Acta physiologica Scandinavica
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Acta Physiol. Scand. · Jan 1991
Effect of training on central factors in fatigue following two- and one-leg static exercise in man.
Leg strength and fatigue developed during 150 repeated two- and one-leg isometric maximal voluntary contractions were determined before and after a 5-week one- (n = 6) or two- (n = 7) leg training programme including a control group of five subjects. Two- and one-leg training increased two- and one-leg strength by 59 (range 8-107) and 36% (-1-69) respectively (P less than 0.01) with no significant difference between the two groups. Two-leg training decreased (P less than 0.05) fatigue only during two-leg maximal voluntary contractions (from 20 [11-26] to 13% [6-27]); and one-leg training fatigue only during one-leg maximal voluntary contractions (from 20 [15-23] to 11% [9-24]) despite the fact that both legs were trained. ⋯ No training effects were seen in the control group. The results show that an approximately 47% increase in muscle strength may take place without a significant change in the relative percentage of muscle fibre types or in the average muscle fibre size. Furthermore, the specificity of the training response to fatigue developed during repeated two- and one-leg maximal voluntary contractions suggests a change in the nervous influence on the motor units.
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Acta Physiol. Scand. · Dec 1990
Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.
The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (FIO2 = 21%) was 78 +/- 16 cmH2O ml-1 min 1000-1 (mRUL). Hypoxic ventilation (FIO2 = 10%) increased pulmonary vascular resistance to 117 +/- 17 mRUL. ⋯ L-arginine reversed the effect of N omega-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 +/- 26 mRUL and at hypoxic ventilation to 239 +/- 42 mRUL. In spontaneously breathing closed-chest rabbits, N omega-nitro-L-arginine methylester evoked a marked decrease in arterial PO2 and increases in respiration frequency and central venous pressure, while blood pH, PCO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
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Acta Physiol. Scand. · May 1990
Comparative StudyVariations in left ventricular volume alter myocardial oxygen consumption more at low than at high inotropy.
Variations in left ventricular (LV) wall tension during changes in LV end-diastolic volume significantly affect myocardial oxygen consumption (MVO2). In the present study we examined if the reduction in MVO2 per beat accompanying a decline in LV end-diastolic volume at constant LV systolic pressure (LVSP) is dependent on the level of myocardial inotropy. In six anaesthetized open-chest pigs, the blood volume was expanded by i.v. infusion of a Ringer solution. ⋯ LVSP was about 25 mmHg higher at high than at low inotropy. The fall in LV tension was therefore greater during blood volume reductions at high than at low inotropy because the fall in LV end-diastolic volume was almost identical and was initiated from the same level at both high and low inotropy. Nevertheless, the slope of the MVO2/LV end-diastolic volume relationship was significantly (P less than 0.05) less steep at high (1.26 +/- 0.30 mumol 100 g-1 mm-1) than at low inotropy (2.06 +/- 0.48 mumol 100 g-1 mm-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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Acta Physiol. Scand. · Mar 1990
Influence of splanchnic intravascular volume changes on cardiac output during muscarinic receptor stimulation in the anaesthetized dog.
The direct influence of systemic muscarinic receptor stimulation on total splanchnic intravascular volume and the splanchnic organs responsible for the total splanchnic volume change associated with muscarinic receptor stimulation in the animal with an intact circulation are unknown. Furthermore, the subsequent effect of these volume changes on cardiac output is not known. Thus, acetylcholine was infused at 5 micrograms kg-1 min-1 in 25 anaesthetized dogs in which nicotinic blockade of the ganglia was achieved with mecamylamine, while total and regional splanchnic intravascular volume changes were determined with a radionuclide imaging technique. ⋯ Acetylcholine-associated splanchnic volume changes were abolished after muscarinic receptor blockade with atropine. Thus, muscarinic receptor stimulation causes a decrease in total splanchnic volume due entirely to a decrease in splenic volume. The splanchnic volume changes do not influence cardiac output.
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Acta Physiol. Scand. · Jul 1988
Myocardial oxygen consumption during atrial pacing at various inotropic levels.
In anaesthetized open-chest pigs (n = 15) we examined whether myocardial oxygen consumption (MVO2) per min increased in proportion to heart rate during right atrial pacing at control, high and low inotropy. By modulating aortic constriction and the circulating blood volume, left ventricular (LV) systolic blood pressure, stroke volume and LV dimensions were kept constant. Examinations at control inotropy (n = 7) showed a linear relationship between increments in MVO2 beat-1 and LV dP/dt when heart rate was increased in four steps, each of 10 beats min-1 from 130 +/- 3 beats min-1 (r = 0.76 +/- 0.08). ⋯ Myocardial oxygen consumption beat-1 increased more at control (6.3 +/- 2.0%) than at high inotropy (diff: P less than 0.02). At low inotropy MVO2 beat-1 increased even more (17.4 +/- 2.8%) than at control inotropy (diff: P less than 0.05). Thus, the increase in MVO2 beat-1 during pacing tachycardia is related to the increase in LVdP/dt and is dependent on the level of inotropy; great increments during tachycardia after propranolol administration and no changes during intracoronary isoproterenol infusion.