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1 ty contractile exercise (25% and 80% maximal handgrip).
2 reased within 1 to 2 seconds of the onset of handgrip.
3 d all of the vasodilatation to contralateral handgrip.
4 ed by damage in brain areas activated during handgrip.
5 one (-54 +/- 11 ms), and also with PS during handgrip (+10 +/- 10 ms) compared with PS alone (-74 +/-
6 vascular resistance increases (basal versus handgrip, 17 +/- 1 versus 26 +/- 2 U; P = .01) in respon
7 l cortical vascular resistance (basal versus handgrip, 18 +/- 1 versus 25 +/- 3 U; P = .002); and (4)
8 e (BP; Finapres) were measured during static handgrip (20 s) at 10% and 70% of maximum voluntary cont
10 l cortical vascular resistance (basal versus handgrip, 20 +/- 1 versus 25 +/- 2 U; P = .04); (3) the
11 er post-flight in all subjects before static handgrip (26 +/- 4 post- vs. 15 +/- 4 bursts min(-1) pre
12 pared with metoprolol and placebo (isometric handgrip -3.5 U for carvedilol versus -1.2 U for metopro
15 y decrease in renal blood flow (basal versus handgrip, 4.2 +/- 0.2 versus 3.5 +/- 0.3 mL.min-1.g-1; P
16 cortical blood flow decreases (basal versus handgrip, 4.4 +/- 0.1 versus 3.5 +/- 0.1 mL.min-1.g-1; P
21 e subjects, vasomotor responses to isometric handgrip and cold pressor test did not differ between tr
22 m vascular resistance responses to isometric handgrip and cold pressor test were determined by plethy
23 55.3%), we compared the responses to dynamic handgrip and during a 3-minute period of posthandgrip re
28 limb function and increased activations with handgrip and median nerve stimulation, but reduced activ
29 ty and blood pressure responses to fatiguing handgrip and post-exercise circulatory occlusion were si
30 he left primary motor cortex leg area during handgrip and the left primary sensory cortex face area d
31 al activation in response to right-sided (i) handgrip; and (ii) median and tibial nerve stimulation w
32 patient (I.G.) was quite unable to open her handgrip appropriately when directly reaching out to pic
33 unctional composite scores: muscle strength (handgrip, arm, and leg) and mobility (timed-up-and-go, c
35 thy volunteers performed fatiguing isometric handgrip before and after a local infusion of pyridoxine
36 e (FVC) during infusion of ADO to FVC during handgripping before and after infusion of dipyridamole (
37 ed exercise hyperaemia during heavy rhythmic handgripping, but vasodilator responses to exogenous ADO
41 lthy subjects in two tasks: (1) intermittent handgrip contractions at 20, 40, 60, and 80% of maximal
42 thy subjects performed repetitive unilateral handgrip contractions that induced significant muscle fa
45 X-ray absorptiometry, muscle strength with a handgrip dynamometer, and blood biochemical indexes of n
46 sment (cognition), manual muscle testing and handgrip dynamometry (muscle and/or nerve function), and
47 ater reliability of handheld dynamometry and handgrip dynamometry was assessed in one study, and resu
49 subjective global assessment, anthropometry, handgrip dynamometry, biochemical and amino acid profile
51 2 agonist) in 10 healthy men during rhythmic handgrip exercise (10-15 % of maximum) and during a cont
52 energic receptor stimulation during rhythmic handgrip exercise (15% maximum voluntary contraction) an
53 (alpha(2)-agonist) during moderate rhythmic handgrip exercise (15% maximum voluntary contraction), d
54 etomidine (alpha(2)-agonist) during rhythmic handgrip exercise (15% MVC), a control non-exercise vaso
55 Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction)
56 cle (forearm) blood flow (FBF) during graded handgrip exercise (5, 15, 25% maximal voluntary contract
57 alsalva manoeuvre (by approximately 45%) and handgrip exercise (by approximately 27%) with unaffected
58 sed by vasomotor reactivity during isometric handgrip exercise (IHE), was recently quantified noninva
60 d when forearm ischemia was maintained after handgrip exercise (posthandgrip circulatory arrest).
61 forearm vascular resistance at rest, during handgrip exercise and after transient arterial occlusion
62 (ml/min/100 ml) at rest and during rhythmic handgrip exercise and after transient arterial occlusion
63 energic receptor stimulation during rhythmic handgrip exercise and during a control non-exercise vaso
65 r transduction was evaluated during ischemic handgrip exercise and postexercise ischemia, and it was
66 nce (FVC) responses during 5 min of rhythmic handgrip exercise at 20% maximal voluntary contraction i
68 .5 tesla before, during, and after isometric handgrip exercise at a level that was 30 percent of the
71 vidence of an abnormal metabolic response to handgrip exercise in at least some women with chest pain
73 conductance (CVC) decreases during isometric handgrip exercise in heat stressed individuals, and we h
74 the influence of blood flow occlusion during handgrip exercise on neuromuscular fatigue development a
76 tic traffic to the resting forearm, rhythmic handgrip exercise to fatigue followed by post-exercise i
77 rther aim was to examine the effect of local handgrip exercise training on radial artery L-FMC and fl
78 ted and randomly assigned to either a 6-week handgrip exercise training program (N=9) or a nonexercis
79 ng a sympatho-excitatory stimulus (isometric handgrip exercise) after either exercise (60 min cycling
80 e deoxygenation (systemic hypoxia and graded handgrip exercise) with age, which was caused by reduced
81 ed brachial artery blood flow during maximal handgrip exercise, 6-minute walk test, maximal oxidative
82 RI was performed before and during isometric handgrip exercise, an endothelial-dependent stressor, an
83 were quantified before and during isometric handgrip exercise, an endothelial-dependent stressor.
84 (2)) in cubital venous blood at rest, during handgrip exercise, and during recovery in 13 patients wi
85 forearm vascular conductance during ischemic handgrip exercise, despite a normal pressor response, su
86 Retina/choroid BF increases during brief handgrip exercise, paralleling increases in mean arteria
88 r data indicate that during graded intensity handgrip exercise, the reduced FVC and subsequently lowe
97 s 26 +/- 2 U; P = .01) in response to static handgrip exercise; (2) central command and/or the mechan
98 KCl) at rest; (2) mild or moderate intensity handgrip exercise; and (3) combined mild exercise + ACh,
99 adrenergic stimulation achieved through post-handgrip-exercise ischaemia (PEI) and beta1 -adrenergic
105 ings of scalp electroencephalographic (EEG), handgrip force, and finger flexor surface electromyograp
107 (BMI) and lean body mass (LBM) depletion on handgrip (HG) force and inspiratory muscle function (IMF
110 ate were measured during fatiguing isometric handgrip (IHG) at 30% maximum voluntary contraction and
113 as they executed their fastest and strongest handgrips in response to a visual cue, which was accompa
115 um and phentolamine prior to another bout of handgripping, little or no vasodilatation was seen eithe
117 ry responses to stressful stimuli (sustained handgrip, maximal forearm ischemia, mental stress, and t
119 lly from those obtained in a 2-min sustained handgrip MVC published in a recent report, in which the
120 icant fatigue were induced; (2) intermittent handgrip MVCs (100 trials) that resulted in significant
121 man participants performed approximately 100 handgrip MVCs (each 2-s contraction was followed by a 1-
122 The fMRI data from the task of intermittent handgrip MVCs differed dramatically from those obtained
123 CI, -4.07 to -1.30; P < .001) and decreased handgrip myotonia on clinical examination (mexiletine, 0
125 myotonia assessment; quantitative measure of handgrip myotonia; and Individualized Neuromuscular Qual
127 line leg power (p trend = 0.046), and poorer handgrip (p trend = 0.005) were associated with higher a
128 sing post-exercise ischaemia (PEI) following handgrip partially maintains exercise-induced increases
129 (PEI-M) and high (PEI-H) intensity isometric handgrip performed at 25% and 40% maximum voluntary cont
131 rested for 1 minute followed by 1 minute of handgrip, repeating three times, while maintaining stabl
133 e activity (SSNA) during intermittent static handgrip (SHG; at 45% of maximal voluntary contraction;
135 gh muscle volume (3.6%; 95% CI: 0.2%, 7.0%), handgrip strength (2.3 kg; 95% CI: 0.8, 3.7 kg), and 1-R
137 idarm and calf circumference, serum albumin, handgrip strength (HGS), and patient-self assessment of
138 9), android distribution of fat (P = 0.021), handgrip strength (P = 0.001), standardized summary scor
139 Longer ICU stay was associated with lower handgrip strength (P<0.01) and lower aromatic amino acid
144 cant increase of about 11% in quadriceps and handgrip strength at mid-cycle compared with both the fo
147 were the median change in lean body mass and handgrip strength over 12 weeks and were measured in all
148 ombined resting energy expenditure (REE) and handgrip strength provided a valuable assessment in data
149 was assessed by means of a maximal isometric handgrip strength test and a test of lower-back trunk mu
151 patency of the ulnopalmar arches, as well as handgrip strength tests to examine the isometric strengt
154 , systolic and diastolic blood pressure, and handgrip strength), behavioural (smoking, alcohol consum
155 by anthropometric assessment, bioimpedance, handgrip strength, and dietary intake (before and 30, 90
156 mpedance, quadriceps, respiratory muscle and handgrip strength, and physical performance with the Sho
168 nificantly increased lean body mass, but not handgrip, strength in patients with advanced non-small-c
170 MSNA) were recorded before and during static handgrip sustained to fatigue at 40 % of maximum volunta
171 ography during a visually cued, incentivized handgrip task in subjects with Parkinson's disease (n =
172 sure by 25%+/-6% (averaged across the entire handgrip task) (P<0.01), but did not change intraocular
173 e by 22%+/-5% (measured at the middle of the handgrip task), and ocular perfusion pressure by 25%+/-6
175 the reference group (normal BMI and highest handgrip tertile), the risk of all-cause mortality incre
177 ot affected by melatonin during an isometric handgrip test (30% maximum voluntary contraction) and a
180 179 +/- 4 cm) completed four constant power handgrip tests to exhaustion under conditions of control
181 Most patients had markedly impaired TUG and handgrip tests, and 21% recalled having fallen more than
184 ubjects (3 women, 7 men) performed ischaemic handgripping to fatigue before and after acute local ana
185 Manoeuvres such as contralateral ischaemic handgripping to fatigue that cause vasoconstriction in t
188 trations may not rise enough during rhythmic handgripping to have a major impact on these responses.
193 In the patients, MSNA responses to static handgrip were markedly attenuated (33 +/- 14 % at 33 % M
194 ure and mean arterial pressure during static handgrip were not different before, during and after spa
195 fter practice, I.G. became able to scale her handgrip when grasping a real target object that she had
196 ced mean arterial pressure response to right handgrip, whereas the pressor response to left handgrip
197 coronary vasoconstriction occurs with static handgrip with a time course that suggests a sympathetic
198 during handgrip under free-flow conditions, handgrip with partial flow restriction and PEI following
200 unilateral thigh-cuff release and isometric handgrip) would be greater after the administration of t
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