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1 sympathoexcitation in the vasculature of the exercising muscle.
2 ved fatty acids and their sparing for use by exercising muscle.
3 ical activity increases energy metabolism in exercising muscle.
4 rease in sympathetic vasoconstriction in the exercising muscles.
5 ercise capacity is the delivery of oxygen to exercising muscles.
6 ch between blood/oxygen demand and supply in exercising muscles.
7 glycogen and do not generate lactic acid in exercising muscles.
8 t is not dependent on movement feedback from exercising muscles.
9 because of decreased fatty acid delivery to exercising muscles.
10 hypothesis that lactic acid accumulation in exercising muscle acted on ASICs located on thin fibre m
11 ect on the distribution of cardiac output to exercising muscle and an age-related reduction in cardia
12 l administration of lactic acid (to simulate exercising muscle and evoke a pressor reflex), endomorph
13 nosine is released into the venous efflux of exercising muscle and that adenosine is responsible for
14 control, and thus the provision of oxygen to exercising muscles and vital organs, because of enhanced
15 ty of metabolically sensitive afferents from exercising muscle are the principal determinants of symp
16 vasoconstriction in the microcirculation of exercising muscle, because such modulation is abrogated
17 tributes to the age-associated impairment in exercising muscle blood flow and vascular tone in humans
18 r than the amount of O(2) in plasma, and ii) exercising muscle blood flow can almost double (from 260
19 n muscle SNA had no effect on oxygenation in exercising muscles but produced robust decreases in oxyg
20 c vasoconstriction is normally attenuated in exercising muscle, but this functional sympatholysis is
22 e nNOS is proposed to regulate blood flow in exercising muscle by diffusing from the skeletal muscle
24 s, the high levels of PGC-1alpha in dark and exercising muscles can explain their resistance to atrop
27 ugh multiple metabolites are concentrated in exercising muscle in CHF, only prostaglandins correlated
28 sympathetic vasoconstriction is enhanced in exercising muscle in heart failure as a result of impair
30 cellular P(O(2)) regulates PCr hydrolysis in exercising muscle is not due to the initial kinetic fall
31 ion induces physiological adaptations in the exercising muscle, it should become more fatigue resista
32 In contrast, the induction of ANGPTL4 in exercising muscle likely is counteracted via AMP-activat
36 central neural factors, afferent input from exercising muscle plays an important role in modulating
37 de, while extrapolation of these data to the exercising muscle predicts a significant role of Ca(2+)
38 exercise, central command and reflexes from exercising muscles produce the breathing stimulation req
39 rylation in vivo and can limit ATP supply in exercising muscle to below the mitochondrial capacity.
40 synapses is reminiscent of that occurring in exercising muscle to sustain cellular function and ident
41 etic vasoconstriction is markedly blunted in exercising muscles to optimize blood flow to the metabol
42 ards more predominant local control over the exercising muscle vasculature, systemic arterial blood p
43 ted by recent (13)C and (31)P NMR studies of exercising muscle, we propose a model of the energetics
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