Electrophysiology and ...

Electrophysiology and Kinesiology for Health and Disease, Science Based

[ Pobierz całość w formacie PDF ]
Journal of Electromyography and Kinesiology 15 (2005) 240–255
www.elsevier.com/locate/jelekin
Electrophysiology and kinesiology for health and disease
Toshio Moritani
*
, Tetsuya Kimura, Taku Hamada, Narumi Nagai
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan
Abstract
This paper summarizes my Basmajian keynote presentation at the 2004 International Society of Electrophysiology and Kinesi-
ology Conference. I dedicate this paper to Dr. Herbert A. deVries, the mentor of my research career. The following topics will be
covered from the standpoint of Electrophysiology and Kinesiology for health and disease: (1) electromechanical manifestations of
neuromuscular fatigue and muscle soreness, (2) cardiac depolarization–repolarization characteristics of normal and patients, (3) eti-
ology of obesity and diabetes and autonomic nervous system, and (4) functional electrical stimulation for health and disease,
respectively.
2005 Elsevier Ltd. All rights reserved.
1. Electromechanical manifestations of neuromuscular
fatigue and muscle soreness
theory. Although a number of different mechanisms
were proposed in the past, the exact nature of this
DOMS and its association to the spinal alpha motoneu-
ron excitability and blood circulation has not yet clearly
been established.
We investigated the physiological effects of static
stretching upon DOMS in conjunction with the spinal
alpha motoneuron pool excitability and peripheral mus-
cle blood flow in seven healthy male subjects. All sub-
jects performed heel raises (30 rep, 5 sets) with 20 kg
load 24 h prior to testing. Electrophysiological measure-
ments included the Hoffman reflex amplitude (H ampli-
tude) as a measure of spinal alpha motoneuron pool
excitability. The directly evoked muscle action potential
(M-wave) remained constant for each subject through-
out the experiments. The posterior tibia nerve was elec-
trically stimulated for this purpose
[38]
. Blood flow was
performed by near infrared spectroscopy (NRS). In the
experimental condition (EXP), those measurements
were obtained before/after static stretching (35 s, 3 sets)
under experimentally induced muscle soreness. During
the control condition (CON), the same measurements
were made before/after standing rest for a period of 4
min. The order of the experimental treatments (EXP
or CON) were chosen at random.
1.1. Delayed onset of muscle soreness
Every sports participant would experience muscle
soreness after training. A typical feature of muscle sore-
ness is its delayed onset, and therefore this type of mus-
cle soreness is usually called delayed onset of muscle
soreness (DOMS)
[27]
. It is the sensation of discomfort
or pain in the skeletal muscles that occur following
unaccustomed eccentric exercise
[3]
. It can usually be felt
within 8 or 10 h after exercise, peaks between 24 and 48
h and it is gone in about 5–7 days post-exercise. Sore
muscle can be described as being stiff or tender because
there is a sense of reduced mobility or flexibility, and the
muscles are sensitive, particularly upon palpation or
movement, sometimes feeling swollen
[47]
. The most
commonly raised possibly cause of DOMS are: (i) dam-
age to the muscle fibers themselves, connective tissue, (ii)
edema, inflammation and swelling, and (iii) a vicious cy-
cle of reflex muscle activity, ischemia and pain–spasm
*
Corresponding author. Tel./fax: + 81 75 753 6888.
E-mail address:
T. Moritani).
1050-6411/$ - see front matter 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jelekin.2005.01.001
T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240–255
241
Fig. 1
represents a typical set of H-reflex data ob-
tained 24 h after experimentally induced muscle soreness
prior to muscle stretching and immediately after muscle
stretching. The data clearly indicated that H-reflex
amplitude was considerably reduced after muscle
stretching. Group data demonstrated that the static
stretching brought about a statistically significant reduc-
tion in the H/M ratio (23.5%, p < 0.01) of the EXP con-
ditions while no such changes were observed in CON
trials. These changes were accompanied by nearly
78.5% increase (p < 0.01) in blood flow after stretching
of the leg with the experimentally induced soreness.
The result of reduction in alpha motoneuron excitability
was entirely consistent with earlier studies, suggesting
that the inverse myotatic reflex (Ib inhibition) may be
the basis for the relief of muscle soreness by static
stretching. The increase in blood flow after stretching
found in the present study suggested that static stretch-
ing could bring about a relief of spasm, which could
have caused local muscles ischemia and pain. Our data
strongly suggest that static stretching plays a significant
role in relief of DOMS by reducing spinal motoneuron
pool excitability and enhancing muscle blood flow (see
Fig. 2
).
reflex amplitudes showed clear-cut rising (p < 0.001)
and by contrast, the T-reflex amplitude did not show
such a significant elevation. All the EMG amplitudes
recovered to the preexercise level in 24 h. The impact
force on the Achilles tendon (coecient of rebound
force) showed a reduction immediately after the running
(p < 0.05) and recovered in 24 h. The difference between
H- and T-reflex amplitudes 2-h after the exhaustive run-
ning might suggest that the sensitivity of fusimotor
activity was reduced by 2-h of running. Furthermore
the reduced impact force might signify deteriorated stiff-
ness regulation of muscle-tendon complex. This may
also suggest the degradation of spindle activity. There-
fore, present results support the hypothesis claiming that
the stretch reflex reduction might be attributed to disfa-
cilitation of alpha motoneuron pool caused by with-
drawal of spindle-mediated fusimotor support and/or
fatigue of the intrafusal fibers of muscle spindle itself
[4,5]
.
1.3. Use of mechanomyogram for analysis of motor unit
activity
Previous studies have indicated that mechanomyo-
gram (MMG) amplitude and frequency components
might represent the underlying motor unit (MU) recruit-
ment and firing rate (rate coding)
[6,49–52]
. Interest-
ingly, MMG amplitude actually decreases at higher
force levels at which MUs might be firing at tetanic
rates, causing a fusion-like contraction leading to dimin-
ished MMG amplitude, while its frequency increases
[41,73,74]
. These data suggest that MMG analyses
might offer not only MU recruitment and rate coding
characteristics, but also their mechanical properties,
i.e., the fusion properties of activated MUs that could
not be obtained by conventional EMG analyses
[41,74]
.
1.2. Fusimotor sensitivity after prolonged stretch
shortening cycle exercise
We have recently performed comparative analyses of
T-reflex, elicited by Achilles tendon tap and H-reflex,
elicited by electrical stimulation of tibial nerve before
and immediately after, 2- and 24-h after two hours of
exhaustive running (n = 10). Results revealed that imme-
diately after the running T and H wave amplitudes were
significantly depressed while maximal M-wave remained
constant. On the other hand, 2-h after the running H-
Fig. 1. Spinal motoneuron excitability (H-reflex) changes following experimentally-induced muscle soreness (a) and after static muscle stretching (b).
242
T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240–255
Fig. 2. A simplified schematic representation of basic neural components involved in stretch reflex and Golgi tendon organ Ib inhibition.
To further shed some light on this matter, we studied
14 isolated MUs in the medial gastrocnemius (MG) mus-
cle of 7 healthy male subjects. Two identical microphone
sensors (10 mm diameter, mass 5 g, bandwidth 3–2000
Hz) for MMG recording were fixed to the center of the
belly of the MG and soleus (SOL). Single twitch and
repetitive stimulations (10 Hz) were performed during
room temperature and hypothermic conditions (15, 20,
and 25 C)
[26]
. During voluntary contractions,
MU and MMG activities were recorded at 20%, 40%,
60%, and 80%MVC. Effects of mixed micro-stimulations
were also studied by stimulating two MUs at 5–10, 10–
20, 8–12, and 12–24 Hz, respectively; while simulta-
neously recorded evoked mass action potentials
(M-wave) remained constant. In addition, isolated MU
fatigue trials were performed at 12 Hz for a period of
2-min in order to determine the relationship between
muscle contractile slowing and the corresponding
MMG amplitude and frequency components (see
Fig. 3
).
The group data indicated that rms-MMG of MG in-
creased as a function of force (p < 0.01). On the con-
trary, these values for SOL increased up to 60% MVC
(p < 0.01), but then decreased at 80% MVC due to pos-
sible MU fusion resulting in smaller muscle dimensional
changes
[41,73]
. Similarly, a significant reduction in the
muscle contractile properties (peak force, maximal rate
of force development and relaxation, contraction and
half-relaxation times, etc.) caused by the experimental
hypothermia also resulted in significant reduction in
MMG amplitude with subsequent fusion at a low stim-
ulation frequency
[26]
. Different stimulation frequency
trials indicated that there were highly significant and
progressive reductions in the force fluctuations from 5
to 50 Hz that were almost mirrored by the similar and
significant reductions in the MMG amplitudes. Mixed
stimulations to different MUs clearly demonstrated that
both MMG and force recordings showed two distin-
guished peak frequencies that were delivered to the
underlying MUs. Lastly, our MU fatigue study with
prolonged stimulation at 12 Hz demonstrated that
MMG amplitude decreased progressively as contractile
slowing occurred as a function of time (see
Fig. 4
).
1.4. Mechanomyogram changes during low back muscle
fatigue
As a practical application of this MMG analysis, we
have recently investigated the etiology of low back mus-
cle fatigue by means of simultaneous recordings of
EMG, MMG, and near infrared spectroscopy (NIRS)
in an attempt to shed some light on the electrophysio-
logic, mechanical, and metabolic characteristics, respec-
tively
[75]
. Eight male subjects performed back
extension isometrically at an angle 15 with reference
to the horizontal plane for a period of 60s. Surface
EMG, MMG and NIRS signals were recorded simulta-
neously from the center of the belly of L3. NIRS were
measured to determine the level of muscle blood volume
(BV) and oxygenation (Oxy-Hb). The root mean square
amplitude value (rms) of EMG significantly increased at
the initial phase of contraction and then fell significantly
while mean power frequency (MPF) of EMG was signif-
icantly and progressively decreased as a function of
time. There were also significant initial increases in
rms-MMG, which was followed by progressive
decreases at the end of fatiguing contractions. MPF-
MMG remained unchanged. BV and Oxy-Hb dramati-
cally decreased at the onset of the contraction and then
T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240–255
243
Fig. 3. Mechanomyogram changes obtained from isolated motor unit during direct stimulation at different frequencies.
remained almost constant throughout the rest of con-
traction. These results obtained by simultaneous record-
ings of EMG, MMG, and NIRS tools demonstrates that
restriction of blood flow due to the high intramuscular
mechanical pressure is one of the most important factors
to evoke the muscle fatigue particularly in low back
muscle. In addition, our simultaneous recording system
described here can obtain more reliable information
regarding the mechanism(s) of low back muscle fatigue.
tality in healthy populations as well
[60]
. Although the
importance of the QTc interval is clearly recognized, it
is often dicult to determine the end of the T(U) wave
and to measure the QT interval precisely because of a
variety of morphological T(U) wave abnormalities such
as biphasic, or notched T-waves in patients
[60]
. In the
latent or borderline patients, exercise stress testing, iso-
proterenol infusion, or autonomic maneuvers such as
the Valsalva maneuver or the cold pressure test are re-
ported to be helpful in unmasking a prolonged QT inter-
val. However these provocative maneuvers are stressful
and may occasionally be dangerous in some LQTS
patients.
Therefore, attempts to identify new quantitative ECG
characteristics of LQTS using a computer algoritlm have
recently been made
[7,21]
. For example, the activation
recovery interval (ARI), defined as the interval between
the minimum dV/dt of the QRS and the maximum dV/dt
in the ST–T segment on ECG, has been proposed as a
useful measure of local repolarization duration. Like-
wise, transmembrane activation time (AT) has been re-
ported to occur at the intrinsic deflection, the interval
between ECG QRS onset to the time of maximal dV/
dt of the T waves. More recent studies including our
own work
[67,70]
have estimated the myocardial depo-
larization–repolarization process in terms of recovery
2. Cardiac depolarization–repolarization characteristics
of normal and patients with long QT syndrome (LQTS)
Cardiac autonomic dysfunction is prevalent in car-
diac and diabetic patients and associated with prolonga-
tion of the myocardial repolarization period. It has been
speculated that changes in autonomic nervous system
activity, particularly the sympatho-vagal balance con-
tributes to the prolongation of myocardial repolariza-
tion. Therefore, a prolonged heart rate-adjusted ECG
QT duration (QTc) has been used as a marker for sud-
den cardiac death in myocardial infarction patients
[61,62]
. There is also increasing evidence that a pro-
longed QTc is predictive of coronary heart disease mor-
244
T. Moritani et al. / Journal of Electromyography and Kinesiology 15 (2005) 240–255
Fig. 4. Mechanomyogram changes obtained from isolated motor unit during 12 Hz prolonged fatigue stimulation.
time (RT) defined as the total time of AT and ARI and
assessed quantitatively the degree of myocardial ische-
mia instead of evaluating changes in ST-segment and
QT interval (see
Fig. 5
).
tion reflected in QTc prolongation may result in ventric-
ular electrical instability and increase the risk of fatal
myocardial infarction. It can thus be speculated that
changes in autonomic nervous system (ANS) activity,
particularly the sympatho-vagal balance contributes to
the prolongation of QTc. We have therefore conducted
a series of studies to develop computer algorithms to
measure cardiac depolarization–repolarization times
and to accomplish the analysis of ECG R–R interval
power spectral analysis simultaneously by using the
CM5 lead ECG
[70]
. Additionally, we have applied
2.1. Cardiac recovery time of normal and patients
It has been suggested that QTc prolongation may be
a consequence of an unfavorable balance between sym-
pathetic and parasympathetic activities. Sympathetic
predominance accompanied by dispersion of repolariza-
Fig. 5. Electrocardiographic determination of cardiac depolarization/repolarization process.
[ Pobierz całość w formacie PDF ]

zanotowane.pl

doc.pisz.pl

pdf.pisz.pl

dietanamase.keep.pl