Aerobic and resistance training improves mood state among adults living with HIV.

The purpose of this investigation was to examine the effects of combined aerobic and resistance exercise training among self-reported mood disturbances, perceived stress, frequency of self-reported symptoms, and symptom distress in a sample of HIV+ adults. For this purpose, 49 participants were randomly assigned into an exercise (EX) or control (CON) group. Those in the EX group completed 50 min of supervised aerobic and resistance training at a moderate intensity twice a week for 6 weeks. The CON group reported to the university and engaged in sedentary activities. Data were collected at baseline before randomization and 6 weeks post intervention. Measures included the symptom distress scale (SDS), perceived stress scale (PSS), profile of mood states (POMS) total score, and the POMS sub-scale for depression and fatigue. A 2 way ANOVA was used to compare between and within group interactions. The EX group showed a significant decrease in reported depression scores (p=0.03) and total POMS (p=0.003). The CON group reported no change in POMS or SDS, but showed a significant increase in PSS. These findings indicate that combination aerobic and resistance training completed at a moderate intensity at least twice a week provides additional psychological benefits independent of disease status and related symptoms.

Physical activity, eating traits and weight in young adulthood: a cross-sectional and longitudinal study.

OBJECTIVE: To investigate the association between eating traits (e.g. dietary restraint or opportunistic eating) and weight - both cross-sectionally and longitudinally - and whether physical activity (PA) moderates these associations. METHODS: Two-hundred seventy young adults (21-35 years; BMI: 25.40 kg/m2 [SD = 3.90 kg/m2]; 48.90% female) participated in this 12-month observational cohort study. Cognitive Restraint (CR), Disinhibition (DI) and Hunger (HU) were measured using the Three-Factor Eating Questionnaire at baseline and 12 months. Participants were measured at quarterly intervals for objectively measured PA and anthropometrics. Cross-sectional and longitudinal models determined if eating traits were associated with weight or weight change, and whether these associations were moderated by PA. RESULTS: At baseline, higher CR (B = 0.429, p < 0.01) and DI (B = 0.942, p < 0.01) were associated with higher weight. The associations of DI (B = -0.008 p = 0.02) and HU (B = -0.006, p = 0.04) with weight were moderated by PA at baseline. The longitudinal model for CR determined PA altered the relationship between change in CR and weight change (B = 0.004, p < 0.01). CONCLUSIONS: Eating traits and PA are associated with weight and weight change. However, to elucidate how PA and eating traits directly affect weight changes, future weight loss interventions should investigate whether improving eating traits and concomitantly increasing PA amplify weight loss.

Prospective association between body composition, physical activity and energy intake in young adults.

BACKGROUND/OBJECTIVES: Despite considerable research on the association between physical activity (PA) and body composition, there remains limited information on the directionality of the relationship. The present study examined the prospective associations among objectively measured PA, energy intake (EI) and body composition. SUBJECTS/METHODS: A convenience sample of 430 adults (49% male) between 21 and 35 years of age was followed over 1 year with repeated measurements taken every 3 months. BMI (kg/m(2)) and percent body fat (%BF) were calculated based on anthropometric measurements and dual energy X-ray absorptiometry. A multi-sensor device was worn over a period of 10 days to estimate total daily energy expenditure and time spent in different intensities. EI was calculated based on change in body composition and total daily energy expenditure. RESULTS: A total of 379 participants provided valid data. On average, participants experienced a significant weight gain of 1.2±4.3 kg during the 12-month observation period, which was associated with an increase in %BF (0.8±3.2 %). Average time spent in moderate-to-vigorous PA (MVPA) decreased significantly, whereas EI remained constant. Optimal linear mixed models, adjusting for age and sex, showed an inverse effect of MVPA on BMI and %BF, whereas EI only directly affected BMI (P<0.001). There was also a significant inverse effect of BMI and %BF on MVPA (P<0.001). CONCLUSIONS: Results of this study indicate an inverse reciprocal association between MVPA and measures of adiposity. Thus, primary preventive actions are warranted to avoid excess weight gain, which may result in a vicious cycle of weight gain and low PA.

High respiratory quotient is associated with increases in body weight and fat mass in young adults.

BACKGROUND/OBJECTIVES: Metabolic disturbances, such as reduced rates of fat oxidation (high respiratory quotient (RQ)) or low energy expenditure (low resting metabolic rate (RMR)), may contribute to obesity. The objective was to determine the association between a high RQ or a low RMR and changes in body weight and body composition over 1 year. SUBJECTS/METHODS: We measured RQ and RMR in 341 adults using indirect calorimetry, along with body weight/body composition using dual-energy X-ray absorptiometery, energy expenditure using an arm-based activity monitor and energy intake using dietary recalls. Participants were classified into low, moderate or high RQ and RMR (adjusted for age, sex, race and body composition) groups according to tertiles by sex. Follow-up measurements were completed every 3 months. RESULTS: Individuals with a high RQ had larger gains in body weight and fat mass compared with individuals with a low/moderate RQ at month 3, and increases in fat mass were more than double among individuals with a high RQ at 12 months (1.3±3.0 vs 0.6±3.7 kg, P=0.03). Individuals with a low RMR did not gain more body weight nor fat mass compared with individuals with a moderate/high RMR. CONCLUSION: The primary finding is a high RQ is predictive of gains in body weight and fat mass over a 12-month period among young adults, with changes occurring as soon as 3 months. In addition, a low RMR was not associated with gains in body weight or fat mass over the same period.

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.

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.

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.

Excitatory amino acid concentrations in the spinal dorsal horn of cats during muscle contraction.

In anesthetized cats, static hindlimb muscle contraction reflexly increases mean arterial pressure (MAP) and heart rate (HR). Pharmacological and immunohistochemical evidence suggests that excitatory amino acids are involved in the spinal transmission of this reflex. Using microdialysis and high-performance liquid chromatography technology, we tested the hypothesis that static contraction of the triceps surae muscle increases the extracellular concentration of glutamate (Glu) and aspartate (Asp) at the L7 level of the dorsal horn of the spinal cord. With the exception of the L7 dorsal root, the L5-S2 dorsal and ventral roots were cut ipsilateral to the contracting muscle. After the insertion of microdialysis probes and a 3-h recovery period, a 2-min static contraction was electrically evoked. MAP and HR increased by 53 +/- 8 mmHg and 20 +/- 4 beats/min. The concentration of Glu increased from 324 +/- 59 to 857 +/- 80 nM, whereas Asp increased from 199 +/- 57 to 499 +/- 113 nM. These results were repeatable, in that Glu and Asp rose by similar amounts in two subsequent contractions. In both of these latter contractions, MAP and HR were also significantly increased. By contrast, in a subset of cats whose L7 dorsal roots were cut after the first contraction, neither MAP, HR, Glu, nor Asp was significantly increased over baseline levels. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu and Asp in the dorsal horn. In summary, the results from this study are in agreement with previous findings suggesting that excitatory amino acids are involved in the spinal transmission of sensory information from the hindlimb muscle.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Central injection of physostigmine attenuates exercise-induced pressor response in conscious cats.

The effects of intracerebroventricular administration of physostigmine, a cholinesterase inhibitor, on the cardiovascular responses evoked by static voluntary exercise were investigated using conscious cats. Four cats were trained to press a bar (200-650 g) with one forelimb for at least 20 s. The changes in mean arterial pressure (MAP), heart rate (HR), and developed force during the first five trials in 30 min by each individual cat were averaged, and a mean of the four values was then calculated. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or physostigmine (5 micrograms) was administered intracerebroventricularly. Before physostigmine, exercise trials by the cats increased MAP and HR by 17 +/- 3 mmHg and 42 +/- 4 beats/min, respectively. Administration of physostigmine did not alter the resting MAP and HR but attenuated the MAP and HR responses to exercise (5-30 min postphysostigmine: MAP = 8 +/- 3 mmHg, HR = 25 +/- 7 beats/min; 30-60 min postphysostigmine: MAP = 4 +/- 3 mmHg, HR = 19 +/- 8 beats/min). Intracerebroventricular administration of CSF had no effect on the cardiovascular responses to static exercise. Pretreatment with the muscarinic antagonist, atropine (25 micrograms icv), blocked the attenuating effects of subsequent intracerebroventricular administration of physostigmine. These results demonstrate that stimulation of central muscarinic receptors attenuates the cardiovascular responses to static exercise by conscious cats. In addition, the present study suggests that there is no tonic effect of central muscarinic receptors on the cardiovascular responses to voluntary exercise.

Cardiovascular responses to static exercise in conscious cats: effects of intracerebroventricular injection of clonidine.

1. Static exercise elicits increases in arterial blood pressure and heart rate (HR) in humans and conscious animals. In this study, the effects of intracerebroventricular (I.C.V.) administration of clonidine, an alpha 2-adrenergic agonist, on these cardiovascular responses were investigated using conscious cats. Four cats were operantly trained to extend a forelimb and press a bar (200-650 g) for 15-60 s. A stainless-steel cannula was inserted into the right lateral ventricle for I.C.V. injection of drugs, and a common carotid artery was catheterized to measure mean arterial pressure (MAP) and HR. The number of exercise trials and changes in MAP, HR and force were pooled for 30 min periods. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or clonidine (2 or 5 micrograms) were administered intracerebroventricularly. 2. Before clonidine injection, fifty-two exercise trials increased MAP and HR by 15 +/- 3 mmHg and 41 +/- 5 beats min-1, respectively. Administration of clonidine (2 micrograms) did not alter the resting MAP and HR, but attenuated the increases in MAP and HR in response to exercise (0-30 min post-clonidine: n = 81; delta MAP, 6 +/- 3 mmHg; delta HR, 20 +/- 6 beats min-1; 30-60 min post-clonidine: n = 71; delta MAP, 4 +/- 4 mmHg; delta HR, 17 +/- 8 beats min-1). Administration of artificial CSF I.C.V. had no effect on the cardiovascular responses to static exercise. 3. An increased dose of clonidine (5 micrograms) decreased resting MAP and HR by 31 +/- 7 mmHg and 37 +/- 7 beats min-1, respectively, and markedly blunted the cardiovascular responses to exercise (pre-clonidine: n = 52; delta MAP, 17 +/- 3 mmHg; delta HR, 38 +/- 5 beats min-1; post-clonidine 0-30 min: n = 66; delta MAP, 4 +/- 2 mmHg; delta HR, 15 +/- 5 beats min-1; post-clonidine 30-60 min: n = 60; delta MAP, 4 +/- 2 mmHg; delta HR, 14 +/- 6 beats min-1). Pretreatment with the alpha 2-adrenergic antagonist, yohimbine (8 micrograms, I.C.V.), blocked the attenuating effects of I.C.V. administration of clonidine (5 micrograms). 4. These results show that stimulation of central alpha 2-adrenoceptors by clonidine attenuates the cardiovascular responses to static exercise in conscious cats. In addition, this study suggests that alpha 2-adrenoceptors blocked by yohimbine injected I.C.V. do not appear to have a tonic influence on HR and blood pressure.