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In the past, ratios of local to global muscle activity were only analysed in specific isolated local muscle contraction tasks (abdominal drawing in manoeuvre) [ 20] and general movement and isometric contraction activities (flexion, extension and lateral flexion from a semiseated position in an apparatus) [ 21].
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This allows for a slow lowering of the body through eccentric (lengthening muscle contraction) activity of the calf muscles.
The data were remarkably consistent across the three cohorts tested, and control trials showed that the methods used to measure heart and abdominal contraction activity did not significantly affect normal physiological functions.
In particular, the lactate threshold is a well known feature of muscle physiology, whereby muscle cells switch to partial anaerobic glucose catabolism when their contraction activity, and their corresponding ATP demand for converting chemical energy to mechanical work exceeds certain intensity [10], [11], even when oxygen abundance is not a limiting factor [12], [13], [14].
Disease cells exhibited enhanced collagen contraction activity compared to control cells.
Sequential redox changes are coupled to muscle contraction activity and disruption of redox equilibria is observed in diverse muscle diseases.
Neutralizing anti-TGF-β2 antibodies abolished exogenous TGF-β2 stimulated collagen contraction, but did not inhibit the enhanced basal collagen contraction activity of disease FPCL cultures.
This has the advantage of presenting a ready picture of single actin contraction activity without common molecular background 'noise' originating from rigor modes in contraction data during measurements.
At Phase IV, spike potential activity and contraction activity rapidly declined, but the starting potentials loaded with action potentials still accounted for >5% of the total starting potentials.
We first examined the basal collagen contraction activity of three independent patient-matched early passage control and disease primary FPCL cultures.
This enhanced collagen contraction activity observed in disease FPCL cultures was not due to differences in cell proliferation/viability between control or disease FPCL cultures.
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