Publication date: Available online 31 December 2016
Source:Archives of Physical Medicine and Rehabilitation
Author(s): M.F. Reneman, M. Roelofs, H.R. Schiphorst Preuper
ObjectiveTo analyze test-retest reliability and agreement, and to explore safety of Neck Functional Capacity Evaluation tests (Neck-FCE) in patients with chronic multifactorial neck pain.Designtest-retest; 2 FCE sessions were held with a 2 week interval.Settinguniversity based outpatient rehabilitation center.Participantsn=18 participants, 14 females, mean age of 34 years.Interventionsnot applicable.Main Outcome MeasureThe Neck-FCE protocol consists of 6 tests: lifting waist to overhead (kg), two-handed carrying (kg), overhead working (s), bending and overhead reaching (s), and repetitive side reaching (left and right) (s). Intraclass Correlation Coefficients (ICCs) and limits of agreement (LoA). ICC point estimates between 0.75 and 0.90 was considered as good and >0.90 was considered as excellent reliability.ResultsICC point estimates ranged between 0.39 and 0.96. Ratios of the LoA ranged between 32.0% and 56.5%. Mean NRS pain scores in neck and shoulder 24-hours after the test were respectively 6.7 (SD 2.6) and 6.3 (SD 3.0).ConclusionBased on ICC point estimates and 95%CI, it was concluded that that 3 tests had excellent reliability and 3 had poor reliability. LoA were substantial in all 6 tests. Safety was confirmed.
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Κυριακή 1 Ιανουαρίου 2017
Reliability and agreement of Neck Functional Capacity Evaluation tests in patients with chronic multifactorial neck pain
Microcirculatory Assessment of Arterial Below-Knee Stumps: Near-Infrared Spectroscopy vs. Transcutaneous Oxygen Tension. A Preliminary Study in Prosthesis Users
Publication date: Available online 31 December 2016
Source:Archives of Physical Medicine and Rehabilitation
Author(s): Davy Laroche, José-Luis Barnay, Bastien Tourlonias, Cyril Orta, Christine Obert, Jean-Marie Casillas
ObjectivesTo examine metrological properties of near-infrared spectroscopy (NIRS) vs. transcutaneous oxygen tension (TcPO2) for microcirculatory assessment of vascular transtibial stumps at the stabilized period of prosthesis fitting, as a preliminary step before exploring its ability to predict stump healing, considering the previously identified limits of TcPO2 (borderline area between 15 and 35 mmHg).DesignProspective single-centre observational study.SettingUniversity-based rehabilitation center.ParticipantsIndividuals with unilateral transtibial amputation for peripheral artery disease, at the definitive stage of prosthesis fitting, able to perform a two-minute walk test (30).InterventionNot applicable.Main Outcome MeasuresTest-retest, the stump being evaluated in supine and inclined position, first by NIRS (Tissue Saturation Index (TSI), oxy-haemoglobin, deoxy-haemoglobin, total haemoglobin) and second by TcPO2. Subjects carried out a 2-minute walk test and visual analogue scales (wound healing, pain).ResultsFeasibility and tolerance of NIRS were satisfactory. The reliability of NIRS and TcPO2 values was good (ICC>0.7, p<0.05). No significant relationship was found between NIRS and TcPO2. No responsiveness (inclined vs. supine) was reported (p>0.05). Significant relationship between TSI and the 2-minute walk test (r>0.49, p<0.05) was found.ConclusionsNIRS is painless, complication-free and feasible, with good reliability. NIRS evaluate other domain than TcPO2, more linked to metabolic adaptation. Its capacity to predict the stump healing and tolerance to early prosthesis fitting is thus interesting to estimate in future studies.
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Cognitive motor interference on upper extremity motor performance in a robot-assisted planar reaching task among patients with stroke
Publication date: Available online 31 December 2016
Source:Archives of Physical Medicine and Rehabilitation
Author(s): Joon-Ho Shin, Gyulee Park, Duk Youn Cho
ObjectiveTo explore motor performance on two different cognitive tasks during robotic rehabilitation in which motor performance was longitudinally assessed.DesignProspective studySettingRehabilitation hospitalParticipantsPatients with chronic stroke and upper extremity impairment (N=22)InterventionA total of 640 repetitions of robot-assisted planar reaching, five times a week for 4 weeksMain Outcome MeasuresLongitudinal robotic evaluations regarding motor performance included smoothness, mean velocity, path error, and reach error by the type of cognitive task. Dual-task effects (DTE) of motor performance were computed in order to analyze the effect of the cognitive task on dual-task interference.ResultsCognitive task type influenced smoothness (p = 0.006), the DTE of smoothness (p = 0.002), and the DTE of reach error (p = 0.052). Robotic rehabilitation improved smoothness (p = 0.007) and reach error (p = 0.078), while stroke severity affected smoothness (p = 0.01), reach error (p < 0.001), and path error (p = 0.01). Robotic rehabilitation or severity did not affect the DTE of motor performance.ConclusionsThe present results provide evidence for the effect of cognitive-motor interference on upper extremity performance among participants with stroke using a robotic-guided rehabilitation system.
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May the year be brighter than the one gone by; enveloped in goodness, well being, bliss and wealth. Happy New Year!
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182
Reduced compensatory responses to maintain central blood volume during hypovolemic stress in women with vasovagal syncope
Although vasovagal syncope (VVS) is a common clinical condition, the underlying pathophysiology is not fully understood. A decrease in cardiac output has recently been suggested as a factor in orthostatic VVS. The aim was to investigate compensatory mechanisms to maintain central blood volume and venous return during hypovolemic stress in women with VVS. Fourteen VVS women (25.7 ± 5.0 yr) and 15 matched controls (22.8 ± 3.2 yr) were investigated. Single-step and graded lower body negative pressure (LBNP) to presyncope were used to create hypovolemic stress. Peripheral mobilization of venous blood from the arm (capacitance response and net capillary fluid absorption) and lower limb blood pooling (calf capacitance response) were evaluated using a volumetric technique. Cardiovascular responses and plasma norepinephrine (P-NE) were measured. Resting P-NE was elevated in VVS women (P < 0.01). Despite a similar hypovolemic stimulus, the increase in P-NE was blunted (P < 0.01) and the maximal percent increase in total peripheral resistance was reduced (P < 0.05) during graded LBNP in VVS women. The arm capacitance response was slower (P < 0.05) and reduced in VVS women at higher levels of LBNP (P < 0.05). Capillary fluid absorption from extra- to intravascular space was reduced by ~40% in VVS women (P < 0.05). Accordingly, the reduction in cardiac output was more pronounced (P < 0.05). In conclusion, in VVS women, mobilization of peripheral venous blood and net fluid absorption from tissue to blood during hypovolemic stress were decreased partly as a result of an attenuated vasoconstrictor response. This may seriously impede maintenance of cardiac output during hypovolemic stress and could contribute to the pathogenesis of VVS.
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Aerobic system analysis based on oxygen uptake and hip acceleration during random over-ground walking activities
Deteriorated aerobic response to moderate exercise might precede the manifestation of clinical symptoms of noncommunicable diseases. The purpose of the current study was to verify that the use of current wearable technologies for analysis of pulmonary oxygen uptake (Vo2) dynamics during a pseudorandom ternary sequence (PRTS) over-ground walking protocol is a suitable procedure for the investigation of the aerobic response in more realistic settings. A wearable accelerometer located at the hip assessed the magnitude of the input changes delivered to the aerobic system. Eight adults (24 ± 4 yr old, 174 ± 7 cm, and 71.4 ± 7.4 kg) performed two identical PRTS over-ground walking protocols. In addition, they performed on the cycle ergometer two identical pseudorandom binary sequence (PRBS) protocols and one incremental protocol for maximal Vo2 determination. In the frequency domain, mean normalized gain amplitude (MNG in %) quantified Vo2 dynamics. The MNG during PRTS was correlated (r = –0.80, P = 0.01) with the Vo2 time constant () obtained during cycling. The MNG estimated during PRBS was similar to the MNG estimated during PRTS (r = 0.80, P = 0.01). The maximal Vo2 correlated with the MNG obtained during the PRBS (r = 0.79, P = 0.01) and PRTS (r = 0.78, P = 0.02) protocols. In conclusion, PRTS over-ground walking protocol can be used to evaluate the aerobic system dynamics by the simultaneous measurement of Vo2 and hip acceleration. In addition, the aerobic response dynamics from PRBS and PRTS were correlated to maximal Vo2. This study has shown that wearable technologies in combination with assessment of MNG, a novel indicator of system dynamics, open new possibilities to monitor cardiorespiratory health under conditions that better simulate activities of daily living than cardiopulmonary exercise testing performed in a medical environment.
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Metabolic abnormalities and obesitys impact on the risk for developing preeclampsia
Preeclampsia (PE), a hypertensive disorder of pregnancy, is increasing as a major contributor to perinatal and long-term morbidity of mother and offspring. PE is thought to originate from ischemic insults in the placenta driving the release of prohypertensive anti-angiogenic [soluble fms-like tyrosine kinase-1 (sFlt-1)] and proinflammatory [tumor necrosis factor-α (TNF-α)] factors into the maternal circulation. Whereas the increased incidence of PE is hypothesized to be largely due to the obesity pandemic, the mechanisms whereby obesity increases this risk are unknown. The maternal endothelium is targeted by placental and adipose tissue-derived factors like sFlt-1 and TNF-α that promote hypertension during pregnancy, resulting in vascular dysfunction and hypertension. Interestingly, not all obese pregnant women develop PE. Data suggest that obese pregnant women with the greatest metabolic abnormalities have the highest incidence of PE. Identifying obesity-related mechanisms driving hypertension in some obese pregnant women and pathways that protect normotensive obese pregnant women, may uncover novel protocols to treat PE. Metabolic abnormalities, such as increased circulating leptin, glucose, insulin, and lipids, are likely to increase the risk for PE in obese women. It is not only important to understand whether each of these metabolic factors contribute to the increased risk for PE in obesity, but also their cumulative effects. This is particularly relevant to obese pregnant women with gestational diabetes mellitus (GDM) where all of these factors are increased and the risk for PE is highest. It is speculated that these factors potentiate the anti-angiogenic and proinflammatory mechanisms of placental ischemia-induced vascular dysfunction thereby contributing to the increasing incidence of PE.
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Dietary nitrate supplementation and exercise tolerance in patients with heart failure with reduced ejection fraction
Endothelial dysfunction and reduced nitric oxide (NO) signaling are key abnormalities leading to skeletal muscle oxygen delivery-utilization mismatch and poor physical capacity in patients with heart failure with reduced ejection fraction (HFrEF). Oral inorganic nitrate supplementation provides an exogenous source of NO that may enhance locomotor muscle function and oxygenation with consequent improvement in exercise tolerance in HFrEF. Thirteen patients (left ventricular ejection fraction ≤40%) were enrolled in a double-blind, randomized crossover study to receive concentrated nitrate-rich (nitrate) or nitrate-depleted (placebo) beetroot juice for 9 days. Low- and high-intensity constant-load cardiopulmonary exercise tests were performed with noninvasive measurements of central hemodynamics (stroke volume, heart rate, and cardiac output via impedance cardiography), arterial blood pressure, pulmonary oxygen uptake, quadriceps muscle oxygenation (near-infrared spectroscopy), and blood lactate concentration. Ten patients completed the study with no adverse clinical effects. Nitrate-rich supplementation resulted in significantly higher plasma nitrite concentration compared with placebo (240 ± 48 vs. 56 ± 8 nM, respectively; P < 0.05). There was no significant difference in the primary outcome of time to exercise intolerance between nitrate and placebo (495 ± 53 vs. 489 ± 58 s, respectively; P > 0.05). Similarly, there were no significant differences in central hemodynamics, arterial blood pressure, pulmonary oxygen uptake kinetics, skeletal muscle oxygenation, or blood lactate concentration from rest to low- or high-intensity exercise between conditions. Oral inorganic nitrate supplementation with concentrated beetroot juice did not present with beneficial effects on central or peripheral components of the oxygen transport pathway thereby failing to improve exercise tolerance in patients with moderate HFrEF.
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Loss of UCP1 exacerbates Western diet-induced glycemic dysregulation independent of changes in body weight in female mice
We tested the hypothesis that female mice null for uncoupling protein 1 (UCP1) would have increased susceptibility to Western diet-induced "whitening" of brown adipose tissue (AT) and glucose intolerance. Six-week-old C57BL/6J wild-type (WT) and UCP1 knockout (UCP1–/–) mice, housed at 25°C, were randomized to either a control diet (10% kcal from fat) or Western diet (45% kcal from fat and 1% cholesterol) for 28 wk. Loss of UCP1 had no effect on energy intake, energy expenditure, spontaneous physical activity, weight gain, or visceral white AT mass. Despite similar susceptibility to weight gain compared with WT, UCP1–/– exhibited whitening of brown AT evidenced by a striking ~500% increase in mass and appearance of large unilocular adipocytes, increased expression of genes related to inflammation, immune cell infiltration, and endoplasmic reticulum/oxidative stress (P < 0.05), and decreased mitochondrial subunit protein (COX I, II, III, and IV, P < 0.05), all of which were exacerbated by Western diet (P < 0.05). UCP1–/– mice also developed liver steatosis and glucose intolerance, which was worsened by Western diet. Collectively, these findings demonstrate that loss of UCP1 exacerbates Western diet-induced whitening of brown AT, glucose intolerance, and induces liver steatosis. Notably, the adverse metabolic manifestations of UCP1–/– were independent of changes in body weight, visceral adiposity, and energy expenditure. These novel findings uncover a previously unrecognized metabolic protective role of UCP1 that is independent of its already established role in energy homeostasis.
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Intradermal administration of endothelin-1 attenuates endothelium-dependent and -independent cutaneous vasodilation via Rho kinase in young adults
We recently showed that intradermal administration of endothelin-1 diminished endothelium-dependent and -independent cutaneous vasodilation. We evaluated the hypothesis that Rho kinase may be a mediator of this response. We also sought to evaluate if endothelin-1 increases sweating. In 12 adults (25 ± 6 yr), we measured cutaneous vascular conductance (CVC) and sweating during 1) endothelium-dependent vasodilation induced via administration of incremental doses of methacholine (0.25, 5, 100, and 2,000 mM each for 25 min) and 2) endothelium-independent vasodilation induced via administration of 50 mM sodium nitroprusside (20–25 min). Responses were evaluated at four skin sites treated with either 1) lactated Ringer solution (Control), 2) 400 nM endothelin-1, 3) 3 mM HA-1077 (Rho kinase inhibitor), or 4) endothelin-1+HA-1077. Pharmacological agents were intradermally administered via microdialysis. Relative to the Control site, endothelin-1 attenuated endothelium-dependent vasodilation (CVC at 2,000 mM methacholine, 80 ± 10 vs. 56 ± 15%max, P < 0.01); however, this response was not detected when the Rho kinase inhibitor was simultaneously administered (CVC at 2,000 mM methacholine for Rho kinase inhibitor vs. endothelin-1 + Rho kinase inhibitor sites: 73 ± 9 vs. 72 ± 11%max, P > 0.05). Endothelium-independent vasodilation was attenuated by endothelin-1 compared with the Control site (CVC, 92 ± 13 vs. 70 ± 14%max, P < 0.01). However, in the presence of Rho kinase inhibition, endothelin-1 did not affect endothelium-independent vasodilation (CVC at Rho kinase inhibitor vs. endothelin-1+Rho kinase inhibitor sites: 81 ± 9 vs. 86 ± 10%max, P > 0.05). There was no between-site difference in sweating throughout (P > 0.05). We show that in young adults, Rho kinase is an important mediator of the endothelin-1-mediated attenuation of endothelium-dependent and -independent cutaneous vasodilation, and that endothelin-1 does not increase sweating.
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Sympathetic responsiveness is not increased in women with a history of hypertensive pregnancy
Hypertensive pregnancy (HTNP) is a risk factor for future cardiovascular disease. Exaggerated cardiovascular responses to physical stress are also considered an independent marker of cardiovascular disease risk. However, there are limited data regarding the blood pressure (BP) responses to acute stress in women, who have a history of HTNP. Hence, the aim of the study is to compare BP responses to a physical stress in postmenopausal women with a history of HTNP to age- and parity-matched women with a history of normotensive pregnancy (NP). Beat-to-beat BP and heart rate was recorded in 64 postmenopausal women with [age = 58.5 (55.2, 62.2) yr, where values are the median, 25th percentile, and 75th percentile] and without [age = 59.4 (55.9, 62.4) yr] a history of HTNP before and during isometric handgrip (IHG) exercise (30% of maximal voluntary contraction) to fatigue. Muscle metaboreflex was measured during postexercise ischemia following IHG exercise. BP variables increased similarly in response to IHG exercise [systolic: NP = 11.5 (8.9, 17.6) %, HTNP = 11.3 (9.5, 15.9) %; diastolic NP = 11.2 (7.9, 13.3) %, HTNP = 9.5 (7.1, 14.3) %; mean blood pressure: NP = 9.8 (5.0, 13.6) %, and HTNP = 7.2 (4.4, 10.4) %] and postexercise ischemia [systolic: NP = 14.1 (10.3, 23.0) %, HTNP = 15.8 (10.6, 21.4) %; diastolic NP = 12.2 (4.8, 17.0) %, HTNP = 10.4 (5.3, 17.1) %; and mean blood pressure: NP = 11.1 (6.1, 17.9) %, HTNP = 9.4 (2.9, 14.8) %] in both groups. Although having a history of HTNP is associated with future cardiovascular disease risk, results from this study suggest that the risk may not be manifested through altered cardiovascular metaboreflex response to physical stressors.
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Cardiac remodeling and increased central venous pressure underlie elevated stroke volume and cardiac output of seawater-acclimated rainbow trout
Substantial increases in cardiac output (CO), stroke volume (SV), and gastrointestinal blood flow are essential for euryhaline rainbow trout (Oncorhyncus mykiss) osmoregulation in seawater. However, the underlying hemodynamic mechanisms responsible for these changes are unknown. By examining a range of circulatory and cardiac morphological variables of seawater- and freshwater-acclimated rainbow trout, the present study revealed a significantly higher central venous pressure (CVP) in seawater-acclimated trout (~0.09 vs. –0.02 kPa). This serves to increase cardiac end-diastolic volume in seawater and explains the elevations in SV (~0.41 vs. 0.27 ml/kg) and CO (~21.5 vs. 14.2 ml·min–1·kg–1) when compared with trout in freshwater. Furthermore, these hemodynamic modifications coincided with a significant increase in the proportion of compact myocardium, which may be necessary to compensate for the increased wall tension associated with a larger stroke volume. Following a temperature increase from 10 to 16.5°C, both acclimation groups exhibited similar increases in heart rate (Q10 of ~2), but SV tended to decrease in seawater-acclimated trout despite the fact that CVP was maintained in both groups. This resulted in CO of seawater- and freshwater-acclimated trout stabilizing at a similar level after warming (~26 ml·min–1·kg–1). The consistently higher CVP of seawater-acclimated trout suggests that factors other than compromised cardiac filling constrained the SV and CO of these individuals at high temperatures. The present study highlights, for the first time, the complex interacting effects of temperature and water salinity on cardiovascular responses in a euryhaline fish species.
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Metabolic effects of prazosin on skeletal muscle insulin resistance in glucocorticoid-treated male rats
High-dose glucocorticoids (GC) induce skeletal muscle atrophy, insulin resistance, and reduced muscle capillarization. Identification of treatments to prevent or reverse capillary rarefaction and metabolic deterioration caused by prolonged elevations in GCs would be therapeutically beneficial. Chronic administration of prazosin, an α1-adrenergic antagonist, increases skeletal muscle capillarization in healthy rodents and, recently, in a rodent model of elevated GCs and hyperglycemia. The purpose of this study was to determine whether prazosin administration would improve glucose tolerance and insulin sensitivity, through prazosin-mediated sparing of capillary rarefaction, in this rodent model of increased GC exposure. Prazosin was provided in drinking water (50 mg/l) to GC-treated or control rats (400 mg implants of either corticosterone or a wax pellet) for 7 or 14 days (n = 5–14/group). Whole body measures of glucose metabolism were correlated with skeletal muscle capillarization (C:F) at 7 and 14 days in the four groups of rats. Individual C:F was found to be predictive of insulin sensitivity (r2 = 0.4781), but not of glucose tolerance (r2 = 0.1601) and compared with water only, prazosin treatment decreased insulin values during oral glucose challenge by approximately one-third in corticosterone (Cort)-treated animals. Cort treatment, regardless of duration, induced significant glycolytic skeletal muscle atrophy (P < 0.05), decreased IRS-1 protein content (P < 0.05), and caused elevations in FOXO1 protein expression (P < 0.05), which were unaffected with prazosin administration. In summary, it appears that α1-adrenergic antagonism improves Cort-induced skeletal muscle vascular impairments and reduces insulin secretion during an oral glucose tolerance test, but is unable to improve the negative alterations directly affecting the myocyte, including muscle size and muscle signaling protein expression.
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Do high-salt microenvironments drive hypertensive inflammation?
Hypertension is a global epidemic affecting over one billion people worldwide. Despite this, the etiology of most cases of human hypertension remains obscure, and treatment remains suboptimal. Excessive dietary salt and inflammation are known contributors to the pathogenesis of this disease. Recently, it has been recognized that salt can accumulate in the skin and skeletal muscle, producing concentrations of sodium greater than the plasma in hypertensive animals and humans. Such elevated levels of sodium have been shown to alter immune cell function. Here, we propose a model in which tissue salt accumulation causes an immune response leading to renal and vascular inflammation and hypertension.
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Altered muscle satellite cell activation following 16 wk of resistance training in young men
Skeletal muscle satellite cells (SC) play an important role in muscle adaptation. In untrained individuals, SC content and activation status have been observed to increase in response to a single bout of exercise. Muscle fiber characteristics change considerably when resistance exercise is performed chronically, but whether training status affects the activity of SC in response to a single bout of exercise remains unknown. We examined the changes in SC content and activation status following a single bout of resistance exercise, before and following a 16-wk progressive resistance training (RT) program in 14 young (25 ± 3 yr) men. Before and after RT, percutaneous biopsies from the vastus lateralis muscle were taken before a single bout of resistance exercise and after 24 and 72 h of postexercise recovery. Muscle fiber size, capillarization, and SC response were determined by immunohistochemistry. Following RT, there was a greater activation of SC after 24 h in response to a single bout of resistance exercise (Pre, 1.4 ± 0.3; 24 h, 3.1 ± 0.3 Pax7+/MyoD+ cells per 100 fibers) compared with before RT (Pre, 1.4 ± 0.3; 24 h, 2.2 ± 0.3 Pax7+/MyoD+ cells per 100 fibers, P < 0.05); no difference was observed 72 h postexercise. Following 16 wk of RT, MyoD mRNA expression increased from basal to 24 h after the single bout of exercise (P < 0.05); this change was not observed before training. Individual capillary-to-fiber ratio (C/Fi) increased in both type I (1.8 ± 0.3 to 2.0 ± 0.3 C/Fi, P < 0.05) and type II (1.7 ± 0.3 to 2.2 ± 0.3 C/Fi, P < 0.05) fibers in response to RT. After RT, enhanced activation of SC in response to resistance exercise is accompanied by increases in muscle fiber capillarization.
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The protective effect of apolipoprotein in models of trophoblast invasion and preeclampsia
Preeclampsia is a hypertensive disorder of pregnancy. It is associated with abnormal placentation via poor placental invasion of the uterine vasculature by trophoblast cells, leading to poor placental perfusion, oxidative stress, and inflammation, all of which are implicated in its pathogenesis. A dyslipidemia characterized by low plasma levels of high-density lipoproteins (HDL) and elevated triglycerides has been described in preeclampsia. Apolipoprotein A-I (apoA-I), a constituent of HDL is an anti-inflammatory agent. This study investigated whether apoA-I protects against hypertension and adverse placental changes in a proinflammatory cytokine (TNF-α)-induced model of preeclampsia. Further, this study investigated whether apoA-I protects against the inhibitory effect of TNF-α in a human in vitro model of trophoblast invasion. Administration of apoA-I to pregnant mice before infusion with TNF-α resulted in a significant reduction in the cytokine-induced increase in systolic blood pressure. MRI measurement of T2 relaxation, a parameter that is tissue specific and sensitive to physiological changes within tissues, showed a reversal of TNF-α-induced placental changes. Preincubation of endothelial cells with apoA-I protected against the TNF-α-induced inhibition of HTR-8/SVneo (trophoblast) cell integration into endothelial (UtMVEC) networks. These data suggest that a healthy lipid profile may affect pregnancy outcomes by priming endothelial cells in preparation for trophoblast invasion.
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Effect of increased and maintained frequency of speed endurance training on performance and muscle adaptations in runners
The aim of the study was, in runners accustomed to speed endurance training (SET), to examine the effect of increased and maintained frequency of SET on performance and muscular adaptations. After familiarization (FAM) to SET, 18 male (n = 14) and female (n = 4) runners (Vo2max: 57.3 ± 3.4 ml/min; means ± SD) completed 20 sessions of maintained low-frequency (LF; every fourth day; n = 7) or high-frequency (HF; every second day; n = 11) SET. Before FAM as well as before and after an intervention period (INT), subjects completed a series of running tests and a biopsy from m. vastus lateralis was collected. Ten-kilometer performance improved (P < 0.05) ~3.5% during FAM with no further change during INT. Time to exhaustion at 90% vVo2max was 15 and 22% longer (P < 0.05) during FAM and a further 12 and 16% longer (P < 0.05) during INT in HF and LF, respectively. During FAM, muscle expression of NHE1 and maximal activity of citrate synthase (CS) and phosphofructokinase (PFK) increased (P < 0.05), running economy (RE) improved (P < 0.05), and Vo2max was unchanged. During INT, both HF and LF increased (P < 0.05) muscle expression of NKAβ1, whereas maximal activity of CS and PFK, RE, and Vo2max were unchanged. Furthermore, during INT, muscle expression of FXYD1 and SERCA1, and FXYD1 activity increased (P < 0.05) in HF, while muscle expression of SERCA2 decreased (P < 0.05) in LF. Thus increased or maintained frequency of SET leads to further improvements in short-term exercise capacity, but not in 10-km running performance. The better short-term exercise capacity may be associated with elevated expression of muscle proteins related to Na+/K+ transportation and Ca2+ reuptake.
NEW & NOTEWORTHY Ten speed endurance training (SET) sessions improved short-term exercise capacity and 10-km performance, which was followed by further improved short-term exercise capacity, but unchanged 10-km performance after 20 SET sessions performed with either high frequency (4 per 8 days) or continued low frequency (2 per 8 days) in trained runners. The further gain in short-term exercise capacity was associated with changes in muscle expression of proteins of importance for the development of fatigue.
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Flow velocity is relatively uniform in the coronary sinusal venous tree: structure-function relation
The structure and function of coronary venous vessels are different from those of coronary arteries and are much less understood despite the therapeutic significance of coronary sinus interventions. Here we aimed to perform a hemodynamic analysis in the entire coronary sinusal venous tree, which enhances the understanding of coronary venous circulation. A hemodynamic model was developed in the entire coronary sinusal venous tree reconstructed from casts and histological data of five swine hearts. Various morphometric and hemodynamic parameters were determined in each vessel and analyzed in the diameter-defined Strahler system. The findings demonstrate an area preservation between the branches of the coronary venous system that leads to relatively uniform flow velocity in different orders of the venous tree. Pressure and circumferential and wall shear stresses decreased abruptly from the smallest venules toward vessels of order –5 (80.4 ± 39.1 µm) but showed a more modest change toward the coronary sinus. The results suggest that vessels of order –5 denote a hemodynamic transition from the venular bed to the transmural subnetwork. In contrast with the coronary arterial tree, which obeys the minimum energy hypothesis, the coronary sinusal venous system complies with the area-preserving rule for efficient venous return, i.e., da Vinci's rule. The morphometric and hemodynamic model serves as a physiological reference state to test various therapeutic rationales through the venous route.
NEW & NOTEWORTHY A hemodynamic model is developed in the entire coronary sinusal venous tree of the swine heart. A key finding is that the coronary sinusal venous system complies with the area preservation rule for efficient venous return while the coronary arterial tree obeys the minimum energy hypothesis. This model can also serve as a physiological reference state to test various therapeutic rationales through the venous route.
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Resistance training with instability is more effective than resistance training in improving spinal inhibitory mechanisms in Parkinsons disease
This study assessed 1) the effects of 12 wk of resistance training (RT) and resistance training with instability (RTI) on presynaptic inhibition (PSI) and disynaptic reciprocal inhibition (DRI) of patients with Parkinson's disease (PD); 2) the effectiveness of RT and RTI in moving PSI and DRI values of patients toward values of age-matched healthy controls (HC; Z-score analysis); and 3) associations between PSI and DRI changes and clinical outcomes changes previously published. Thirteen patients in RT group, 13 in RTI group, and 11 in a nonexercising control group completed the trial. While RT and RTI groups performed resistance exercises twice a week for 12 wk, only the RTI group used unstable devices. The soleus H reflex was used to evaluate resting PSI and DRI before and after the experimental protocol. The HC (n = 31) was assessed at pretest only. There were significant group x time interactions for PSI (P < 0.0001) and DRI (P < 0.0001). RTI was more effective than RT in increasing the levels of PSI (P = 0.0154) and DRI (P < 0.0001) at posttraining and in moving PSI [confidence interval (CI) 0.1–0.5] and DRI (CI 0.6–1.1) levels to those observed in HC. There was association between DRI and quality of life changes (r = –0.69, P = 0.008) and a strong trend toward association between PSI and postural instability changes (r = 0.60, P = 0.051) after RTI. RTI increased PSI and DRI levels more than RT, reaching the average values of the HC. Thus RTI may cause plastic changes in PSI and DRI pathways that are associated with some PD clinical outcomes.
NEW & NOTEWORTHY Patients with Parkinson's disease (PD) have motor dysfunction. Spinal inhibitory mechanisms are important for modulating both supraspinal motor commands and sensory feedback at the spinal level. Resistance training with instability was more effective than resistance training in increasing the levels of presynaptic inhibition and disynaptic reciprocal inhibition of lower limb at rest of the patients with PD, reaching the average values of the healthy controls.
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Habitual aerobic exercise does not protect against micro- or macrovascular endothelial dysfunction in healthy estrogen-deficient postmenopausal women
Aging causes micro- and macrovascular endothelial dysfunction, as assessed by endothelium-dependent dilation (EDD), which can be prevented and reversed by habitual aerobic exercise (AE) in men. However, in estrogen-deficient postmenopausal women, whole forearm microvascular EDD has not been studied, and a beneficial effect of AE on macrovascular EDD has not been consistently shown. We assessed forearm blood flow in response to brachial artery infusions of acetylcholine (FBFACh), a measure of whole forearm microvascular EDD, and brachial artery flow-mediated dilation (FMD), a measure of macrovascular EDD, in 12 premenopausal sedentary women (Pre-S; 24 ± 1 yr; Vo2max = 37.5 ± 1.6 ml·kg–1·min–1), 25 estrogen-deficient postmenopausal sedentary women (Post-S; 62 ± 1 yr; Vo2max = 24.7 ± 0.9 ml·kg–1·min–1), and 16 estrogen-deficient postmenopausal AE-trained women (Post-AE; 59 ± 1 yr; Vo2max = 40.4 ± 1.4 ml·kg–1·min–1). FBFACh was lower in Post-S and Post-AE compared with Pre-S women (135 ± 9 and 116 ± 17 vs. 193 ± 21 AUC, respectively, both P < 0.008), whereas Post-S and Post-AE women were not different (P = 0.3). Brachial artery FMD was 34% (5.73 ± 0.67%) and 45% (4.79 ± 0.57%) lower in Post-S and Post-AE, respectively, vs. Pre-S women (8.69 ± 0.95%, both P ≤ 0.01), but not different between Post-S and Post-AE women (P = 0.3). Post-AE women had lower circulating C-reactive protein and oxidized low-density lipoprotein compared with Post-S women (0.5 ± 0.1 vs. 1.1 ± 0.2 mg/l and 40 ± 4 vs. 55 ± 3 U/l, respectively, both P = 0.01), but these markers were not correlated to FBFACh (P = 0.3) or brachial artery FMD (P = 0.8). These findings are consistent with the idea that habitual AE does not protect against age/menopause-related whole forearm micro- and macrovascular endothelial dysfunction in healthy nonobese estrogen-deficient postmenopausal women, despite being associated with lower systemic markers of inflammation and oxidative stress.
NEW & NOTEWORTHY This is the first study to demonstrate that habitual aerobic exercise may not protect against age/menopause-related whole forearm microvascular endothelial dysfunction in healthy nonobese estrogen-deficient postmenopausal women, consistent with recent findings regarding macrovascular endothelial function. This is in contrast to what is observed in healthy middle-aged and older aerobic exercise-trained men.
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Intermittent parathyroid hormone administration attenuates endothelial dysfunction in old rats
Aging is an independent risk factor for cardiovascular disease and is characterized by a decline in endothelial function. Parathyroid hormone (PTH) administration has been shown to increase endothelial nitric oxide synthase (eNOS) expression. The purpose of this investigation was to determine the effect of intermittent PTH administration on aortic endothelial function in old rodents. We hypothesized that intermittent PTH administration would improve endothelial function in older rodents. Old (24-mo-old) and young (4-mo-old) Fischer-344 rats were given 10 injections of PTH 1–34 (43 μg·kg–1·day–1) or phosphate-buffered saline (100 μl/day) over 15 days. Endothelium-dependent relaxation of aortic rings in response to acetylcholine (10–9 to 10–5 M) was significantly impaired in old control (OC) compared with young control (YC) as indicated by a reduced area under the curve (AUC, 100 ± 6.28 vs. 54.08 ± 8.3%; P < 0.05) and impaired maximal relaxation (Emax, 70.1 ± 4.48 vs. 92.9 ± 4.38%; P < 0.05). Emax was improved in old animals treated with PTH (OPTH) (OC, 70.1 ± 4.48 vs. OPTH, 85 ± 7.48%; P < 0.05) as well as AUC (OC, 54.08 ± 8.3 vs. OPTH, 82.5 ± 5.7%; P < 0.05) while logEC50 was not different. Endothelial-independent relaxation in response to sodium nitroprusside was not different among groups. Aortic eNOS protein expression was significantly decreased in OC compared with YC (P < 0.05). PTH treatment restored eNOS expression in OPTH animals (P < 0.05). These data suggest that PTH may play a role in attenuating age-related impairments in aortic endothelial function.
NEW & NOTEWORTHY We have demonstrated that intermittent parathyroid hormone administration can rescue age-related vascular dysfunction by improving endothelial-dependent dilation in the aorta of older rodents. This demonstrates a novel potential benefit of parathyroid hormone administration in aging.
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Neuromuscular electrical stimulation prior to presleep protein feeding stimulates the use of protein-derived amino acids for overnight muscle protein synthesis
Short periods of muscle disuse result in substantial skeletal muscle atrophy. Recently, we showed that both neuromuscular electrical stimulation (NMES) as well as presleep dietary protein ingestion represent effective strategies to stimulate muscle protein synthesis rates. In this study, we test our hypothesis that NMES can augment the use of presleep protein-derived amino acids for overnight muscle protein synthesis in older men. Twenty healthy, older [69 ± 1 (SE) yr] men were subjected to 24 h of bed rest, starting at 8:00 AM. In the evening, volunteers were subjected to 70-min 1-legged NMES, while the other leg served as nonstimulated control (CON). Immediately following NMES, 40 g of intrinsically l-[1-13C]-phenylalanine labeled protein was ingested prior to sleep. Blood samples were taken throughout the night, and muscle biopsies were obtained from both legs in the evening and the following morning (8 h after protein ingestion) to assess dietary protein-derived l-[1-13C]-phenylalanine enrichments in myofibrillar protein. Plasma phenylalanine concentrations and plasma l-[1-13C]-phenylalanine enrichments increased significantly following protein ingestion and remained elevated for up to 6 h after protein ingestion (P < 0.05). During overnight sleep, myofibrillar protein-bound l-[1-13C]-phenylalanine enrichments (MPE) increased to a greater extent in the stimulated compared with the control leg (0.0344 ± 0.0019 vs. 0.0297 ± 0.0016 MPE, respectively; P < 0.01), representing 18 ± 6% greater incorporation of presleep protein-derived amino acids in the NMES compared with CON leg. In conclusion, application of NMES prior to presleep protein feeding stimulates the use of dietary protein-derived amino acids for overnight muscle protein synthesis in older men.
NEW & NOTEWORTHY Neuromuscular electrical stimulation (NMES) as well as presleep dietary protein ingestion represent effective strategies to stimulate muscle protein synthesis rates. Here we demonstrate that in older men after a day of bed rest, the application of NMES prior to presleep protein feeding stimulates the use of dietary protein-derived amino acids for overnight muscle protein synthesis by 18% compared with presleep protein feeding only.
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Single passive leg movement-induced hyperemia: a simple vascular function assessment without a chronotropic response
Passive leg movement (PLM)-induced hyperemia is a novel approach to assess vascular function, with a potential clinical role. However, in some instances, the varying chronotropic response induced by PLM has been proposed to be a potentially confounding factor. Therefore, we simplified and modified the PLM model to require just a single PLM (sPLM), an approach that may evoke a peripheral hemodynamic response, allowing a vascular function assessment, but at the same time minimizing central responses. To both characterize and assess the utility of sPLM, in 12 healthy subjects, we measured heart rate (HR), stroke volume, cardiac output (CO), mean arterial pressure (MAP), leg blood flow (LBF), and calculated leg vascular conductance (LVC) during both standard PLM, consisting of passive knee flexion and extension performed at 1 Hz for 60 s, and sPLM, consisting of only a single passive knee flexion and extension over 1 s. During PLM, MAP transiently decreased (5 ± 1 mmHg), whereas both HR and CO increased from baseline (6.0 ± 1.1 beats/min, and 0.8 ± 0.01 l/min, respectively). Following sPLM, MAP fell similarly (5 ± 2 mmHg; P = 0.8), but neither HR nor CO responses were identifiable. The peak LBF and LVC response was similar for PLM (993 ± 189 ml/min; 11.9 ± 1.5 ml·min–1·mmHg–1, respectively) and sPLM (878 ± 119 ml/min; 10.9 ± 1.6 ml·min–1·mmHg–1, respectively). Thus sPLM represents a variant of the PLM approach to assess vascular function that is more easily performed and evokes a peripheral stimulus that induces a significant hyperemia, but does not generate a potentially confounding, chronotropic response, which may make sPLM more useful clinically.
NEW & NOTEWORTHY Using the single passive leg movement (PLM) technique, a variant of the vascular function assessment PLM, we have identified a novel peripheral vascular assessment method that is more easily performed than PLM, which, by not evoking potentially confounding central hemodynamic responses, may be more useful clinically.
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A pilot study examining the impact of exercise training on skeletal muscle genes related to the TLR signaling pathway in older adults following hip fracture recovery
Older adults after hip fracture surgery experience progressive muscle atrophy and weakness, limiting full recovery. Further understanding of the molecular mechanisms in muscle with adaptation to exercise training in this vulnerable population is necessary. Therefore, we conducted a pilot study to investigate the skeletal muscle inflammatory and ceramide biosynthesis gene expression levels associated with the toll-like receptor (TLR) pathway before (Pre) and following a 3-mo multicomponent exercise training program in older adults (3M, 4F; 78.4 ± 13.3 yr; 25.5 ± 2.3 kg/m2) ~4 mo after repair from hip fracture (HipFx). Vastus lateralis biopsies from the surgical limb were obtained before (Pre) and after training. Molecular end points and muscle function data were also compared with matched nonexercise healthy controls (CON). As a follow-up analysis, we evaluated specific sphingolipid pools in HipFx and CON muscle. Following training, quadriceps cross-sectional area, strength, and 6-min walk (6MW) increased in the surgical limb (P < 0.05). Additionally, MYD88, TAK1, NFKB1, IL6, SPT2, and CERS1 gene expression decreased after training (P ≤ 0.05), but some remained elevated above CON levels. Interestingly, MYD88 mRNA was inversely correlated to quadriceps CSA, strength, and 6MW. Finally, muscle dihydroceramides and phosphoceramides in HipFx were lower than CON at Pre (P ≤ 0.05), but after training differences from CON were removed. Together, our pilot data support that exercise training alters skeletal muscle inflammation and ceramide metabolism associated with TLR signaling in older adults recovering from hip fracture surgery and may be related to improvements in muscle function recovery.
NEW & NOTEWORTHY These pilot data demonstrate that 3 mo of exercise training in older adults recovering from hip fracture surgery was able to mitigate skeletal muscle gene expression related to inflammation and ceramide metabolism while also improving surgical limb lean tissue, strength, and physical function.
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Obesity, type 2 diabetes, and impaired insulin-stimulated blood flow: role of skeletal muscle NO synthase and endothelin-1
Increased endothelin-1 (ET-1) and reduced endothelial nitric oxide phosphorylation (peNOS) are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), but studies examining these links in humans are limited. We sought to assess basal and insulin-stimulated endothelial signaling proteins (ET-1 and peNOS) in skeletal muscle from T2D patients. Ten obese T2D [glucose disposal rate (GDR): 6.6 ± 1.6 mg·kg lean body mass (LBM)–1·min–1] and 11 lean insulin-sensitive subjects (Lean GDR: 12.9 ± 1.2 mg·kg LBM–1·min–1) underwent a hyperinsulinemic-euglycemic clamp with vastus lateralis biopsies taken before and 60 min into the clamp. Basal biopsies were also taken in 11 medication-naïve, obese, non-T2D subjects. ET-1, peNOS (Ser1177), and eNOS protein and mRNA were measured from skeletal muscle samples containing native microvessels. Femoral artery blood flow was assessed by duplex Doppler ultrasound. Insulin-stimulated blood flow was reduced in obese T2D (Lean: +50.7 ± 6.5% baseline, T2D: +20.8 ± 5.2% baseline, P < 0.05). peNOS/eNOS content was higher in Lean under basal conditions and, although not increased by insulin, remained higher in Lean during the insulin clamp than in obese T2D (P < 0.05). ET-1 mRNA and peptide were 2.25 ± 0.50- and 1.52 ± 0.11-fold higher in obese T2D compared with Lean at baseline, and ET-1 peptide remained 2.02 ± 1.9-fold elevated in obese T2D after insulin infusion (P < 0.05) but did not increase with insulin in either group (P > 0.05). Obese non-T2D subjects tended to also display elevated basal ET-1 (P = 0.06). In summary, higher basal skeletal muscle expression of ET-1 and reduced peNOS/eNOS may contribute to a reduced insulin-stimulated leg blood flow response in obese T2D patients.
NEW & NOTEWORTHY Although impairments in endothelial signaling are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), human studies examining these links are limited. We provide the first measures of nitric oxide synthase and endothelin-1 expression from skeletal muscle tissue containing native microvessels in individuals with and without T2D before and during insulin stimulation. Higher basal skeletal muscle expression of endothelin-1 and reduced endothelial nitric oxide phosphorylation (peNOS)/eNOS may contribute to reduced insulin-stimulated blood flow in obese T2D patients.
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Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study
Patients with chronic obstructive pulmonary disease (COPD) endure excessive resistive and elastic loads leading to chronic respiratory failure. Oxygen supplementation corrects hypoxemia but is not expected to reduce mechanical loads. Nasal high-flow (NHF) therapy supports breathing by reducing dead space, but it is unclear how it affects mechanical loads of patients with COPD. The objective of this study was to compare the effects of low-flow oxygen and NHF therapy on ventilation and work of breathing (WOB) in patients with COPD and controls during sleep. Patients with COPD (n = 12) and controls (n = 6) were recruited and submitted to polysomnography to measure sleep parameters and ventilation in response to administration of oxygen and NHF. A subset of six patients also had an esophageal catheter inserted for the purpose of measuring WOB. Patients with COPD had similar minute ventilation (Ve) but lower tidal volumes than matched controls. With oxygen, SaO2was increased and Ve was reduced in both controls and patients with COPD, but there was an increase in transcutaneous CO2 levels. NHF produced a greater reduction in Ve and was associated with a reduction in CO2 levels. Although NHF halved WOB, oxygen produced only a minor reduction in this parameter. We conclude that oxygen produced little change in WOB, which was associated with CO2 elevations. On the other hand, NHF produced a large reduction in Ve and WOB with a concomitant decrease in CO2 levels. Our data indicate that NHF improves alveolar ventilation during sleep compared with oxygen and room air in patients with COPD and therefore can decrease their cost of breathing.
NEW & NOTEWORTHY Nasal high-flow (NHF) therapy can support ventilation in patients with chronic obstructive pulmonary disease during sleep by decreasing the work of breathing and improving CO2 levels. On the other hand, oxygen supplementation corrects hypoxemia, but it produces only a minimal reduction in work of breathing and is associated with increased CO2 levels. Therefore, NHF can be a useful method to assist ventilation in patients with increased respiratory mechanical loads.
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Chorangioma (benign capillary hemangioma) of the placenta
2017-01-01T02-26-10Z
Source: Cukurova Medical Journal
Sibel Özler, Efser Öztaş, Başak Gümüş Güler, Dilek Uygur, Nuri Danışman.
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