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Biomedical subjects

G A Hand

Publications and source records attributed to G A Hand.

At least 19 recordsLinked to original sources

Perceived stress in HIV-infected individuals: physiological and psychological correlates.

The purpose of this study was to determine the correlation of perceived stress with selected physiological and psychological factors in an HIV-infected, predominantly African American population and to assess the multivariable effects on perceived stress. The variables that correlated significantly with perceived stress were entered into a backward stepwise regression model. Pearson's r analysis showed significant correlations between perceived stress and state and trait anxiety, depression, HIV-related symptoms, sleep quality, daytime sleepiness and fatigue. State and trait anxiety, depression and fatigue retained significance (p<0.1) in the final regression model. These factors explained approximately 80% of the variance in perceived stress. The significant interactions of multiple physiological and psychological correlates suggest that perceived stress is a complex outcome with a multifactorial etiology. Further, the model suggests that psychological factors may contribute to perceived stress in this population more than physiological factors such as HIV-related symptomatology or stage of disease.

Adaptation, Psychological↗

Counteracting muscle wasting in HIV-infected individuals.

HIV-infected persons often experience a loss of lean tissue mass, which includes decreases in skeletal muscle mass. This HIV-associated wasting is significant because it has been associated with accelerated disease progression and increased morbidity. Signalling related to several circulating molecules, including tumour necrosis factor (TNF)-alpha, growth hormone, insulin-like growth factor (IGF)-1 and testosterone, has been associated with the aetiology of muscle wasting. Additionally, nutritional status related to malnutrition and specific dietary deficiencies may be involved. In an attempt to counter muscle wasting in HIV-infected persons, treatments have been suggested that target these mechanisms. Nutritional supplementation, cytokine reduction, hormone therapy and resistance exercise training are potential treatments for this condition. Resistance exercise training, which is more easily accessible to this population than other treatments, holds promise in counteracting the process of HIV wasting, as it has been successfully used to increase lean tissue mass in healthy and clinical populations. This review will explore the HIV/AIDS muscle-wasting syndrome, its aetiology, and the treatments used to counteract wasting.

Cytokines↗

Depression in HIV-infected patients: allopathic, complementary, and alternative treatments.

OBJECTIVES: The purpose of this review article is to synthesize the current knowledge related to depression and HIV disease. METHODS: The research literature was critically evaluated for several selected therapies that are prescribed for HIV-infected persons to treat depression. These therapies included pharmacotherapy, psychotherapy, alternative, and complementary therapies. RESULTS: Several therapies are currently available for the treatment of depression in HIV disease. When prescribing treatments, clinicians should be aware of problems associated with diagnoses, drug-drug interactions, and the benefits of some of the new therapies that are now available. Treatment regimes should be carefully designed to meet the individual needs of the patient and will optimally include a combination of approaches including psychotherapy, pharmacotherapy, education, and/or complementary therapies. CONCLUSIONS: Although HIV is now a treatable disease, the prevalence of depression in the HIV population remains high and should be continually addressed.

Acupuncture Therapy↗

Chronic physical exercise reduces anxiety-like behavior in rats.

While many individuals with anxiety disorders receive drug therapy, many do not respond or adversely respond to drugs. An alternative treatment, exercise, has been shown to relieve negative feelings and induce positive shifts in mood. The purpose of this study was to establish an animal model to specifically test the effects of chronic physical exercise on anxiety-related behaviors. Thirty-two male Sprague Dawley rats were divided into two groups: runners (R) and nonrunners (NR). Runners ran on a treadmill for 45 minutes a day, five days a week, for ten weeks at a moderate intensity. Nonrunners remained in their cages in the treadmill room during the running period and were handled for an equal amount of time. After ten weeks of training, two behavioral tests were administered including the elevated plus maze and open field tests. Results comparing R and NR showed higher responses by R in percent open arm time and center square time during the elevated plus maze test, as well as in number of entries into the center, number of rears, and lower fecal boli count during the open field test, p < 0.05. In addition, there were no differences in total activity levels between groups as indicated by similar closed arm entries in the elevated plus maze test and total lines crossed in the open field test. These results indicate that treadmill training reduces anxiety-like behaviors in two animal tests of anxiety, without a significant change in total activity levels. These data are in support of treadmill training as a model to test the anxiolytic effects of exercise.

Animals↗

Physical activity and immunity in HIV-infected individuals.

The purpose of this study was to determine what relationship exists among physical activity levels and viral load and CD4+ cell count in HIV-infected individuals. Increased viral load is associated with disease progression and symptom severity. A convenience sample of 66 male and female subjects between the ages of 18 and 64 years of age (mean 39 +/- 8) was recruited from a hospital-based HIV/AIDS clinic. Components of PA were assessed for three continuous days using a mini-motion logger wrist actigraph. These components included mean PA level, and PA index and acceleration index. Pearson's correlational analysis was used to test the strength of association between PA components and viral load or CD4+ cell count. A significant inverse relationship was found between mean PA level and viral load (p=0.047). An inverse relationship was also observed between PA index and viral load (p=0.0061). Neither mean PA nor PA index scores correlated with CD4+ cell counts. Acceleration index, a measure of PA intensity, showed no correlation to viral load or CD4+ cell counts. These findings suggest that increasing levels of physical activity might have beneficial effects on viral load in HIV-infected individuals.

Adolescent↗

Overload-induced androgen receptor expression in the aged rat hindlimb receiving nandrolone decanoate.

This study's purpose was to examine whether functional overload with nandrolone decanoate (ND) administration increased muscle mass and steroid receptor concentration in aged rat soleus (Sol) and plantaris (Plan) muscle. ND (6 mg/kg body wt) was administered once a week for 4 wk, whereas control rats received sesame seed oil injections. Functional overload of the hindlimb Sol and Plan was induced by synergistic gastrocnemius muscle ablation at the beginning of the fourth week. Adult (5 mo of age) and aged rats (25 mo of age) were randomly assigned to four groups: control, overload, control-ND, and overload-ND. Seven days of functional overload increased adult Sol muscle mass 27%, whereas the aged Sol muscle mass did not change. The aged overloaded Sol muscle receiving ND significantly increased muscle weight by 35% and total muscle protein by 24%. Aged Plan muscle did not increase muscle weight with overload or ND treatment. Androgen receptor protein was induced by ND treatment and functional Ov, and combining the two treatments induced Sol androgen receptor protein concentration above either alone. Sol glucocorticoid receptor protein concentration increased in overload groups of both ages. ND administration can increase aged Sol muscle mass and protein content after 7 days of functional overload, and the cooperative induction of androgen receptor may be important for this response.

Anabolic Agents↗

Effect of creatine supplementation on cardiac muscle of exercise-stressed rats.

The role of creatine supplementation in altering the physiological parameters regulating cardiac muscle's functional capacity through the initiation of cardiac hypertrophy and altered contractile protein expression has not been determined. The purpose of this study was to determine the effect of creatine supplementation, with and without exercise stress, on physiological parameters regulating functional capacity through alterations in rat cardiac mass and contractile-protein expression. Thirty male Sprague-Dawley rats were subjected to 30 min of exercise stress 5 days/week for 3 weeks with 2% of total body mass attached to the tail. Animals were randomly assigned to one of four treatment groups: group 1 (Con) received (1 ml/day) sucrose water by intubation tube (n=8); group 2 (Cr) received (1 ml/day) sucrose/creatine solution (n=6); group 3 (EX) received 1 ml/day sucrose water and the exercise stimulus (n=8), and group 4 (Cr/EX) received (1 ml/day) sucrose/creatine solution and the exercise stimulus (n=8). At the conclusion of the 21-day exercise-training period, the heart was collected and weighed for determination of wet weight, total protein, total RNA, and myosin heavy chain protein expression. RNA concentration decreased significantly (13%) in the EX group, but not in the CR/EX group, indicating an interactive effect of creatine and exercise. Total RNA significantly decreased (15%) in the EX group. Protein concentration significantly increased (9%) in the exercising treatments, while total protein did not change. Cardiac myosin heavy chain expression significantly shifted towards a predominant expression of the beta-isoform in the Cr/EX group [54.53% (3.42) beta]. These results indicate an interaction of creatine supplementation and swimming exercise stress that potentially alters cardiac protein synthesis and demonstrates a possible mechanism through which the combination of creatine supplementation and swimming stress stimuli act to alter the physiological parameters regulating cardiac functional capacity.

Administration, Oral↗

Determinants of metabolic cost during submaximal cycling.

The metabolic cost of producing submaximal cycling power has been reported to vary with pedaling rate. Pedaling rate, however, governs two physiological phenomena known to influence metabolic cost and efficiency: muscle shortening velocity and the frequency of muscle activation and relaxation. The purpose of this investigation was to determine the relative influence of those two phenomena on metabolic cost during submaximal cycling. Nine trained male cyclists performed submaximal cycling at power outputs intended to elicit 30, 60, and 90% of their individual lactate threshold at four pedaling rates (40, 60, 80, 100 rpm) with three different crank lengths (145, 170, and 195 mm). The combination of four pedaling rates and three crank lengths produced 12 pedal speeds ranging from 0.61 to 2.04 m/s. Metabolic cost was determined by indirect calorimetery, and power output and pedaling rate were recorded. A stepwise multiple linear regression procedure selected mechanical power output, pedal speed, and pedal speed squared as the main determinants of metabolic cost (R(2) = 0.99 +/- 0.01). Neither pedaling rate nor crank length significantly contributed to the regression model. The cost of unloaded cycling and delta efficiency were 150 metabolic watts and 24.7%, respectively, when data from all crank lengths and pedal speeds were included in a regression. Those values increased with increasing pedal speed and ranged from a low of 73 +/- 7 metabolic watts and 22.1 +/- 0.3% (145-mm cranks, 40 rpm) to a high of 297 +/- 23 metabolic watts and 26.6 +/- 0.7% (195-mm cranks, 100 rpm). These results suggest that mechanical power output and pedal speed, a marker for muscle shortening velocity, are the main determinants of metabolic cost during submaximal cycling, whereas pedaling rate (i.e., activation-relaxation rate) does not significantly contribute to metabolic cost.

Adult↗

Changes in defensive behaviors following olfactory bulbectomy in male and female rats.

The present study examined if olfactory bulbectomy (OBX) altered defensive behaviors on the elevated plus-maze and the open-field differently in male and female rats. Similar increases in defensive behaviors in male and female rats were observed in both tests following OBX. No significant correlations were detected between defensive behaviors and activity, supporting the hypothesis that some behavioral changes following OBX may be due to decreased defensive behaviors and not increased activity.

Aggression↗

The association between physical activity, cardiorespiratory fitness, and lipoprotein(a) concentrations in a tri-ethnic sample of women: The Cross-Cultural Activity Participation Study.

The purpose of this cross-sectional study was threefold: (1) to examine ethnic differences in plasma lipoprotein(a) [Lp(a)] concentrations; (2) to examine the relationship between physical activity levels (moderate, moderate-vigorous, and total MET-min/day) and Lp(a) concentrations; and (3) to determine the relationship between maximal treadmill time and Lp(a) concentrations among African-American, Native American, and Caucasian women (n=140, ages 40-70 years: 54.5+/-10.7). Physical activity records were kept for two 4-day periods, scheduled 1 month apart, a total of 8 days, and each activity was assigned a code from the 'Compendium of physical activity'. Subjects completed a graded exercise test to determine maximal treadmill time, and a fasted blood sample was collected to quantify Lp(a) concentration. Lp(a) concentrations were negatively skewed with a geometric mean of 28.3 mg/dl (25-75%: 10.4-43.1 mg/dl) in African-Americans (n=47), 2.9 mg/dl (25-75%: 1.2-7.4 mg/dl) in Native Americans (n=45), and 9.4 mg/dl (25-75%: 2.6-22.4 mg/dl) in Caucasians (n=48). African-American women had significantly higher (p<0.05) Lp(a) concentrations than either Native Americans or Caucasians. No relationships were observed among moderate, moderate-vigorous, and total MET-min/day of physical activity, maximal treadmill time, and Lp(a) concentrations. Significant ethnic differences in Lp(a) concentrations were found, with African-American women having higher Lp(a) concentrations than Native American and Caucasian women. Lp(a) concentrations were not associated with any physical activity variables. Therefore, physical activity and maximal treadmill time did not influence Lp(a) concentrations in this tri-ethnic population of women.

Adult↗

Spinal cholinergic inhibition of the pressor response to muscle activation is mediated by muscarinic, but not nicotinic, receptors.

This study examined the influence of spinal muscarinic and nicotinic receptors on the cardiovascular adjustments to skeletal muscle activation in anesthetized cats. Microdialyzing into the L(7) dorsal horn increasing doses of the muscarinic receptor agonist bethanechol, but not the nicotinic receptor antagonist mecamylamine, reduced increases in mean arterial pressure (MAP) and heart rate (HR) during hindlimb contraction or passive stretch. Atropine administration accentuated the cardiovascular responses during contraction, but not during passive stretch. These data indicate that muscarinic, but not nicotinic, receptors at the dorsal horn level blunt the pressor response to muscle activity. Further, the data suggest that the two neural pathways involved in muscle contraction or stretch are anatomically distinct.

Acetylcholine↗

Spinal cholinergic inhibition of the pressor response to skeletal muscle activation.

The purpose of this study was to delineate the role of the cholinergic pathway within the spinal cord in the reflex cardiovascular responses to muscle activity. Based on dose-response experiments, we microdialyzed a 0.1 mM solution of the acetylcholinesterase inhibitor neostigmine into the L7 level of the dorsal horn of anesthetized cats to determine its effects on the mean arterial blood pressure (MAP) and heart rate (HR) responses to static muscle contraction or passive stretch. The peak responses to 1-min contractions and stretches were reduced from control levels after 1 h of drug administration. In four experiments, the cardiovascular responses returned to control levels after a 2-h recovery period. Perfusion of the cholinergic receptor antagonist atropine accentuated the peak MAP response to muscle contraction. By contrast, atropine administration had no effect on the peak MAP adjustment to passive muscle stretch. These data support the hypothesis that increased acetylcholine (ACh) concentrations in the spinal cord inhibit the reflex cardiovascular responses to static muscle contraction. Further, the results suggest that the spinal cholinergic system is activated by metabolic changes in skeletal muscle, but likely unaffected by mechanical muscle changes.

Analysis of Variance↗

Segmental effect of spinal NK-1 receptor blockade on the pressor reflex.

The physiological effects of substance P (SP) are mediated via activation of neurokinin-1 (NK-1) receptors. The purpose of this study was to test the hypothesis that blockade of NK-1 receptors in the dorsal horn, both at the site of entry for the primary afferent neurons and adjacent spinal segments, attenuates the pressor reflex evoked by static contraction and stretch of skeletal muscle. Cats were anesthetized with alpha-chloralose and urethan, and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side of the spinal cord. Thus the primary afferent fibers mediating the pressor reflex enter the spinal cord via the L7 dorsal root in these experiments. Based on dose-response data, dialysis of the NK-1 receptor antagonist CP-96,345 (5 mM for 2 h) into the L7 dorsal horn ipsilateral to the contracting muscle attenuated the pressor response to static contraction (75 +/- 15 vs. 46 +/- 7 mmHg; n = 5 cats) but not muscle stretch (60 +/- 12 vs. 50 +/- 8 mmHg). Administration of the inactive enantiomer of CP-96,345, CP-96,344 (5 mM for 2 h), into the L7 dorsal horn failed to alter the cardiovascular changes elicited by contraction (45 +/- 7 vs. 43 +/- 6 mmHg) and stretch (31 +/- 8 vs. 32 +/- 11). Dialysis of 5 mM CP-96, 345 into the dorsal horn at the L6 and S1 segments for 2 h decreased the peak pressor response to static contraction (58 +/- 9 vs. 31 +/- 6 mmHg; n = 7) and muscle stretch (61 +/- 6 vs. 44 +/- 8 mmHg). These data suggest that the activation of NK-1 receptors, both at the site of entry and in regions outside of the entry site for afferent neurons, is involved in the spinal processing that produces the pressor reflex evoked by static contraction of skeletal muscle.

Animals↗

Central interaction between carotid baroreceptors and skeletal muscle receptors inhibits sympathoexcitation.

To determine the potential of an inhibitory interaction between the carotid sinus baroreflex (CSB) and the exercise pressor reflex (EPR), both pathways were activated to produce sympathoexcitation. It was hypothesized that, under conditions when the baroreflex increased sympathetic outflow, the interaction between CSB and EPR would be inhibitory. Bilateral carotid occlusion (BCO), electrically induced muscle contraction (EMC), and passive muscle stretch (PMS) were used to evoke sympathoexcitation. BCO decreased sinus pressure 50 +/- 5 mmHg, and the levels of muscle tension generated by EMC and PMS were 7 +/- 2 and 8 +/- 1 kg, respectively. This resulted in significant increases in mean arterial pressure (MAP) of 55 +/- 9, 50 +/- 7, and 50 +/- 6 mmHg (P = not significant, BCO vs. EMC vs. PMS) and in heart rate (HR) of 7 +/- 2, 19 +/- 4, and 17 +/- 2 beats/min (P < 0. 05, BCO vs. EMC and PMS). When BCO was combined with EMC or PMS, the reflex increase in MAP was augmented (80 +/- 8 and 79 +/- 10 mmHg; BCO+EMC and BCO+PMS, respectively; P < 0.05). However, summation of the individual MAP responses was greater than the response evoked during coactivation (106 +/- 11 and 103 +/- 12 mmHg, respectively, P < 0.05). Because summing the individual blood pressure responses exceeded the response during coactivation, the net effect was that the CSB and EPR interacted in an occlusive manner. In contrast, summation of the individual chronotropic responses was the same as the response evoked during coactivation. Moreover, there was no difference in summation of the individual MAP or HR responses when muscle afferents were activated by either EMC or PMS. In conclusion, the interaction between the CSB and the EPR in control of MAP was occlusive when both reflexes were stimulated to evoke sympathoexcitation. However, summation of the reflex changes in HR was simply additive.

Animals↗

Identification of hypothalamic vasopressin and oxytocin neurons activated during the exercise pressor reflex in cats.

Blood pressure and heart rate reflexly increase during static muscle contraction in anesthetized cats. Previous studies have demonstrated that vasopressin (AVP) and oxytocin (OT) may act as neuromodulators to regulate cardiovascular responses elicited by contraction of skeletal muscle. In this study, we tested the hypothesis that neurons containing AVP and OT in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) of the hypothalamus are activated during static muscle contraction. A laminectomy was performed to expose the spinal cord and the peripheral cut ends of L7 and S1 ventral roots were stimulated electrically to induce muscle contraction. Hypothalamic neurons activated during the muscle contraction were identified by Fos-like immunoreactivity (FLI). Static muscle contraction significantly increased FLI in the PVN and SON, compared with sham-operated cats. Double-staining of neurons in the PVN for AVP and OT showed that 22 +/- 4% of the AVP and 26 +/- 3% of the OT neurons in the PVN expressed FLI. In contrast, only 4 +/- 1% of the AVP and 3 +/- 1% of the OT neurons in the PVN were labeled with FLI in sham-operated animals. These results indicate that neurons in the PVN and SON of the hypothalamus were activated during static muscle contraction. Furthermore, as FLI was present in AVP and OT neurons, this suggests these neurons may constitute a part of the neural pathway involved in cardiovascular regulation during static muscle contraction.

Animals↗

Static muscle contraction elicits a baroreflex-dependent increase in glutamate concentration in the ventrolateral medulla.

In anesthetized cats, static contraction of the hindlimb reflexly increases mean arterial pressure (MAP). This cardiovascular adjustment is reduced by the arterial baroreflex. Both of these reflex responses are mediated through activation of ventrolateral medullary (VLM) regions. We tested the hypothesis that the concentration of glutamate (Glu) increases in the caudal ventrolateral medulla (cVLM) during static hindlimb contractions in anesthetized cats, and that barodenervation reduces this elevation in Glu levels. Static contractions of the triceps surae muscle of one hindlimb were evoked by electrical stimulation of the peripheral ends of cut L7 and S1 ventral roots. After the insertion of the microdialysis probes and a 3-h recovery period, a 2-min static contraction increased MAP by 47 +/- 7 mmHg. The concentration of Glu increased from 606 +/- 189 to 1042 +/- 228 nM. These results were repeatable in that Glu, as well as MAP, rose by a similar amount in two subsequent contractions. By contrast, in a subset of cats paralyzed prior to the third contraction, neither MAP nor Glu were significantly increased over baseline levels during the third stimulation period. In a third group of cats, hindlimb contraction increased MAP and Glu levels. However, the Glu release was attenuated in subsequent contractions after these cats were barodenervated. During the same periods of stimulation, the denervation accentuated the rise in MAP. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu in the cVLM. Further, our study implicates this neurotransmitter in the baroreflex mediated reduction of the pressor reflex response to static muscle contraction.

Animals↗

The pressor reflex evoked by static contraction: neurochemistry at the site of the first synapse.

Stimulation of somatic sensory neurons activates the sympathetic nervous system, in turn enhancing cardiovascular function. This has been repeatedly demonstrated when afferent fibers arising from skeletal muscle serve as the sensory neurons. Over the past several years, studies have been performed examining the central nervous system (CNS) mechanisms that cause the reflex increases in arterial blood pressure and heart rate when skeletal muscle contracts. These studies have provided insights into how the CNS alters cardiovascular function, and have helped to enhance our understanding of central sensory transduction processes. Using a variety of techniques, several sites have been identified within the brain and spinal cord that are responsible for producing the reflex pressor response to static contraction. However, the purpose of this manuscript is to review the recent developments concerning only one CNS site: the dorsal horn of the spinal cord. This region serves as the first synapse for afferent fibers from skeletal muscle. The release of neurotransmitters, and possibly neuromodulators, into this region initiates the CNS component of this reflex. In addition, the magnitude of the reflex cardiovascular changes can be modulated at this site. The studies described in this review suggest that the dorsal horn of the spinal cord serves as an important site of integration for sensory signals that influence the cardiovascular system.

Animals↗

c-Fos expression in the medulla induced by static muscle contraction in cats.

In this study, we examined Fos-like immunoreactivity (FLI) in the medulla after static muscle contraction induced by stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized cats. The results show that FLI increases in the lateral reticular nucleus, nucleus of the solitary tract, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, and A1 region of the medulla in comparison with these same areas in sham-operated animals (P < 0.05 in each region). In the rostral ventrolateral medulla, FLI distribution in neurons containing phenylethanolamine-N-methyltransferase (PNMT, the synthetic enzyme for epinephrine) was also observed utilizing double-labeling methods. The majority of neurons with PNMT also expressed FLI (66 +/- 4%). These data are in contrast to the results from sham-operated animals showing that 24 +/- 3% of the neurons costained with PNMT (P < 0.05). Our findings indicate that expression of FLI can be used to identify neurons activated during static muscle contraction and support previous studies implicating the ventrolateral medulla as a critical region for expression of the exercise pressor reflex. Furthermore, neurons in the rostral ventrolateral medulla containing PNMT were activated during static muscle contraction.

Animals↗