Static Contraction Research Articles

Myocardial load at 30% and 50% of Maximal Voluntary Isometric Contraction in healthy individuals with Active and Sedentary Lifestyle

Background: Activities of daily living consists of isometric & isotonic contraction. Isometric contraction is a static contraction that exerts pressure overload on the heart. Studies have been carried out demonstrating hemodynamic effects of isotonic exercises however limited studies are available on myocardial load with isometric exercises. Aims and Objectives: To study the myocardial load at 30% and 50% of maximal voluntary isometric contraction (MVIC) in individuals with active and sedentary lifestyle. Study design and setting: Observational cross-sectional study was carried out in a tertiary care hospital. Materials and Methods: 140 healthy subjects (70 each in active & sedentary group) were recruited for the study. Baseline demographics of both groups were comparable. Hemodynamic parameters were taken at rest. Subject performed 30% and 50% MVIC and hemodynamic parameters were recorded during and post contraction. Statistical Analysis: Paired t test was used to compare the myocardial load between 30% and 50% MVIC in both groups. Repeated measures ANOVA was used to compare the myocardial load between active & sedentary groups at 30% and 50% MVIC. Result: There was a statistically significant difference in heart rate, systolic blood pressure &rate pressure product between 30% and 50% in active as well as sedentary groups. There was statistically no significant difference in heart rate, systolic blood pressure & rate pressure product between active & sedentary groups at 30% and 50% MVIC. Conclusion: The myocardial load during activities at submaximal intensities (<50%) is within the physiological limits and can be performed safely in individuals with active and sedentary lifestyle.

Effects of prolonged muscle stretch on reflex and voluntary muscle activations in children with spastic cerebral palsy

We studied the short term effects of a single session of prolonged muscle stretch (PMS) on reflex and voluntary muscle activations in 22 children with spastic cerebral palsy (CP) assigned to an experimental (n = 12) and a control group (n = 10). Children of the experimental group underwent PMS of the triceps surae (TS) by standing with the feet dorsiflexed on a tilt-table for 30 min, whereas children of the control group were kept at rest. The effects were determined by measuring the associated changes in torque and in electromyographic (EMG) activity of the TS and tibialis anterior (TA) muscles during both passive ankle movements and maximal static voluntary contractions. The results indicate that PMS led to reduced spasticity in ankle muscles as demonstrated by the significant reductions (p less than 0.05) of the neuromuscular responses (torque and EMG) to passive movement. These inhibitory effects lasted up to 35 min after cessation of PMS. In addition, the capacity to voluntarily activate the plantar flexors was significantly (p less than 0.05) increased post-PMS, but the capacity to activate the dorsiflexors was apparently not affected. These findings suggest that repeated sessions of PMS may have beneficial effects in the management of spasticity in children with CP.

One‐Time Acute Elevation of Muscle Temperature Is Effective for Attenuation of Exaggerated Exercise Pressor Reflex in Rats with Peripheral Artery Disease

BackgroundThe blood pressure (BP) response is augmented during static exercise in peripheral artery disease (PAD). Heating treatment was found to be effective for the attenuation of the BP response in PAD patients. However the underlying mechanism for the muscle temperature (Tm) on BP responses in PAD is still unclear.AimsWe first determined the effect of one‐time acute Tm elevation on the exaggerated exercise pressor reflex in PAD rats with 72 hours of femoral artery occlusion. We further determined if P2X receptor was engaged during this process because a lower Tm in occluded muscle can alter expression and function of P2X.MethodsThe BP response to static muscle contraction was recorded to examine the exercise pressor reflex. Also, αβ‐methylene ATP (αβ‐me ATP) was injected into the arterial blood supply of the hindlimb muscles to stimulate P2X receptors in the muscle afferent nerves. To elevate the Tm, a heating pad was placed locally on the hindlimb and the Tm was increased by ~1.5 °C. Then the Tm was stabilized and maintained for 5 min.ResultsThe BP response to static muscle contraction was examined 20 minutes before (pre‐heat), immediately following (acute heat) and 20 minutes after the end of elevation of Tm (recovery). Compared with control rats, a greater mean arterial pressure (MAP) response was observed in PAD rats in the pre‐heat session (27.50±2.07 mmHg in PAD rats/n=12 vs. 18.00±1.67 mmHg in control rats/n=9; P<0.05). However, following elevation of the Tm, the amplification of MAP response was similar in PAD rats and in control rats (21.25±3.00 mmHg in PAD rats/n=12 vs. 18.00±2.56 mmHg in control rats/n=8; P>0.05). During the recovery, a greater MAP response remained in PAD rats (27.54±0.90 mmHg in PAD rats/n=11 vs. 20.14±1.43 mmHg in control rats/n=7; P<0.05). Note that no significant difference in developed muscle tension during contraction was seen in control rats and PAD rats (P>0.05). When αβ‐me ATP (0.125mM) was given, the MAP responses were higher in PAD rats (n=7) than in control rats (n=7) (56.03±4.70 mmHg in PAD vs. 39.12±4.59 mmHg in control for pre‐heat, 59.63±3.55 mmHg in PAD vs. 39.92±5.20 mmHg in control after heating, and 63.33±2.51 mmHg in PAD vs. 35.57±4.38 mmHg in control for recovery; P<0.05 for all sessions between two groups).ConclusionOne‐time acute elevation of the Tm inhibits the exaggeration of the exercise pressor reflex in PAD rats. The effects of one‐time heat may not be through alternating muscle afferent nerves’ P2X receptors.Support or Funding InformationThis study was supported by NIH P01 HL134609 & R01 HL141198

ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats

The role of the acid‐sensing ion channel 1a (ASIC1a) in evoking the exercise pressor reflex is unknown despite the fact that ASIC1a is opened by decreases in pH in the physiological range. This fact prompted us to test the hypothesis that ASIC1a plays an important role in evoking the exercise pressor reflex in decerebrated rats with freely perfused hindlimb muscles. To test this hypothesis, we measured the effect of injecting two ASIC1a blockers into the arterial supply of the triceps surae muscles on the reflex pressor responses to four maneuvers, namely (1) static contraction of the triceps surae muscles (i.e., the exercise pressor reflex), (2) calcaneal tendon stretch, and (3) intra‐arterial injection of lactic acid and (4) diprotonated phosphate. We found that the two ASIC1a blockers, psalmotoxin‐1 (200 ng kg−1) and mambalgin‐1 (6.5 μg −1), decreased the pressor responses to static contraction as well as the peak pressor responses to injection of lactic acid and diprotonated phosphate. In contrast, neither ASIC1a blocker had any effect on the pressor responses to tendon stretch. Importantly, we found that ASIC1a blockade significantly decreased the pressor response to static contraction after a latency of at least 8 s. Our results support the hypothesis that ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflexSupport or Funding Information Funding for this study was provided by the National Institute of Arthritis and Muskuloskeletal and Skin Diseases (Grant R01‐AR‐059397) and National Heart, Lung, and Blood Institute (Grant P01‐HL‐134609).

Dynamic contraction dependence on the instantaneous motor unit firing rates

The effect of voluntary muscle contraction is to regulate position change about a joint involving recruitment and rate coding of motor units (MU) to produce torque results in the shortening velocity component. Unlike isometric (static) muscle contractions, isotonic (dynamic) muscle contractions can involve feedback to slow the shortening velocity as the joint reaches the terminal position. During dynamic conditions of increasing velocity targets, evidence indicates that the neuromuscular initiation of movement is greater than at isometric conditions, possibly being enhanced by the motor neuron secondary firing rate range. Our objective was to further characterize voluntary neuromuscular control at the level of instantaneous motor unit action potential firings during dynamic shortening muscle contractions. During isometric and isotonic contractions, intramuscular fine‐wire electromyography (EMG) was used to record MU potentials from the anconeus and triceps brachii muscles in healthy younger men and women (range 20–35 years, n= 15). Isotonic contractions were normalized to the maximal isotonic velocity and were loaded at 20% of the maximal isometric voluntary contraction torque. For analysis, the EMG was digitally high‐pass filtered (1 kHz, 3rd order Butterworth) and MU action potential waveforms were determined and sorted by template matching (Spike2 Wavemark, version 7) with manual inspection. Torque, velocity and position were also measured and at each individual firing rate time‐point and these vectors were aligned. From this, 627 MU trains (mean±standard deviation 42±19, n= 15) during the isotonic contractions in the anconeus muscle and 226 MU trains (38±14, n= 6) in the long head of the triceps brachii muscle were measured. To explore a more comprehensive model related to firing rates, the torque, velocity and position were modelled by linear regression with the residuals of MU train number, participant, testing session, sex, muscle and target velocity removed. From the full model when comparing slope coefficients, there was no significant interactions between torque (β= 48.1x) and velocity (β= −28.5x) on firing rate dependence (p= 0.2). Position (β= 0.4x) had a smaller coefficient on firing rates as compared to torque and velocity and a significant interaction effect with torque (p< 0.05), but not velocity (p= 0.4). These results indicate that a model of instantaneous firing rate dependence on torque, velocity and position requires a re‐examination, especially because the interaction of torque and velocity were significantly correlated (r= 0.5, p< 0.05). Shortening velocity of muscles causing elbow joint extension must be first initiated by a rate of torque development, further supporting that a different conceptual approach may be necessary to understand MU output during dynamic contractions. It may be important in this task to model firing rates as the independent variable (time vector) that will affect succeeding dependent changes of torque, velocity and position.Support or Funding InformationSupported by NSERC.

Heat treatment improves the exaggerated exercise pressor reflex in rats with femoral artery occlusion via a reduction in the activity of the P2X receptor pathway.

During exercise, the blood pressure (BP) response is exaggerated in peripheral artery disease (PAD). We examined whether heat treatment (HT) has beneficial effects on the exaggerated exercise pressor reflex in PAD rats. With HT (increase in basal muscle temperature of ∼1.5°C for 30min, twice daily for three continuous days), the amplified BP response to muscle contraction is alleviated in PAD. We demonstrated that HT attenuates the enhancement of the BP response induced by stimulation of P2X in muscle afferent nerves of PAD rats. HT also attenuates the upregulation of the P2X3 and the increase in P2X currents in the muscle afferent neurons of PAD rats. Previous heat exposure plays a beneficial role in modifying the exaggeration of the exercise pressor reflex in PAD and a reduction in the activity of the P2X receptor pathway is probably a part of the mechanism mediating this improvement. The current study was performed to examine if heat treatment (HT) has beneficial effects on the exaggerated exercise pressor reflex in rats with peripheral artery disease (PAD). We further determined if the temperature-sensitive P2X receptor is involved in the effects of HT. The pressor response to static muscle contraction and α,β-methylene ATP (αβ-me ATP, a P2X agonist) was examined. Western blot analysis was used to determine the protein levels of P2X3 in the dorsal root ganglion (DRG), and the whole cell patch clamp was used to examine the amplitude of P2X currents in the DRG neurons. The basal muscle temperature (Tm ) was lower in PAD rats than in control rats. Tm was increased by ∼1.5°C and this increase was maintained for 30min. This HT protocol was performed tweice daily for three continuous days. A greater blood pressure (BP) response to contraction was observed in PAD rats. HT attenuated the amplification of the BP response in PAD rats. HT also attenuated the enhancement of the BP response induced by the arterial injection of αβ-me ATP in PAD rats. In addition, HT attenuated the upregulation of the P2X3 and increased P2X currents in the DRG neurons of PAD rats. In conclusion, previous heat exposure plays an inhibitory role in modifying the exaggeration of the exercise pressor reflex in PAD and a reduction of the activity of the P2X receptor pathway is probably a part of mechanisms leading to the beneficial effects of HT.

Experimental study on the sEMG of "joint angle effect" of human muscle strength—Taking biceps brachii as an example

In the experiment, the author used wave plus wireless surface electromyography system (SEMs + 3-axis acceleration sensor) made in Italy and wave wireless EMG software system, high-definition high-speed camera and human joint angle measuring instrument. Taking human biceps brachii as an example, the static and dynamic isometric contraction of biceps brachii was completed surface electromyography. In the experiment, the surface electromyography of biceps brachii was measured at 30°, 60°, 90°, 120°, 150°, 180° and the surface electromyography of biceps brachii was measured at the same time when the biceps brachii was not loaded or when the biceps brachii was loaded. Secondly, the surface electromyography of biceps brachii was measured at the same time when the biceps brachii completed the whole process of flexion and extension of the elbow (centripetal and centrifugal). Finally, the paper combined with HD The effect of joint angle on the contraction of biceps brachii muscle was analyzed by camera technique. The results show that the static contraction force of biceps brachii is different when the elbow joint is at different angles; in addition, when the dynamic contraction, the contraction force of biceps brachii is inversely proportional to the angle of elbow joint.

Analysis of Electrical Impedance Myography Electrodes Configuration for Local Muscle Fatigue Evaluation Based on Finite Element Method

Local muscle fatigue (LMF) is a common physiological phenomenon that occurs in daily exercise training and medical rehabilitation. Without timely treatment it can easily lead to muscle spasm, ligament rupture, and even stress fractures. Electrical impedance myography (EIM) is a noninvasive bioelectrical impedance technique suitable for the wearable LMF monitoring anytime and anywhere. In this paper, a novel EIM electrode configuration was proposed by establishing a four-layer simulation model of the human upper arm in FEM software. Sensitivity parameters were introduced to optimize muscle selectivity. The effect of fat thickness on impedance change rate was explored to reduce the influence of individual fat differences on EIM results. Dynamic and static contraction experiments of muscle fatigue were performed on the biceps brachii muscles of 10 volunteers to verify the effectiveness and feasibility of the proposed electrode configuration. The proposed electrode configuration reduced the measurement area by 25%, whereas the impedance amplitude and sensitivity remained the same. The influence of individual fat differences on EIM results was significantly reduced. When the fat thickness increased from 6 mm to 18 mm, the impedance change decreased by 31.78% compared with the traditional electrode configuration. When the muscles were extremely exhausted, the decrease in resistance varied around $10~\Omega $ and within 10−1 order of magnitude in different volunteers. In a word, the proposed electrode configuration effectively evaluated the degree of LMF, providing more feasibility for the design of wearable devices.

ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex in rats.

The role of the acid-sensing ion channel 1a (ASIC1a) in evoking the exercise pressor reflex is unknown, despite the fact that ASIC1a is opened by decreases in pH in the physiological range. This fact prompted us to test the hypothesis that ASIC1a plays an important role in evoking the exercise pressor reflex in decerebrated rats with freely perfused hindlimb muscles. To test this hypothesis, we measured the effect of injecting two ASIC1a blockers into the arterial supply of the triceps surae muscles on the reflex pressor responses to four maneuvers, namely 1) static contraction of the triceps surae muscles (i.e., the exercise pressor reflex), 2) calcaneal tendon stretch, 3) intra-arterial injection of lactic acid, and 4) intra-arterial injection of diprotonated phosphate. We found that the 2 ASIC1a blockers, psalmotoxin-1 (200 ng/kg) and mambalgin-1 (6.5 μg/kg), decreased the pressor responses to static contraction as well as the peak pressor responses to injection of lactic acid and diprotonated phosphate. In contrast, neither ASIC1a blocker had any effect on the pressor responses to tendon stretch. Importantly, we found that ASIC1a blockade significantly decreased the pressor response to static contraction after a latency of at least 8 s. Our results support the hypothesis that ASIC1a plays a key role in evoking the metabolic component of the exercise pressor reflex.NEW & NOTEWORTHY The role played by acid-sensing ion channel 1a (ASIC1a) in evoking the exercise pressor reflex remains unknown. In decerebrated rats with freely perfused femoral arteries, blocking ASIC1a with psalmotoxin-1 or mambalgin-1 significantly attenuated the pressor response to static contraction, lactic acid, and diprotonated phosphate injection but had no effect on the pressor response to stretch. We conclude that ASIC1a plays a key role in evoking the exercise pressor reflex by responding to contraction-induced metabolites, such as protons.

The magnitude of the exercise pressor reflex is influenced by the active skeletal muscle mass in the decerebrate rat.

The exercise pressor reflex is composed of two components, namely the muscle mechanoreflex and the muscle metaboreflex. The afferents evoking the two components are either thinly myelinated (group III) or unmyelinated (group IV); in combination they are termed "thin fiber afferents." The exercise pressor reflex is often studied in unanesthetized, decerebrate rats. However, the relationship between the magnitude of this reflex and the number of thin fiber afferents stimulated by muscle contraction is unknown. This lack of knowledge prompted us to test the hypothesis that the magnitude of the exercise pressor reflex was directly proportional to the amount of muscle mass activated. Muscle mechanoreceptors were stimulated by stretching the calcaneal tendon. Likewise, muscle metaboreceptors were stimulated by injecting lactic acid into the arterial supply of the hindlimb muscles. In addition, both muscle mechanoreceptors and metaboreceptors were stimulated by statically contracting the hindlimb muscles. We found that simultaneous bilateral (both hindlimbs) stimulation of thin fiber afferents with stretch, lactic acid, and static contraction evoked significantly greater pressor responses than did unilateral (one hindlimb) stimulation of these afferents. In addition, the magnitude of the pressor responses to bilateral simultaneous stimulation of thin fiber afferents evoked by stretch, lactic acid, and contraction was not significantly different from the magnitude of the sum of the pressor responses evoked by unilateral stimulation of these afferents by stretch, lactic acid, and contraction. We conclude that the magnitude of the exercise pressor reflex and its two components is dependent on the number of afferents stimulated.

Effect of knockout of the ASIC3 on cardiovascular reflexes arising from hindlimb muscle in decerebrated rats.

The exercise pressor reflex is initiated by the contraction-induced activation of group III and IV muscle afferents. The reflex is manifested by increases in arterial blood pressure and cardiac output, which, in turn, are generated by increases in the sympathetic outflow to the heart and vasculature and decreases in the vagal outflow to the heart. In previous experiments, we used a pharmacological approach to assess the role played by the acid-sensing ion channel 3 (ASIC3) on group III and IV afferents in evoking the exercise pressor reflex. In the present experiments, we used an alternative approach, namely functional knockout (KO) of the ASIC3 gene, to confirm and extend our previous finding that pharmacological blockade of the ASIC3 had only a small impact on the expression of the exercise pressor reflex when the arterial supply to the contracting hindlimb muscles of rats was patent. Using this alternative approach, we compared the magnitude of the exercise pressor reflex evoked in ASIC3 KO rats with that evoked in their wild-type (WT) counterparts. We found both WT and ASIC3 KO rats displayed similar pressor responses to static contraction (WT, n = 10, +12 ± 2 mmHg; KO, n = 9, +11 ± 2 mmHg) and calcaneal tendon stretch (WT, n = 9, +13 ± 2 mmHg; KO, n = 7, +11 ± 2 mmHg). Likewise, both WT and ASIC3 KO displayed similar pressor responses to intra-arterial injection of 12 mM lactic acid (WT, n = 9, +14 ± 3 mmHg; KO, n = 8, +18 ± 5 mmHg), 24 mM lactic acid (WT, n = 9,+24 ± 2 mmHg; KO, n = 8, +20 ± 5 mmHg), capsaicin (WT, n = 9,+27 ± 5 mmHg; KO, n = 10, +29 ± 5 mmHg), and diprotonated phosphate ([Formula: see text]; WT, n = 6,+22 ± 3 mmHg; KO, n = 6, +32 ± 6 mmHg). We conclude that redundant receptors are responsible for evoking the pressor reflexes arising from group III and IV afferents.

Exaggerated cardiovascular responses to muscle contraction and tendon stretch in UCD type-2 diabetes mellitus rats

Patients with type-2 diabetes mellitus (T2DM) have exaggerated sympathetic activity and blood pressure responses to exercise. However, the underlying mechanisms for these responses, as well as how these responses change throughout disease progression, are not completely understood. For this study, we examined the effect of the progression of T2DM on the exercise pressor reflex, a critical neurocardiovascular mechanism that functions to increase sympathetic activity and blood pressure during exercise. We also aimed to examine the effect of T2DM on reflexive cardiovascular responses to static contraction, as well as those responses to tendon stretch when an exaggerated exercise pressor reflex was present. We evoked the exercise pressor reflex and mechanoreflex by statically contracting the hindlimb muscles and stretching the Achilles tendon, respectively, for 30 s. We then compared pressor and cardioaccelerator responses in unanesthetized, decerebrated University of California Davis (UCD)-T2DM rats at 21 and 31 wk following the onset of T2DM to responses in healthy nondiabetic rats. We found that the pressor response to static contraction was greater in the 31-wk T2DM [change in mean arterial pressure (∆MAP) = 39 ± 5 mmHg] but not in the 21-wk T2DM (∆MAP = 24 ± 5 mmHg) rats compared with nondiabetic rats (∆MAP = 18 ± 2 mmHg; P < 0.05). Similarly, the pressor and the cardioaccelerator responses to tendon stretch were significantly greater in the 31-wk T2DM rats [∆MAP = 69 ± 6 mmHg; change in heart rate (∆HR) = 28 ± 4 beats/min] compared with nondiabetic rats (∆MAP = 14 ± 2 mmHg; ∆HR = 5 ± 3 beats/min; P < 0.05). These findings suggest that the exercise pressor reflex changes as T2DM progresses and that a sensitized mechanoreflex may play a role in exaggerating these cardiovascular responses.NEW & NOTEWORTHY This is the first study to provide evidence that as type-2 diabetes mellitus (T2DM) progresses, the exercise pressor reflex becomes exaggerated, an effect that may be due to a sensitized mechanoreflex. Moreover, these findings provide compelling evidence suggesting that impairments in the reflexive control of circulation contribute to exaggerated blood pressure responses to exercise in T2DM.

P2X3 receptors contribute to muscle pain induced by static contraction by a mechanism dependent on neutrophil migration.

P2X3 receptors are involved with several pain conditions. Muscle pain induced by static contraction has an important socioeconomic impact. Here, we evaluated the involvement of P2X3 receptors on mechanical muscle hyperalgesia and neutrophil migration induced by static contraction in rats. Also, we evaluated whether static contraction would be able to increase muscle levels of TNF-α and IL-1β. Male Wistar rats were pretreated with the selective P2X3 receptor antagonist, A-317491, by intramuscular or intrathecal injection and the static contraction-induced mechanical muscle hyperalgesia was evaluated using the Randall-Selitto test. Neutrophil migration was evaluated by measurement of myeloperoxidase (MPO) kinetic-colorimetric assay and the cytokines TNF-α and IL-1β by enzyme-linked immunosorbent assay. Intramuscular or intrathecal pretreatment with A-317491 prevented static contraction-induced mechanical muscle hyperalgesia. In addition, A-317491 reduced static contraction-induced mechanical muscle hyperalgesia when administered 30 and 60min of the beginning of static contraction, but not after 30 and 60min of the end of static contraction. Intramuscular A-317491 also prevented static contraction-induced neutrophil migration. In a period of 24h, static contraction did not increase muscle levels of TNF-α and IL-1β. These findings demonstrated that mechanical muscle hyperalgesia and neutrophil migration induced by static contraction are modulated by P2X3 receptors expressed on the gastrocnemius muscle and spinal cord dorsal horn. Also, we suggest that P2X3 receptors are important to the development but not to maintenance of muscle hyperalgesia. Therefore, P2X3 receptors can be pointed out as a target to musculoskeletal pain conditions induced by daily or work-related activities.

Effect of acute high-phosphate intake on muscle metaboreflex activation and vascular function.

Increased consumption of inorganic phosphate (Pi), an abundant ingredient in processed foods, has been associated with elevated cardiovascular disease risk; however, studies investigating underlying mechanisms are limited. Recently, high dietary Pi was shown to exaggerate the pressor response to static muscle contraction in rodents in part because of overactivation of metabolically sensitive skeletal muscle afferents. Whether acute high Pi consumption affects muscle metaboreflex activation in humans remains unknown. Furthermore, although acute high Pi consumption has been shown to impair vascular function in young healthy men, equivocal results have been reported. Therefore, we hypothesized that acute high Pi consumption augments mean arterial pressure (MAP) responses during muscle metaboreflex activation, impairs endothelial function, and increases arterial stiffness in young healthy men. Subjects performed 35% maximal voluntary contraction static handgrip (HG), followed by postexercise ischemia (PEI) to isolate muscle metaboreflex activation. Resting flow-mediated dilation (FMD) and arterial stiffness were assessed. Measures were made before (pre) and 60 min after (post) subjects consumed either a high-phosphate drink (2,000 mg phosphorus and 1,520 mg sodium) or a sodium drink (1,520 mg sodium; control). MAP responses during HG (preΔ = +23 ± 3 mmHg; postΔ = +21 ± 2 mmHg; P = 0.101) and PEI (preΔ = +21 ± 4 mmHg; postΔ = +18 ± 3 mmHg; P = 0.184) were similar before and after Pi consumption. In contrast, FMD was significantly attenuated following Pi (pre = 5.1 ± 0.5%; post = 3.5 ± 0.5%; P = 0.010), whereas arterial stiffness remained unchanged. There were no changes in any measured variable after control drink consumption. In summary, although the muscle metaboreflex remains unaffected following acute high Pi consumption in young healthy men, endothelial function is impaired. NEW & NOTEWORTHY This study was the first to investigate the influence of acute high-phosphate consumption on the pressor response during isometric handgrip and isolated muscle metaboreflex activation during postexercise ischemia in young healthy humans. We demonstrated that a single high dose of phosphate (2,000 mg) did not augment blood pressure in response to exercise or isolated muscle metaboreflex activation, but endothelial function was blunted in young healthy men.

Influence of age on motor control accuracy during static ramp contractions.

We investigated the influence of the ageing process on the performance of the motor control system accuracy during a challenging motor task throughout the analysis of force output oscillations. The force signal of the first dorsal interosseous during linearly varying static contraction, 0-100-0% of the maximal volitional abduction in 15s, was studied in 11 young and older adults. The relative error between the target and the actual force as well as several parameters of the force oscillations (corrections) were estimated. To understand the experimental results, we analyzed the force output generated by a set of computational simulations of a pool of motor units controlled by a proportional-integral-derivative system. Compared to young adults the older subjects presented larger errors and a lower number of corrections with longer duration and larger relative amplitude. The motor control system modelling varied the error update frequency (UF) of the controller (from 1 to 2.5Hz) as well as the range of contraction time (CT) of the recruited motor unit (30-90ms and 60-120ms reflecting young and old ranges, respectively). The simulation generated force profiles with parameters similar to experimental recordings in young (UF = 1.5; CT 30-90ms) and older (UF = 1; CT 60-120ms) adults. Interestingly, the results of the simulations suggested that the improvement in the error update frequency of the controller was not able to compensate for the contractile changes in the motor unit twitches. In conclusion, the peripheral contractile changes with age can influence motor unit control strategies and represent a crucial phenomenon in the generation of larger force oscillations in older adults.

Stimulation of spinal δ-opioid receptors attenuates the exercise pressor reflex in decerebrate rats

A reflex arising from contracting hindlimb muscle is responsible in part for the increases in arterial pressure and heart rate evoked by exercise. The afferent arm of this reflex comprises group III and IV afferents. δ-Opioid receptors are expressed predominately on the spinal endings of group III afferents, whereas μ-opioid receptors are expressed predominately on the spinal endings of group IV afferents. Using stimuli that activated group III afferents, namely static contraction, calcaneal tendon stretch, and lactic acid injection into the superficial epigastric artery, we tested the hypothesis that, in rats with either patent or ligated femoral arteries, activation of pre- and postsynaptic δ-opioid receptors in the dorsal horn attenuated pressor reflex responses to these stimuli. In rats with patent arteries or ligated femoral arteries, [d-Pen2,5]enkephalin (DPDPE), a δ-opioid agonist injected intrathecally (10 μg in 10 μl), significantly attenuated the pressor responses to contraction, stretch, and lactic acid (all P < 0.05). Naltrindole, a δ-opioid receptor antagonist, prevented the attenuation. In contrast, DPDPE did not attenuate the pressor response to capsaicin injection into the superficial epigastric artery in either group of rats (both P > 0.05). Intrathecal injection of saline (10 μl), the vehicle for DPDPE, had no effect on the pressor responses in either group of rats. We conclude that activation of spinal δ-opioid receptors attenuates reflexes evoked by group III afferents in both freely perfused and ligated rats.

The Exercise Pressor Reflex Evoked by Static Contraction is influenced by the Active Skeletal Muscle Mass in Decerebrated Rats

The decerebrated rat is a useful preparation to study the neural mechanisms controlling the circulation during exercise. One of these mechanisms, the exercise pressor reflex, is evoked by statically contracting the hindlimb muscles. However, contraction of only one hindlimb may not always be enough to achieve threshold for activation of the exercise pressor reflex in the decerebrated rat preparation. Here we demonstrate that simultaneous contraction of both hindlimbs evoked a greater pressor response than did contraction of one hindlimb. This was found to be the case when we analyzed the pressor response to contraction as either the area under the curve or the peak (n=4). Static contraction was induced by electrically stimulating the sciatic nerve for thirty seconds at currents that did not activate the axons of group III and IV afferents. When analyzing the area under the curve, we found that simultaneous contraction of both hindlimbs yielded a pressor response averaging 138 ± 64 mmHg seconds, whereas individual contraction of either hindlimb yielded a pressor response averaging either 48 ± 48 or 76 ± 23 mmHg seconds (right limb vs left limb, respectively). When analyzing the peak, simultaneous contraction of both hindlimbs yielded a pressor response averaging 12 ± 4 mmHg, whereas individual contraction of either hindlimb yielded a pressor response averaging 8 ± 6 mmHg or 9 ± 4 mmHg (right limb vs left limb, respectively). Additionally, the sum of the pressor responses to contraction analyzed as either the area under the curve or as the peak appeared to be additive. Our results suggest that the total active muscle mass influences the magnitude of the exercise pressor reflex.Support or Funding InformationSupported by NIH grant P01 HL 134609.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

δ‐Opioid agonist, [D‐Pen2,5]enkephalin (DPDPE) attenuates the exercise pressor reflex in both freely perfused and ligated rats

A reflex, which is elicited by mechanical and metabolic stimuli arising in contracting muscles, is responsible in part for the increases in cardiac output, heart rate, and arterial pressure evoked by exercise. In patients with peripheral artery disease, this reflex is exaggerated and may contribute to their increased risk of adverse cardiovascular events. The afferent arm of this reflex, which is called the exercise pressor reflex (EPR), is comprised of group III and IV afferents. Both μ and δ opioid receptors are expressed on the spinal endings of these afferents which terminate in the dorsal horn of the spinal cord. Evidence suggests that δ‐opioid receptors (DOR) are expressed predominately on the spinal endings of thinly myelinated Aδ fibers (group III), whereas μ‐opioid receptors (MOR) are expressed predominately on the spinal endings of C‐fibers (group IV). Using stimuli that activated group III afferents, namely static contraction, tendon stretch, and lactic acid, we tested the hypothesis that activation of pre and postsynaptic DOR in the dorsal horn attenuated the pressor reflexes in both rats with freely perfused hindlimb muscles and in rats with hindlimb muscles whose arterial supply had been ligated for 72 hours. We activated DOR by intrathecal injection (10μg in 10μl) of the selective δ‐opioid agonist, [DPen2,5] enkephalin (DPDPE).We found that in freely perfused rats, DPDPE significantly attenuated the EPR evoked by static contraction ( n=7; P &lt;0.005) and the muscle mechanoreflex, the latter of which was evoked by stretching the calcaneal tendon (n=9; P &lt;0.05). Likewise, DPDPE attenuated the pressor response to injection of lactic acid into the arterial supply of the hindlimb (n=7; P &lt;0.05). in contrast, DPDPE did no attenuate the pressor response to arterial injection of capsaicin (n=7; P&gt;0.5), which is a more selective stimulus to group IV afferents than it is to group III afferents. In ligated rats, DPDPE attenuated the EPR, the muscle mechanoreflex (both n=6; P&lt;0.05) as well as the pressor response to arterial injection of lactic acid (n=6; P&lt; 0.05). In ligated rats, however, DPDPE did not attenuate the pressor response to capsaicin (n=8; P&gt;0.05). Intrathecal injection of saline (10μl), the vehicle for DPDPE, did not affect the EPR, the muscle mechanoreflex or the pressor responses to lactic acid or capsaicin in either FP or ligated rats. We conclude that activation of δ‐opioid receptors in the dorsal horn attenuates reflexes evoked by group III muscle afferents in both freely perfused and ligated rats.Support or Funding InformationThis work was funded by National Institutes of Health grants R01 AR059397 and P01 HL134609. The NIH is thanked for their support of this work.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Acute Effect of Hyperglycemia on the Exercise Pressor Reflex

Previous work has shown that the exercise pressor reflex is exaggerated in type 2 diabetic rats that present with hyperglycemia. Although it is likely that chronic hyperglycemia plays a role, no studies have isolated the acute effects of high blood glucose levels on this reflex. Therefore, the purpose of the current study was to determine the acute effects of hyperglycemia on the exercise pressor reflex. We first determined the glucose concentration needed to increase local blood glucose level in the hindlimb vasculature to a similar level seen in our type 2 diabetic rats that had an exaggerated exercise pressor reflex. To do this, healthy Sprague‐Dawley rats were infused over 20 min with one of two different concentrations of glucose (125 mg/ml, male n=3 or 250 mg/ml, male n=3) into the arterial supply of the left hindlimb with blood flow to and from the hindlimb restricted. At the same time somatostatin (3.9 ug/100 ul) was infused systemically in order to prevent an endogenous insulin response. Blood glucose was measured every two minutes from both hindlimbs to determine how long it would take to bring blood glucose concentration up to the desired level. We then determined the acute effect of glucose on the pressor and cardioaccelerator responses during static contraction of the hindlimb. The exercise pressor reflex was evoked in healthy, unanesthetized, decerebrated Sprague‐Dawley rats by statically contracting the hindlimb muscle for 30 seconds before and after 15 minutes of either glucose (250 mg/ml) or saline infusion, while mean arterial pressure and heart rate were recorded. We found that infusing 250 mg/ml of glucose significantly raised blood glucose levels to 486 ± 84 mg/dl by the 3rd minute compare to the control leg. However, infusing 125 mg/ml of glucose did not raise blood glucose concentration to 546 ± 33 mg/dl until the 11th minute compare to the control leg (p&lt;0.05). Therefore, we decided to use 250 mg/ml glucose for the exercise pressor experiment. We then found that acutely infusing 250 mg/ml of glucose into the arterial supply of the hindlimb did not significantly affect the pressor (ΔMAP before glucose: 13 ± 0.4 mmHg; after glucose: 12 ± 0.8 mmHg, n=4; before saline: 11 ± 2 mmHg; after saline: 10 ± 2 mmHg, n=3; p&gt;0.05) or cardioaccelerator (ΔHR before glucose: 14 ± 1 bpm; after glucose: 12 ± 2 bpm, n=4; before saline: 14 ± 3 bpm; after saline: 12 ± 4 bpm, n=3; p&gt;0.05) responses to static contraction. We conclude that the acute presence of glucose in the circulation of the hindlimb muscles plays no role in exaggerating the exercise pressor reflex.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Exaggerated Pressor Response to Intermittent Contraction in Type 1 Diabetic Rats

Type 1 diabetes mellitus (T1DM) is associated with an impaired regulation of autonomic and cardiovascular responses during exercise, an effect attributable, in part, to the exercise pressor reflex. Previously, we have found that the pressor responses to both static muscle contraction and to tendon stretch are exaggerated in the early stage of T1DM. However, it is not known whether a similar response is present during dynamic exercise. Moreover, other studies have suggested that endothelial dysfunction manifests early in T1DM, which may impair muscle perfusion during exercise leading to an increased stimulation of the exercise pressor reflex. Therefore, the purpose of this study was to test whether T1DM rats have an exaggerated pressor and an attenuated blood flow response to intermittent contraction. To do this, we measured the exercise pressor reflex in unanesthetized, decerebrated T1DM (Streptozotocin 50mg/kg i.p; STZ: body weight: 328 ± 39g) and healthy (CTL: body weight: 264 ± 17g, n=5) Sprague Dawley rats by intermittently contracting the hindlimb for 30 s while continuously measuring mean arterial pressure (MAP), heart rate (HR) and popliteal arterial blood flow (BF). Popliteal vascular conductance was estimated by dividing popliteal BF by MAP. BF and VC are reported as mean change from baseline.Muscle contraction significantly increased peak MAP (STZ: 32 ± 4 mmHg, n=3; CTL: 17 ± 4 mmHg, n=5, p&lt;0.05) but not HR (STZ: 20 ± 4 mmHg, n=3; CTL: 14 ± 6 mmHg, n=5, p&gt;0.05) to similar developed tensions (p&gt;0.05) in T1DM rats compared to CTL rats. Muscle contraction increased hindlimb BF (STZ: 858 ± 379 μl/min, n=3; CTL: 220 ± 40 μl/min, n=2) and hindlimb vascular conductance (STZ: 7.4 ± 4.1 μl/min/mmHg, n=3; CTL: 2.2 ± 0.3 μl/min/mmHg, n=2) from baseline in STZ and CTL rats, however, this was not significantly different between groups (p&gt;0.05). These findings are consistent with our previous studies that found that early stage T1DM rats had an exaggerated pressor response to static muscle contraction. Furthermore, the finding that blood flow delivery was not impaired in the T1DM rats may suggest that a mismatch between metabolic demand and oxygen delivery is not contributing to the exaggerated response.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.