Blood flow response to muscle contractions is more closely related to metabolic rate than contractile work.

The magnitude of the blood flow response to exercise has been linked to both the contractile work performed and the metabolic cost of the activity. Under certain conditions, contractile work and metabolic cost may be dissociated. This study examined the blood flow response to trains of contractions when contraction duration was manipulated under conditions of similar tension-time indexes (isometric analog of work). Previous investigations have shown that trains of short-duration contractions have a greater ATP utilization, which may result from an augmented ion transport required for muscle activation and relaxation. On the basis of these findings, we hypothesized that the blood flow response would be greater to a train of short-duration contractions than a train of long-duration contractions. Canine gastrocnemius-plantaris muscle (n = 8) was isolated, and blood flow assessed with an ultrasound flow probe placed around the popliteal artery. The sciatic nerve was stimulated to produce two contraction protocols that resulted in similar contraction-to-rest ratios: short duration: 0.25 s/0.75 s vs. long duration: 1 s /3 s. In accord with the design of the experiment, the tension-time indexes were identical for the two contraction protocols (short: 18.6 +/- 1.0 vs. long: 18.6 +/- 1.0 kN.s). Steady-state oxygen consumption was greater in the short-duration contractions (17.2 +/- 0.9 ml.100 g(-1).min(-1)) than in the long-duration contractions (11.7 +/- 0.7 ml.100 g(-1).min(-1)). Similarly, the steady-state blood flow was greater in contractions of short duration (125 +/- 7 ml/min) compared with long-duration contractions (92 +/- 7 ml/min). Contractions of short duration resulted in significantly higher oxygen consumptions and blood flows compared with contractions of long duration despite the same total contractile work. The blood flow response to muscle contraction appears to be more closely associated with muscle metabolism than contractile work performed.     

M wave potentiation during and after muscle activity

The M wave (muscle compound action potential) has been shown to enlarge between successive 3-s voluntary contractions of the human thenar and extensor digitorum brevis (EDB) muscles. The changes, which affected both the amplitude and the area of the M wave, were more obvious in the thenar than in the EDB muscles. In the thenar muscles the mean amplitude was already significantly enlarged after the first voluntary contraction and close to the maximal value by the third (mean maximal increase 23.6 +/- 12.6% of control). The increase in mean M wave area was more gradual, reaching a maximum of 29.3 +/- 14.1% at 100 s. After the voluntary thenar contractions ceased, the amplitude of the M wave subsided more rapidly than the area and had regained the control value within 50 s. The magnitude and time course of the increase in EDB M wave area (maximum change 25.9 +/- 15.2%) were similar to those of the thenar muscles; however, the subsequent decline was slower. The amplitude of the EDB M wave showed the least change, and the maximum increase (11.4 +/- 9.6%) occurred early in the postcontraction period. In both muscles the changes in M wave amplitude and area were significantly different from the control values.     

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion.

Potential protective effects of aerobic exercise training on the myocardium, before an ischemic event, are not completely understood. The purpose of the study was to investigate the effects of exercise training on contractile function after ischemia-reperfusion (Langendorff preparation with 15-min global ischemia/30-min reperfusion). Trabeculae were isolated from the left ventricles of both sedentary control and 10- to 12-wk treadmill exercise-trained rats. The maximal normalized isometric force (force/cross-sectional area; Po/CSA) and shortening velocity (Vo) in isolated, skinned ventricular trabeculae were measured using the slack test. Ischemia-reperfusion induced significant contractile dysfunction in hearts from both sedentary and trained animals; left ventricular developed pressure (LVDP) and maximal rates of pressure development and relaxation (+/-dP/dtmax) decreased, whereas end-diastolic pressure (EDP) increased. However, this dysfunction (as expressed as percent change from the last 5 min before ischemia) was attenuated in trained myocardium [LVDP: sedentary -60.8 +/- 6.4% (32.0 +/- 5.5 mmHg) vs. trained -15.6 +/- 8.6% (64.9 +/- 6.6 mmHg); +dP/dtmax: sedentary -54.1 +/- 4.7% (1,058.7 +/- 124.2 mmHg/s) vs. trained -16.7 +/- 8.4% (1,931.9 +/- 188.3 mmHg/s); -dP/dtmax: sedentary -44.4 +/- 2.5% (-829.3 +/- 52.0 mmHg/s) vs. trained -17.9 +/- 7.2% (-1,341.3 +/- 142.8 mmHg/s); EDP: sedentary 539.5 +/- 147.6%; (41.3 +/- 6.0 mmHg) vs. trained 71.6 +/- 30.6%; 11.4 +/- 1.2 mmHg]. There was an average 26% increase in Po/CSA in trained trabeculae compared with sedentary controls, and this increase was not affected by ischemia-reperfusion. Ischemia-reperfusion reduced Vo by 39% in both control and trained trabeculae. The relative amount of the beta-isoform of myosin heavy chain (MHC-beta) was twofold greater in trained trabeculae as well as in the ventricular free walls. Despite a possible increase in the economy in the trained heart, presumed from a greater amount of MHC-beta, ischemia-reperfusion reduced Vo, to a similar extent in both control and trained animals. Nevertheless, the trained myocardium appears to have a greater maximum force-generating ability that may, at least partially, compensate for reduced contractile function induced by a brief period of ischemia.     

Impulse propagation and muscle activation in long maximal voluntary contractions

With fatigue, force generation may be limited by several factors, including impaired impulse transmission and/or reduced motor drive. In 5-min isometric maximal voluntary contraction, no decline was seen in the peak amplitude of the tibialis anterior compound muscle mass action potential (M wave) either during or immediately after the voluntary effort, provided maximal nerve stimulation was retained. For first dorsal interosseous (FDI) muscle, M wave amplitudes declined by 19.4 +/- 1.6% during the first 2 min but did not change significantly thereafter, despite the continued force reduction (up to 94% in 5 min for both muscles). The duration of the FDI M waves increased (greater than 30%), suggesting that the small decline in amplitude was the result of increased dispersion between the responses of different motor units. Some subjects kept FDI maximally activated throughout, but when they used tibialis anterior, twitch occlusion and tetanic muscle stimulation showed that most subjects were usually only able to do so for the first 60 s and thereafter only during brief "extra efforts." Thus force loss during isometric voluntary contractions sustained at the highest intensities results mainly from failure of processes within the muscle fibers.     

Cardiovascular responses to static and dynamic contraction during comparable workloads in humans

Previous studies suggest that the blood pressure response to static contraction is greater than that caused by dynamic exercise. In anesthetized cats, however, pressor responses to electrically induced static and dynamic contraction of the same muscle group are similar during equivalent workloads and peak tension development [i.e., similar tension-time index (TTI)]. To determine if the same relationship exists in humans, where contraction is voluntary and central command is present, dynamic (180 s; 1/s) and static (90 s) contractions at 30% of maximal voluntary contraction (MVC) were performed. Dynamic contraction also was repeated at the same TTI for 90 s at 60% MVC. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), MAP during postexercise arterial occlusion (an index of the metaboreceptor-induced activation of the exercise pressor reflex), and relative perceived exertion (RPE) (an index of central command) were assessed. No differences in these variables were found between static and dynamic contraction at a tension of 30% MVC. During dynamic contraction at 60% MVC, changes in MAP (16 +/- 3 vs. 19 +/- 4 mmHg) and absolute HR (92 +/- 6 vs. 69 +/- 5 beats/min), CO (7.9 +/- 0.4 vs. 6.3 +/- 0.3 l/min), RPE (16 +/- 1 vs. 13 +/- 1), and MAP during postexercise arterial occlusion (115 +/- 3 vs. 100 +/- 4 mmHg) were greater than during static contraction (P < 0.05). Thus increases in MAP and HR, activation of central command, and muscle metabolite-induced stimulation of the exercise pressor reflex during static and dynamic contraction in humans seem to be similar when peak tension and TTI are equal. Augmented responses to dynamic contraction at 60% MVC are likely related to greater activation of these two mechanisms.     

Voluntary activation of human quadriceps during and after isokinetic exercise.

The extent of voluntary activation in fresh and fatigued quadriceps muscles was investigated during isometric and isokinetic voluntary contractions at 20 and 150 degrees/s in 23 normal human subjects. The muscles were fatigued by a total of 4 min of maximal knee extension at an angular velocity of 85 degrees/s. Voluntary activation was determined by the superimposition of tetanic electrical stimulation at 100 Hz for 250 ms, initiated at a constant knee angle. The relationship between voluntary and stimulated force was similar to that found with the established twitch superimposition technique used on isometric contractions. In fresh muscle all the subjects showed full voluntary activation during isometric contractions. Some activation failure was seen in five subjects at 20 degrees/s [2.0 +/- 0.9 degrees (SE)] and in two subjects at 150 degrees/s (0.7 +/- 0.5). After fatigue all subjects showed some activation failure at 0 and 20 degrees/s (36.4 +/- 3.1 and 28.8 +/- 4.1 degrees, respectively), but only two showed any at 150 degrees/s (1.4 +/- 5.7). We conclude that brief high-intensity dynamic exercise can cause a considerable failure of voluntary activation. This failure was most marked during isometric and the lower-velocity isokinetic contractions. Thus a failure of voluntary activation may have greater functional significance than previous studies of isometric contractions have indicated.     

Effects of (artificial) boar stimuli on uterine activity in estrous sows

This study aims to examine influences of specific boar stimuli on uterine activity in estrous sows, by comparing uterine activity in presence of a mature teaser boar and a robot boar with variable stimuli. Nineteen multiparous, cyclic, commercial crossbred sows were used. Intra-luminal uterine pressure was measured using a non-surgical method for 45 min before applying one of four treatments in combination with a back-pressure-test (BPT): (1) robot with olfactory and auditory stimuli (R+O+A) (n=16), (2) robot with auditory stimuli (R+A) (n=16), (3) robot without additional stimuli (R) (n=16), (4) a mature boar (boar) (n=15). After treatment, measurements continued for 30 min. For each measurement, frequency, mean amplitude and mean duration of uterine contractions were determined. Spontaneous frequency of uterine contractions was 18.6+/-0.7 h(-1) on average and did not differ between treatments. Frequency of contractions increased significantly for the boar (+5.6+/-1.3 h(-1); P<0.01), R+O+A (+3.9+/-1.3; P<0.01) and R+A (+2.6+/-1.3; P<0.05). The effect of boar presence on frequency of contractions was greater than the effect of R (P<0.05). Amplitude and duration of contractions were not affected by treatment. The change in frequency was dependent on spontaneous frequency (P<0.01). In conclusion, the higher the level of boar stimuli, the greater the increase in frequency of uterine contractions. The results indicate that the used combinations of artificial boar stimuli do not mimic a 'whole' boar. It is unclear which boar stimuli stimulate maximal uterine activity during estrus.     

Determinants of transpyloric fluid transport: a study using combined real-time ultrasound,manometry, and impedance recording

Intraluminal impedance recording has made it possible to record fluid transport across the pylorus during the interdigestive state without filling the stomach. During antral phase II, fluid transport occurs with and without manometrically detectable antral contraction. Our aim was to investigate the relationships between ultrasonographic patterns of antral contraction, manometric pressure waves, and transpyloric fluid transport during antral phase II. Antral wall movements were recorded by real-time ultrasound (US) in eight healthy volunteers (mean age 24 +/- 7 yr) during 17 +/- 5 min of antral phase II. Concomitantly, a catheter positioned across the pylorus, monitored by transmucosal potential difference measurement, recorded five impedance signals (1 antral, 1 pyloric, and 3 duodenal) and six manometric signals (2 antral, 1 pyloric, and 3 duodenal). Antral contractions detected by US at the level of the two antral impedance electrodes were classified according to their association with a pyloric opening or a duodenal contraction. Transpyloric liquid transport events (impedance drop of >40% of the baseline with an antegrade or retrograde propagation) and manometric pressure waves (amplitude and duration) were identified during the whole study and especially during each period of US antral contraction. A total of 110 antral contractions was detected by US. Of these, 79 were also recorded by manometry. Fluid transport across the pylorus was observed in 70.9% of the US-detected antral contractions. Pyloric opening was observed in 98.6% of the contractions associated with fluid transport compared with 50% in the absence of fluid transport (P < 0.05). Antral contractions associated with fluid transport were significantly (P < 0.05) more often propagated to the duodenum (92%) than those without fluid transport (53%). Pressure waves associated with fluid transport were of higher amplitude (208 mmHg, range 22-493) and longer duration (7 s, range 2.5-13.5 s) than those not associated with fluid transport (102 mmHg, range 18-329 mmHg, and 4.1 s, range 2-8.5 s; P < 0.05). The propagation of the antral contractions in the duodenum in US was always associated with a pyloric opening, whereas only 8 of the 25 contractions without duodenal propagation were associated with a pyloric opening (P < 0.05). The presence of duodenal contractile activity before the onset of an antral contraction in US was always accompanied by pyloric opening and with fluid transport in 93.3%, compared with 56.8% in its absence (P < 0.05). In antral phase II, US is the most sensitive technique to detect antral contractions. Transpyloric fluid transport observed in relation to antral contractions occurs mainly in association with contractions of high amplitude and long duration and is associated with pyloric opening and/or duodenal propagation.     

Cholinergic stimulation induces asynchrony between the circular and longitudinal muscle contraction during esophageal peristalsis

In healthy subjects, a close temporal correlation exists between contractions of the circular muscle (CM) and longitudinal muscle (LM) layers of the esophagus. Patients with nutcracker esophagus show disassociation between the peak of contractions of the CM and LM layers and the peak of contraction 1-3 s apart (Jung HY, Puckett JL, Bhalla V, Rojas-Feria M, Bhargava V, Liu J, Mittal RK. Gastroenterology 128: 1179-1186, 2005). The purpose of the present study was to evaluate the effect of acetylcholinesterase inhibitor (edrophonium) and acetylcholine receptor antagonist (atropine) on human esophageal peristalsis in normal subjects. High-frequency intraluminal ultrasound imaging and manometry were performed simultaneously during swallow-induced peristalsis in ten normal subjects. Standardized 5-ml water swallows were recorded 2 cm above the lower esophageal sphincter under three study conditions: control, edrophonium (80 microg/kg iv), and atropine (10 microg/kg iv). A close temporal correlation exists between the peak pressure and peak wall thickness during the control period. The mean time lag between the peak LM and peak CM contraction was 0.03 s. After edrophonium administration, the mean contraction amplitude increased from 101 +/- 9 mmHg to 150 +/- 20 mmHg (P < 0.05) and mean peak muscle thickness increased from 3.0 +/- 0.2 mm to 3.6 +/- 0.3 mm (P < 0.01), and duration of both CM and LM contractions were also increased. Furthermore, the mean time difference between the peak LM and CM was increased to 1.1 s, (ranging 0.2 to 3.4 s) (P < 0.0001). We conclude that cholinomimetic agent induces discoordination between the two muscle layers of the esophagus.     

Calcium channel blockade prevents pressure-dependent inward remodeling in isolated subendocardial resistance vessels

The capacity for myocardial perfusion depends on the structure of the coronary microvascular bed. Coronary microvessels may adapt their structure to various stimuli. We tested whether the local pressure profile affects tone and remodeling of porcine coronary microvessels. Subendocardial vessels (approximately 160 microm, n=53) were cannulated and kept in organoid culture for 3 days under different transvascular pressure profiles: Osc 80: mean 80 mmHg, 60 mmHg peak-peak sine wave pulsation amplitude at 1.5 Hz; St 80: steady 80 mmHg; Osc 40: mean 40 mmHg, 30 mmHg amplitude; St 40: steady 40 mmHg. Under the Osc 80 profile, modest tone developed, reducing the diameter to 81+/-14% (mean+/-SE, n=6) of the maximal, passive diameter. No inward remodeling was found here, as determined from the passive pressure-diameter relation after 3 days of culture. Under all other profiles, much more tone developed (e.g., Osc 40: to 26+/-3%, n=7). In addition, these vessels showed eutrophic (i.e., without a change in wall cross-sectional area) inward remodeling (e.g., Osc 40: passive diameter reduction by 24+/-3%). The calcium blocker amlodipine induced maintained dilation in St 40 vessels and reversed the 22+/-3% (n=6) inward remodeling to 15+/-3% (n=8) outward remodeling toward day 3. Vessels required a functional endothelium to maintain structural integrity in culture. Our data indicate that reduction of either mean pressure or pulse pressure leads to microvascular constriction followed by inward remodeling. These effects could be reversed by amlodipine. Although microvascular pressure profiles distal to stenoses are poorly defined, these data suggest that vasodilator therapy could improve subendocardial microvascular function and structure in coronary artery disease.     

Effects of transmural pressure on brachial artery mean blood velocity dynamics in humans.

The effects of changes in transmural pressure on brachial artery mean blood velocity (MBV) were examined in humans. Transmural pressure was altered by using a specially designed pressure tank that raised or lowered forearm pressure by 50 mmHg within 0.2 s. Brachial MBV was measured with Doppler directly above the site of forearm pressure change. Pressure changes were evoked during resting conditions and after a 5-s handgrip contraction at 25% maximal voluntary contraction. The handgrip protocol selected was sufficiently vigorous to limit flow and sufficiently brief to prevent autonomic engagement. Changes in transmural pressure evoked directionally similar changes in MBV within 2 s. This was followed by large and rapid adjustments [-2.14 +/- 0.24 cm/s (vasoconstriction) during negative pressure and +2.14 +/- 0.45 cm/s (vasodilatation) during positive pressure]. These adjustments served to return MBV to resting levels. This regulatory influence remained operative after 5-s static handgrip contractions. Of note, changes in transmural pressure were capable of altering the timing of the peak MBV response (5 +/- 0, 2 +/- 0, 6 +/- 1 s ambient, negative, and positive pressure, respectively) as well as the speed of MBV adjustment (-2.03 +/- 0.18, -2.48 +/- 0.15, -0.84 +/- 0.19 cm x s(-1) x s(-1) ambient, negative, and positive pressure, respectively) after handgrip contractions. Vascular responses, seen with changes in transmural pressure, provide evidence that the myogenic response is normally operative in the limb circulation of humans.     

Relationships between spatial patterns of colonic pressure and individual movements of content

The aim of this study was to examine the relationship between colonic pressure waves and movement of content. In 11 healthy subjects, pressures were recorded at 10-cm intervals from cecum to rectum for 32 h. In six subjects, transit was simultaneously measured for 8 h after direct cecal instillation of 1.5 mCi of (99m)Tc sulfur colloid. Thirty-two percent of isotope movements were related to nonpropagating activity and twenty-eight percent to propagating sequences. The extent of isotope movement related to propagating sequences (25.1 +/- 2.1 cm) was greater than that due to nonpropagating activity (12.8 +/- 0.7 cm; P = 0.0001). Propagating sequences originated significantly more frequently (P = 0.004) and propagated further (P = 0.0006) in the proximal compared with the distal colon. Only 36% of propagating sequences were propulsive of content, and compared with nonpropulsive sequences, these propagated further (41 +/- 6 vs. 27 +/- 2 cm; P < 0.05) and had a higher probability of originating proximally (P = 0.0003), a higher pressure wave amplitude (50 +/- 5 vs. 34 +/- 4 mmHg; P = 0.0001), and slower velocity (2.2 +/- 0.3 vs. 3.6 +/- 0.47 cm/s; P = 0.02). We conclude that most movements of colonic content are related to pressure waves. There is marked regional variation in the prevalence, velocity, and extent of propagation of propagating pressure wave sequences, which are an important mechanism for transporting content over long distances. The effectiveness of transport by a propagating sequence is influenced by its site of origin, amplitude, and velocity.     

Effects of caffeine on neuromuscular function.

This double-blind, repeated-measures study examined the effects of caffeine on neuromuscular function. Eleven male volunteers [22.3 +/- 2.4 (SD) yr] came to the laboratory for control, placebo, and caffeine (6 mg/kg dose) trials. Each trial consisted of 10 x 1-ms stimulation of the tibial nerve to elicit maximal H reflexes of the soleus, four attempts at a maximal voluntary contraction (MVC) of the right knee extensors, six brief submaximal contractions, and a 50% MVC held to fatigue. Isometric force and surface electromyographic signals were recorded continuously. The degree of maximal voluntary activation was assessed with the twitch-interpolation technique. Single-unit recordings were made with tungsten microelectrodes during the submaximal contractions. Voluntary activation at MVC increased by 3.50 +/- 1.01 (SE) % (P < 0. 01), but there was no change in H-reflex amplitude, suggesting that caffeine increases maximal voluntary activation at a supraspinal level. Neither the force-EMG relationship nor motor unit firing rates were altered by caffeine. Subjects were able to hold a 50% MVC for an average of 66.1 s in the absence of caffeine. Time to fatigue (T(lim)) increased by 25.80 +/- 16.06% after caffeine administration (P < 0.05). There was no significant change in T(lim) from pretest to posttest in the control or placebo trials. The increase in T(lim) was associated with an attenuated decline in twitch amplitude, which would suggest that the mechanism is, at least in part, peripheral.     

Splenic baroreceptors control splenic afferent nerve activity

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 +/- 0.5 to 22.9 +/- 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 +/- 0.1 to 0.9 +/- 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 +/- 0.1 to 0.6 +/- 0.1 ml/min, n = 6), and increased SANA (1.7 +/- 0.4 to 2.2 +/- 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 +/- 0.1 to 0.7 +/- 0.05, n = 6) or splenic venous blood flow (1.2 +/- 0.1 to 0.5 +/- 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (-0.4 +/- 0.9 mmHg, n = 6 and +0.1 +/- 0.3 mmHg, n = 5) or SANA (-0.11 +/- 0.15 spikes/s, n = 6 and -0.05 +/- 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure (r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous (r = 0.371, P = 0.236, n = 12) or arterial (r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.     

Spike-triggered average torque and muscle fiber conduction velocity of low-threshold motor units following submaximal endurance contractions.

The motor unit twitch torque is modified by sustained contraction, but the association to changes in muscle fiber electrophysiological properties is not fully known. Thus twitch torque, muscle fiber conduction velocity, and action potential properties of single motor units were assessed in 11 subjects following an isometric submaximal contraction of the tibialis anterior muscle until endurance. The volunteers activated a target motor unit at the minimum discharge rate in eight 3-min-long contractions, three before and five after an isometric contraction at 40% of the maximal torque, sustained until endurance. Multichannel surface electromyogram signals and joint torque were averaged with the target motor unit potential as trigger. Discharge rate (mean +/- SE, 6.6 +/- 0.2 pulses/s) and interpulse interval variability (33.3 +/- 7.0%) were not different in the eight contractions. Peak twitch torque and recruitment threshold increased significantly (93 +/- 29 and 12 +/- 5%, P <0.05) in the contraction immediately after the endurance task with respect to the preendurance values (0.94 +/- 0.26 mN.m and 3.7 +/- 0.5% of the maximal torque), whereas time to peak of the twitch torque did not change (74.4 +/- 10.1 ms). Muscle fiber conduction velocity decreased and action potential duration increased in the contraction after the endurance (6.3 +/- 1.8 and 9.8 +/- 1.8%, respectively, P <0.05; preendurance values, 3.9 +/- 0.2 m/s and 11.1 +/- 0.8 ms), whereas the surface potential peak-to-peak amplitude did not change (27.1 +/- 3.1 microV). There was no significant correlation between the relative changes in muscle fiber conduction velocity or surface potential duration and in peak twitch torque (R2= 0.04 and 0.10, respectively). In conclusion, modifications in peak twitch torque of low-threshold motor units with sustained contraction are mainly determined by mechanisms not related to changes in action potential shape and in its propagation velocity.     

Individualization of transfer function in estimation of central aortic pressure from the peripheral pulse is not required in patients at rest

Central aortic pressure gives better insight into ventriculo-arterial coupling and better prognosis of cardiovascular complications than peripheral pressures. Therefore transfer functions (TF), reconstructing aortic pressure from peripheral pressures, are of great interest. Generalized TFs (GTF) give useful results, especially in larger study populations, but detailed information on aortic pressure might be improved by individualization of the TF. We found earlier that the time delay, representing the travel time of the pressure wave between measurement site and aorta is the main determinant of the TF. Therefore, we hypothesized that the TF might be individualized (ITF) using this time delay. In a group of 50 patients at rest, aged 28-66 yr (43 men), undergoing diagnostic angiography, ascending aortic pressure was 119 +/- 20/70 +/- 9 mmHg (systolic/diastolic). Brachial pressure, almost simultaneously measured using catheter pullback, was 131 +/- 18/67 +/- 9 mmHg. We obtained brachial-to-aorta ITFs using time delays optimized for the individual and a GTF using averaged delay. With the use of ITFs, reconstructed aortic pressure was 121 +/- 19/69 +/- 9 mmHg and the root mean square error (RMSE), as measure of difference in wave shape, was 4.1 +/- 2.0 mmHg. With the use of the GTF, reconstructed pressure was 122 +/- 19/69 +/- 9 mmHg and RMSE 4.4 +/- 2.0 mmHg. The augmentation index (AI) of the measured aortic pressure was 26 +/- 13%, and with ITF and GTF the AIs were 28 +/- 12% and 30 +/- 11%, respectively. Details of the wave shape were reproduced slightly better with ITF but not significantly, thus individualization of pressure transfer is not effective in resting patients.     

Supraspinal fatigue does not explain the sex difference in muscle fatigue of maximal contractions.

Young women are less fatigable than young men for maximal and submaximal contractions, but the contribution of supraspinal fatigue to the sex difference is not known. This study used cortical stimulation to compare the magnitude of supraspinal fatigue during sustained isometric maximal voluntary contractions (MVCs) performed with the elbow flexor muscles of young men and women. Eight women (25.6 +/- 3.6 yr, mean +/- SD) and 9 men (25.4 +/- 3.8 yr) performed six sustained MVCs (22-s duration each, separated by 10 s). Before the fatiguing contractions, the men were stronger than the women (75.9 +/- 9.2 vs. 42.7 +/- 8.0 N.m; P < 0.05) in control MVCs. Voluntary activation measured with cortical stimulation before fatigue was similar for the men and women during the final control MVC (95.7 +/- 3.0 vs. 93.3 +/- 3.6%; P > 0.05) and at the start of the fatiguing task (P > 0.05). By the end of the six sustained fatiguing MVCs, the men exhibited greater absolute and relative reductions in torque (65 +/- 3% of initial MVC) than the women (52 +/- 9%; P < 0.05). The increments in torque (superimposed twitch) generated by motor cortex stimulation during each 22-s maximal effort increased with fatigue (P < 0.05). Superimposed twitches were similar for men and women throughout the fatiguing task (5.5 +/- 4.1 vs. 7.3 +/- 4.7%; P > 0.05), as well as in the last sustained contraction (7.8 +/- 5.9 vs. 10.5 +/- 5.5%) and in brief recovery MVCs. Voluntary activation determined using an estimated control twitch was similar for the men and women at the start of the sustained maximal contractions (91.4 +/- 7.4 vs. 90.4 +/- 6.8%, n = 13) and end of the sixth contraction (77.2 +/- 13.3% vs. 73.1 +/- 19.6%, n = 10). The increase in the area of the motor-evoked potential and duration of the silent period did not differ for men and women during the fatiguing task. However, estimated resting twitch amplitude and the peak rates of muscle relaxation showed greater relative reductions at the end of the fatiguing task for the men than the women. These results indicate that the sex difference in fatigue of the elbow flexor muscles is not explained by a difference in supraspinal fatigue in men and women but is largely due to a sex difference of mechanisms located within the elbow flexor muscles.     

Cardiovascular responses to voluntary and nonvoluntary static exercise in humans.

We have measured the cardiovascular responses during voluntary and nonvoluntary (electrically induced) one-leg static exercise in humans. Eight normal subjects were studied at rest and during 5 min of static leg extension at 20% of maximal voluntary contraction performed voluntarily and nonvoluntarily in random order. Heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were determined, and peripheral vascular resistance (PVR) and stroke volume (SV) were calculated. HR increased from approximately 65 +/- 3 beats/min at rest to 80 +/- 4 and 78 +/- 6 beats/min (P < 0.05), and MAP increased from 83 +/- 6 to 103 +/- 6 and 105 +/- 6 mmHg (P < 0.05) during voluntary and nonvoluntary contractions, respectively. CO increased from 5.1 +/- 0.7 to 6.0 +/- 0.8 and 6.2 +/- 0.8 l/min (P < 0.05) during voluntary and nonvoluntary contractions, respectively. PVR and SV did not change significantly during voluntary or nonvoluntary contractions. Thus the cardiovascular responses were not different between voluntary and electrically induced contractions. These results suggest that the increases in CO, HR, SV, MAP, and PVR during 5 min of static contractions can be elicited without any contribution from a central neural mechanism (central command). However, central command could still have an important role during voluntary static exercise.     

Cardiac contractility modulation by electric currents applied during the refractory period

Inotropic effects of electric currents applied during the refractory period have been reported in cardiac muscle in vitro using voltage-clamp techniques. We investigated how electric currents modulate cardiac contractility in normal canine hearts in vivo. Six dogs were instrumented to measure regional segment length, ventricular volume (sonomicrometry), and ventricular pressure. Cardiac contractility modulating (CCM) electric currents (biphasic square pulses, amplitude +/-20 mA, total duration 30 ms) were delivered during the refractory period between pairs of electrodes placed on anterior and posterior walls. CCM significantly increased index of global contractility (E(es)) from 5.9 +/- 2.9 to 8.3 +/- 4.6 mmHg/ml with anterior CCM, from 5.3 +/- 1.8 to 8.9 +/- 4.0 mmHg/ml with posterior CCM, and from 6.1 +/- 2.6 to 11.0 +/- 7.0 mmHg/ml with combined CCM (P < 0.01, no significant change in volume axis intercept). End-systolic pressure-segment length relations showed contractility enhancement near CCM delivery sites, but not remotely. Relaxation was not influenced. CCM increased mean aortic pressure, but did not change peripheral resistance. Locally applied electrical currents enhanced global cardiac contractility via regional changes in myocardial contractility without impairing relaxation in situ.     

Effects of age on brachial artery myogenic responses in humans

The myogenic response, the inherent ability of blood vessels to rapidly respond to changes in transmural pressure, is involved in local blood flow autoregulation. Animal studies suggest that aging impairs the myogenic response. The purpose of this study was to compare the effects of changes in transmural pressure on mean blood velocity (MBV, cm/s) in young and older subjects. Twelve younger men and women (25 +/- 1 yr) were gender and body composition matched to twelve older men and women (65 +/- 1 yr). A specially designed tank raised or lowered forearm pressure by 50 mmHg within 0.2 s. Brachial artery MBV was measured directly above the site of forearm pressure change using Doppler methods. In response to increasing transmural pressure (i.e., release of +50 mmHg), older subjects compared with younger subjects had significantly lower peak MBV (Delta 12.43 +/- 1.16 vs. Delta 17.97 +/- 2.01 cm/s; P < 0.05), reduced rates in the dynamic fall of MBV after peak values were achieved (vasoconstriction) (-1.88 +/- 0.17 vs. -2.90 +/- 0.28 cm.s(-1).s(-1); P < 0.05), and lower MBV values with sustained suction. In response to decreasing transmural pressure (i.e., change to +50 mmHg), there was a significantly greater increase in MBV (Delta peak flow from trough 7.71 +/- 1.32 vs. 4.38 +/- 0.71 cm/s; P < 0.05) and a trend toward a greater rate of rise in MBV (vasodilation; 1.61 +/- 0.29 vs. 0.96 +/- 0.21 cm.s(-1).s(-1); P = 0.08) in the older subjects. Older subjects compared with the younger subjects exhibited decreased dynamic vasoconstriction, enhanced steady-state constriction, as well as evidence for enhanced dynamic vasodilation responses to sustained alterations in forearm transmural pressure.