Electrophysiology and Kinesiology for Health and Disease.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.

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: moritani@virgo.jinkan.kyoto-u.ac.jp ( T. Moritani).

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.

Plik z chomika:

Inne pliki z tego folderu:

Inne foldery tego chomika: