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.

Thermoregulatory control of sympathetic fibres supplying the rat's tail.

We investigated the thermoregulatory responses of sympathetic fibres supplying the tail in urethane-anaesthetised rats. When skin and rectal temperatures were kept above 39 degrees C, tail sympathetic fibre activity was low or absent. When the trunk skin was cooled episodically by 2-7 degrees C by a water jacket, tail sympathetic activity increased in a graded fashion below a threshold skin temperature of 37.8 +/- 0.6 degrees C, whether or not core (rectal) temperature changed. Repeated cooling episodes lowered body core temperature by 1.3-3.1 degrees C, and this independently activated tail sympathetic fibre activity, in a graded fashion, below a threshold rectal temperature of 38.4 +/- 0.2 degrees C. Tail blood flow showed corresponding graded vasoconstrictor responses to skin and core cooling, albeit over a limited range. Tail sympathetic activity was more sensitive to core than to trunk skin cooling by a factor that varied widely (24-fold) between animals. Combined skin and core cooling gave additive or facilitatory responses near threshold but occlusive interactions with stronger stimuli. Unilateral warming of the preoptic area reversibly inhibited tail sympathetic activity. This was true for activity generated by either skin or core cooling. Single tail sympathetic units behaved homogeneously. Their sensitivity to trunk skin cooling was 0.3 +/- 0.08 spikes s(-1) degrees C(-1) and to core cooling was 2.2 +/- 0.5 spikes s(-1) degrees C(-1). Their maximum sustained firing rate in the cold was 1.82 +/- 0.35 spikes s(-1).

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.

Effects of estrogen on thermoregulatory tail vasomotion and heat-escape behavior in freely moving female rats.

Effects of estrogen on thermoregulatory vasomotion and heat-escape behavior were investigated in ovariectomized female rats supplemented with estrogen (replaced estrogen rats) or control saline (low estrogen rats). First, we measured tail temperature of freely moving rats at ambient temperatures (T(a)) between 13 and 31 degrees C. Tail temperature of the low estrogen rats was higher than that of the replaced estrogen rats at T(a) between 19 and 25 degrees C, indicating that the low estrogen rats exhibit more skin vasodilation than the replaced estrogen rats. There was no significant difference in oxygen consumption and core temperature between the two groups. Second, we analyzed heat-escape behaviors in a hot chamber where rats could obtain cold air by moving in and out of a reward area. The low estrogen rats kept T(a) at a lower level than did the replaced estrogen rats. These results imply that the lack of estrogen facilitates heat dissipation both by skin vasodilation and by heat-escape behavior. Ovariectomized rats may mimic climacteric hot flushes not only for autonomic skin vasomotor activity but also for thermoregulatory behavior.

Increased heat-escape/cold-seeking behavior following hypertonic saline injection in rats.

We examined the effect of hypertonic saline injection on heat-escape/cold-seeking behavior in desalivated rats. Rats were exposed to 40 degrees C heat after normal (154 mM NaCl, control) or hypertonic saline (2,500 mM NaCl) injection (1 ml/100 g body wt). The rats received a 0 degrees C air for 30 s when they entered a specific area in an experimental box. Core temperature (T(c)) surpassed 40 degrees C in both conditions when 0 degrees C air was not available. Hypertonic saline injection produced a lower baseline T(c) than control [36.9 +/- 0.2 and 37.9 +/- 0.2 degrees C (means +/- SE), P < 0.05] and a greater number of 0 degrees C air rewards during the 2-h heat with lower T(c) at the end (48 +/- 1 and 34 +/- 2, 37.6 +/- 0.1, and 37.3 +/- 0.1 degrees C in the control and hypertonic saline injection trial, respectively, P < 0.05, n = 6). However, T(c) was similar (37.7 +/- 0.2 and 37.6 +/- 0.4 degrees C in the control and hypertonic saline injection trial, n = 5) when 0 degrees C air was automatically and intermittently (35 times) given during the heat. Rats augment heat-defense mechanisms in response to osmotic stress by lowering the baseline T(c) and increasing heat-escape/cold-seeking behavior.

Autonomic and behavioural thermoregulation in starved rats.

1. We investigated the mechanism of starvation-induced hypothermia in rats. 2. Threshold core temperatures (Tcor) for tail skin vasodilatation and cold-induced thermogenesis were determined after a 3 day starvation using a chronically implanted intravenous thermode. Food deprivation significantly lowered the threshold Tcor for heat production, but did not affect the heat loss threshold. 3. Thermogenic response to a fall in Tcor below its threshold was enhanced by starvation. 4. Preferred ambient temperatures (Tpref) and Tcor were measured before and during a 3 day starvation in a thermal gradient. The 3 day starvation significantly lowered Tcor only in the light phase of the day. The level of hypothermia was the same throughout the fasting period, while Tpref gradually increased during the 3 days of starvation. 5. When rats were starved at a constant ambient temperature of 25 C (no thermal gradient), their Tcor levels were comparable with those of the rats kept in the thermal gradient. 6. The results suggest that, in rats, hypothermia caused by starvation was not due to a decrement in thermogenic capability, but was due to a decrease in the threshold for the activation of thermogenesis.

Radiation effects in dry ice: models for a peak on the Arrhenius curve

Dry ice (solid CO2) occurs in the polar caps of Mars, on the surface of Triton, and in places in the outer planets of our solar system. Radicals in gamma-irradiated solid CO2 have been studied by ESR for future applications of ESR dating on outer planets. The annealing curves for CO3- radical (ESR signal at g = 2.0126) can be described neither by the first-order nor the second-order decay kinetics. The peak observed in the Arrhenius plot can result from two parallel first-order kinetic processes. Radicals that provide overlapping signals are CO3- (g1 = 2.0057, g2 = 2.0126, g3 = 2.0161; activation energy E = 0.10 eV; frequency factor v0 = 4 x 10(1) s(-1)) and HO2 (g1 = 2.0040, g2 = 2.0055, g3 = 2.0360), which have E = 0.28 eV and v0 = 7 x 10(5) s(-1)). Hence, HO2 is more thermally stable, and use of HO2 is promising for ESR dating.

Effects of food deprivation on daily changes in body temperature and behavioral thermoregulation in rats.

Homeothermic animals regulate body temperature (T(b)) by using both autonomic and behavioral mechanisms. In the latter process, animals seek out cooler or warmer places when they are exposed to excessively hot or cold environments. Thermoregulation is affected by the state of energy reserves in the body. In the present study, we examine the effects of 4-day food deprivation on circadian changes in T(b) and on cold-escape and heat-escape behaviors in rats. Continuous measurement of T(b) during food deprivation indicated that the peak T(b) amplitude was not different from baseline values, but the trough amplitude continuously decreased after the onset of food deprivation. Cold-escape behavior was facilitated by food deprivation, whereas heat-escape behavior was unchanged. After the termination of food deprivation, the lowered T(b) returned to normal on the first day. However, cold-escape behavior was still facilitated on the third day after food reintroduction. Autonomic and behavioral thermoregulatory effectors are modulated in the face of food shortage so as to maintain optimal performance during the active period, whereas increasing energy conservation occurs during the quiescent phase.

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.

Neuronal actions of oxytocin on the subfornical organ of male rats.

The aim of this study was to investigate effects of oxytocin (OT) on electrical neuronal activities in rat subfornical organ (SFO) and compare its action with the well-described excitatory effects of blood-borne angiotensin II (ANG II) on the same SFO neurons. With the use of extracellular recordings from spontaneously active neurons in slice preparations of the SFO of male rats, 11.7% of tested neurons (n = 206) were excited and 9.7% were inhibited by superfusion with 10(-6) M OT. Both excitatory and inhibitory effects of OT were dose dependent with similar threshold concentrations and were blocked by a specific OT-receptor antagonist but not by a vasopressin receptor antagonist. Blocking synaptic transmission with low calcium medium suppressed only inhibitory effects of OT. All but one of the OT-sensitive neurons were also excited by superfusion with ANG II at a concentration much lower than required for OT, suggesting that synaptically released OT rather than blood-borne OT alters the activity of SFO neurons in vivo. The results support the hypothesis that neurally released OT may modulate SFO-mediated functions by acting on OT-sensitive neurons.

Efferent projection from the preoptic area for the control of non-shivering thermogenesis in rats.

1. To investigate the characteristics of efferent projections from the preoptic area for the control of non-shivering thermogenesis, we tested the effects of thermal or chemical stimulation, and transections of the preoptic area on the activity of interscapular brown adipose tissue in cold-acclimated and non-acclimated anaesthetized rats. 2. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) elicited non-shivering thermogenesis in the brown adipose tissue (BAT); warming the preoptic area to 41.5 C completely suppressed the thermogenic response. 3. Injections of d, l-homocysteic acid (DLH; 0.5 mM, 0.3 microliter) into the preoptic area also significantly attenuated BAT thermogenesis, whereas injections of control vehicle had no effect. 4. Transections of the whole hypothalamus in the coronal plane at the level of the paraventricular nucleus induced rapid and large rises in BAT and rectal temperatures. This response was not blocked by pretreatment with indomethacin. The high rectal and BAT temperatures were sustained more than 1 h, till the end of the experiment. Bilateral knife cuts that included the medial forebrain bundle but not the paraventricular nuclei elicited similar rises in BAT and rectal temperatures. Medial knife cuts had no effect. 5. These results suggest that warm-sensitive neurones in the preoptic area contribute a larger efferent signal for non-shivering thermogenesis than do cold-sensitive neurones, and that the preoptic area contributes a tonic inhibitory input to loci involved with non-shivering thermogenesis. This efferent inhibitory signal passes via lateral, but not medial, hypothalamic pathways.

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.

Effect of midbrain stimulations on thermoregulatory vasomotor responses in rats.

1. Efferent projections eliciting vasodilatation when the preoptic area is warmed were investigated by monitoring tail vasomotor responses of ketamine-anaesthetized rats when brain areas were stimulated electrically (0.2 mA, 200 microseconds, 30 Hz) or with the excitatory amino acid D,L-homocysteic acid (1 mM, 0.3 microliter). 2. Both stimulations elicited vasodilatation when applied within a region extending from the most caudal part of the lateral hypothalamus to the ventrolateral periaqueductal grey matter (PAG) and the reticular formation ventrolateral to the PAG. 3. Vasodilatation elicited by preoptic warming was suppressed when either stimulation was applied within the rostral part of the ventral tegmental area (VTA). 4. Sustained vasodilatation was elicited by knife cuts caudal to the VTA, and vasodilatation elicited by preoptic warming was suppressed by cuts either rostral to the VTA or in the region including the PAG and the reticular formation ventrolateral to it. 5. These results, together with the results of earlier physiological and histological studies, suggest that warm-sensitive neurones in the preoptic area send excitatory signals to vasodilatative neurones in the caudal part of the lateral hypothalamus, ventrolateral PAG and reticular formation, and send inhibitory signals to vasoconstrictive neurones in the rostral part of the VTA.

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.

Warm and cold signals from the preoptic area: which contribute more to the control of shivering in rats?

1. To find out whether the thermosensitive neurones in the preoptic area that control shivering are predominantly warm or cold sensitive, we tested the effects of injecting the excitatory amino acid L-glutamate at various sites in and adjacent to the preoptic area of anaesthetized rats shivering at ambient temperatures of 15-21 degrees C. 2. L-Glutamate injections (0.2 mM in 0.5-1.0 microliter), as well as preoptic warming and electrical stimulation, suppressed shivering, whereas control saline injections had no effect. Effective sites were restricted to the anterior part of the preoptic area, and a tenfold lower concentration of L-glutamate did not influence shivering. 3. Injections of procaine (0.2 M) into the sites where L-glutamate suppressed shivering did not affect strong shivering activity, but facilitated shivering in three out of seven cases when shivering was weak or absent at higher ambient temperatures (25-30 degrees C). 4. L-Glutamate injections, as well as preoptic warming and electrical stimulation, also elicited vasodilatation of the paw skin and the tail. Procaine elicited vasoconstriction when it was applied during vasodilatation induced by local preoptic warming. 5. These results indicate that the contribution of the preoptic area to the control of shivering and vasomotion is influenced more by signals from warm-sensitive neurones than by signals from cold-sensitive neurones.

Hypothalamic network for thermoregulatory shivering.

Warming one side of a rat's preoptic area and anterior hypothalamus (POAH) suppresses shivering on both sides of the body, and the present study evaluated the extent to which signals mediating this suppression cross the midline within and below the POAH. Hind paw shivering during unilateral POAH thermal stimulation was measured for rats in which the POAH had been midsagittally transected and for rats in which one side of the hypothalamus had been coronally transected just caudal to the POAH. In midsagittally transected rats, unilateral warming on either side of the POAH suppressed shivering equally on both sides of the body. In unilaterally transected rats, POAH warming on the transected side did not affect shivering, but warming the intact side suppressed shivering equally on both sides of the body. When a unilateral transection of only the lateral part of the hypothalamus included the medial forebrain bundle, the effect was the same as that of a unilateral transection of the whole hypothalamus. These results indicate that no information controlling shivering is exchanged between the left and right POAH and that efferent signals from the POAH, descending through the medial forebrain bundle, cross the midline somewhere below the hypothalamus to innervate both sides of the body equally.