Lab #3: Hoffman Reflex

EPHE 380
Section: A01

Brianna Crighton
V00745066
February. 10, 2015
Instructor: Chelsea Kaupp
Introduction

The Hoffman reflex, or H-reflex, is often considered to be an electrical analogue of the

stretch reflex, but it bypasses the effects of the gamma motor neurons and muscle spindle
discharge (Zahr, 2002). It is an artificially stimulated response that has been used to
measure spinal reflex excitability, and is a useful method to study the characteristics of
the monosynaptic connections from Ia sensory afferent fibres to the alpha motor neurons
of the spinal cord (Kandel, Schwartz, Jessel, Siegelbaum & Hudspeth, 2013).
The technique commonly used to elicit the H-reflex involves the electrical
stimulation of a mixed peripheral nerve, activating both afferent sensory (from the point
of stimulation to the spinal cord) and efferent motor (from the alpha motor neurons in the
spinal cord to the neuromuscular junction) arcs as well as a direct efferent motor response
(from the point of stimulation to the neuromuscular junction), which is referred to as the
M-wave (Zehr, 2002). When the electrical stimulation is above threshold it causes
sufficient depolarization of the afferent terminals to release neurotransmitters at the Ia
afferent-alpha motor neuron synapse. This can then lead to post-synaptic depolarization
of the alpha motor neurons, release of neurotransmitters at the neuromuscular junction
and the contraction of muscle fibers (Zehr). The resulting H-reflex is typically recorded
by electromyography (EMG).
When stimulus of increasing intensity is applied the Ia afferents are be recruited
before alpha motor neurons, due to their larger diameter, and thus, a H-reflex can be
observed without an M-wave (Zehr, 2002). The amplitudes of the H-reflex and M-wave
will both increase in a fairly linear fashion with the stimulation intensity until the
maximum H reflex (Hmax), representing the fullest extent of reflex activation, and, at

higher stimulation levels, the maximum M-wave, representing the maximal muscle
activation, are reached (Zehr, 2002).
The H-reflex is a useful tool in evaluating the changes in human reflex pathways
and the plasticity of the neuromuscular system, but it is important to understand its
limitations (Zehr, 2002). Due to the direct anatomical connection between the Ia afferents
and the alpha motor neurons the H-reflex has been studied in both motor control research,
as well as exercise and clinical studies, however it is the issue of motor neuron
excitability that is continually misunderstood (Zehr). The synaptic connections between
Ia afferents and alpha motor neurons are subject to modification, specifically mechanisms
that cause changes in the presynaptic inhibition (PSI) of Ia afferent transmission.
Increases and decreases in PSI directly affects the release of neurotransmitters at the
Ia/alpha-motoneuron synapse (Zehr). Presynaptic inhibition is mediated by the action of
an inhibitory interneuron acting on Ia afferent terminals by decreasing their excitation
when stimulated (Zehr). Many factors affect PSI of the H-reflex pathway, including
afferent feedback from other peripheral receptors (e.g., muscle spindles, Golgi tendon
organs, cutaneous mechanoreceptors) and descending supraspinal commands (Zehr).
Many additional factors influence the amplitude of the H-reflex including the
level of motor neuron pool depolarization (or background muscle activity) and the
influence of post activation depression (Zehr, 2002). Post activation depression occurring
after repetitive activation of the Ia afferent pathway due to a depletion of neurotransmitter
stores and thereby requiring more time to evoke an action potential (Zehr).
H-reflex amplitude has also been observed to change between motor tasks, such
as standing and walking, as well as within various phases of a single motor task (Zehr,

2002). The amplitude of the H-reflex is a product of complex interactions and it appears
that either homonymous muscle activity, muscle activity from antagonistic muscles or
other more distant neural mechanisms may be capable of having a significant effect on H
reflex magnitude (Verrier, 1985) through mechanisms that influence the PSI and motor
neuron depolarization level (Zehr). It has also been shown that the contraction of the
muscles in the human upper body could markedly facilitate reflexes in the lower limbs
(Zehr & Stein, 1999). Specifically, the facilitation of stretch reflexes by remote muscle
contractions of the forearm and the jaw together has become known as the Jendrassik
maneuver, or JM (Zehr & Stein).
The purpose of this study was to observe the H-reflex, M-wave and the factors
that influence the generated responses evoked by electrical stimulation of the human
soleus muscle. Factors investigated included variables of local muscle contraction, as
well as remote influences. The independent variables that were manipulated in the study
were the stimulus intensity, local muscle contraction condition (at rest, 10% plantar
flexion and 10% dorsiflexion), and remote influences (the Jendrassik maneuver, the
Jendrassik maneuver with 10% plantar flexion, high vibration to the tibialis anterior
muscle and the removal of vibration from the tibialis anterior muscle). The dependent
variable of the study was the amplitude of the H-reflex, measured in millivolts and
recorded by an EMG. It was hypothesized that both local muscle contraction and remote
influences would have an effect on the size of the H-reflex. It was hypothesized that the
H-reflex amplitude of the soleus muscle would increase during 10% plantar flexion and
decrease during 10% dorsiflexion due to differences in the motor neuron pool
depolarization. Compared to rest, it was also hypothesized that the JM conditions would

result in an increased H-reflex amplitude and that stimulation to the antagonist, the
tibialis anterior muscle, would result in a decreased H-reflex amplitude.
Methods
The ankle joint was used in this experiment to observe the effect of various conditions on
the H-reflex amplitude of the human soleus muscle. The tibial nerve was stimulated and
surface EMG activity of the soleus muscles was recorded to investigate the characteristics
of the H-reflex and the M-wave. The subject was a twenty-year-old female, in apparently
good health. She was 175 cm tall and her right leg was dominant. Refer to pages 28-33 of
Human Motor Control Laboratory Manual (Zehr, 2015) for procedural details.
Modifications to the procedure were made in that data was only collected from one
subject.
Results
At rest, the soleus muscle produced a H-reflex threshold of 0.040 mV at a
stimulus of 25.82 V and a M-wave threshold 0.61 mV at a stimulus of 28.87 V. The Hreflex reached a maximum value of 7.2 mV at a stimulus of 30.27 V and then decreased
until a final reading of 0.35 mV was recorded at a stimulus of 37.15 V. The M-wave
amplitude continued to increase to the max recorded value of 7.54 mV at a stimulus of
37.15 V (Figure 1).

M-Wave
H-Reflex

60

65

70

75

80

85

90

95

100

105

Stimulus Amplitude (% M-max)

Figure 1. H-reflex and M-wave amplitudes, measured in millivolts, mV, versus the
stimulus intensity, recorded in voltages, V, recorded for the soleus muscle in the
participants dominant leg during rest. The nerve stimulated was the tibial nerve.
During 10% maximal voluntary plantar flexion, the soleus muscle produced a Hreflex threshold of 0.067 mV at a stimulus of 22.32 V and a M-wave threshold 1.47 mV
at a stimulus of 31.50 V. The H-reflex reached a maximum value of 7.69 mV at a
stimulus of 29.93 V and then decreased until a final reading of 1.47 mV was recorded at a
stimulus of 37.54 V. The M-wave amplitude continued to increase to the max recorded
value of 10.03 mV at a stimulus of 39.61 V (Figure 2). When both recruitment curves
were plotted it was determined that Figure 2 was shifted to the left.

9
8
7
6
5

M-Wave

H-Reflex

EMG Amplitude (mV)

3
2
1
0

Figure 2. H-reflex and M-wave amplitudes, measured in millivolts, mV, versus the
stimulus intensity, recorded in voltages, V, recorded for the soleus muscle in the
participants dominant leg during 10% maximal voluntary plantar flexion. The nerve
stimulated was the tibial nerve.
With a stimulus intensity setting producing a constant M-wave of 3.40 mV, the
following H-reflex amplitudes 5.02 mV, 6.45 mV, and 1.20 mV were observed at rest,
during 10% maximal voluntary plantar flexion on the dominant side and during 10%
maximal voluntary dorsiflexion on the dominant side, respectively (Table 1).
Remote influences on the amplitude of the H-reflex were also observed at a
stimulus intensity setting producing a constant M-wave of 3.40 mV. The following values
2.30 mV, 4.70 mV, 0.69 mV, and 2.27 mV were observed for the Jendrassik maneuver,
the Jendrassik maneuver with 10% plantar flexion of the ipsilateral soleus muscle, high
vibration to the ipsilateral tibialis anterior muscle and withdrawal of vibration from the
tibialis anterior muscle, respectively (Table 2).

Table 1
The Influences of Local Muscle Contraction of the Dominant Side (at Rest, at 10%
Maximal Voluntary Plantar Flexion and at 10% Maximal Voluntary Contraction
Dorsiflexion) on H-reflex Size at a Stimulus Intensity with a Constant M-wave at 3.40
mV.
Local Muscle Contraction

H-reflex size (mV)

Rest

5.02

10% MVC Plantar Flexion

6.45

10% MVC Dorsiflexion

1.20

Note. MVC is an abbreviation for maximal voluntary contraction.

Table 2
The Effect of Remote Influences (the Jendrassik Maneuver, the Jendrassik Maneuver with
10% Plantar Flexion of the Ipsilateral Soleus Muscle, High Vibration to the Ipsilateral
Tibiali Anterior tendon and Withdrawal of Vibration from the Tibialis Anterior Tendon)
on H-reflex Size at a Stimulus Intensity with a Constant M-wave at 3.40 mV.
Remote Influence

H-reflex size (mV)

Jendrassik Maneuver

2.30
4.70

Jendrassik Maneuver with 10% PF of Ipsilateral Soleus Muscle

High Vibration to Ipsilateral TA Tendon

0.69

Withdrawal of Vibrator from Ipsilateral TA Tendon

2.27

Note. PF and TA are abbreviations for plantar flexion and tibialis anterior respectively.
Discussion
At rest the subjects H-reflex threshold amplitude was measured to be 0.040 mV
and it reached a maximum value of 7.2 mV at a stimulus of 30.27 V before beginning to
decrease (Figure 1). This amplitude was less than at 10% maximal voluntary plantar
flexion where a H-reflex threshold was measured to be 0.067 mV and reached a
maximum value of 7.69 mV at a stimulus of 29.93 V before beginning to decrease
(Figure 2). Additionally, at 10% plantar flexion threshold occurred at a lesser stimulus
(22.32 mV) than at rest (25.82 mV) indicating that voluntary agonist activation facilitates
the H-reflex. With a constant M-wave of 3.40 mV, the H-reflex amplitudes changed from
rest (5.02 mV), to an increased 6.45 mV during 10% maximal voluntary plantar flexion
and a decreased 1.20 during 10% maximal voluntary dorsiflexion (Table 1). Generally, it
has been observed that the H-reflex amplitude will increase linearly with the number of
motor neurons recruited in the target motor neuron pool, which occurs during contraction
of the agonist muscle (Burke, Gandevia & McKeon, 1983). Increased motor neuron
depolarization allows muscle contraction to occur at a lower stimulus voltage, due to a
greater excitatory pre-synaptic potential before stimulus activation. However, it has also
been shown that when the input stimulus is increased beyond certain levels the effect of
9

baseline EMG activity on the change in H reflex magnitude diminishes (Verrier, 1985).
This increase observed at 10% maximal voluntary plantar flexion, or contraction of the
soleus muscle, when the H-reflex amplitude (0.067 mV) was larger than the threshold
value at rest (0.040), and appeared at a lower voltage, supporting the initial hypothesis
that contraction of the agonist muscle will facilitate the H-reflex amplitude (Figure 1 &
2). During voluntary contraction there is an increase in descending cortical effects on the
spinal interneurons, specifically those mediating reciprocal inhibition and the inability to
elicit H reflexes in certain muscles was due to the lack of facilitation to motor neurons
(Zehr, 2002; Verrier, 1985). These findings support the initial hypothesis that contraction
of the agonist muscle and increase in the motor neuron pool depolarization facilitates the
H-reflex. The hypothesis that activation of the antagonist muscles decreases H-reflex
amplitude was also supported.
This concept was further supported in a study looking at the effect of variations in
baseline EMG activity produced by voluntary muscle contractions of the flexor carpi
radialis muscle. It has been observed that increases in baseline EMG activity increase the
H-reflex magnitude as well as the probability of the occurrence of an H-reflex at subthreshold values (Verrier, 1985). Changes in the excitability of the interposed
interneurons in the polysynaptic pathway, rather than by direct changes in motor neuron
excitability, could be the mechanism responsible for this reflex modulation, especially at
higher stimuli (Verrier).
All conditions involving remote muscles resulted in decreased amplitude values
from the resting value of 5.02 mV, with the smallest amplitude, 0.69 mV, observed during
high vibration of the ipsilateral tibialis anterior tendon, which increased slightly to 2.27

10

mV when the vibration was removed. This supports the hypothesis that contraction of an
antagonist muscle will decrease H-reflex amplitude. The two conditions involving the
Jendrassik maneuver resulted in greater amplitudes, with the largest value (4.70 mV)
resulting from the combined action of the JM and 10% ipsilateral plantar flexion, and a
lesser amplitude of 2.30 mV when the JM was applied on its own (Table 2). This finding,
however, does not support they hypothesis that the JM would facilitate the H-reflex.
Deviations of the observed results from the current literature are likely due to equipment
and data collection errors, including the measurement equipment being held and the
subject having to hold a controlled contraction at 10% of maximum. Both of these
conditions are subject to human error and fluctuations between trials.
The decreases in the H-reflex during dorsiflexion and stimulation of the tibialis
anterior muscle have been attributed to alterations of the pre-synaptic inhibition (PSI) on
the afferent fibers that synapse directly on alpha motor neurons, leading to the H-reflex
response (Zehr, 2002). Increasing antagonist contraction has been identified as one
mechanism that increases PSI, suppressing the H-reflex amplitude (Zehr). Additionally,
PSI can be increased by direct stimulation of the nerves supplying the antagonist muscle,
or by vibration of the antagonist muscle tendon (Zehr), which was demonstrated by the
decrease in H-reflex during vibration of the tibialis anterior tendon and the increase in
amplitude when the vibration was removed (Table 2). In the case of the soleus muscle,
threshold electrical stimulation of the tibial nerve (to induce a homonymous facilitation
of the soleus H reflex) is strongly affected by vibration of the tibialis anterior muscle and
tendon. This increases the discharge of the Ia afferents that increase the PSI of Ia
afferents in the tibial nerve supplying the soleus, thereby decreasing firing rate of the

11

afferents onto the alpha motor neurons and resulting in less motor neurons reaching
threshold (Zehr).
While the complete mechanisms for facilitation are not completely understood, it
is believed that the Jendrassik maneuver potentiates the soleus H-reflex by reducing
segmental presynaptic inhibition (Zehr & Stein, 1999). The mechanism involves
blockage of the segmental PSI that is a product of antagonistic nerve stimulation,
specifically by common peroneal nerve (CP), innervating dorsiflexors of the ankle (Zehr
& Stein). It has been found that after CP activation there was a significant suppression of
the soleus H-reflex amplitude and a significant facilitation to the amplitude after the JM
(Zehr & Stein). When these stimuli were applied simultaneously the resulting reflex was
close to the algebraic sum of the affects of each stimulus alone, demonstrating that a
degree of convergence exists between the JM and segmental PSI, contributing to the
modulation of the H-relex amplitude (Zehr & Stein). It is likely that excitatory and
inhibitory synaptic inputs sum linearly on the inhibitory interneuron, changing the firing
rate of motor neurons post-synaptically. This provides various methods to modulate the
H-reflex, depending on the contextual requirements of the movement (Zehr & Stein).
Similarly, studies on the modulation of the H-reflex amplitude in response to
movement and postural conditions have identified the process of Ia afferent PSI as a
major mechanism involved in the control and fine-tuning of afferent feedback from the
leg during locomotor tasks (Zehr). It has been shown that as posture changes from lying
down, to standing, to walking, and then to running, the PSI of Ia afferent transmission is
steadily increased, thereby decreasing the amplitude of the H-reflex, allowing for a
greater amount of cortical control of segmental reflexes (Zehr, 2002).

12

Zehr and Stein (1999) suggested that Ia PSI is reduced at the onset of a focused
muscle contraction, as seen in the Jendrassik maneuver and voluntary plantar flexion.
This permits more afferent input for reflex and voluntary control of movement, to
optimize control (Zehr & Stein). Since there is interaction to some degree, there may be
some clinical utility (Zehr & Stein). A reduction in presynaptic inhibition of the soleus Hreflex, after spinal cord injury, may be due to a loss of tonic descending input to
segmental inhibitory interneurons, using these interactions as a probe for the state of
spinal control mechanisms after injury or stroke (Zehr & Stein).
In conclusion, this study supports the existing evidence that many factors
modulate the H-reflex, including motor neuron excitability and presynaptic inhibition,
which have been shown responsive to both local and remote contractions. It is important
to consider these influences to determine the implications they have on the development
of methods and the inferences that can be made from the data obtained, when used as a
tool in a research or clinical setting.

(1) By definition the H-reflex is a monosynaptic reflex of the Ia afferent onto

alpha motor neurons. As the neural circuitry is largely the same as the monosynaptic
stretch reflex, the H-reflex has often been described as the electrical analog of the stretch
reflex (Misiaszek, 2003). In reality, the H-reflex is confounded by oligosynaptic
contributions from Ia and other large diameter afferents (Misiaszek). The composite
excitatory postsynaptic potential (EPSP) of the H-reflex in the motor neurons have a
sufficient long rising phase that permits oligosynaptic to reach the motorneuron before
the EPSP begins to fade, indicating they have ample time to affect the later portions of

13

the H-reflex (Burke et al, 1983). In particular, inhibitory Ib effects from Golgi tendon
organ afferents were suggested as possible confounding contributors to the H-reflex
waveform (Burke et al. 1983). In addition, it has been shown that monosynaptic
excitation is greater in the smaller motor neurons of the flexor and extensor carpi radialis
muscles of the forearm, while non-monosynaptic excitation seems to be more preferential
to the larger motor units (Marchand-Pauvert, Mazevet, Nielsen, Petersen & PierrotDeseilligny, 2000).
(2) Due to the direct synaptic connection of Ia afferents and alpha motor neurons
it has been tempting for researchers to assume that the H reflex represents the excitability
of the motor neuron pool under study (Zehr, 2002). However, the synaptic connection
between Ia afferents and alpha motor neurons is subject to modification, such as
mechanisms that cause changes in the pre synaptic inhibition of the Ia afferent
transmission affecting the neurotransmitter release at the Ia afferent/alpha-motor neuron
synapse (Zehr).
Presynaptic inhibition (PSI) is mediated by the action of an inhibitory interneuron
acting on the Ia afferent terminals, leading to a reduction of neurotransmitter release and
thus a reduction in motor neuron depolarization induced by Ia activity (Zehr, 2002).
However, it has been shown that afferent transmission can be altered without a
corresponding affect on the post-synaptic membrane due to motor neurons remaining
receptive to other inputs unaffected by the PSI (Zehr). It is due to this reason that the
level of motor neuron excitability cannot be determined unambiguously by measuring the
H-reflex (Zehr).

14

(3) The response of the H-reflex and M-wave depends on the stimulus strength
(Kandel et al., 2013). At low stimulus strengths a pure H-reflex is evoked because the
threshold for activation of the large diameter Ia fibers is less than that of the smaller
diameter alpha motor axons (Kandel et al). Recruitment of motor neurons by
corticospinal, or Ia afferernts (as in the H-reflex), proceeds according to the size
principle from smallest to largest (Zehr, 2002). In the soleus muscle, it has been
suggested that the smaller, lower threshold, or slow motor units predominate in the Hreflex response (Buchthal & Schmalbruch, 1970). At higher stimulus intensities, the
direct stimulation of the motor axon fibers results in the production of the M-wave
(Kandel et al).
Increasing the stimulus strength eventually excites the motor axons, in this case of
the soleus muscle, resulting in two successive responses. The first response results from
the direct activation of the motor axons (M-Wave), and the second (H-reflex) is evoked
by stimulation of the Ia afferent fibers (Kandel et al., 2013). The H-reflex wave occurs
later because it results from a signal that travels to the spinal cord, across a synapse and
back to the muscle, while the M-wave results from direct stimulation of the motor axon
innervating the muscle (Kandel et al).
As the stimulus continues to increase, the M-wave continues to get larger while
the H-reflex progressively declines (Kandel et al., 2013). The decline in the H-reflex
amplitude is due to antidromic conduction, when the action potentials in the motor axons
propagate toward the cell body and cancel the reflexively evoked action potentials in the
same motor axons (Kandel et al). At very high stimulus strengths only the M-wave

15

persists and a maximum value will be reached when all motor units are active (Kandel et
al).

(4) The recruitment curve during the contraction of the soleus muscle was not
that same as the recruitment curve at rest. It was observed that 10% plantar flexion, or
contraction of the soleus muscle, resulted in H-reflex threshold value of 0.067 mV at 56.3
V compared to the threshold value of 0.040 mV at 65.9 V when at rest. The entire
recruitment curve for 10% plantar flexion is shifted to the left, implying that the
amplitude is higher at any given intensity than at rest. The increase in amplitude increases
linearly with the number of motor neurons activated in a target motor neuron pool, and
thus is due to an increase in motor neuron excitability (Zehr, 2002). Voluntary flexion
itself exerted a major excitatory input on the alpha motor neurons, while voluntary
extension exerted an inhibitory input (Chen et al., 1999). Several types of neural activity
modifies the excitability of the motor neuron pool during both plantar flexion and
dorsiflexion contractions through the summation of excitatory and inhibitory inputs
(Zehr). During plantar flexion, or contraction of the agonist, the motor neurons of the
soleus are facilitated by direct motor commands, descending from the cortex, and
increasing peripheral Ia afferent feedback (Zehr).

(5) It is important to rest between the different procedural steps of the recruitment
curve to prevent post activation depression. Repetitive activation of the Ia afferent
pathway can lead to reductions in neurotransmitter stores and release at the alpha motor
neurons. This post activation depression can persist for many seconds after the activation

16

of the Ia afferents (Zehr, 2002), requiring a greater stimulus than normal to evoke a
reflex. When evoking an unconditioned H-reflex it is recommended that a stimulation
interval of no less than three seconds be used, to allow time for the replenishing of
neurotransmitters (Rossi-Durand, Jones, Adams & Bawa, 1983)

(6) When the M-wave was a constant 3.40 mV, a rest H-reflex amplitude of 5.02
mV was recorded. Increasing agonist activation (ie. 10% plantar flexion) increased the
amplitude to 6.45 mV while increasing antagonist activation (ie. 10% dorsiflexion)
decreased the amplitude to 1.20 mV. Changes in the excitability of the interposed
interneurons in the polysynaptic pathway, rather than by direct changes in motor neuron
excitability, are likely the mechanism responsible for this reflex modulation, where
increasing voluntary agonist contraction decreases presynaptic inhibition and increasing
voluntary antagonist contraction increases presynaptic inhibition (Zehr, 2002).
All remote influences resulted in a decrease from the rest value of 3.40 mV. This
was expected for vibration to the tibialis anterior tendon (0.69 mv), due to increases in
presynaptic inhibition and reciprocal inhibition on the Ia afferents that excite the agonist
muscle (Zehr, 2002). This was further supported as the amplitude increased to 2.27 mV
with the withdrawal of the high vibration. It was expected that the Jendrassik maneuver
would facilitate the amplitude, but this was not observed in our study. It has been shown
that the JM potentiates the soleus H-reflex by reducing segmental presynaptic inhibition
(Zehr & Stein, 1999). The mechanism involves blockage of the segmental PSI that is a
product of antagonistic nerve stimulation, specifically by common peroneal nerve (CP),
innervating dorsiflexors of the ankle (Zehr & Stein). The JM alone produced an

17

amplitude of 2.30 mV and increased with 10% plantar flexion to 4.70 mV. This increase
was expected since the motor neuron pool was depolarized to a greater amount during
agonist activation, thus requiring less stimuli to invoke a greater reflex response (Zehr).
Sources of error described above likely contributed to the differences between the
collected JM data and the current literature.
The level of motor neuron pool excitability (as measured using the background
EMG activation level of the soleus muscle) is held at a constant level by voluntary
contraction, and is measured by keeping the M-wave constant. This ensures the change in
H-reflex amplitude represents a change in pre-synaptic inhibition and not a change in
motor neuron excitability (Zehr, 2002).

(7) Both contraction of the tibialis anterior and vibration of its tendon decrease
the amplitude of the H-reflex. Two mechanisms that cause this effect are the increase in
presynaptic inhibition and reciprocal inhibition. Increasing antagonist contraction has
been identified as one mechanism that increases PSI, suppressing the H-reflex amplitude
(Zehr, 2002). This increases the discharge of the tibialis anterior Ia afferents increases the
PSI of Ia afferents in the tibial nerve supplying the soleus, thereby decreasing firing rate
of the afferents onto the alpha motor neurons and resulting in less motor neurons reaching
threshold (Zehr). Specifically, inhibitory Ib effects from Golgi tendon organ afferents
were suggested as possible confounding contributors to the increase in PSI (Burke et al.
1983). These inhibitory effects would have been increased when the TA tendon was
stretched.

18

Reciprocal inhibition occurs when Ia inhibitory interneurons receive inputs from

collaterals of axons descending from neurons in the motor cortex that make direct
excitatory connections with spinal motor neurons. This organizational feature simplifies
the control of voluntary movements, for higher centers do not have to send separate
commands to the opposing muscles (Kandel et al., 2013). In this experiment, activation
of the tibialis anterior afferents (antagonist of the soleus), by either method, led to the
increased activation of an inhibitory interneuron that caused relaxation of the antagonist
muscle (the soleus) for the applied stimulus.
Another important class of inhibitory interneurons, Renshaw cells, also regulates
activity of spinal motor neurons (Kandel et al., 2013). Renshaw cells are excited by by
collaterals of the axons of motor neurons, and make inhibitory synaptic connections with
several populations of motor neurons, including the motor neurons that excite them and
the Ia inhibitory interneurons (Kandel et al). The connections with the Ia inhibitory
interneurons may regulate the strength of inhibition of antagonistic motor neurons, and
thus likely receive input during TA excitation. Renshaw cells also receive input from
descending pathways and distribute inhibition to task-related groups of motor neurons
and Ia interneurons (Kandel et al).
An increase in pre-synaptic inhibition due to signals from the afferent Ia fibers of
the tibialis anterior are likely more responsible for the modulation of the H-reflex in the
soleus muscle. Reciprocal inhibition and Renshaw cells both receive cortical input, which
requires more time to complete. Since a reflex response is often very fast, the direct presynaptic inhibition from the antagonist level occurs more readily.

19

References
Buchthal, F., Schmalbruch, H. (1970). Contraction times of twitches evoked by Hreflexes. Acta Physiologica Scandinavica, 80, 378382.
Burke, D., Gandevia, S.C., McKeon, B. (1983). The afferent volleys responsible for
spinal proprioceptive reflexes in man. Journal of Physiology, 33(9), 535552.
Chen, F., Lin, T., Chu, Y., & Chen, C. (1999). The H-reflex changes during wrist flexion
and wrist extension. Journal of Electromyography and Kinesiology, 16(5), 220228.
Kandel, E.R., Schwartz, J.H., Jessel, T.M., Siegelbaum, S.A., Hudspeth, A.J. (2013).
Principles of Neural Science. (5th Ed). New York, USA: McGraw Hill
Companies.
Marchand-Pauvert, V., Mazevet, D., Nielsen, J., Petersen, N., Pierrot-Deseilligny, E.
(2000). Distribution of non-monosynaptic excitation to early and late recruited
units in human forearm muscles. Experimental Brain Research, 134, 274278.

20

Masiaszek, J.E. (2003). The H-reflex as a tool in neurophysiology: Its limitations and
uses in understanding nervous system function. Muscle Nerve, 28, 144-160.
Rossi-Durand, C., Jones, K.E., Adams, S., Bawa, P. (1999). Comparison of the
depression of H-reflexes following previous activation in upper and lower limb
muscles in human subjects. Experimental Brain Research, 126, 117127.
Verrier, M. (1985). Alterations in H reflex magnitude by variations in baseline EMG
excitability. Electroencephalography and Clinical Neurophysiology, 60, 492-499.
Zehr, P.E. (2015). EPHE 380 Human Motor Control Laboratory Manual. Victoria,
Canada: Univeristy of Victoria.
Zehr, P.E. (2002). Considerations for the use of the hoffmann reflex in exercise studies.
European Journal of Applied Physiology. 86, 455-468.
Zehr, P.E., Stein, R.B. (1999). Interaction of the jendrassik maneuver with segmental
presynaptic inhibiton. Experimental Brain Research.124, 474-480.

21

Appendix A
Table of M-Wave and H-Reflex Amplitude Data, Measured in Millivolts, for Each
Stimulus Intensity, Measured in Volts for the Recruitment Curve at Rest.
Stimulus

Converted Stimulus

M-Wave

H-Reflex

(V)

(% Mmax)

(mV)

(mV)

25.82

65.9

0.040

26.59

71.6

1.86

27.22

73.3

3.72

28.87

77.7

0.61

6.61

29.48

79.4

1.05

7.06

30.27

81.5

1.96

7.2

86.6

2.83

6.80

33.35

89.8

5.30

3.35

35.01

94.2

6.56

1.69

37.15

100

7.54

0.35

32.16

22

Appendix B
Table of M-Wave and H-Reflex Amplitude Data, Measured in Millivolts, for Each
Stimulus Intensity, Measured in Volts for the Recruitment Curve at 10% Maximal Plantar
Flexion.

Stimulus

Converted Stimulus

(V)

(% Mmax)

22.32
24.64
26.59
28.49
29.93
31.50

M-Wave
(mV)

(mV)
0.067

56.3
62.2

0.52

67.1

5.05
7.59

71.9

7.69

75.6
79.5

H-Reflex

1.47

7.37

23

32.53

82.1

2.96

6.03

34.89

87.9

9.22

2.78

37.54

94.8

9.73

1.47

39.61

100

10.03

24