps
indicating superior neural adaptations to high in-
tensity sprint exercise. These studies, however, were
cross-sectional in nature and, as such, the relative
importance of genetic and training influences re-
mains uncertain. This question can be addressed
only by a detailed longitudinal analysis of the ad-
aptations to running technique with training.
1.2 Electromyographic Studies
The difficulties in ensuring reliable electrode
placement between sessions make longitudinal stud-
ies of the changes in EMG technically challenging.
As a result there are few such studies in the current
literature. However, electromyographic studies in-
vestigating the temporal sequencing of muscle ac-
tivation or relative activity of various muscles have
reported significant changes when speed is increased
to maximal or supra-maximal velocities.[24,25] Sim-
ilarly, in controlled laboratory conditions, changes
in the speed of muscle contraction have been reported
to alter the ratio of contribution of co-agonist mus-
cles.[26] Furthermore, relative temporal changes in
muscle activation as a result of practice have been
observed even in simple single arm movements.[12,27]
Schneider and associates[27] reported increased use
of the stretch shortening cycle (SSC) in late prac-
tice. Such an adaptation would have obvious ad-
vantages for sprinting efficiency as evidence sug-
gests that the SSC contributes to propulsive force
during running.[8] These results suggest that there
is considerable scope for temporal changes in mus-
cle activation to occur with sprint training and that
such changes could enhance performance.
1.3 Fibre Type Recruitment
The ability to fully or selectively recruit fast twitch
motor units has been examined under various con-
ditions[19,28-30] and may have implications for sprint
performance. Anumber of studies have shown ev-
idence of preferential fast twitch fibre recruitment,
particularly in eccentric exercise.[28,29] However,
the results from Desmedt and Godaux[30] suggested
that in rapid concentric contractions there is no ev-
idence of selective or preferential recruitment of fast
twitch units. In contrast, one cross-sectional study
has demonstrated that sprint athletes may have a
significantly greater ability to selectively recruit
fast twitch motor units compared with endurance
or untrained individuals.[19] However, Saplinskas
and associates[19] limited their investigation to only
one muscle (tibialis anterior) and reported little de-
tail of the type of contraction used. Hence, it is diffi-
cult to fully assess the validity of their findings.
Furthermore, the possibility of a greater proportion
of fast twitch motor units in the sprint athlete’s tib-
ialis anterior may bias the result. Nevertheless, the
possibility of recruiting selectively those motor units
that can rapidly contract and relax remains as a
potential adaptation to the demands of sprint exer-
cise.
In summary,differencesinrunningtechniqueand
in muscle activation patterns have been reported
among trained sprint athletes compared with con trols
or endurance-trained individuals. This evidence pro-
vides some support for neurally influenced changes
in sprint performance, though definitive data in this
area are currently unavailable. Longitudinal train-
ing studies are required to determine the influence
of training on these parameters.
412 Ross et al.
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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 sprintexercise 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 studiesof 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] Arapid
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 differenceswere 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 theproximal 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
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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 ofhigh 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 exercisestress
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,NCVwouldappeartodifferbe-
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.
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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
apossibleexplanation.Analternativesuggestion
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
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of what the power athletes were in the Kyröläinen
and Komi[72] study were limited and no reference
was made to their training age or competitive sta-
tus. Nevertheless, the pattern of the above results
is at the very least less clear cut than in the case of
the H-reflex, suggesting that a positive adaptation
in the gain of the muscle spindle may occur. That
is, the muscle spindle is likely more sensitive to
stretch as a result of the prolonged sprint and/or
power training inducing a greater reflex response.
As yet, no sprint training studies have been con-
ducted to examine modification of the stretch re-
flex; however, it has been shown that it is possible
to enhance the stretch reflex response using a con-
ditioning routine consisting of multiple rapid short
stretches and biofeedback on the stretch reflex re-
sponse.[73,74] While this research is still somewhat
removed from sprint work, clearly there is potential
for the stretch reflex response to be enhanced as a
result of ballistic type activity such as sprinting.
As discussed in this section, most the work us-
ing sprint athletes and reflex investigation has been
cross-sectional in design, hence genetic and training-
induced differences are difficult to discriminate.
However, the small amount of longitudinal work in
conjunction with the prevailing cross-sectional work,
suggests that the H-reflex decreases in response to
sprint training – reflecting a decrease in motoneu-
ron activation either caused by changes in presyn-
aptic inhibition or potentially linked to a slow to
fast motor unit transition. Stretch reflexes, how-
ever, are either unaffected or may increase post-
sprint exercise, possibly indicating an increase in
muscle spindle sensitivity to compensate for the
decreased motoneuron excitability.
2.2.2 Reflex Potentiation by Contraction
Acommonresultofanisometricmusclecon-
traction is potentiation of both H- and tendon re-
flexes.[75-79] This may be caused by either central
or peripheral mechanisms acting on the reflexpath-
way. Centrally, possible mechanisms for reflex po-
tentiation include an increase in excitability of the
motoneuron pool and decreased presynaptic inhi-
bition of Ia terminals.[75,77] Peripherally, changes
in the threshold of spindles after or during contrac-
tion may also affect stretch reflexes particularly.[79]
Reflex potentiation during a steady contraction[41]
has been used to directly compare sprint athletes to
other populations. The results suggested that reflexes
were potentiated to a greater extent in elite sprint
athletes than in control participants. While at rest,
the higher percentage of fast twitch or high thresh-
old motor units in sprint athletes require greater stim-
ulation from the Ia afferents for a reflex to be elic-
ited. Hence, during a contraction, the fast twitch units
may be closer to threshold and thus the reflex stim-
ulus may be sufficient to elicit a response.Whether
enhanced reflex potentiation has performance ad-
vantages or applications beyond indicating fibre type
is debatable. However, it is possible that potenti-
ated reflex contribution, as a result of muscle ac-
tivity at and immediately before footstrike, may aid
force production in sprinting.[32] Furthermore, sprint-
trained athletes may potentiate the stretch reflex to
agreaterextentthananuntrainedpopulation,giv-
ing sprinters a further performance advantage.
Immediately following the contraction there is
abriefdepressionoftheH-reflex,followedbypo-
tentiation after approximately 4 minutes.[54,80] Gül-
lich and Schmidtblicher[54] demonstrated a greater
increase in reflex response after maximal contrac-
tions in sprint and power athletes compared with
controls. Notably, the increase in H-reflex followed
the same time course as did enhancements in ex-
plosive voluntary force production, possibly in-
dicating potentiated stretch reflex contribution to
power output. This may be caused by an increase
in post-synaptic discharge caused by an increased
effectiveness of the afferent volley following a high
frequency burst of impulses, in turn leading to an
increased liberation of transmitter from the Ia ter-
minals.[80] Alternatively, the post-maximal activa-
tion potentiation (PAP) may be caused by phos-
phorylation of myosin light chains (MLC) during
maximum voluntary contraction (MVC) which rend-
ers actin-myosin more sensitive to Ca2+ in a sub-
sequent twitch.[81] This PAP appears to be greatest
in type II fibres and is thought to be related to their
greater capacity for MLC phosphorylation in re-
416 Ross et al.
Adis Inter national Limited. A ll rights reserve d. Sports Med 2001; 31 (6)
sponse to high frequency activation.[81] These lat-
ter possibilities may also provide a mechanistically
based explanation for the greater potentiation seen
in elite sprint athletes, given the known high pro-
portions of fast twitch muscle in such populations.[82]
The mode of contraction also strongly affects
the reflex response.[83-85] The studies above gener-
ally show that H-reflex is potentiated during an
isometric contraction. Similar findings have been
reported with a concentric contraction.[83] Converse-
ly, eccentric muscle actions have been reported in
anumberofstudiestoshowsmallerH-orstretch
reflex responses compared with isometric or con-
centric contractions.[83-85] These results appear to
be independent of the level of background EMG
although the control mechanism remains somewhat
unclear.[85] This has implications for sprinting which
will be further discussed in section 2.2.3.
To summarise,theH-reflexispotentiateddur-
ing isometric and concentric muscle action and is
potentiated to a greater extent in sprint athletes.
Similarly, the stretch reflex is also potentiated by
isometric muscle action; the H-reflex is potentiated
more in sprint athletes after contraction, and explo-
sive voluntary muscle action follows a similar time
course. The H-reflex is depressed during eccentric
muscle action in the soleus muscle. These findings
may have implications for both talent identifica-
tion as well as pre-competition warm-up leading to
performance enhancement for sprint athletes.
2.2.3 Reflex Influence on Gait: Implications
for Sprinting
An extensive review of reflex function during
the phases of gait is beyond the scope of this review
(see Zehr and Stein,[86] for a more comprehensive
review in this area). Nevertheless, reflexes and, in
particular, short latency stretch reflexes have a num-
ber of important influences that are pertinent for
sprint running performance. These are addressed
briefly below.
(i) Force production.Duringstancephase,evidence
suggests that the stretch reflex makes a strong con-
tribution to leg extensor EMG, aiding propulsive
force.[8] The rapid time frame of the reflex contri-
bution makes it highly applicable to its use in sprint-
ing where ground contact is less than 100 millisec-
onds. Factors influencing force production via the
stretch reflex include:
Muscle pre-activity (activity before ground con-
tact). Pre-activity occurs in numerous leg mus-
cles that are involved in generating propulsive
force, including gastrocnemius, vastus lateralis
and biceps femoris during sprint running.[81] This
pre-activity likely increases muscle spindle sen-
sitivity potentiating the stretch reflex contribu-
tion.[32,79,87]
Ten d o n c ompliance. The degree of comp l i ance of
the tendon affects force through the muscle and
the resultant feedback from the muscle spindles.
Training. It has been speculated that with strength
and power training, the length feedback compo-
nent that originates from the muscle spindles may
be enhanced,[88] possibly improving muscle stiff-
ness on contact (see point ii). A similar spindle/
stretch-reflex moderated adaptation may occur
with high intensity sprint training.[89] Unfortunate-
ly, as yet no studies have examined the effect of
sprint training in a longitudinal study. However,
Voight and associates[90] examined changes in
both H- and stretch reflexes in response to 4
weeks of hopping training. While some adapta-
tions were reported following the training pe-
riod (notably increased soleus tendon reflex and
reduced soleus H-reflex depression during hop-
ping) no measurable changes in either gastroc-
nemius or soleus movement–induced stretch
reflexes were observed. This lack of change in
the movement-induced stretch reflex may be a
function of the short period of training in the
study (4 weeks). A longer period of training may
be required to make significant changes in the
muscle spindle gain.
(ii) Stiffness of the tendo-muscular system.Stiff-
ness of the tendo-muscular system appears to be
related to, and enhanced by,reflex contribution.[59,91]
The stiffness of the tendo-muscular system may
affect the use of the SSC with respect to storage
and use of elastic energy. Stiffness of the tendo-
muscular system has been strongly related to max-
imal running velocity and speed maintenance.[92,93]
Neural Influences on Sprint Running 417
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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.Asmentionedin
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.
Afurtherprocessforcontrolatthislevelis
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,reflexesappeartohavenumerous
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 Inter national Limited. A ll rights reserve d. 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 ofneural 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 evokedcontractions
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
010 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)
SR and SL
Speed (m/sec)
SL (m)
SR (s/sec)
Speed (m/sec)
Fig. 2. Var i ati o n o f spee d s t rid e r a te (S R ) a n d st r i d e le n g th (S L ) d uri n g t he c o u r se of a n e lit e 1 0 0m sp r i n t pe r f orm a n c e (av e r a ge
data from male finalists of the 1991 World Championships 100m final).[21]
Neural Influences on Sprint Running 419
Adis Inter national Limited. A ll rights reserve d. 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
2to3timessoracelengthdistancescanbecovered.
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
afurtherindicationofthemagnitudeoffatiguedis-
tal to the neuromuscular junction. Such data are yet
to be collected on elite individuals.
Afinalpossiblecauseofacuteneuralfatigueis
adecreaseinreflexsensitivity.Assuggestedinsec-
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.
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3.2 Long Lasting Neural Fatigue
In contrast to acute fatigue, long lasting neural
fatigue is fatigue of neural origin that continues for
some time after the cessation of exercise. Neural
fatigue and its time course for recovery has been
cited by leading coaches as a factor to be consid-
ered when assessing the timing and frequency of
maximal speed sessions.[110,111] However, specific
research to assess such claims, is yet to be con-
ducted. This lack of research may be largely because
of the difficulty in assessing maximal activation in
ataskascomplexassprinting.Whileinterpolated
twitch has recently been used during contractions
other than isometric[112-114] to assess the degree of
voluntary muscle activation it is unlikely to be suit-
able for a skill as complex as sprinting. Neverthe-
less there are a number of previous studies that do
have implications for sprint training.[107,115-119]
Muscle damage can affect neural function at cer-
tain levels, with both reflex changes and disruption
of the electrical excitability of the muscle mem-
brane potentially causing changes in the EMG sig-
nal for up to 7 days after trauma.[115,116] Extensive
muscle damage has been reported following sprint
running even among trained individuals,[117] par-
ticularly among type IIb muscle fibres. Research
suggests that the IIb fibre is the fastest and strong-
est type of muscle fibre[120,121] giving it obvious
applicability to sprint performance. Given that the
IIb fibre, in particular, may sustain damage during
maximal sprint training it is likely that full recov-
ery of the ability to appropriately activate IIb fibres
would be required for a subsequent maximal speed
session to be optimal. As with the acute situation,
muscle damage has long term implications with
respect to reflex changes and muscle activation,
with type III and IV muscle afferents being affected
by chemical agents associated with muscle pain.[109]
Stretch and H-reflex values have shown full recov-
ery after long distance running, and may take up to
4daysforcompleterecovery.
[107] While sprint ex-
ercise is of much shorter duration, the more intense
SSC exercise may mean that similar effects can
occur with a much smaller total volume of exer-
cise. Furthermore, activation of the type III and IV
muscle afferents may provide increased inhibitory
drive to the α-motoneuron pool, resulting in per-
formance decrements in the SSC exercise.[118]
Evidence of muscle damage causing prolonged
neuromuscular dysfunction after eccentric exercise i s
evidenced by poor proprioception and perceived
exertion difficulties experienced by individuals af-
ter eccentric exercise.[119] Changes in position sense
and perceived force generation would likely ad-
versely influence an athlete’s technical model and
again make maximum velocity type training in such
astatelessthanoptimal.
To su m ma r i s e ,fatigueofneuraloriginclearlyaf-
fects force production and sprint performance, hence,
training drills have been developed to accommod-
ate its influence. The origin of neural fatigue is
likely multifaceted with much of it occurring via
afferent feedback loops either as a result of muscle
damage or peripheral fatigue. Evidence suggests
that centres at least as proximal as the motor cortex
are directly affected. Fatigue of the neuromuscular
system also has implications for recovery and train-
ing frequency during high intensity training peri-
ods. Coaches and athletes currently assess muscle
fatigue from training using anecdotal evidence, such
as, performance and muscle soreness, in a effort to
measure response to a training stimulus. These meas-
ures may also be indicative of the neural response
to training stimuli. Further research is required to op-
timise both the understanding of neural fatigue and
the development of training regimens that accom-
modate its effects.
4. Conclusion
The nervous system and its state of training is
an integral component with respect to sprint per-
formance. While the current state of research is less
than comprehensive, it can be concluded that:
(i) Relative sequencing of muscle activation during
gross movement changes with practice, therefore,
sprint technique is modifiable
(ii) NCV may increase in response to a period of
sprint training
Neural Influences on Sprint Running 421
Adis Inter national Limited. A ll rights reserve d. Sports Med 2001; 31 (6)
(iii) Excessive training may result in negative ad-
aptations with respect to NCV, reflex responses and
proprioception
(iv) Stretch reflex appears to aid force production
during sprinting
(v) Stretch reflex output is trainable
(vi) Acute fatigue during sprinting may have aneu-
ral component though this would appear to be
strongly influenced by metabolic changes in the
muscle
(vii) Longer lasting fatigue as a result of sprint ex-
ercise may also have neural implications with re-
spect to reflex output and proprioception and, there-
fore, sprinting technique.
There are implications for optimising sprint train-
ing from the above points; however, these have to
be weighed against metabolic and contractile adap-
tations to training, with the combination of these
factors ultimately determining the performance out-
come.
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Neural Influences on Sprint Running 425
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... These previous observations raise some questions on whether these particular loading regimes would have positive adaptations after midterm to long-term training programs, especially when not accompanied by lighter sled loads or unresisted sprints. Regarding motor unit recruitment, the potential mechanisms for neural-influenced improvements in sprint performance include changes in temporal sequencing of muscle activation and motor-unit recruitment pattern (i.e., preferential recruitment of the fastest motor units), increased nerve conduction velocity, increased ability to maintain muscle recruitment, and rapid firing throughout the sprint (103). Therefore, it is likely that a stiffer system would have positive implications for sprint performance, such as an increased rate of force development at contact that results in decreased CT and higher peak force (103). ...
... Regarding motor unit recruitment, the potential mechanisms for neural-influenced improvements in sprint performance include changes in temporal sequencing of muscle activation and motor-unit recruitment pattern (i.e., preferential recruitment of the fastest motor units), increased nerve conduction velocity, increased ability to maintain muscle recruitment, and rapid firing throughout the sprint (103). Therefore, it is likely that a stiffer system would have positive implications for sprint performance, such as an increased rate of force development at contact that results in decreased CT and higher peak force (103). Indeed, an increase in the force applied in the first 100 ms has been observed during concentric jumps after 4 weeks of ST using a load that induced a 7.5% V dec relative to traditional sprints, whereas the same training under unresisted conditions resulted in a significant decrease in this parameter (3). ...
... An additional aspect to consider is that fatigue at the neuromuscular junction may also prevent full muscle activation during sprinting (103). Regarding neural fatigue, variations in technique, altered recruitment, and changes in firing rate are elements and mechanisms influenced by neural factors which affect sprint performance (103). ...
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Sprinting is a key component for many individual and team sports. Therefore, to enhance sprint performance, various training methods are widely used by coaches and practitioners, including maximum sprint speed and resisted sprint training. Resisted sprinting with sled towing is a method that has recently received considerable attention from the sport science community. However, to date, no consensus exists regarding its acute and chronic effects in team sport athletes. This narrative review aimed to (a) review and analyze the mechanics of sprinting under unresisted and resisted conditions with a specific focus on team sport disciplines; (b) provide a thorough and applied discussion on the importance of considering acute and chronic effects of sled loading on technique, electromyographic activity, and force production, as well as on the role of muscle architecture and neural factors in sled training; (c) analyze the effects of increasing sled loads during acceleration and maximum velocity phases on contact and flight phases, while concomitantly examining kinetic, kinematic, and neuromuscular aspects, because all these factors affect each other and cannot be properly understood in isolation.
... Contradictions to these findings have also been presented [13] identifying a clear association between step frequency (group mean: 4.85 Hz) and 100-meter performance (10.16 ± 0.16 s), with lower step frequency noted in specific training blocks (4.34 Hz). It has previously been suggested that step length is more related to increased force production, whereas step frequency is associated with higher rates of force production during ground contact and leg turnover requiring greater neural adaptations [29,50], which may also be a reflection of training load and training content during the COMP phase. It could therefore be concluded, that limiting the volume of speed endurance and strength endurance leading into important competitions has maximized mechanical characteristics and step kinematics necessary to drive 100-meter performance outcomes. ...
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Objective: This case study aimed to explore changes to sprint force-velocity characteristics across a periodized training year (45 weeks) and the influence on sprint kinematics and performance in national level 100-meter athletes. Force-velocity characteristics have been shown to differentiate between performance levels in sprint athletes, yet limited information exists describing how characteristics change across a season and impact sprint performance, therefore warranting further research. Methods: Two male national level 100-meter athletes (Athlete 1: 22 years, 1.83 m, 81.1 kg, 100 m time: 10.47 s; Athlete 2: 19 years, 1.82 cm, 75.3 kg, 100 m time: 10.81 s) completed 12 and 11 force-velocity assessments, respectively, using electronic timing gates. Sprint mechanical characteristics were derived from 30-meter maximal sprint efforts using split times (i.e., 0–10 m, 0–20 m, 0–30 m) whereas step kinematics were established from 100-meter competition performance using video analysis. Results: Between the preparation (PREP) and competition (COMP) phase, Athlete 1 showed significantly large within-athlete effects for relative maximal power (PMAX), theoretical maximal velocity (v0), maximum ratio of force (RFMAX), maximal velocity (VMAX), and split time from 0 to 20 m and 0 to 30 m (−1.70 ≤ ES ≥ 1.92, p ≤ 0.05). Athlete 2 reported significant differences with large effects for relative maximal force (F0) and RFMAX only (ES: ≤ −1.46, p ≤ 0.04). In the PREP phase, both athletes reported almost perfect correlations between F0, PMAX and 0–20 m (r = −0.99, p ≤ 0.01), however in the COMP phase, the relationships between mechanical characteristics and split times were more individual. Competition performance in the 100-meter sprint (10.64 ± 0.24 s) showed a greater reliance on step length (r ≥ −0.72, p ≤ 0.001) than step frequency to achieve faster performances. The minimal detectable change (%) across mechanical variables ranged from 1.3 to 10.0% while spatio-temporal variables were much lower, from 0.94 to 1.48%, with Athlete 1 showing a higher ‘true change’ in performance across the season compared to Athlete 2. Conclusions: The estimated sprint force-velocity data collected across a training year may provide insight to practitioners about the underpinning mechanical characteristics which affect sprint performance during specific phases of training, plus how a periodized training design may enhance sprint force-velocity characteristics and performance outcomes.
... Literatüre bakıldığında, takım sporcularında doğrusal sprint performansını değerlendirmek için çeşitli mesafeler kullanılmıştır (Castillo vd., 2021;de Hoyo vd., 2015;Suarez-Arrones vd., 2018). Bu anlamda, daha kısa mesafeler (örneğin 5-10 m) daha çok hızlanma yeteneği ile ilişkilendirilirken, özellikle yetişkin sporcularda maksimum hızı değerlendirmek için daha uzun mesafeler ( İlk başta, sprint testlerindeki performansın büyük ölçüde genetik faktörlere bağlı olduğuna ve antrenman etkisi sayesinde sadece nispeten küçük gelişmeler elde edildiğine inanılmaktadır (Ross, Leveritt, & Riek, 2001). İkincisi, her sporcunun bireysel adaptasyon potansiyeli, bir antrenman programının etkilerini açıkça etkiler ve bu da yüksek düzeyde antrenmanlı profesyonel sporcularda iyileştirmeler elde etmeyi zorlaştırır (Keul vd., 2013). ...
... Sprinting is defined as the generation of maximum velocity (Slater, Sygo and Jorgensen, 2019). Sprint performance is defined as an ability to have quick reaction times, acceleration, maximum running velocity, and the ability to sustain performance in the presence of increasing fatigue (Ross, Leveritt and Riek, 2001). ...
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Background: The purpose of this paper is to describe the effects on preparation for sprinting performance in Hong Kong university-level athletes during the COVID-19 pandemic. Changes in training methods, and well-being of athletes due to COVID-19 pandemic were also investigated. Methods: Using Google Form, the study recall period was established during the closure of sports facilities in Hong Kong (2/2020–2/2021) during the COVID-19 pandemic. Physical state preparation (PSP), Mental state preparation (MSP), Nutritional preparation (NP), and Major changes in training methods (MTM) were analyzed. Results: The results demonstrated no significant mean difference between male and female athletes on the effects of COVID-19 regarding the PSP, MSP, NP, and MTM. However, both males and females were highly disrupted in relation to performance preparation. Conclusions: The pandemic affected physical performance, stress, and mental state, impacted on nutritional regimes, changed training locations and recovery strategies, and lowered training quantity and quality. In addition, athletes received less coaching, and had less accessibility to training equipment. Athletes and coaches should reflect on the effects of the COVID-19 pandemic to address personal training needs, while sports professionals need to carefully prepare themselves for sprinting performance, in relation to the current COVID-19 situation.
... Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. [6] The primary objectives were to compare nerve conduction parameters of the common peroneal nerve and surface electromyography parameters of gastrocnemius muscles in active and nonactive individuals. The effect of physical activity on nerve conduction and surface EMG parameters were mostly done on the professional athletes. ...
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Introduction: Physical activity is defined as any bodily movement produced by skeletal muscles that requires energy expenditure. Nerve conduction studies and surface EMG provides a comprehensive evaluation of nerve, muscle or neuromuscular impairment. However, such studies are mostly done on professional athletes. Methods: Healthy physically active (n=17) and non-active (n=17) medical undergraduate students from B.P. Koirala Institute of Health Sciences (BPKIHS), Nepal were enrolled in the study using convenient sampling technique. Anthropometric and motor nerve conduction parameters of common peroneal nerves and surface EMG of gastrocnemius muscle were recorded using standard technique in Neurophysiology Lab II, BPKIHS. Descriptive analysis was done. Unpaired t-test was applied for comparing the nerve conduction and surface EMG variables between the groups. Pearson's correlation was applied between anthropometric and nerve conduction & surface EMG variables. Objectives: To compare nerve conduction parameters of common peroneal nerve and surface EMG of Gastrocnemius muscle between active and non-active individuals. Results: The distal and proximal amplitudes of left common peroneal nerve were significantly higher in physically active compared to non-active individuals (LCPDA-p value: 0.026, LCPPA-p value: 0.009). Anthropometric parameters showed significant correlation with nerve conduction parameters.
... Physical training induces adaptive changes within the nervous system that allow trainees to better coordinate activation of all relevant muscles resulting in maximal force production. 1 A rapid Nerve Conduction Velocity (NCV) is an indicator of a short refractory period which allows for greater impulse frequency, thereby elevating muscle activation levels. 2 A number of studies have found higher NCV in trained than untrained ones. 3,4 It has also been mentioned that NCV is greater in the dominant limb as compared to the non-dominant limb. ...
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Introduction: Neural adaptation to physical training allows a person to better coordinate the activation of all relevant muscles producing maximum force. Nerve conduction velocity measures the speed of impulse along the motor neuron and is strongly associated with muscle contraction time. This study aimed to find out the mean motor nerve conduction velocity of the right ulnar nerve among physically trained adult males in a tertiary care centre. Methods: This descriptive cross-sectional study was conducted in the Neurophysiology Laboratory of a tertiary care centre from 3rd November, 2019 to 2nd November, 2020. Thirty young adult males who were engaged in the physical training at a training centre for more than 3 months were studied after receiving ethical approval from the Institutional Review Committee (Reference number: 1578/019). Motor nerve conduction parameters of the right ulnar nerve were measured and data were entered in Microsoft Excel. Statistical analysis was done using the Statistical Packages for the Social Sciences version 25.0. Point estimate at 95% Confidence Interval was calculated along with frequency and percentages for binary data, and mean and standard deviation for continuous data. Results: Among 30 males studied, the mean motor nerve conduction velocity of the ulnar nerve was found to be 61.02±5.86 m/sec (58.92-63.11 at 95% Confidence Interval). The mean distal latency and amplitude of the muscle action potential were 2.33±0.53 ms and 8.08±1.17 mv respectively. Conclusions: Our study found that the mean nerve conduction velocity of the ulnar nerve was similar when compared to studies conducted in similar settings. Keywords: Nepal; nerve conduction; ulnar nerve.
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For this research, we analyzed the immediate effects of warm-up condition (WC) or without warm-up condition (WWC) on amateur referees’ physical and cognitive functioning. Eight professional soccer referees from the Balearic Committee of Football Referees were the participants of this study. Body composition characteristics were measured and the scores on three tests were recorded: the Yo-Yo intermittent recovery, repeated-sprint ability, and psychomotor vigilance task. Regarding results, the psychomotor vigilance task was performed better after warm-up training ( p = .002, η ² = .79) with faster reaction times following WC ( M = 318.2, SD = 27.1 ms) than WWC ( M = 334.9, SD = 26.1). Similarly, the referees’ performance was better on the repeated-sprint ability test after WC ( p = .002, d = 0.53) than WWC, with minimum and average power values higher after WC ( M = 626.77, SD = 112.57) than WWC ( M = 562.35, SD = 79.63). We conclude that re-warm-up training may mitigate the vigilance performance changes caused by effects of rest on soccer referees.
Chapter
This chapter reviews the molecular and metabolic responses in human skeletal muscle to exercise training. Acute changes in various stimuli that trigger adaptations largely depend on the type of exercise performed and particularly the intensity and duration of discrete sessions. These stimuli are linked to the activation and/or repression of an array of intracellular signal transduction pathways, pre- and posttranscriptional processes, and the regulation of protein translation. Given the considerable overlap in these underlying molecular processes, the mechanistic basis for how repeated, acute changes are translated into specific training responses remains a topic of much investigation. Endurance training is primarily associated with an enhanced capacity for oxidative energy provision and a shift in substrate utilization, from carbohydrate to lipid, at a given absolute exercise intensity. Strength training mainly results in increased muscle size, force-generating capacity, and enhanced capacity for non-oxidative energy provision. Sprint training also increases the capacity for non-oxidative energy provision, but can elicit a range of responses, including some that resemble endurance or strength training. Training generally enhances fatigue resistance and performance in a manner that is specific, but not exclusive, to the type of exercise performed. These improvements are owed, in part to training-induced changes in both the maximal capacity for, and the specific utilization of, various substrates during exercise.
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Background Photobiomodulation therapy (PBMT) is defined as non-thermal electromagnetic irradiation through laser or light-emitting diodes sources. In recent decades, PBMT has attracted attention as a potential pre-conditioning method. The current meta-analysis was conducted to assess the effectiveness of PBMT in improving mode-specific exercise performance in healthy young adults. Methods A computerized literature search was conducted, ending on 15 May 2022. The databases searched were PubMed, Cochrane Central Register of Controlled Trials, Embase, SPORTDiscus, and Physiotherapy Evidence Database. Inclusion/exclusion criteria limited articles to crossover, double-blind, placebo-controlled studies investigating the PBMT effects as a pre-conditioning method. The included trials were synthesised according to exercise mode (single-joint, cycling, running, and swimming). All results were combined with the standardized mean differences (SMDs) method and the 95% confidence intervals (95% CI) were described. Results A total of 37 individual studies, employing 78 exercise performance measurements in 586 participants, were included in the analyses. In single-joint exercises, PBMT improved muscle endurance performance (SMD = 0.27, 95% CI = 0.12 to 0.41; p < 0.01) but not muscle strength performance (p = 0.92). In cycling, PBMT improved time to exhaustion performance (SMD = 0.35; 95% CI = 0.10 to 0.59; p < 0.01), but had no effect on all-out sprint performance (p = 0.96). Similarly, PBMT had no effect on time to exhaustion (p = 0.10), time-trial (p = 0.61), or repeated-sprint (p = 0.37) performance in running, and no effect on time-trial performance in swimming (p = 0.81). Conclusion PBMT improves muscle endurance performance in single-joint exercises and time to exhaustion performance in cycling, but it is not effective for muscle strength performance in single-joint exercises, running, or swimming performance metrics.
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