Resistance training volume and post exercise energy expenditure.

The main purpose of this study was to determine if increasing the volume of a resistance training program, while keeping the intensity the same would significantly increase the recovery energy expenditure, as measured by the excess post-exercise energy expenditure (EPEE). Fifteen resistance-trained women completed two resistance training protocols. Both protocols consisted of nine exercises performed to volitional fatigue, at the previously determined eight RM. The only difference between the two protocols was the number of sets (1-set or 3-sets). All subjects completed both protocols in a randomized and counterbalanced fashion. Energy expenditure, as determined by oxygen consumption and respiratory exchange ratio (RER), was measured continuously prior to exercise, during the exercise session, and during the entire 120 min of recovery. Fingertip blood lactate concentration was determined at baseline, immediately post-exercise, and every 30 min in recovery. The net energy expenditure during exercise was significantly greater during the 3-set protocol (661.9 +/- 43.9 kj) than the 1-set protocol (234.7 +/- 13.4 kj). However, per minute of exercise, there was no significant difference between the two protocols. During the 120 min of recovery, the net EPEE was not significantly different between the two protocols (93.3 +/- 20.1 kj following the 1-set protocol, and 94.1 +/- 7.1 kj following the 3-set protocol). However, when comparing the EPEE to the number of minutes spent in the exercise session, the 1-set protocol led to a significantly greater energy expenditure in the recovery period (1.0 +/- 0.22 kj/min) than did the 3-set protocol (0.4 +/- 0.03 kj/min). These data indicate that in previously trained women, increasing the volume of resistance training, from 1-set to 3-sets, while keeping the intensity the same will not significantly increase EPEE above what is found in a lower volume of work.

Influence of therapeutic ultrasound on skeletal muscle regeneration following blunt contusion.

Athletic trainers typically use therapeutic ultrasound to treat skeletal muscle contusion injuries. However, the structural outcomes underlying this treatment are not well understood. Our working hypothesis was that following a blunt contusion injury to the gastrocnemius muscle, ultrasound treatment would facilitate recovery, as indicated by changes in several biological markers of skeletal muscle regeneration. Eighty male Wistar rats (three-month) were studied. Following anesthetic administration, each animal received a bilateral contusion injury to the gastrocnemius muscle. Pulsed ultrasound treatment was subsequently initiated six hours post-contusion injury unilaterally on the right gastrocnemius muscle, and ultrasound treatment was continued once daily for seven days. The left (non-ultrasound treated) and right (ultrasound treated) gastrocnemius muscles of 10 animals per group were excised at 1-, 3-, 5-, 7-, 14-, 21-, 28-, and 40-days post-contusion injury. There were no differences in muscle mass, total protein concentration, or fiber cross-sectional area between the right and left gastrocnemius muscles at any post-injury time point examined. Further, when fiber cross-sectional area was normalized to muscle mass, there were no differences. Myonuclear number and cross-sectional area per myonuclei between the right and left gastrocnemius muscles were not different. These results suggest that ultrasound, as administered, does not hasten or improve the regeneration of skeletal muscle following contusion injury.

Activation of supraoptic magnocellular neurons by gamma 2-melanocyte stimulating hormone (gamma 2-MSH).

The effects of intracarotid infusions of the peptide gamma 2-melanocyte stimulating hormone (gamma 2-MSH) on electrophysiologically and immunohistochemically identified supraoptic nucleus (SON) units were investigated. Over a wide dose range this agent always excited SON units, while control infusions of vehicle had no effect. Because neural responses invariably preceded blood pressure elevation, it appears that gamma 2-MSH excitation of the magnocellular system was due to a direct effect on the central nervous system and was not a result of systemic cardiovascular responses. These results suggest a forebrain gamma 2-MSH sensitive site in the activation of SON magnocellular neurons.

The supraoptic nucleus: afferents from areas involved in control of body fluid homeostasis.

Physiological evidence indicates that the supraoptic nucleus may be an important integrating region for information relating to body fluid homeostasis. It is known that the supraoptic nucleus receives neural influences from brain receptive zones for plasma osmolality and angiotensin II, as well as from relay centers for blood pressure and blood volume. It is also known that these influences interact to modulate vasopressin release from the supraoptic nucleus. Therefore, a detailed investigation of the neurochemical afferents to the supraoptic nucleus from regions of the lamina terminalis and the brainstem was undertaken. Injection of a fluorescent retrograde tracer, doxorubicin, into the supraoptic nucleus was combined with histochemistry of angiotensin II and catecholamines. Following supraoptic nucleus injection, retrograde label was found in forebrain neurons of the subfornical organ, median preoptic nucleus, and organum vasculosum of the lamina terminals. Some labeled cells in the subfornical organ and organum vasculosum of the lamina terminalis were also found to contain angiotensin II immunoreactivity. In the brainstem, retrograde label was found in neurons of the A1, A2 and A6 cell groups. Many of these cells were also found to contain catecholamine fluorescence or tyrosine hydroxylase immunoreactivity. Corroboration of the A2 projection was obtained by lesions of this nucleus, which reduced catecholamine fluorescence in the supraoptic nucleus. These findings provide an anatomical basis for the functional observations that the supraoptic nucleus plays a key integrative role in the maintenance of body fluid homeostasis.

Increased norepinephrine turnover in the median preoptic nucleus following reduced extracellular fluid volume.

The role of noradrenergic input to fluid balance regulatory systems in the anterior hypothalamus was studied by examination of norepinephrine (NE) turnover during reduction of systemic extracellular fluid volume. Extracellular fluid volume was decreased iso-osmotically by subcutaneous polyethylene glycol (PEG), known to increase thirst and vasopressin secretion. NE turnover was assessed by measuring the decline of NE concentration in brain micropunches after administration of alpha-methyl tyrosine in PEG- or sham-treated groups. Several hypothalamic areas were investigated, including the median preoptic area (MnPO), preoptic area (POA), paraventricular nucleus, supraoptic nucleus (SON), subfornical organ, ventromedial hypothalamus, and posterior hypothalamus. Volume-depleted animals showed significantly increased NE turnover in the MnPO, an important area for integration of fluid balance information. The POA and the SON also showed trends toward increased NE turnover. All other areas showed no difference in NE turnover between volume-depleted and normal animals. These results are consistent with previous findings that NE innervation to the MnPO is important in the control of fluid balance and also support the hypothesis that basal forebrain NE projections facilitate thirst and vasopressin secretion.

Forebrain and brainstem afferents to the arcuate nucleus in the rat: potential pathways for the modulation of hypophyseal secretions.

Doxorubicin, an anti-oncogenic agent, was used as a retrograde marker to identify arcuate nucleus afferent projections. Injections of this tracer into the arcuate nucleus indicated that the subfornical organ, the organum vasculosum of the lamina terminalis, the nucleus raphe dorsalis and median raphe send projections to the arcuate nucleus. Immunocytochemical procedures were used to demonstrate that the raphe projections to the arcuate nucleus are serotoninergic. This anatomical investigation provides evidence that neural pathways exist between forebrain body fluid and mineral nuclei, mesencephalic serotonin nuclei and the arcuate nuclei.

Response of supraoptic magnocellular neurons to stimulation of forebrain alpha-adrenoceptors.

Effects of alpha-adrenoceptor agents on electrophysiologically and immunohistochemically identified supraoptic nucleus (SON) vasopressin (VP) units were investigated by intracarotid infusion. Clonidine, an alpha 2-adrenoceptor agonist always excited SON units and alpha 2-adrenoceptor antagonists consistently inhibited them. alpha 1-Adrenoceptor agents produced inconsistent responses. The results implicate forebrain alpha 2-adrenergic receptors in the excitation of SON VP neurons.

Neurohypophyseal hormone release and biosynthesis in rats with lesions of the anteroventral third ventricle (AV3V) region.

Lesions of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) have been shown to disrupt body fluid homeostasis. The acute post-lesion phase in rats is characterized by adipsia, the lack of an appropriate antidiuretic response, and plasma vasopressin levels which do not rise. Electron micrographs of the supraoptic nucleus and neural lobe of lesioned adipsic rats suggest no stimulation of biosynthetic activity, and large stores of neurosecretory material in the axon terminals. To directly investigate the status of these neurons, we determined neural lobe vasopressin and oxytocin content and the incorporation of [35S]cysteine into hypothalamic proteins in rats with sham-lesions or lesions of the AV3V after 3 days of adipsia or water deprivation, and in water replete sham-lesioned rats. The results demonstrate that adipsic rats with AV3V lesions have neural lobe vasopressin and oxytocin content equivalent to water-replete sham-lesioned rats. Neural lobe vasopressin and oxytocin levels of water-deprived sham-lesioned rats were significantly below those of all other groups. In addition, this group had a radioactivity incorporation rate into hypothalamic proteins which was two-fold greater than either of the other groups. The results indicate that 3-day adipsic AV3V-lesioned rats do not increase neurohypophyseal hormone release or biosynthesis as do 3-day water-deprived sham-lesioned rats. The periventricular tissue of the AV3V would therefore appear to be crucial in providing information to the hypothalamo-neurohypophyseal neurons on body fluid homeostasis.

Changes in magnocellular-neurohypophyseal vasopressin following anteroventral third-ventricle (AV3V) lesions.

Lesions of the brain region surrounding the anteroventral third ventricle (AV3V) have been shown to result in adipsia without a corresponding antidiuretic response or rise in plasma vasopressin levels. Electron microscopic examination of the supraoptic nucleus and neural lobe of the pituitary has shown that large stores of neurosecretory material build up in the neurohypophysis. In the present study, the increased neurosecretory material was characterized by immunocytochemistry. Vasopressin immunoreactivity was examined and compared between adipsic rats with AV3V lesions, water-deprived rats, and normal rats. Two days after surgery, sham-lesioned, water-deprived rats displayed decreased vasopressin immunostaining density compared to normal controls, and adipsic AV3V-lesioned rats displayed increased vasopressin immunoreactivity throughout the magnocellular-hypophyseal system. These results indicate that AV3V lesions interrupt neural inputs that stimulate the magnocellular system to release vasopressin in response to normal humoral stimuli.

Demonstration of regional blood-brain barrier permeability in human brain.

The brain of a 78-year-old woman with argyria was examined at autopsy. Silver nitrate deposition was observed in circumventricular organs (CVO) and in the paraventricular and supraoptic nuclei of the hypothalamus. These findings parallel animal experiments of other investigators and are the best demonstration so far of regional absence of the blood-brain barrier in humans. These observations demonstrate similarities between humans and other mammals of CVO anatomy, permeability to blood-borne agents, and perhaps neural connections between CVOs and magnocellular nuclei.

Systemic angiotensin II, blood pressure and supraoptic neuronal activity.

Recordings of SON single unit activity and systemic arterial blood pressure (B.P.) were taken from 10 rats while systemic infusions of angiotensin II (AII), 1-1000 ng/kg body weight/min in 7 steps, or phenylephrine, 1-100 ng in 3 steps were administered. The relationship between AII concentrations and neuronal activity was biphasic. Within the physiological range (1 ng to 100 ng) AII excited single units in a dose dependent manner, but it had little effect on B.P. At higher concentrations, B.P. rose and neuronal activity was decreased. Phenylephrine, however, did not excite neuronal activity. With increasing phenylephrine concentrations, B.P. rose and neuronal activity slowed. We conclude that increased B.P. may dampen the SON neuronal output by baroreceptor inhibition. Under physiological conditions, therefore, AII may serve to reinforce tonic vasopressin release while inhibiting vasopressin release at pressor doses. This further suggests a role for plasma AII as an important link of the renal-hypothalamic-hormonal feedback loop.

The role of substance P-containing fibers in sympathetic ganglia: effect of capsaicin.

Capsaicin was given subcutaneously to guinea pigs and the effect on substance P-immunoreactive (SP-I) fibers in the celiac/superior mesenteric and inferior mesenteric ganglia was observed at 2 day and 8-10 day intervals. Capsaicin (125 mg) treatment led to almost total disappearance of SP-I fibers from all areas examined in both short- and long-term animals. This effect applied equally to the dense network of varicose SP-I fibers and to basket-like SP-I contacts with principal ganglionic neurons. The effect of capsaicin on SP-I fibers in the mesenteric ganglia provides a strong indication that these fibers represent a homogeneous population of visceral sensory afferents. This is supported by other lines of anatomical evidence in the literature. Taken together with studies that have shown axodendritic contact of SP-I terminals on principal ganglionic neurons and neuro-modulatory effects of SP on these neurons, it may be hypothesized that SP-I fibers in the mesenteric ganglia represent collaterals of visceral sensory afferents forming a subspinal feedback arc.

Pavlovian conditioning with ethanol and lithium: effects on heart rate and taste aversion in rats.

Rats received paired injections of either ethanol or saline as the conditioned stimulus and lithium chloride as the unconditioned stimulus (US) in a Pavlovian differential conditioning paradigm. Lithium chloride evoked a large deceleration in heart rate (80-100 beats per minute) as an unconditioned response. As a result of 10 conditioning trials, the substance paired with LiCl elicited a lower average heart rate than that elicited by the unpaired substance. Moreover, animals that received ethanol-LiCl injections subsequently were more averse to the taste of ethanol than animals receiving saline-LiCl pairings. However, there were no differences in ethanol's ability to serve as the US to induce an aversion to a novel flavor solution (i.e., the Avfail phenomenon was not observed). The overall pattern of results underscores the value of using multiple indexes of learning in drug-drug conditioning paradigms.