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Correlating resting discharge with small signal sensitivity and discharge variability in primary endings of cat soleus muscle spindles.

1. In a previous report we proposed that primary endings of cat soleus muscle spindles can be separated into two kinds. One kind, called by us silent endings, at muscle lengths shorter than Lm -10 (maximum body length -10 mm), fell silent after a 5 mm shortening step. Spontaneous endings, on the other hand, were able to resume a resting discharge after a brief pause at all muscle lengths down to Lm -20. This report examines further differences between the two kinds of endings. 2. There were consistent differences in the muscle length dependence of the maintained level of resting discharge of the two kinds of endings, measured after a conditioning contraction or a contraction followed by a shortening step. The resting discharge of spindles with spontaneous endings, after both forms of conditioning increased progressively with length. For silent endings, after a conditioning contraction, resting discharge fell slightly at longer lengths. 3. Discharge variability, measured at a number of muscle lengths, showed a dependence both on mean interimpulse interval and on spindle type, being higher in silent than spontaneous spindles. 4. Small signal sensitivity was measured with the use of 1 Hz sinusoidal stretches applied longitudinally to the tendon. Sine wave amplitude was adjusted to give a 30% depth of modulation of the resting discharge. Spontaneous endings were consistently less sensitive to the stretches than silent endings at all muscle lengths. Average sensitivities, measured over a range of lengths between Lm -4 and Lm -20 mm were 0.30 imp.s-1.microns -1 for spontaneous endings and 0.66 imp.s-1.microns -1 for silent endings.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Is parkinsonian arm tremor a resting tremor?

Arm tremor in Parkinson's disease occurs during rest which has been explained by a specific tremulous mechanism activated during rest. During action or posture maintenance, the tremor may persist or recur, but with reduced amplitude. We present 2 patients with idiopathic Parkinson's disease who showed persisting arm tremor which was most marked during action rather than during rest. The patterns of upper limb tremor were investigated during rest, maintenance of fixed posture, and slow movement, using an advanced computerized movement-monitoring system (Coda 3). Four parkinsonian patients showing tremor under all conditions were studied, comparing 2 patients whose tremor was most marked during rest with 2 whose tremor was most marked during action. All showed intermediate amplitudes during posture maintenance. Patterns of tremor frequency were very similar between patients, irrespective of amplitude characteristics. These features suggest that tremors in all patients originate in a single, complex mechanism which may involve both central and peripheral mechanisms.

Aged↗

Long-term haemodynamic effects of amlodipine at rest and during exercise in essential hypertension.

Haemodynamic responses at rest and during exercise were studied in 18 patients with essential hypertension following long-term treatment with amlodipine. Patients underwent a 2-week placebo run-in period followed by a mean duration of 11 months' treatment with amlodipine 5-10 mg (mean dose 9 mg) once daily. Blood pressure was measured intra-arterially, cardiac output by dye dilution and heart rate by electrocardiogram. Amlodipine produced a mean reduction in systolic and diastolic arterial pressure of 27 and 16 mm Hg, respectively, at rest and after exercise. At rest sitting, mean systolic and diastolic arterial pressures were reduced by 16 and 14% (p less than 0.01), respectively, from initial mean values of 182.4/111.2 mm Hg. This reduction in blood pressure was associated with a marked reduction in the total peripheral resistance index of 19% (p less than 0.001). Similar responses were observed at rest supine and during exercise. No significant changes were seen in heart rate. Stroke index showed a small increase at rest and during exercise together with a trend towards an increase in cardiac index after treatment with amlodipine. Ambulatory blood pressure monitoring was carried out in 10 patients after the placebo run-in and at the end of the study. Amlodipine showed effective blood pressure control throughout the 24 h after one daily dose. The incidence of side effects was low (ankle oedema in 2 patients).

Adult↗

Respiration in conscious dogs at rest and during exercise.

25 mongrel dogs (average b.w. 24.6 kg) were studied on several occasions at rest and during treadmill exercise of up to 10 mph (15% incline). Minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), tidal volume (VT) and respiratory frequency (f) were determined at rest and at each level of exercise. Individual variability in resting VO2 was considerable (71--695 ml/min). Most often the dogs panted, with VE's above 25 liters/min and f's above 100 min-1. The averate VE/VO2 was 109 at rest. VO2 was linearly related to VE (VO2 = 9.17 VE + 66.9; r = 0.80). Differences in resting VE were largely due to differences in f (f = 3.57 VE + 21.2; r = 0.82). Considerable individual variability in VO2 for a given work load was also observed during exercise. Some dogs showed significant differences in VO2 from experiment to experiment while running at a given treadmill speed. These differences were largely related to the levels of VE. VE/VO2 decreased to 50. We found a leveling off of VO2 (at about 60 ml/min/kg) at treadmill speeds of 5 mph, suggesting that the maximal VO2 in dogs is less than previously reported.

Animals↗

Enhanced peripheral vasoconstrictor response and increased thromboxane A2 synthesis after the cold pressor test in patients with angina at rest.

Peripheral vascular resistance (PVR) and thromboxane A2(TxA2) synthesis after the cold pressor test were investigated in different subsets of patients with angina (10 with stable effort angina, 36 with resting angina [24 in an active phase and 12 in an inactive phase], and five with Prinzmetal's variant angina) and in 41 control subjects of equivalent age and risk factors. Left ventricular end-diastolic pressure, ejection fraction, extent of coronary angiographic lesions, and baseline PVR were not significantly different among the various patient groups. In all patient groups, except those with variant angina, the cold pressor test resulted in a higher increase in PVR than in the control subjects (p less than .001 for all groups). In patients with variant angina the vasoconstrictor response was increased only in proximity (about 1 hr) to ischemic attacks. In patients with active resting angina the vasoconstrictor response was on the average four times longer than that in patients with effort angina and with inactive resting angina (p less than .001). This exaggerated vasoconstrictor response was associated with elevated TxA2 resting levels in plasma and with increased TxA2 synthesis after the cold pressor test. A linear relationship was found between the area of the vascular response and the area of TxA2 production after the cold pressor test in patients with active resting angina (r = .87, p less than .001). The increased TxA2 synthesis and the inappropriate increase of peripheral vascular response to sympathetic stimulation revert back to normal in the inactive phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

13N ammonia myocardial imaging at rest and with exercise in normal volunteers. Quantification of absolute myocardial perfusion with dynamic positron emission tomography.

Positron emission tomography (PET) was applied to the measurement of myocardial perfusion using the perfusion tracer 13N-labeled ammonia. 13N ammonia was delivered intravenously to 13 healthy volunteers both at rest and during supine bicycle exercise. Dynamic PET imaging was obtained in three cross-sectional planes for 10 minutes commencing with each injection. The left ventricle was divided into eight sectors, and a small region of interest was assigned to the left ventricular blood pool to obtain the arterial input function. The net extraction of 13N ammonia was obtained for each sector by dividing the tissue 13N concentration at 10 minutes by the integral of the input function from the time of injection to 10 minutes. With this approach for calculating net extractions, rest and exercise net extractions were not significantly different from each other. To obviate possible overestimation of the true 13N ammonia input function by contamination by 13N-labeled compounds other than 13N ammonia or by spillover from myocardium into blood pool, the net extractions were calculated using only the first 90 seconds of the blood and tissue time-activity curves. This approach for calculating net extractions yielded significant differences between rest and exercise, with an average ratio of exercise to rest of 1.38 +/- 0.34. Nonetheless, the increase was less than predicted from the average 2.7-2.8-fold increase in double product at peak exercise or the 1.7-fold increase in double product at 1 minute after exercise. However, when the first 90 seconds of dynamic data were fit with a two compartment tracer kinetic model, average perfusion rates of 0.75 +/- 0.43 ml/min/g at rest and 1.50 +/- 0.74 ml/min/g with exercise were obtained. This average increase in perfusion of 2.2-fold corresponded to similar average increases in double product. Thus, the noninvasive technique of PET imaging with 13N ammonia shows promise for future applications in determining absolute flows in patients with coronary artery disease.

Adult↗

Differential 18F-2-deoxyglucose uptake in viable dysfunctional myocardium with normal resting perfusion: evidence for chronic stunning in pigs.

BACKGROUND: Viable, chronically dysfunctional myocardium can have normal or reduced resting flow. We previously produced hibernating myocardium with reduced resting flow in pigs with a chronic stenosis and hypothesized that hibernation is preceded by chronic stunning with normal resting perfusion. METHODS AND RESULTS: Pigs instrumented with a proximal left anterior descending coronary artery (LAD) stenosis were studied 1 or 2 months later in the closed-chest anesthetized state. Stenosis severity increased from 74+/-5% at 1 month to 83+/-6% at 2 months and was accompanied by anteroapical hypokinesis (wall motion score, 2.1+/-0.1 at 1 month and 1.5+/-0.3 at 2 months; normal=3). Resting perfusion was similar in normal and dysfunctional regions, but the deposition of 18F-2-deoxyglucose (FDG) varied. At 1 month, subendocardial FDG deposition by excised tissue counting was similar in each region (0. 034+/-0.006 mL. g-1. min-1 LAD region versus 0.032+/-0.004 mL. g-1. min-1 in normal regions, P=NS). At 2 months, subendocardial FDG deposition was increased (0.084+/-0.025 mL. g-1. min-1 LAD region versus 0.042+/-0.017 mL. g-1. min-1 in normal regions, P<0.05). Increases in FDG uptake were inversely related to LAD subendocardial flow reserve during adenosine (3.5+/-0.6 at 1 month versus 1.4+/-0.2 at 2 months, P<0.01). CONCLUSIONS: These data indicate a progression of physiological adaptations in pigs with viable, chronically dysfunctional myocardium. As coronary flow reserve decreases, fasting FDG uptake increases. Flow at rest remains normal, consistent with "chronic stunning," and contrasts with reduced flow and increased FDG characteristic of hibernating myocardium in similarly instrumented pigs after 3 months. This temporal progression of adaptations supports the hypothesis of a transition from a physiological phenotype of stunning to hibernation.

Animals↗

Effect of ATP-sensitive potassium channel inhibition on resting coronary vascular responses in humans.

Experimental data suggest that vascular ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow (CBF), but their role in regulating human CBF is unclear. We sought to determine the contribution of K(ATP) channels to resting conduit vessel and microvascular function in the human coronary circulation. Twenty-five patients (19 male/6 female, aged 56 +/- 12 years) were recruited. Systemic and coronary hemodynamics were assessed in 20 patients before and after K(ATP) channel inhibition with graded intracoronary glibenclamide infusions (4, 16, and 40 microg/min), in an angiographically smooth or mildly stenosed coronary artery following successful elective percutaneous coronary intervention to another vessel. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. Adenosine-induced hyperemia was determined following bolus intracoronary adenosine injection (24 microg). Time control studies were undertaken in 5 patients. Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting conduit vessel diameter from 2.5 +/- 0.1 to 2.3 +/- 0.1 mm (P<0.01), resting CBF by 17% (P=0.05), and resting CBF corrected for rate pressure-product by 18% (P=0.01) in a dose-dependent manner. A corresponding 24% increase in coronary vascular resistance was noted at the highest dose (P<0.01). No alteration to resting CBF was noted in the time control studies. Glibenclamide reduced peak adenosine-induced hyperemia (P=0.01) but did not alter coronary flow reserve. Plasma insulin increased from 5.6 +/- 1.2 to 7.6 +/- 1.3 mU/L (P=0.02); however, plasma glucose was unchanged. Vascular K(ATP) channels are involved in the maintenance of basal coronary tone but may not be essential to adenosine-induced coronary hyperemia in humans.

Adenosine↗

Treatment of pulmonary arteriovenous malformations by therapeutic embolization. Rest and exercise physiology in eight patients.

Pulmonary arteriovenous malformations (AVM) lead to chronic hypoxemia and systemic emboli. These lesions can now be treated by catheter embolization. In order to examine physiologic abnormalities during exercise in AVM patients, and to evaluate functional improvement after therapeutic embolization, eight patients underwent detailed physiologic studies at rest and during exercise before and after therapeutic embolization. Before treatment, six patients noted dyspnea on exertion and three had symptoms suggesting paradoxical embolism. Resting studies showed hypoxemia, abnormally increased shunt fractions, chronic alveolar hyperventilation, mild decreases in diffusing capacity, and abnormal wasted ventilation (VD). During exercise, oxygenation changed little from the resting values but VD increased markedly. Functional impairment was observed in most patients, and was correlated with shunt fraction. Obliteration of the AVM was accomplished by therapeutic embolization with placement of coils or balloons in the feeder vessels. This treatment resulted in immediate relief of dyspnea and improvement in resting PaO2 and shunt fraction. Exercise studies after embolization showed improvement in exercise capacity and gas exchange. However, chronic alveolar hyperventilation and reduced diffusing capacity remained unchanged. In summary, therapeutic embolization effectively reduces the degree of shunting, with improvement in respiratory symptoms, exercise capacity, and gas exchange at rest and during exercise. The abnormally decreased diffusing capacity and increased VD suggest the presence of a diffuse pulmonary vascular abnormality, of which further study is warranted.

Adult↗

Effects of breathing through external dead space on ventilation at rest and during exercise. II.

We used a new non-invasive monitor of ventilation, the respiratory inductive plethysmograph, to determine the effects of breathing through a mouthpiece (with nose clip) and breathing through external dead spaces on ventilation at rest and during exercise. Six normal young subjects were studied during 5-min sequential periods at rest, submaximal exercise on a bicycle at a work load of 800 kgm/min, and recovery. Not surprisingly, the imposition on the respiratory system of breathing through a mouthpiece (with nose clip) and with external dead spaces of 150, 250, and 350 ml produced progressively greater ventilation than natural breathing during rest and submaximal bicycle exercise. However, when the actual tidal volumes were corrected for the increase in ventilation caused by the external dead space, ventilation both at rest and during exercise with mouthpiece breathing still remained higher than natural breathing. These data suggest that breathing through a mouthpiece (with nose clip) and breathing through external dead spaces stimulates ventilation both at rest and during exercise.

Adult↗

5-Lipoxygenase is located in the euchromatin of the nucleus in resting human alveolar macrophages and translocates to the nuclear envelope upon cell activation.

5-Lipoxygenase (5-LO) and 5-lipoxygenase-activating protein (FLAP) are two key proteins involved in the synthesis of leukotrienes (LT) from arachidonic acid. Although both alveolar macrophages (AM) and peripheral blood leukocytes (PBL) produce large amounts of LT after activation, 5-LO translocates from a soluble pool to a particulate fraction upon activation of PBL, but is contained in the particulate fraction in AM irrespective of activation. We have therefore examined the subcellular localization of 5-LO in autologous human AM and PBL collected from normal donors. While immunogold electron microscopy demonstrated little 5-LO in resting PBL, resting AM exhibited abundant 5-LO epitopes in the euchromatin region of the nucleus. The presence of substantial quantities of 5-LO in the nucleus of resting AM was verified by cell fractionation and immunoblot analysis and by indirect immunofluorescence microscopy. In both AM and PBL activated by A23187, all of the observable 5-LO immunogold labeling was found associated with the nuclear envelope. In resting cells of both types, FLAP was predominantly associated with the nuclear envelope, and its localization was not affected by activation with A23187. The effects of MK-886, which binds to FLAP, were examined in ionophore-stimulated AM and PBL. Although MK-886 inhibited LT synthesis in both cell types, it failed to prevent the translocation of 5-LO to the nuclear envelope. These results indicate that the nuclear envelope is the site at which 5-LO interacts with FLAP and arachidonic acid to catalyze LT synthesis in activated AM as well as PBL, and that in resting AM the euchromatin region of the nucleus is the predominant source of the translocated enzyme. In addition, LT synthesis is a two-step process consisting of FLAP-independent translocation of 5-LO to the nuclear envelope followed by the FLAP-dependent activation of the enzyme.

Arachidonate 5-Lipoxygenase↗

Transition into daylight saving time influences the fragmentation of the rest-activity cycle.

BACKGROUND: Daylight saving time is widely adopted. Little is known about its influence on the daily rest-activity cycles. We decided to explore the effects of transition into daylight saving time on the circadian rhythm of activity. METHODS: We monitored the rest-activity cycles with the use of wrist-worn accelerometer on a sample of ten healthy adults for ten days around the transition into summer time. Identical protocols were carried out on the same individuals in two consecutive years, yielding data on 200 person-days for analysis in this study. RESULTS: There was no significant effect on the rest-activity cycle in the sample as a whole. Fragmentation of the rest-activity cycle was enhanced in a subgroup of persons having sleep for eight hours or less (P = 0.04) but reduced in those who preferred to sleep for more than eight hours per night (P = 0.05). The average level of motor activity was increased in persons having the morning preference for daily activity patterns (P = 0.01). CONCLUSION: Transition into daylight saving time may have a disruptive effect on the rest-activity cycle in those healthy adults who are short-sleepers or more of the evening type.

Journal Article↗

Arachidonic acid directly mediates the rapid effects of 24,25-dihydroxyvitamin D3 via protein kinase C and indirectly through prostaglandin production in resting zone chondrocytes.

Prior studies have shown that 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] plays a major role in resting zone chondrocyte differentiation and that this vitamin D metabolite regulates both phospholipase A2 and protein kinase C (PKC) specific activities. Arachidonic acid is the product of phospholipase A2 action and has been shown in other systems to affect a variety of cellular functions, including PKC activity. The aim of the present study was to examine the interrelationship between arachidonic acid and 24,25-(OH)2D3 on markers of proliferation, differentiation, and matrix production in resting zone chondrocytes and to characterize the mechanisms by which arachidonic acid regulates PKC, which was shown previously to mediate the rapid effects of 24,25-(OH)2D3 and arachidonic acid on these cells. Confluent, fourth passage resting zone cells from rat costochondral cartilage were used to evaluate these mechanisms. The addition of arachidonic acid to resting zone cultures stimulated [3H]thymidine incorporation and inhibited the activity of alkaline phosphatase and PKC, but had no effect on proteoglycan sulfation. In contrast, 24,25-(OH)2D3 inhibited [3H]thymidine incorporation and stimulated alkaline phosphatase, proteoglycan sulfation, and PKC activity. In cultures treated with both agents, the effects of 24,25-(OH)2D3 were reversed by arachidonic acid. The PKC isoform affected by arachidonic acid was PKCalpha; cytosolic levels were decreased, but membrane levels were unaffected, indicating that translocation did not occur. Arachidonic acid had a direct effect on PKC in isolated plasma membranes and matrix vesicles, indicating a nongenomic mechanism. Plasma membrane PKCalpha was inhibited, and matrix vesicle PKCzeta was stimulated; these effects were blocked by 24,25-(OH)2D3. Studies using cyclooxygenase and lipoxygenase inhibitors indicate that the effects of arachidonic acid are due in part to PG production, but not to leukotriene production. This is supported by the fact that H8-dependent inhibition of protein kinase A, which mediates the effects of PGE2, had no effect on the direct action of arachidonic acid but did mediate the role of arachidonic acid in the cell response to 24,25-(OH)2D3. Diacylglycerol does not appear to be involved, indicating that phospholipase C and/or D do not play a role. Gamma-linolenic acid, an unsaturated precursor of arachidonic acid, elicited a similar response in matrix vesicles but not plasma membranes, whereas palmitic acid, a saturated fatty acid, had no effect. These data suggest that arachidonic acid may act as a negative regulator of 24,25-(OH)2D3 action in resting zone chondrocytes.

24,25-Dihydroxyvitamin D 3↗

MEK5 and ERK5 are localized in the nuclei of resting as well as stimulated cells, while MEKK2 translocates from the cytosol to the nucleus upon stimulation.

The ERK5 signaling cascade acts through sequential activation of MEKK2/3, MEK5 and ERK5 and transmits signals to a variety of stress and mitogenic related targets. In this study we examined the subcellular localization of the components of the ERK5 cascade and found that in resting, as well as in EGF-stimulated HeLa and Rat-1 cells, endogenous ERK5 is localized mainly in the nucleus. This location is different from the previously described location of exogenous ERK5, in the cytosol of resting cells, which is confirmed in this study. The reason for the different localization could be a saturation of anchoring moieties by the endogenous ERK5. Indeed, in situ detergent extraction analysis using Nonidet P-40, revealed that ERK5 is bound to detergent resistant moieties in the nucleus, while the exogenous protein fails to interact with those anchors. The upstream activator MEK5 is also localized in the nucleus both before and after EGF stimulation and is resistant to NP-40 extraction in resting cells. ERK5 remains bound to these nuclear moieties even after stimulation, while MEK5 is detached from the anchors but remains localized in the nucleus. Unlike ERK5 and MEK5, their upstream activator MEKK2 is localized mainly in the cytosol of resting cells, and translocates into the nucleus upon EGF stimulation, allowing transmission of signals to the nuclear MEK5. The nuclear localization of MEK5 and ERK5 is different from that of ERK1/2 and MEK1/2 in resting cells, indicating that each MAPK cascade uses distinct mechanisms to transmit extracellular signals to their nuclear targets.

Animals↗

Plasma catecholamines in the lesser spotted dogfish and rainbow trout at rest and during different levels of exercise.

The hypothesis that there is an increase in plasma catecholamines during exercise in fish and that they play an important role in the cardiovascular adjustments during exercise was investigated in the lesser spotted dogfish and rainbow trout. In resting fish plasma catecholamines were at a concentration of 10(-9)-10(-8) mol l-1. During spontaneous swimming in the dogfish, adrenaline increased by 3.3 times to 1.9 X 10(-8) mol l-1 and noradrenaline increased by 2.3 times to 3.2 X 10(-8) mol l-1. In rainbow trout swimming at a steady 1 body length s-1 (Ls-1) in a water channel, the levels of both amines decreased to approximately 25% of the resting values. When swimming to apparent exhaustion at approximately 2 Ls-1, adrenaline was 10 times the resting value at 1.4 X 10(-8) mol l-1, whereas noradrenaline was 2.2 times the resting value at 2.3 X 10(-8) mol l-1. Only after repeated burst swimming for 2-3 min did the levels of plasma catecholamines increase substantially above the resting values. In the dogfish, both amines were at 10(-7) mol l-1, whereas in the rainbow trout, noradrenaline was at 8.5 X 10(-8) mol l-1 and adrenaline was at 2 X 10(-7) mol l-1. These levels were compared with the concentrations of catecholamines used by other workers to elicit changes in the branchial vasculature, gas exchange at the gills or gas transport to the tissues. In lesser spotted dogfish, the levels of adrenaline and noradrenaline present in the plasma during spontaneous swimming have 80% and 50% of maximum effect on gill blood vessels, respectively, whereas in rainbow trout the levels present when swimming to apparent exhaustion have approximately 20% of maximum effect on the branchial vasculature. The levels present in the trout after repeated burst swimming have 40% of maximum effect on blood vessels in the gills. The difference between the dogfish and the trout may be related to the lack of innervation of the gill blood vessels in the former. Enhancement of gas exchange across the gills of rainbow trout can be demonstrated by using adrenaline at the concentration found after repeated burst swimming. It is possible, however, that the concentration of adrenaline found in the plasma of trout after swimming to apparent exhaustion may cause an increase in the concentration of oxygen in arterial blood, thus enhancing oxygen delivery to the tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Cardiovascular responses to acute and subchronic treatment with oxprenolol in spontaneously hypertensive rats at rest and at stress.

To further examine the mechanism of antihypertensive action, effects of a single (50mg/kg) and repeated oral administration (50 mg/kg per day, for 14 days) of oxprenolol on mean arterial pressure (MAP) and heart rate (HR) were studied in spontaneously hypertensive (SHR) rats at rest and during handling stress. MAP was measured through a indwelling aortic cannula and HR was determined via chronically implanted electrodes. A single oral dose of oxprenolol produced a gradual fall in resting MAP. Although repeated dose of oxprenolol did not alter the developmental course of hypertension in SHR rats, a prompt and significant fall in MAP at rest was observed after the dose on the 14th day of the experiment. A single and repeated dose of oxprenolol attenuated the increase in MAP during handling stress, but these effects were less apparent when compared to the fall in resting MAP. Significant reductions in stress-induced tachycardia were observed both after a single and repeated dose, whereas resting HR tended to increase. These results indicate that some of the postulated antihypertensive mechanisms such as central inhibition of sympathetic outflow, peripheral inhibition of sympathetic nerve functions and suppression of cardiac output are not directly related to a fall in MAP observed in SHR rats after oxprenolol treatment. Time courses of the hypotensive effect of a single and repeated doses suggest that the accumulation of oxprenolol in active sites which appear to be located in deep compartments is required to develop hypotensive effect.

Animals↗

Validity of a multi-sensor armband in estimating rest and exercise energy expenditure.

UNLABELLED: The SenseWear Armband (SWA; BodyMedia, Inc.), using multiple sensors, was designed to estimate energy expenditure (EE) in free-living individuals. PURPOSE: To examine the reliability and validity of the SWA during rest and exercise compared with indirect calorimetry (IC). METHODS: EE was assessed with SWA and IC in 13 males during two resting and one cycle ergometry (40 min at 60% VO2peak) sessions. In a second experiment, 20 adults walked on a treadmill for 30 min at three intensities (80.5 m x min, 0% grade; 107.3 m x min, 0% grade; 107.3 m x min, 5% grade) while IC and SWA measured EE. RESULTS: At rest, no significant differences were found between EE measurements from the SWA (1.3 +/- 0.1 kcal x min) and IC (1.3 +/- 0.1 kcal x min), and the two methods were highly correlated (r = 0.76; P < 0.004). The SWA EE estimation was reliable when comparing the two resting visits (r = 0.93; P < 0.001). For the ergometer protocol, no significant differences were found between the SWA and IC measurements of EE early, mid, or late in exercise or for the total bout, although the measurements were poorly correlated (r = 0.03-0.12). The SWA EE estimate of walking increased with treadmill speed but not with incline. The SWA significantly overestimated (13-27%) the EE of walking with no grade (P < 0.02) and significantly underestimated (22%) EE on the 5% grade (P < 0.002). The SWA estimation of EE correlated moderately with IC (r = 0.47-0.69). CONCLUSION: The SWA provided valid and reliable estimates of EE at rest and generated similar mean estimates of EE as IC on the ergometer; however, individual error was large. The SWA overestimated the EE of flat walking and underestimated inclined walking EE.

Adolescent↗

Heart rate variability of recently concussed athletes at rest and exercise.

PURPOSE: The objective of this study was to assess the neuroautonomic cardiovascular regulation in recently concussed athletes at rest and in response to low-moderate steady-state exercise, using heart rate variability (HRV). METHODS: A 5-min ECG sample was taken at rest from the 14 concussed athletes at 1.8 (+/- 0.2) days postinjury and again at 5 d later. Once asymptomatic at rest, the concussed athletes and their matched controls (N = 14) participated in an exercise protocol. The protocol consisted of a 2-min warm-up with a pedaling frequency between 50 and 60 rpm against a load of 40 W. After the warm-up, the athletes engaged in a low-moderate intensity steady state 10-min exercise bout where the pedaling frequency and load increased to 80-90 rpm and 1.5 W x kg(-1) body weight, respectively. The protocol was repeated 5 d later. A 5-min ECG sample from minutes 4 to 9 of the low-moderate intensity steady state exercise bout was used to assess HRV during exercise. Mixed model ANOVA were used to analyze the data. RESULTS: No difference at rest was detected between the concussed athletes and their matched controls in any of the HRV variables measured. However, across both exercise tests, the concussed group demonstrated a significant decrease in the mean RR interval, and low- and high-frequency power (P < 0.05) in relation to their matched controls. CONCLUSION: Low-moderate steady-state exercise elicits a neuroautonomic cardiovascular dysfunction in concussed athletes that is not present in a rested state. This dysfunction alludes to an exercise induced uncoupling between the autonomic and cardiovascular systems.

Adolescent↗