Unstable rocker shoes promote recovery from marathon-induced muscle damage in novice runners.

We recently reported that wearing unstable rocker shoes (Masai Barefoot Technology: MBT) may enhance recovery from marathon race-induced fatigue. However, this earlier study only utilized a questionnaire. In this study, we evaluated MBT utilizing objective physiological measures of recovery from marathon-induced muscle damages. Twenty-five university student novice runners were divided into two groups. After running a full marathon, one group wore MBT shoes (MBT group), and the control group (CON) wore ordinary shoes daily for 1 week following the race. We measured maximal isometric joint torque, muscle hardness (real time tissue elastography of the strain ratio) in the lower limb muscles before, immediately after, and 1, 3, and 8 days following the marathon. We calculated the magnitude of recovery by observing the difference in each value between the first measurement and the latter measurements. Results showed that isometric torques in knee flexion recovered at the first day after the race in the MBT group while it did not recover even at the eighth day in the CON group. Muscle hardness in the gastrocnemius and vastus lateralis showed enhanced recovery in the MBT group in comparison with the CON group. Also for muscle hardness in the tibialis anterior and biceps femoris, the timing of recovery was delayed in the CON group. In conclusion, wearing MBT shoes enhanced recovery in lower leg and thigh muscles from muscle damage induced by marathon running.

Motor imagery beyond the motor repertoire: Activity in the primary visual cortex during kinesthetic motor imagery of difficult whole body movements.

To elucidate the neural substrate associated with capabilities for kinesthetic motor imagery of difficult whole-body movements, we measured brain activity during a trial involving both kinesthetic motor imagery and action observation as well as during a trial with action observation alone. Brain activity was assessed with functional magnetic resonance imaging (fMRI). Nineteen participants imagined three types of whole-body movements with the horizontal bar: the giant swing, kip, and chin-up during action observation. No participant had previously tried to perform the giant swing. The vividness of kinesthetic motor imagery as assessed by questionnaire was highest for the chin-up, less for the kip and lowest for the giant swing. Activity in the primary visual cortex (V1) during kinesthetic motor imagery with action observation minus that during action observation alone was significantly greater in the giant swing condition than in the chin-up condition within participants. Across participants, V1 activity of kinesthetic motor imagery of the kip during action observation minus that during action observation alone was negatively correlated with vividness of the kip imagery. These results suggest that activity in V1 is dependent upon the capability of kinesthetic motor imagery for difficult whole-body movements. Since V1 activity is likely related to the creation of a visual image, we speculate that visual motor imagery is recruited unintentionally for the less vivid kinesthetic motor imagery of difficult whole-body movements.

Fos activation in hypothalamic neurons during cold or warm exposure: projections to periaqueductal gray matter.

The hypothalamus, especially the preoptic area, plays a crucial role in thermoregulation, and our previous studies showed that the periaqueductal gray matter is important for transmitting efferent signals to thermoregulatory effectors in rats. Neurons responsible for skin vasodilation are located in the lateral portion of the rostral periaqueductal gray matter, and neurons that mediate non-shivering thermogenesis are located in the ventrolateral part of the caudal periaqueductal gray matter. We investigated the distribution of neurons in the rat hypothalamus that are activated by exposure to neutral (26 degrees C), warm (33 degrees C), or cold (10 degrees C) ambient temperature and project to the rostral periaqueductal gray matter or caudal periaqueductal gray matter, by using the immunohistochemical analysis of Fos and a retrograde tracer, cholera toxin-b. When cholera toxin-b was injected into the rostral periaqueductal gray matter, many double-labeled cells were observed in the median preoptic nucleus in warm-exposed rats, but few were seen in cold-exposed rats. On the other hand, when cholera toxin-b was injected into the caudal periaqueductal gray matter, many double-labeled cells were seen in a cell group extending from the dorsomedial nucleus through the dorsal hypothalamic area in cold-exposed rats but few were seen in warm-exposed rats. These results suggest that the rostral periaqueductal gray matter receives input from the median preoptic nucleus neurons activated by warm exposure, and the caudal periaqueductal gray matter receives input from neurons in the dorsomedial nucleus/dorsal hypothalamic area region activated by cold exposure. These efferent pathways provide a substrate for thermoregulatory skin vasomotor response and non-shivering thermogenesis, respectively.

Single lung transplantation in rats with fatal pulmonary hypertension.

Effects of single lung transplantation on fatal pulmonary hypertension were evaluated in rats receiving a lethal dose of monocrotaline. Inbred rats treated with monocrotaline (80 mg/kg) received a left lung isograft at 4 weeks (n = 9) and at 6 weeks (n = 6), when moderate and severe pulmonary hypertension, respectively, had developed. Medicated (n = 12) and nonmedicated rats (n = 12) served as control animals. Each rat was tested weekly with treadmill for exercise tolerance and oxygen consumption during a 10-week period after medication and after they were killed. Medicated control rats lost exercise tolerance and highest oxygen consumption per unit time consistently to the range of resting value (or 45% of nonmedicated control rats), and all died from severe pulmonary vascular occlusive disease with right ventricular hypertrophy before 10 weeks (right ventricular/left ventricular weight ratio of 1.16). All rats receiving a left lung isograft at 4 weeks survived and regained highest oxygen consumption per unit time (87% of nonmedicated control rats), with the lung transplant receiving 65% (nonmedicated control rats, 39%) of cardiac output and milder right ventricular hypertrophy (right ventricular/left ventricular weight ratio of 0.46). Except for one, all rats that received a left lung isograft at 6 weeks tolerated single lung transplantation, but they died soon after reperfusion because of pulmonary edema in the graft that received 58% of cardiac output with right ventricular/left ventricular weight ratio of 0.79. Results of single lung transplantation in rats were dependent on severity of pulmonary hypertension. In rats with moderate pulmonary hypertension, single lung transplantation was successful in reversing exercise intolerance and right ventricular hypertrophy. Single lung transplantation was unsuccessful when pulmonary hypertension was severe in the rat model because increased flow toward the lung transplant resulted in graft pulmonary edema.

Ionic responsiveness in third ventricular hypertonic stimulation of antidiuresis in ducks.

Domestic ducks were chronically equipped with a device probing the third cerebral ventricle (VIII) for localized intracerebroventricular (i.c.v.) perfusion. In conscious animals made diuretic by intravenous water loading with 1.0 ml/min hypoosmotic glucose solution (200 mOsm/kg), hyperosmotic i.c.v. stimulations were tested for antidiuretic actions. Artificial cerebrospinal fluid made hypertonic (400 mOsm/kg) by adding sucrose, mannitol, NaCl, LiCl, choline chloride, NaI, NaNO3, LiNO3, CaCl2 or MgCl2 was perfused i.c.v. for 10-15 min at rates of 10-15 microliters/min. Arterial pressure and heart rate were monitored continuously. Hyperosmotic stimulations with non-electrolytes did not induce antidiuresis. Approximately equivalent degrees of antidiuresis were elicited by Na(+)-, Li(+)- and choline salts with a tendency for moderate rises in arterial pressure. Compared to Cl(-)- and I(-)-salts, the effects of NO3(-)-salts were attenuated. Divalent cations caused prolonged antidiuresis, sometimes preceded by initial diuresis, with circulatory side effects unrelated to the changes in renal fluid excretion. It is concluded that the observed antidiuretic effects were mediated by cation-sensitive, rather than osmosensitive neurons on the brain side of the blood-brain-barrier. Their transduction mechanism might consist of poorly selective membrane channels permeable to cations but not to anions.

Neuronal activities in ventrobasal complex of thalamus and in trigeminal main sensory nucleus during EEG desynchronization in anesthetized rats.

Activities of somatosensory relay neurons responding to orofacial mechanical stimulation were examined in the ventrobasal complex of the thalamus (VB) and in the trigeminal main sensory nucleus (MSN) during EEG desynchronization in urethane-anesthetized rats. EEG desynchronization was induced by scrotal warming in a temperature range of 35-40 degrees C. Responses of most VB neurons to receptive-field stimulation were augmented during EEG desynchronization, when compared to responses during synchronization. Spontaneous activity of VB neurons also increased with EEG desynchronization. Responses of MSN neurons to receptive-field stimulation did not change appreciably when the EEG pattern was altered. If a VB neuron was induced by iontophoretic application of glutamate to fire at the same rate as seen during EEG desynchronization, a similar increased response to receptive-field stimuli was also observed. The augmented response of the VB neuron during desynchronization may thus have resulted from increased excitability of the neuron itself.

Responses of thalamic and hypothalamic neurons to scrotal warming in rats: non-specific responses?

Activities of thalamic and hypothalamic neurons in response to scrotal temperature change were investigated in urethanized (1.2-1.5 g/kg) rats with special attention to changes in cortical electroencephalogram (EEG). Somatosensory relay neurons were identified electrophysiologically in the ventrobasal complex (VB) of the thalamus. These neurons had tactile receptive fields in areas outside the scrotum. Forty out of 44 of these neurons responded to scrotal warming by increase in firing rate. The responses occurred abruptly at threshold temperatures ranging from 31 to 40 degrees C (switching response) with simultaneous changes in EEG from high to low voltages (desynchronization). In both the thalamus and the hypothalamus, neurons excited or inhibited by scrotal warming were also excited or inhibited, respectively, by noxious stimulation that produced EEG desynchronization. Neurons showing no response to scrotal warming were not affected by noxious stimulation. In deeply anesthetized (2.5 g/kg urethane) rats, VB relay neurons responded to tactile stimulation of their receptive fields, but scrotal warming produced no change in either EEG or activities of thalamic and hypothalamic neurons. These facts suggest that the responses of thalamic and hypothalamic neurons to scrotal warming may be 'non-specific'. Most thalamic and hypothalamic neurons showing switching responses did not appear to mediate specific information concerning scrotal skin temperature.

Effect of gonadotropin releasing hormone on thermoregulatory vasomotor activity in ovariectomized female rats.

To investigate the effect of gonadotropin releasing hormone (GnRH) on thermoregulatory skin vasomotion, we injected GnRH into various brain regions in both anesthetized and unanesthetized ovariectomized female rats. Local warming of preoptic area (PO) elicited skin vasodilation in anesthetized rats. Injection of 2 microg GnRH into the septal area lowered the threshold hypothalamic temperature for skin vasodilation at least for 2 h. Similar injections of 2 microg GnRH into the lateral ventricle (LV) and PO were ineffective. Although this vasodilative effect was also obtained after the injection of 20 ng GnRH into the septal area, injections of 2 ng GnRH were without effect. Not only injections of 20 ng Antide, a potent GnRH antagonist, but also injections of the mixed solution of 20 ng GnRH and 20 ng Antide were also without effect. In unanesthetized and unrestrained rats at an ambient temperature of 17 degrees C, injections of 20 ng GnRH into the septal area elicited tail vasodilation lasting for 30 minutes, whereas vehicle injections were ineffective. Injections of 20 ng GnRH into LV and PO were also ineffective. These results indicate that GnRH can elicit thermoregulatory skin vasomotion by acting on GnRH receptors in the septal area. This thermoregulatory vasodilative effect of GnRH might be possibly related to the etiology of climacteric hot flush.

Effects of estradiol treatment on responses of rat preoptic warm sensitive neurons to progesterone in vitro.

Single unit activity was recorded extracellularly in preoptic slice preparations from ovariectomized female rats. The rats were pretreated daily with (1) estradiol benzoate (20 micrograms/0.1 ml sesame oil) for 3 consecutive days just prior to the experiment (OVX+E72h), (2) sesame oil (OVX+Oil), or (3) untreated (OVX). In the preparations from OVX rats, 12 (50%) of 24 warm-sensitive neurons were inhibited and 2 (8%) were excited by the application of progesterone (P) in perfusion medium (30 ng/ml). In OVX+Oil preparations, 4 (40%) of 10 warm-sensitive neurons were inhibited and none was excited by P. In OVX+E72h preparations, however, only 4 (10%) were inhibited by P and 16 (38%) of 42 warm-sensitive neurons were excited. When Ru38486, a P-receptor antagonist, was applied together with P, no excitation was observed in warm-sensitive neurons in OVX+E72h preparations. These findings suggest that the P-induced excitation of preoptic warm sensitive neurons is mediated through the estrogen-induced P-receptors.

Grooming, body extension, and vasomotor responses induced by hypothalamic warming at different ambient temperatures in rats.

During heat stress, rats extend their body and spread saliva onto their body surfaces (grooming) for evaporative heat loss in addition to tail vasodilation. We investigated the effects of changing hypothalamic (Thy) and ambient (Ta) temperatures on these thermoregulatory responses. The higher the Ta, the lower the Thy at which grooming started when Ta was changed from the thermoneutral zone (24 degrees C) to 28-40 degrees C. At any Ta grooming was induced only when the posterior hypothalamic region (PH) was warmed by implanted diathermy. Grooming was more strongly induced at a Ta of 28 degrees C than at 24 degrees C. At a Ta of 32 degrees C, PH warming evoked body extension as well, decreasing the duration of grooming as compared to that at 28 degrees C. Warming the preoptic area and anterior hypothalamus induced body extension and tail vasodilation regardless of Ta. The data suggest that grooming was induced by integrated temperature signals from the PH and from the peripheral skin.

Competition between lever-pressing behavior and thermoregulatory behavior on exposure to heat in intracranial self-stimulating rats.

To investigate the relationship between the thermoregulatory system and the brain-reward system, we examined effects of heat exposure and tail amputation on lever-pressing behavior in intracranial self-stimulating rats. Rats that continuously pressed a lever voluntarily for 1 hour at an ambient temperature (Ta) of 22 degrees C interrupted lever pressing and showed heat loss behaviors, such as grooming and body extension, at a Ta of 36 degrees C. Hypothalamic temperature (Thy) at the time of the first body extension was higher than that after 1 hour of lever-pressing at a Ta of 22 degrees C. Tail amputation experiments showed the same result. Thy at the onset of the body extension after tail amputation was higher than that at the end of 1 hour of lever-pressing under control conditions. The data suggest that thermal factors, especially Thy, are important in the control of lever-pressing behavior.

New apparatus for studying behavioral thermoregulation in rats.

The operant system described here contains a box that can be convectively heated or cooled. A rat moves freely in the box. Its location is monitored photoelectrically while its deep body temperature is monitored by a telemetry system. In heat-escape experiments, hot air (40 degrees C) flows through the box. When the rat enters a reward zone the air source is switched and cold air (0 degrees C) flows through the box for a given period (30 s). Conversely, in cold-escape experiments cold air flows through the box and when the rat enters the reward zone the air source is switched to a warm one. Experiments show that rats quickly learn to stay near the reward zone and move in and out of it periodically. This system is based on behavior more natural than the frequently used lever-pressing response, and has many advantages for use in studies involving behavioral thermoregulation.

Neuronal circuitries involved in thermoregulation.

The body temperature of homeothermic animals is regulated by systems that utilize multiple behavioral and autonomic effector responses. In the last few years, new approaches have brought us new information and new ideas about neuronal interconnections in the thermoregulatory network. Studies utilizing chemical stimulation of the preoptic area revealed both heat loss and production responses are controlled by warm-sensitive neurons. These neurons send excitatory efferent signals for the heat loss and inhibitory efferent signals for the heat production. The warm-sensitive neurons are separated and work independently to control these two opposing responses. Recent electrophysiological analysis have identified some neurons sending axons directly to the spinal cord for thermoregulatory effector control. Included are midbrain reticulospinal neurons for shivering and premotor neurons in the medulla oblongata for skin vasomotor control. As for the afferent side of the thermoregulatory network, the vagus nerve is recently paid much attention, which would convey signals for peripheral infection to the brain and be responsible for the induction of fever. The vagus nerve may also participate in thermoregulation in afebrile conditions, because some substances such as cholecyctokinin and leptin activate the vagus nerve. Although the functional role for this response is still obscure, the vagus may transfer nutritional and/or metabolic signals to the brain, affecting metabolism and body temperature.

Modulation of reflex activity of motor units in response to stretch of a human finger muscle.

Changes in stretch reflex responses were examined in two types of motor task, force control and position control, by applying a small quick stretch to the middle finger extensor digitorum communis (EDC) muscle at an unpredicted time and observing activities of single motor units. Subjects were asked to maintain a constant extending isometric force at the metacarpophalangeal (MP) joint for force control, and to maintain a constant middle finger position against an applied force for position control. No significant differences in the tonic activities of EDC motor units were seen between the two types of motor task when the same force was exerted about the MP joint. Tonic activities of the EDC muscle and its antagonists were thus similar for both types of motor task. Ten of the eighteen motor units investigated showed obvious reflex responses (increase in firing rate) with latencies of 30-60 msec after the stretch. This reflex response was greater for position control than for force control, given the same operating conditions of tonic force, finger position, and activities of motor units. Enhancement of the stretch reflex for position control was also observed in surface electromyograms of the same muscle.

Fall in skin temperature during exercise observed by thermography.

Monochromatic and colored thermographies were used to visualize skin temperatures during exercise without involvement of sweating. Skin temperature began to fall immediately at the onset of exercise, remained low during exercise and rose rapidly after cessation of exercise. Increased work intensities produced a proportional fall in skin temperature and greater surface area of lowered temperature.

The number of active motor units and their firing rates in voluntary contraction of human brachialis muscle.

To make clear the control mechanism of force generation in human muscle, the electrical activity of the brachialis muscle was studied at various levels of contraction force by recording single motor unit discharges as well as mass electromyograms (EMGs). The firing rate of motor units increased with force along an S-shaped curve. At low levels of force, motor units increased their firing rates steeply with force. At intermediate levels of force, each motor unit increased its firing rate linearly with force at lower rates. As the maximum of force was approached, the firing rate increased very steeply, reaching as high as 50 Hz or more. By applying a new method of statistical processing to mass EMGs, the number of active motor units and the size of action potential were estimated at each level of force. The number of active motor units increased monotonously with muscle force. Motor units recruited at high levels of force had larger amplitudes of action potentials than those recruited at lower levels. Calculations were made to determine how the relative contribution to an increase in muscle force is varied between recruitment and the increase in firing rate. The contribution of recruitment gradually decreased with the increase in force. Up to about 70% of the maximum force, recruitment is the major mechanism for increasing the force of contraction.

Effect of periaqueductal morphine injection on thermal response in rats.

The effect of morphine injection into the midbrain periaqueductal gray (PAG) was examined on thermal response in rats. Rectal temperature (Tre) was recorded in unanesthetized and unrestrained animals before and after PAG morphine injection of 5 or 10 micrograms in cold (10 degrees C), neutral (22 degrees C), and hot (34 degrees C) environments. Both doses of morphine caused hyperthermia. Sixty to 105 min after the injection, Tre rose by 1.0-1.5 degrees C regardless of ambient temperature. Naloxone (2 mg/kg, i.p.) blocked the hyperthermic effects of morphine. Injection sites producing hyperthermia were distributed mostly in the ventral PAG and its ventral environs. The analgesic effect of morphine was examined by the tail-flick test. Locations of morphine injection effective for producing analgesia were restricted to the ventral area of the region responsible for hyperthermia. Magnitude of the hyperthermia did not significantly differ between animals with or without analgesia. The effect of PAG morphine (5 micrograms) was tested on tail vasomotor response to hypothalamic and scrotal thermal stimulations in urethane anesthetized (1.0 g/kg) animals. Threshold hypothalamic temperature for the vasodilation was lower at a scrotal temperature of 40 degrees C than at 30 degrees C. Following PAG morphine, threshold hypothalamic temperature rose and the difference in threshold hypothalamic temperature at the two scrotal temperatures disappeared.

Hypothalamic region facilitating shivering in rats.

Although the posterior part of the hypothalamus has long been considered important for thermoregulatory shivering, it is unknown whether the neurons there or the passing fibers are implicated in the response. Exposure of urethane-anesthetized rats to cold (15-21 degrees C) elicits shivering. An injection of muscimol (0.5 mM), a GABA(A) receptor agonist, into the medial part of the hypothalamus, including the dorsomedial and posterior nuclei, suppressed the cold-induced shivering. This result suggests that neurons having an excitatory effect on shivering are in this region of the hypothalamus.