Forearm Volume Research Articles

GPU-based real-time generation of large ultrasound volumes from freehand 3D sweeps

Abstract In the recent past, 3D ultrasound has been gaining relevance in many biomedical applications. One main limitation, however, is that typical ultrasound volumes are either very poorly resolved or only cover small areas. We have developed a GPU-accelerated method for live fusion of freehand 3D ultrasound sweeps to create one large volume. The method has been implemented in CUDA and is capable of generating an output volume with 0.5 mm resolution in real time while processing more than 45 volumes per second, with more than 300.000 voxels per volume. First experiments indicate that large structures like a whole forearm or high-resolution volumes of smaller structures like the hand can be combined efficiently. It is anticipated that this technology will be helpful in pediatric surgery where X-ray or CT imaging is not always possible.

Limb suction evoked during arterial occlusion causes systemic sympathetic activity in humans

Venous saline infusions in an arterially occluded forearm evokes reflex increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP). We hypothesized that the application of suction to the human limbs would activate this venous distension reflex and raise sympathetic outflow. We placed airtight pressure tanks and applied 100 mmHg negative pressure to an arterially occluded limb (occlusion and suction, O&S) to induce tissue deformation without fluid translocation. BP, heart rate (HR), and MSNA were assessed in 19 healthy subjects during 2 min of arm or leg O&S. Occlusion without suction served as a control. During a separate visit, saline (5% forearm volume) was infused into veins of the arterially occluded arm (n = 13). The O&S increased limb circumference, MSNA burst rate (arm: Δ6.7 ± 0.7; leg: Δ6.8 ± 0.7 bursts/min), and total activity (arm: Δ199 ± 14; leg: Δ172 ± 22 units/min) and BP (arm: Δ4.3 ± 0.3; leg: Δ9.4 ± 1.4 mmHg) from the baseline. The MSNA and BP responses during arm O&S correlated with those during leg O&S. Occlusion alone had no effect on MSNA and BP. MSNA (r = 0.607) responses during arm O&S correlated with those evoked by the saline infusion into the arm. These correlations suggest that sympathetic activation during limb O&S is likely, at least partially, to be evoked via the venous distension reflex. These data suggest that suction of an occluded limb evokes sympathetic activation and that the limb venous distension reflex exists in arms and legs of normal humans.

Agreement Between Dual Energy X-Ray Absorptiometry and Opto-Electronic Volumetry for Measurement of Forearm Volume

Lymphedema is commonly assessed by measuring the increase in volume of the affected region using methods that are not only accurate and sensitive but also applicable for use in clinical practice. Opto-electronic volumetry (Perometer™) is a rapid and convenient technique recommended as a reference method for this purpose, while the use of dual-energy X-ray absorptiometry is becoming more common. We report here a method agreement study between DXA and perometry for the measurement of forearm volume. Perometric measurements were performed on both whole arms, in the horizontal plane, of a group of healthy young participants. Perometric data were obtained for 4 and 5 mm slices between the malleoli to the anticubital fossa crease. The DXA-measured masses (bone mineral, fat, and lean) for the same forearm region were obtained using recently published algorithms. Perometric and DXA-measured volumes were compared using correlation and limits of agreement analysis. DXA-computed volumes were highly and significantly correlated (r=0.986; p<0.0001) with those measured by perometry. The mean bias between the methods was extremely small; 0.7% underestimation by DXA with limits of agreement of 6.3 to -7.7% (DXA-perometry). This study has demonstrated a high degree of concordance between DXA computed limb volumes and those measured by the reference method of perometry. The relatively small limits of agreement suggest that these methods can be used interchangeably.

Intercostal and forearm muscle deoxygenation during respiratory fatigue in patients with heart failure: potential role of a respiratory muscle metaboreflex

The purpose of this study was to determine the effect of respiratory muscle fatigue on intercostal and forearm muscle perfusion and oxygenation in patients with heart failure. Five clinically stable heart failure patients with respiratory muscle weakness (age, 66±12 years; left ventricle ejection fraction, 34±3%) and nine matched healthy controls underwent a respiratory muscle fatigue protocol, breathing against a fixed resistance at 60% of their maximal inspiratory pressure for as long as they could sustain the predetermined inspiratory pressure. Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm. Data were compared by two-way ANOVA and Bonferroni correction. Respiratory fatigue occurred at 5.1±1.3 min in heart failure patients and at 9.3±1.4 min in controls (P<0.05), but perceived effort, changes in heart rate, and in systolic blood pressure were similar between groups (P>0.05). Respiratory fatigue in heart failure reduced intercostal and forearm muscle blood volume (P<0.05) along with decreased tissue oxygenation both in intercostal (heart failure, -2.6±1.6%; controls, +1.6±0.5%; P<0.05) and in forearm muscles (heart failure, -4.5±0.5%; controls, +0.5±0.8%; P<0.05). These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.

Sex and vasodilator responses to hypoxia at rest and during exercise

In humans, β-adrenergic receptor activation causes a substantial portion of hypoxic vasodilation in skeletal muscle at rest and during forearm exercise. Recent evidence suggests that β-adrenergic receptors are either more sensitive or upregulated in young women vs. men. Therefore, we examined whether sex influences hypoxic vasodilation in 31 young subjects (15 women/16 men; 26 ± 1 yr). We also examined whether potential sex-related differences existed in a group of older adults (6 women/5 men; 61 ± 2 yr). All subjects performed forearm exercise at 10 and 20% of maximum under normoxic and hypoxic [80% arterial O2 saturation (So2)] conditions. Forearm vascular conductance (FVC; ml · min(-1) · 100 mmHg(-1)) was calculated from blood flow (ml/min) and blood pressure (mmHg). At rest, young women demonstrated a greater vasodilator response to hypoxia compared with men (39 ± 12 vs. 13 ± 6%, P < 0.05). The absolute compensatory vasodilator response (hypoxic FVC-normoxic FVC) during exercise was similar between sexes, but the relative change was greater in young women at 10% (28 ± 5 vs. 17 ± 3%, P < 0.05) and 20% exercise (29 ± 4% vs. 15 ± 3%, P < 0.01). Additionally, the absolute changes in vasodilation after normalizing the response to forearm volume or workload were greater in young women during exercise (P < 0.05). Interestingly, the compensatory vasodilator responses between older women and men were similar at 10 and 20% exercise, regardless of whether the response is expressed as absolute, relative, or absolute change normalized for forearm volume or workload (P = 0.054-0.97). Our data suggest that the compensatory vasodilator response to hypoxic exercise is greater in young women compared with men. However, sex-specific differences appear to be lost with aging.

Endogenous estrogen enhances brachial blood conductance during dynamic handgrip in young healthy and metabolic syndrome women

Fadel et al. (2004) reported that in women, estrogen can attenuate sympathetic vasoconstriction as seen in postmenopausal women given estrogen treatment and increased vascular conductance. We hypothesize that women during the low estrogen phase of menses with metabolic syndrome (MetS) have an attenuated brachial conductance compared to normal controls. Participants were tested during the early menses (low estrogen, low progesterone) and the proliferative phase (high estrogen, low progesterone). Participants engaged in dynamic handgrip exercise (30 contactions/min) with a ramped increase in workload (0.5kg resistance/min) until task failure. Vascular velocity and diameter were measured during exercise in the brachial artery by Doppler ultrasound; heart rate and blood pressure were repeatedly recorded. The data demonstrate that MetS (25.3 years +1.58) have an attenuated conductance response (MetS 4.78×10^−3+0.7×10^−3 ml/min/mmHg/L, n=5) vs Control 9.4×10^−3+0.96 ml/min/mmHg/L, n=8)per forearm volume at high intensities(3kg) during early menses. During the proliferaive phase the MetS group increased conductance (6.6×10^−3+0.53×10^−3 mL/min/mmHg/L) at high intensity. Thus metabolically compromised women have reduced vascular conductance which is improved by estrogen. Supported by NM‐INBRE P20RR016480, P20GM103451

Role of Endogenous Vascular Endothelial Growth Factor in Endothelium-Dependent Vasodilation in Humans

Angiogenesis inhibitors have remarkably improved the outcome of patients with several types of cancer. Hypertension is the most reported side effect of angiogenesis inhibitors interfering with vascular endothelial growth factor signaling. In this study, we test the hypothesis that circulating vascular endothelial growth factor at physiological concentrations is essential to preserve normal endothelial control of vasomotor tone. In 7 healthy male volunteers, infusion of bevacizumab (monoclonal vascular endothelial growth factor antibody) into the brachial artery for 15 minutes (144 μg/dL forearm volume per minute) did not affect forearm vasodilator tone as measured with venous occlusion strain gauge plethysmography. In a separate group of 12 male volunteers, a similar bevacizumab infusion reduced the vasodilator response to 2 dosages of acetylcholine from (mean ± SE) 440 ± 157% and 926 ± 252% to 169 ± 40% and 612 ± 154% (P<0.05). Finally, in a third group of 12 volunteers, bevacizumab did not alter the percentage increase in forearm blood flow during infusion of sodium nitroprusside at dosages equipotent to acetylcholine. Bevacizumab acutely and specifically reduced endothelium-mediated vasodilation at local concentrations that resemble plasma concentrations after systemic exposure to bevacizumab. This observation suggests a physiological role for vascular endothelial growth factor in maintaining normal endothelial control of vasomotor tone. The role of the endothelium in the mechanism of bevacizumab-induced hypertension deserves further exploration.

Abstract 613: Interactive Effect of Ace Inhibition and DPP4 Inhibition on Substance P-Stimulated T-PA Release

Dipeptidyl peptidase 4 (DPP4) inhibitors improve glycemic control in patients with T2DM by preventing the degradation of the incretin hormones. DPP4 inhibition prevents the degradation of other peptides with a penultimate proline or alanine, including the vasodilator substance P and the metabolite of bradykinin formed by its cleavage by aminopeptidase P. Substance P and bradykinin are normally inactivated by ACE. This study tested the hypothesis that during ACE inhibition, DPP4 inhibition would potentiate the effects of substance P. Ten healthy, lean (BMI&lt;30 kg/m 2 ) subjects, age 24-60 years of old (2 Black, 8 White, 6 Female) participated in this randomized, double-blinded, placebo-controlled crossover study. On separate study days separated by at least one week, Subjects received sitagliptin 200 mg po or matching placebo. Substance P (2, 4, 8 pmol/min) and bradykinin (25, 50, 100 ng/min) were given via the brachial artery before and after administration of intra-arterial enalaprilat (0.33 mcg/min/100mL forearm volume). Enalaprilat potentiated the FBF and tissue plasminogen activator (t-PA) responses to bradykinin and there was no effect of sitagliptin (Figure). Neither ACE inhibition nor DPP4 inhibition altered the FBF flow response to substance P. In contrast, there was an interactive effect of ACE inhibition and DPP4 inhibition on t-PA release in response to substance P (p=0.026).

Limb venous distension evokes sympathetic activation via stimulation of the limb afferents in humans

We have recently shown that a saline infusion in the veins of an arterially occluded human forearm evokes a systemic response with increases in muscle sympathetic nerve activity (MSNA) and blood pressure. In this report, we examined whether this response was a reflex that was due to venous distension. Blood pressure (Finometer), heart rate, and MSNA (microneurography) were assessed in 14 young healthy subjects. In the saline trial (n = 14), 5% forearm volume normal saline was infused in an arterially occluded arm. To block afferents in the limb, 90 mg of lidocaine were added to the same volume of saline in six subjects during a separate visit. To examine whether interstitial perfusion of normal saline alone induced the responses, the same volume of albumin solution (5% concentration) was infused in 11 subjects in separate studies. Lidocaine abolished the MSNA and blood pressure responses seen with saline infusion. Moreover, compared with the saline infusion, an albumin infusion induced a larger (MSNA: Δ14.3 ± 2.7 vs. Δ8.5 ± 1.3 bursts/min, P < 0.01) and more sustained MSNA and blood pressure responses. These data suggest that venous distension activates afferent nerves and evokes a powerful systemic sympathoexcitatory reflex. We posit that the venous distension plays an important role in evoking the autonomic adjustments seen with postural stress in human subjects.

Limb-specific training affects exercise hyperemia but not sympathetic vasoconstriction

This study used cross-sectional and longitudinal training research designs to determine if (a) exercise hyperemia is enhanced in exercise-trained forearms and (b) sympathetic vasoconstriction of the trained forearm is attenuated (sympatholysis) during handgrip exercise. In the cross-sectional comparison, 10 rock climbers, 10 runners, 10 controls participated while the longitudinal training study examined vascular responsiveness in six untrained men before and after 6weeks of handgrip training. Mean blood velocity, brachial artery diameter, heart rate, and systemic blood pressure were measured at rest, during a cold pressor test (CPT), dynamic handgrip exercise at 30% MVC with and without CPT, and during reactive hyperemia. During the resting CPT, forearm blood flow (FBF) decreased less (P<0.05) in runners than in climbers, the decline being -6.30+30.05 and -34.3+20.54 during the last minute, respectively. During handgrip exercise, FBF and vascular conductance (VC) increased more (P<0.05) in climbers than in runners and controls, the latter reaching 3.98+1.11, 2.22+0.88, and 2.75+1.06 mlmin(-1)mmHg(-1), respectively. When a CPT was added during handgrip exercise, the reduction in FBF and VC was not different between the groups. Handgrip training increased (P < 0.05) forearm volume (5 + 3%) and MVC (25 + 29%), but did not affect FBF or VC during a CPT, with or without exercise. These data suggest that arm-trained athletes have greater exercise hyperemia. However, this training effect is not explained by sympatholysis and is not evident after 6weeks of handgrip training in previously untrained subjects.

Abstract 8302: Lidocaine Abolishes the Sympathetic and Blood Pressure Responses in Limb Venous Distension Reflex

Introduction- We have recently shown that saline infusion into the veins of an arterially occluded human forearm evokes a systemic response with an increase in muscle sympathetic nerve activity (MSNA) and blood pressure (BP). Hypothesis- Limb veins distension per se activates afferent nerves within (or close to) the vessel wall, and evokes a systemic sympathoexcitatory reflex. Methods- Thus, we examined MSNA and BP responses as albumin was infused into the venous circulation of an arterially occluded forearm. These MSNA and BP responses were compared with those seen with a saline infusion. Albumin preferentially remains within the vascular space whereas saline distributes within the entire limb extracellular space. BP (Finometer), heart rate, and MSNA (microneurography) were assessed in 14 young healthy subjects on 3 separate visits. In the saline trial, 5% forearm volume saline was infused into an arterially occluded arm. In the albumin trial (n=11), the same volume of albumin solution (5% concentration) was infused. In separate studies, 90 mg of lidocaine was added to the saline infusion (n=6). Results- MSNA and mean BP rose towards to the end of infusion in both saline and albumin trials. A larger (i.e. the peak response at the end of infusion: delta 14.3±2.7 vs. delta 8.5±1.3 bursts/min, P &lt;0.01) and a sustained (i.e. the 30-60 sec of post infusion: delta 15.0±3.0 vs. delta 5.9±2.4 bursts/min, P &lt;0.05) MSNA response was noted with albumin infusion as compared to saline infusion. The BP response with albumin infusion was also greater and sustained than saline infusion (all P &lt;0.05). The 90 mg of lidocaine added to the saline infusion abolished &gt;90% of the MSNA and BP responses. Discussion and Conclusion- These data suggest that vein distension is crucial to evoking the response seen. The lidocaine trial confirms that this venous distension evokes an autonomic reflex. We suggest that venous distension importantly contributes to autonomic and cardiovascular control in humans.

Perspective in comparisons of skin versus muscle blood flow

Letters to the EditorPerspective in comparisons of skin versus muscle blood flowGeorge BrengelmannGeorge BrengelmannDepartment of Physiology and Biophysics, University of Washington, Seattle, WashingtonPublished Online:01 Oct 2011https://doi.org/10.1152/japplphysiol.00910.2011MoreSectionsPDF (29 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: On grounds of their observations of elevated muscle blood flow in heated muscle, Heinonen et al. (2) call for reconsideration of how cardiac output is apportioned in hyperthermic humans. I hope those doing the reconsidering will bear in mind that venous occlusion plethysmography (VOP), the basis of our quantitative understanding of cutaneous blood flow, records volume accumulation in a limb during venous occlusion in terms of milliliters per minute per 100 milliliters of limb, whereas muscle blood flow (MBF) is expressed as milliliters per minute per 100 milliliters of muscle.How then to compare data from Heinonen et al. (2) for muscle at 37°C with, say, Barcroft and Edholm's (1) classical VOP data? For forearm skin temperatures (Tsk) of 35 and 38°C, blood flow in the forearm (FBF) was 4 and 7 ml·min−1·100 ml−1, respectively. For 37°C, we might interpolate 5 ml·min−1·100 ml−1; at first glance, a level 2.5 times Heinonen et al.'s MBF of ∼2 ml·min−1·100 ml−1.But, if FBF increased from, say 2 to 5 ml·min−1·100 ml−1 with Tsk 37°C and constant MBF, then the 5 ml/min rate comprises a steady 2 ml/min in the proportion of the forearm that is muscle and some higher value in the fraction that is skin. If the proportions were 80% muscle and 20% skin, we have 5 = 0.8 times 2 plus 0.2 times x, from which x = 17 ml·min−1·100 ml−1 of skin (SkBF). Even allowing a doubling of MBF, 5 = 0.8 *4 plus 0.2 times x, and SkBF =9 ml·min−1·100 ml−1.Estimates of relative skin volume vary. For the forearm it may be as low as 10% (doubling the above estimation of SkBF). Even at the conservative 20% estimate, though, the responsiveness of cutaneous vasculature smooth muscle to local temperature stands out as greatly exceeding that of the vasculature of skeletal muscle.Moreover, consider the full potential for SkBF revealed at the extreme that occurs with local Tsk at 42°C. FBF in different individuals reached maxima from 16 to 38 ml·min−1·100 ml−1 of forearm in a study of the reproducibility of this response (3). These levels, multiplied by the inverse of the skin:forearm volume fraction are the basis of estimates of the potential fraction of cardiac output taken up by the skin mentioned by Heinonen et al. (2). They highlight the great difference in sensitivity to local temperature in the vasculatures of skin and muscle. Even in a study (4) in which diathermy elevated temperature to 42°C, MBF was not elevated above baselines similar to levels reported by Heinonen et al. (higher levels were reported for higher temperatures, but this is the range in which thermal injury is expected).In conclusion, reconsideration of how cardiac output is distributed in hyperthermic humans is undoubtedly a valuable endeavor but one in which the different ways that the data are expressed need to be kept in mind.DISCLOSURESNo conflicts of interest, financial or otherwise, are declared by the author.REFERENCES1. Barcroft H , Edholm OG. Temperature and blood flow in the human forearm. J Physiol 104: 366–376, 1946.Crossref | ISI | Google Scholar2. Heinonen I , Brothers RM , Kemppainen J , Knuuti J , Kalliokoski KK , Crandall CG. Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow. J Appl Physiol 111: 818–824, 2011.Link | ISI | Google Scholar3. Savage MV , Brengelmann GL. Reproducibility of the vascular response to heating in human skin. J Appl Physiol 76: 1759–1763, 1994.Link | ISI | Google Scholar4. Sekins KM , Lehmann JF , Esselman P , Dundore D , Emery AF , deLateur BJ , Nelp WB. Local muscle blood flow and temperature responses to 915mhz diathermy as simultaneously measured and numerically predicted. Arch Phys Med Rehabil 65: 1–7, 1984.ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: G. Brengelmann, Professor Emeritus, Mail Stop 357290, Dept. of Physiology and Biophysics, Univ. of Washington, Seattle, WA 98105 (e-mail: [email protected]washington.edu). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationRelated ArticlesReply to Brengelmann 01 Oct 2011Journal of Applied PhysiologyCited BySkin blood flow measurements during heat stress: technical and analytical considerationsGeorgia K. Chaseling, Craig G. Crandall, and Daniel Gagnon23 December 2019 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 318, No. 1Circulation30 October 2018 More from this issue > Volume 111Issue 4October 2011Pages 1225-1225 Copyright & PermissionsCopyright © 2011 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00910.2011PubMed22566689History Published online 1 October 2011 Published in print 1 October 2011 Metrics

Sympathetic and cardiovascular responses to venous distension in an occluded limb

We recently showed that a fixed volume (i.e., 40 ml) of saline infused into the venous circulation of an arterially occluded vascular bed increases muscle sympathetic nerve activity (MSNA) and blood pressure. In the present report, we hypothesized that the volume and rate of infusion would influence the magnitude of the sympathetic response. Blood pressure, heart rate, and MSNA were assessed in 13 young healthy subjects during forearm saline infusions (arrested circulation). The effects of different volumes of saline (i.e., 2%, 3%, 4%, or 5% forearm volume at 30 ml/min) and different rates of infusion (i.e., 5% forearm volume at 10, 20, or 30 ml/min) were evaluated. MSNA and blood pressure responses were linked with the infusion volume. Infusion of 5% of forearm volume evoked greater MSNA responses than did infusion of 2% of forearm volume (Δ11.6 ± 1.9 vs. Δ3.1 ± 1.8 bursts/min and Δ332 ± 105 vs. Δ38 ± 32 units/min, all P < 0.05). Moreover, greater MSNA responses were evoked by saline infusion at 30 ml/min than 10 ml/min (P < 0.05). Sonographic measurements confirmed that the saline infusions induced forearm venous distension. The results suggest that volume and rate of saline infusion are important factors in evoking sympathetic activation. We postulate that venous distension contributes to cardiovascular autonomic adjustment in humans.

Long-term Follow-up of Vascular Reconstructions after Supracondylar Humerus Fracture with Vascular Lesion in Childhood

Introduction Supracondylar humerus fractures in childhood present with a pulseless but well-perfused hand in 2.6% of cases and with limb-threatening ischaemia in <1%. Conservative treatment is widely used in non-limb-threatening ischaemia, in particular if the child is very young (<2.5 years). It has been sufficiently proven that conservative treatment may retard growth. The aim of our study was to determine long-term patency rates after surgical reconstruction and growth impairment, if any, after surgical vascular reconstruction. Patients and methods Between June 1990 and June 2004, 12 children (mean age 6.6 years, eight boys and four girls) with supracondylar fracture with vascular lesions underwent surgical reconstruction at the Department of Vascular Surgery at the University Hospital, Graz. Patient files were reviewed retrospectively. All patients were recalled for physical (forearm length and volume) and ultrasonographic examinations (forearm blood flow) in 2005 and for ultrasonographic examinations (reconstructed vascular area) in 2011, with a final mean follow-up time of 14.0 years (range 6.8–20.9 years). Results Twelve patients, 10 of whom had undergone growth measurements in 2005, were available for the latter examination. All were doing well, with patent vascular reconstructions. Seven reconstructed brachial arteries were enlarged, two of which with intramural calcifications, four did not show abnormalities and one presented with 45% thinning. There were no differences between affected and healthy forearms concerning volume, length and blood flow. Conclusions Our data emphasise that surgical reconstruction is effective in terms of blood supply and growth. In cases with interposition of greater saphenous vein or venous patch plasty, we found a high risk for development of enlargements. We suggest that these patients be followed periodically, with ultrasound studies, to detect aneurysms and/or thrombotic changes as early as possible.

Endurance time of grip-force as a function of grip-span, posture and anthropometric variables

The time to volitional exhaustion (endurance time) for sustained contractions is considered as a valid parameter to quantify fatigue and to determine the required rest pauses between two successive contractions. In this study, the effects of grip-span, shoulder posture and anthropometric characteristics on endurance time of grip-force during sustained 30% of maximal voluntary grip-force were investigated. Both subjective and objective measures of fatigue were used in determining the endurance times. Twelve male subjects performed sustained isometric handgrip contractions using a handgrip dynamometer at the combinations of three different grip span settings and two shoulder postures. The investigated three grip spans were the optimal, 2 cm narrower than the optimal, and 2 cm wider than the optimal. The investigated two shoulder postures were neutral and 25° flexion. The outcome measures were: endurance time, surface electromyography of related forearm muscles, heart rate, blood pressure, and ratings of perceived discomfort/pain. The results indicate that the endurance time decreases significantly as the grip span deviates from the optimal in both directions. On the other hand, the considered shoulder postures did not have a significant effect on the endurance time. Further analysis indicated a significant negative correlation between endurance time and rest pause and a marginal positive correlation between maximum voluntary grip-force and rest pause. Body mass index, and volume of forearm and hand had also significant negative correlation with endurance time. The comparisons are made with a number of existing endurance models and the impact of findings are discussed. Relevance to industry In accurate establishment of the time standards, muscular fatigue allowances need to be taken into account. The endurance time for sustained isometric contractions is correlated with the required rest allowances (pauses) for intermittent static contractions; and therefore, required muscular fatigue allowances can be estimated from the endurance times.

Exercise-mediated changes in conduit artery wall thickness in humans: role of shear stress

Episodic increases in shear stress have been proposed as a mechanism that induces training-induced adaptation in arterial wall remodeling in humans. To address this hypothesis in humans, we examined bilateral brachial artery wall thickness using high-resolution ultrasound in healthy men across an 8-wk period of bilateral handgrip training. Unilaterally, shear rate was attenuated by cuff inflation around the forearm to 60 mmHg. Grip strength, forearm volume, and girth improved similarly between the limbs. Acute bouts of handgrip exercise increased shear rate (P < 0.005) in the noncuffed limb, whereas cuff inflation successfully decreased exercise-induced increases in shear. Brachial blood pressure responses similarly increased during exercise in both the cuffed and noncuffed limbs. Handgrip training had no effect on baseline brachial artery diameter, blood flow, or shear rate but significantly decreased brachial artery wall thickness after 6 and 8 wk (ANOVA, P < 0.001) and wall-to-lumen ratio after week 8 (ANOVA, P = 0.005). The magnitude of decrease in brachial artery wall thickness and wall-to-lumen ratio after exercise training was similar in the noncuffed and cuffed arms. These results suggest that exercise-induced changes in shear rate are not obligatory for arterial wall remodeling during a period of 8 wk of exercise training in healthy humans.

Noninvasive imaging of human skin hemodynamics using a digital red-green-blue camera

In order to visualize human skin hemodynamics, we investigated a method that is specifically developed for the visualization of concentrations of oxygenated blood, deoxygenated blood, and melanin in skin tissue from digital RGB color images. Images of total blood concentration and oxygen saturation can also be reconstructed from the results of oxygenated and deoxygenated blood. Experiments using tissue-like agar gel phantoms demonstrated the ability of the developed method to quantitatively visualize the transition from an oxygenated blood to a deoxygenated blood in dermis. In vivo imaging of the chromophore concentrations and tissue oxygen saturation in the skin of the human hand are performed for 14 subjects during upper limb occlusion at 50 and 250 mm Hg. The response of the total blood concentration in the skin acquired by this method and forearm volume changes obtained from the conventional strain-gauge plethysmograph were comparable during the upper arm occlusion at pressures of both 50 and 250 mm Hg. The results presented in the present paper indicate the possibility of visualizing the hemodynamics of subsurface skin tissue.

Free Fatty Acids Induce Insulin Resistance in Both Cardiac and Skeletal Muscle Microvasculature in Humans

Insulin recruits microvasculature in both cardiac and skeletal muscle, which increases the endothelial exchange surface area. Plasma concentrations of free fatty acids (FFAs) are elevated in patients with diabetes, which impairs insulin-mediated skeletal muscle microvascular recruitment. The objective of the study was to examine whether elevated FFAs likewise cause insulin resistance in cardiac muscle microvasculature. The study was conducted at the General Clinical Research Center at the University of Virginia. Twenty-two healthy, young adults were studied twice in random order after an overnight fast. Each subject received a 5-h systemic infusion of either saline or Intralipid/heparin with a 1 mU/min · kg euglycemic insulin clamp superimposed for the last 2 h. Cardiac and forearm skeletal muscle microvascular blood volume (MBV) and flow velocity were measured and microvascular blood flow (MBF) calculated before and at the end of the insulin infusion. Insulin significantly increased MBV and MBF in both cardiac (P < 0.0001 for both) and skeletal (P = 0.008 and < 0.03, respectively) muscle. Microvascular flow velocity increased slightly but significantly in the skeletal (P = 0.04) but not in cardiac muscle. Lipid infusion lowered insulin-stimulated whole-body glucose disposal and abolished insulin-mediated increases in MBV and MBF in both cardiac and skeletal muscle. Whole-body insulin sensitivity predicted skeletal but not cardiac muscle microvascular responses to insulin. Insulin even decreased skeletal muscle MBV during lipid infusion in subjects who were moderately sensitive to insulin metabolically. In conclusion, high plasma concentrations of FFAs cause insulin resistance in cardiac as well as skeletal muscle microvasculature in healthy humans. This may contribute to the association of cardiac complications with metabolic insulin resistance in diabetes.

Alpha‐receptor blockade improves muscle perfusion and glucose uptake in heart failure

Alpha-adrenergic receptor-mediated vasoconstriction might underlie the insulin resistance seen in conditions associated with increased sympathetic tone, like chronic heart failure (CHF). Alpha-adrenergic receptor blockade by phentolamine could improve forearm blood flow (FBF) and forearm glucose uptake (FGU) in CHF patients. In 8 CHF patients and in 12 healthy volunteers, FBF (plethysmography) and FGU were measured in both forearms during a 150 min hyperinsulinaemic euglycaemic clamp procedure. During the final 30 min of the clamp, phentolamine was infused into one arm (experimental arm) at a dose of 5.0 μg; min(-1) dL(-1) of forearm volume. Insulin infusion (t = 0-120 min) increased FGU in the two groups, without affecting FBF. In the CHF group, α-adrenergic receptor blockade by phentolamine (t = 120-150 min) further increased FGU in the experimental arm from 3.0 ± 0.7 to 5.0 ± 0.9 μmol min(-1) dL(-1) (P = 0.03). Forearm glucose uptake in the contralateral forearm remained unchanged. In the control group, phentolamine infusion did not increase FGU in the experimental forearm. The increase in blood flow in response to phentolamine was similar in both groups (CHF: 2.1 ± 0.3-7.5 ± 1.7 mL min(-1) dL(-1), P < 0.001; controls 1.5 ± 0.2-5.5 ± 0.8 mL min(-1) dL(-1), P < 0.001 for both, CHF vs. control, P = 0.2). Phentolamine did not affect FBF in the control arm in either group. Alpha-adrenergic receptor blockade improves FGU in CHF patients. As the increase in FBF is similar in controls and CHF patients, this might be explained by an improved glucose-extraction capacity in CHF patients.

Mechanisms of strength gain in a handgrip exercise programme in rheumatoid arthritis

In a progressive resistive strengthening programme, healthy individuals gain strength initially through neural adaptation followed by increases in muscle mass. Programmes are designed to maximise these responses. The physiological mechanisms of strength gain in RA are unknown, but their identification will help to develop more effective exercise programmes. The aim of this study was to investigate the responses to a 12-week isometric handgrip strengthening programme in female subjects with RA. Fourteen right-handed female subjects with RA and 14 age-matched female controls participated in a 12-week right handgrip strengthening programme. Maximum grip strength (MGS) and disease activity were measured serially over 12 weeks. Forearm muscle volume was measured using MRI at baseline and 12 weeks. Significant gains in right handgrip strength were noted in both groups, the gains being most marked in those with RA: mean (SD; range) MGS (mmHg) in RA group at baseline 105.1 (48.1; 34-108) and 174.8 (76.4; 50-340) at 12 weeks. Mean (SD; range) MGS in control group at baseline 311.7 (49.6; 220-370) and 357.0 (67.1; 250-540) at 12 weeks. Significant increases in forearm muscle volume occurred in the controls, correlating with gains in strength. No such changes were noted in the RA group, indicating that improvements were solely related to neural adaptation. Response to strength training in RA differs from those of healthy individuals. Significant gains in strength in individuals with RA can occur due to neural adaptation without gains in muscle mass during a strengthening programme. This has implications for the design of rehabilitation programmes for such subjects.