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Biomedical subjects

G Raimondi

Publications and source records attributed to G Raimondi.

At least 37 records · Page 2Linked to original sources

Effects of isokinetic, isotonic and isometric submaximal exercise on heart rate and blood pressure.

The purpose of the present study was to compare arterial pressure (AP) and heart rate (HR) responses to submaximal isokinetic, isotonic and isometric exercises currently employed in physical rehabilitation therapy in terms of both magnitude and time-course. To this aim AP and HR were continuously and noninvasively measured in ten healthy subjects performing isokinetic, isotonic and isometric exercises at the same relative intensity. Isokinetic and isotonic exercises consisted of 30 knee extension/flexion repetitions at 40% of maximal effort. Isokinetic speed was set at 180 degrees s(-1). Isometric exercise consisted of a 60-s knee extension at 40% maximal voluntary contraction. The AP showed a rapid and marked increase from the onset of all types of exercise progressing throughout the exercises. Peak systolic (SAP) and diastolic (DAP) arterial pressure were 190.7 (SEM 8.9) and 121.6 (SEM 7.8) mmHg during isokinetic and 197.6 (SEM 11.2) and 128.3 (SEM 7.7) mmHg during isotonic exercise, respectively. During isometric exercise peak SAP and DAP were 168.1 (SEM 6.3) and 102.1 (SEM 3.7) mmHg, respectively [both lower compared to isokinetic and isotonic exercise (P < 0.05)]. The HR rose abruptly and after five isokinetic and isotonic repetitions it had already increased by about 30 beats min(-1), continuing to rise throughout the exercises. The HR response to isometric exercise was significantly less (P < 0.05) at all times. An immediate fall in AP, undershooting resting levels, was observed at the cessation of all types of exercise, being more marked after isokinetic and isotonic exercise. These results indicate that submaximal exercise of a dynamic type induces greater AP responses than intensity-matched isometric exercise and that even submaximal endurance-type rehabilitation exercise yields an elevated functional stress on the cardiovascular system which could precipitate hazardous events particularly in subjects with unrecognized cardiac diseases.

Adult↗

Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes.

This study evaluated the influence of central command and muscle afferent stimulation (mechanical and chemical) on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Twenty-two healthy men performed voluntary knee extension and electrically induced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) were measured continuously and noninvasively. The arterial baroreflex was evaluated by analyzing the slopes of sequences of three or more consecutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, both voluntary exercise and electrically induced exercise under arrested-flow conditions resulted in a maintained baroreflex sensitivity (BRS; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmHg, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest that the central command and muscle chemoreflex act to preserve the BRS, possibly "resetting" the baroreceptor-cardiac response relationship, whereas stimulation of mechanosensitive receptors appears capable of modifying the integrated baroreflex control of sinus node function in humans. The first two mechanisms seem, however, to overwhelm the latter to maintain BRS, thus permitting a concomitant increase in arterial pressure and heart rate.

Adult↗

Evaluation of reproducibility of spontaneous baroreflex sensitivity at rest and during laboratory tests.

OBJECTIVE: The aim of the present study was to examine the reproducibility of arterial baroreflex sensitivity (BRS) provided by the spontaneous baroreflex method at rest and during laboratory tests. METHODS: Twenty healthy volunteers were studied 24 h apart, in the same laboratory and under the same environmental conditions, at rest, during active standing, while performing mental arithmetics and during static hand-gripping. Systolic blood pressure, mean arterial pressure and pulse interval were continuously and non-invasively measured by using a Finapres device. BRS was evaluated by analysing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and pulse interval of the following beat both increased or decreased, in the same direction, in a linear fashion. Individual BRS were obtained by averaging all slopes computed within a given test. RESULTS: Under each test condition BRS did not differ significantly between the two consecutive days, showing strikingly similar values. The mean group coefficients of variation (CVAR), obtained by averaging individual CVAR, between the two experimental days were 15.0, 13.9 and 19.7% for resting, standing, static hand-gripping and mental arithmetic, respectively. No relationships were found between individual CVAR and individual mean arterial pressure, pulse interval and number of baroreflex sequences under any tested condition, on both experimental days. CONCLUSIONS: These results show that the spontaneous baroreflex method provides good BRS reproducibility under various stimuli that affect the neural control of circulation differently. They also suggest that BRS variability is dependent neither on haemodynamic modifications nor on the degree of baroreflex engagement, but it seems to reflect an inherent feature of the way in which arterial baroreflex modulate the heart period.

Adult↗

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit.

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Anesthesia↗

Noxious stimuli do not determine reflex cardiorespiratory effects in anesthetized rabbits.

The main purpose of this study is to examine whether the stimulation of an exclusively pain-sensing receptive field (dental pulp) could determine cardiorespiratory effects in animals in which the cortical integration of the peripheral information is abolished by deep anesthesia. In 15 anesthetized (alpha-chloralose and urethan) rabbits, low (3-Hz)- and high-frequency (100-Hz) electrical dental pulp stimulation was performed. Because this stimulation caused dynamic and static reflex contractions of the digastric muscles leading to jaw opening jaw-opening reflex (JOR); an indirect sign of algoceptive fiber activation], experimentally induced direct dynamic and static contractions of the digastric muscle were also performed. The low- and high-frequency stimulation of the dental pulp determined cardiovascular [systolic arterial pressure (SAP): -21.7 +/- 4.6 and 10.8 +/- 4.7 mmHg, respectively] and respiratory [pulmonary ventilation (VE): 145.1 +/- 44.9 and 109.3 +/- 28.4 ml/min, respectively] reflex responses similar to those observed during experimentally induced dynamic (SAP: -17.5 +/- 4.2 mmHg; VE: 228.0 +/- 58.5 ml/min) and static (SAP: 5.8 +/- 1.5 mmHg; VE: 148.0 +/- 75.3 ml/min) muscular contractions. The elimination of digastric muscular contraction (JOR) obtained by muscular paralysis did away with the cardiovascular changes induced by dental pulp stimulation, the effectiveness of which in stimulating dental pulp receptors has been shown by recording trigeminal-evoked potentials in six additional rabbits. The main conclusion was that, in deeply anesthetized animals, an algesic stimulus is unable to determine cardiorespiratory effects, which appear to be exclusively linked to the stimulation of ergoreceptors induced by muscular contraction.

Anesthesia↗

[Cardiodepressive effects of muscular exercise in spontaneously hypertensive rats].

Conflicting results have been reported on the differences in the cardiovascular reactivity to muscular exercise between normotensive and hypertensive subjects and normotensive subjects with family history of hypertension and normotensive subjects without familial hypertensive history. Also studies performed in spontaneously hypertensive in comparison with normotensive rats have not led to final conclusions. Therefore, the aim of the present study was twofold: to evaluate cardiorespiratory reactivity to different types of muscular exercise in normotensive (WKY) compared to spontaneously hypertensive rats (SHR) at pre-hypertensive and hypertensive stages; to verify the role played by the "muscular reflex drive" in mediating the cardiorespiratory responses in rats. We utilized four groups of anesthetized rats: 8 young WKY, 8 SHR in pre-hypertensive stage, 6 adult WKY and 6 SHR in hypertensive stage. We evaluated the cardiorespiratory responses to (rhythmic) dynamic and (static) isometric contractions of gastrocnemius muscles induced by electrical stimulation of the tibial nerve. Cardiorespiratory responses during the initial phase of dynamic and static contractions of hindlimb muscles were studied. Muscle contractions were elicited by stimulating the tibial nerves at 3 and 100 Hz. We measured: mean arterial pressure (MAP), heart rate (HR), and pulmonary ventilation (VE). Both types of exercise caused a significant decrease in MAP and a significant increase in VE while HR did not change significantly. The four groups of rats did not show significant differences in the pattern of cardiorespiratory responses to muscular exercise. The cardiorespiratory reflexes initiated by activation of muscle receptors, verified by interrupting the afferents from the contracting muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Evaluation of spontaneous baroreflex modulation of sinus node during isometric exercise in healthy humans.

The purpose of this study was to 1) evaluate the baroreflex (BR) modulation of the sinus node during isometric exercise in humans by analyzing the variations in pulse interval (PI) in response to beat-by-beat spontaneous changes in systolic arterial pressure (SAP), thus avoiding external intervention to alter arterial pressure (AP); and to 2) evaluate the specific influence of muscle chemoreflex on the SAP-PI relationship. Sixteen healthy males were studied during rest, handgrip at 30% of maximum voluntary contraction [isometric handgrip (IHG)], post-IHG arrested forearm circulation (AFC), and recovery. AP and PI were measured continuously and noninvasively. A BR response was defined by series of at least three consecutive beats in which SAP and PI of the following beat either increased or decreased in a linear fashion. In nine subjects, forearm (FVR) and calf vascular resistances (CVR) were determined. Mean slope (by linear regression) of SAP-PI sequences did not significantly differ between rest, IHG, and AFC (14.1 +/- 2.0, 12.2 +/- 1.6, and 13.2 +/- 1.4 ms/mmHg, respectively), i.e., BR sensitivity was unchanged. IHG resulted in a rightward shift of the regression line relating SAP to PI. The shift was maintained during AFC, when PI returned to control and AP fell slightly but remained significantly elevated. CVR, which did not change during IHG, significantly increased during AFC, whereas FVR increased during both IHG and AFC, but not significantly. The data indicate that arterial BR is "reset" to a higher operating point during isometric exercise. Muscle chemoreflex appears to be partially involved in this modification.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Chronic obstructive pulmonary disease].

Several meetings of chest specialists were held in order to update basic knowledge on Chronic Obstructive Pulmonary Disease (COPD) and to establish guidelines regarding its prevention and treatment. This Consensus was prompted by the important morbidity and mortality due to COPD. Pulmonary emphysema, chronic bronchitis and asthma may evolve into COPD when developing chronic, persistent, non reversible airflow obstruction. Its pathologic features, physiopathology, pulmonary function derangements and clinico-radiological picture are summarized. Early detection and prevention accomplished through smoking cessation are essential to stop health damage due to this condition. Strategies directed to smoking cessation are described. Once COPD is established, inhaled bronchodilators (IB)--anticholinergics, beta-2 agonists or both--might be useful. Teophylline is indicated additionally when no improvement is obtained with IB. Inhaled steroids (IE) may stop progression of airways obstruction; they are recommended in patients who remain symttomatic and/or with severe airflow obstruction (FEV1 less than 50% predicted) despite treatment with beta-2 adrenergics and teophylline. Vaccination against influenza and pneumococcal pneumonia is suggested. Other medications (antibiotics, psychoactive drugs, alpha-1 antitrypsine, respiratory stimulants) or surgical interventions, including lung transplantation, might be of help in certain circumstances. In patients with physiotherapy, supplementary nutrition, muscle retraining, prolonged oxygen therapy and, eventually, noninvasive mechanical ventilation might improve survival and quality of life. Acute decompensations leading to respiratory failure should be promptly detected and treated with oxygen, IB, teophylline, corticosteroids, antibiotics and, eventually, mechanical ventilation. The main role of public education in disease prevention is emphasized. Moreover, patient and family education is essential for adequate treatment of COPD.

Humans↗

Effects of alpha-human atrial natriuretic peptide in guinea-pig isolated heart.

The aim of the present investigation has been to ascertain whether or not atrial natriuretic peptides (ANP) can exert a direct effect on myocardial contractility. Alpha-human ANP (alpha-hANP) concentrations ranging from 1 pM to 50 nM have been used to perfuse guinea-pig isolated hearts in a non-recirculating Langendorff apparatus. A dual concentration-related effect has been induced by alpha-hANP on myocardial function. A maximal increase of +LV dP/dtmax (+56%; P < 0.001) has been observed when guinea-pig hearts were perfused with 100 pM alpha-hANP, whereas a 25% decrease (P < 0.01) occurred with 50 nM alpha-hANP. Similar effects have also been induced by alpha-hANP on the coronary flow rate (CFR). A significant CFR increase (maximal at 10 pM alpha-hANP) was induced by picomolar concentrations of alpha-hANP, whereas a progressive decrease, which was maximal (-28%; P < 0.01) at 50 nM alpha-hANP, was observed with nanomolar concentrations of the peptide. No effects have been observed on heart rate. These results suggest that ANP has direct effects on both vascular and myocardial muscle cells. Coronary vasoconstriction induced by nanomolar concentrations of ANP can contribute to the cardiodepression, whereas ANP in picomolar concentrations can induce a coronary vasodilation which is not coupled with the enhanced myocardial contractility. The latter is the likely expression of a direct effect of the peptide on myocardial function.

Animals↗

Physiological unloading of cardiopulmonary mechanoreceptors by posture change does not influence the pressor response to isometric exercise in healthy humans.

In recent studies in humans the role of cardiopulmonary baroreflexes in modulating the cardiovascular responses to isometric exercise (somatic pressor reflex) has been investigated by performing static handgrip exercise during deactivation of cardiopulmonary receptors produced by low levels of lower body negative pressure; however, findings from these studies have not been consistent. The purpose of this study was to investigate whether a more physiological unloading stimulus of cardiopulmonary baroreceptors, obtained by sequentially changing posture, could influence the pressor response to somatic afferent stimulation induced by isometric exercise. To accomplish this, ten healthy subjects performed a 2-min isometric handgrip (IHG) at 30% maximal voluntary contraction after 10 min of supine rest and, in rapid sequence, after 10 min of sitting and 10 min of standing, at the time when, owing to their transitory nature, the cardiovascular effects, due to arterial baroreceptor intervention should have been minimal. During IHG arterial pressure (BPa) was continuously and noninvasively measured to quantify accurately the blood pressure response to IHG both in magnitude and time course. Results showed that the pressor response to IHG was not significantly influenced by change in posture, either in magnitude or in time course. The mean arterial pressure increased by 17.4 (SEM 2.5), 18.6 (SEM 1.2) and 17.0 (SEM 1.3) mmHg in supine, sitting and standing [2.3 (SEM 0.3), 2.5 (SEM 0.2) and 2.3 (SEM 0.2) kPa] positions, respectively. Also the heart rate response to IHG was unaffected by change in posture.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Standards established by consensus for the treatment of bronchial asthma and its exacerbations].

A group of pulmonologists from different sites of Argentina convened to establish consensus guidelines for treatment of acute and chronic bronchial asthma. General acceptance that in fatal asthma diagnosis and hospital admission are usually too late and treatment insufficient prompted the need for this meeting. The purpose of treatment was devised to keep the patient symptomless, decrease frequency of exacerbations and the risk of severe attacks. Peak expiratory flow rate (PEFR) measurement in all patients was decided. inhalation of anti-inflammatory drugs (corticosteroids, CE, and/or disodium cromoglycate, DSG, in those younger than 20 years) was established as first line of treatment. Inhaled CE (even in high doses such as 2 mg/day) do not provoke significant adverse systemic effects (immune depression, Cushing syndrome, hyperglycemia in diabetics or osteopenia). Secondary local adverse effects are however frequent: oral and pharyngeal candidiasis and dysphonia. It is advisable considering present evidence, that bronchodilators (Bd) be used preferentially on demand. On account of small bronchodilator effect and frequent secondary adverse effects, use of theophylline should be limited to patients not adequately responsive to anti-inflammatory drugs in high dosage. Immunotherapy is not useful in asthma. Four clinical levels were defined in chronic asthma considering severity of dyspnea, frequency of nocturnal bronchial obstruction, levels of PEFR and amount of required Bd. Guidelines of treatment were established for each clinical level considering increasing dosage of CGS, inhaled CE (up to 2 mg/day) and regular administration of Bd. Indications for systemic CE administration were also established. Three levels of acute asthma (sudden worsening of symptoms) were accepted based on clinical evidence and PEFR values. Treatment was quantitatively adjusted to severity. Criteria for hospital admission either in emergency or intensive care areas and treatment procedures were established.

Administration, Inhalation↗

[The physiopathological aspects and new therapeutic approaches in cardiac-circulatory failure].

Pathophysiological mechanisms are reviewed concerning the onset and the perpetuation of the clinical features of congestive heart failure. This syndrome is a severe condition of poor prognosis and bad life quality which in the last decades has reached, in the western industrial countries, the highest levels of general mortality, mainly due to the high prevalence of hypertensive and ischaemic myocardiopathies in the last years. To the clinical features of heart failure mainly contributes a deregulation of the physiological compensatory mechanisms contemporarily and concurrently activated following the primary deficiency of the heart pump function. In physiological conditions, following the myogenic adapting mechanisms reflex mechanisms intervene, activated by intracardiac and aortic and carotid-sinus mechanoreceptors following the variations in intracardiac and intravascular pressure and generally evoking negative feed-back effects. In patients with heart failure arterial high pressure mechanoreceptors respond to the reduction in effective arterial pressure thus provoking a deactivation of the tonic inhibition on the sympathetic cardiovascular drive. This leads to an activation of peripheral and renal vasoconstrictor tone, to a raised medullary catecholamine incretion, to heart rate and inotropism stimulation, and to an increase in pituitary gland ADH production as well as to an activation of renin-angiotensin-aldosterone system (RAAS). Analogous vasoconstrictive, and sodium and water retentive effects can be elicited by endothelin produced by endothelial cells and found in high plasma levels in CHF. These excitatory effects, leading to a rise in systemic vascular resistance and to hydro-electrolytic retention with volume expansion, are not efficiently counteracted by the opposite effects triggered by cardiopulmonary vagally mediated mechanoreceptors activated by the raised cardiac filling pressure and leading to sympathetic nervous inhibition, peripheral and renal vasodilation, ADH and RAAS inhibition. Analogous effects should be provoked by the raised production, due to enhanced heart wall distension, of atrial natriuretic factor leading to vasodilation, natriuresis and diuresis. Reduced sensitivity of cardiopulmonary baroreceptors and lowered production of ANF due to structural cardiac changes could represent, according to most opinions, the main factors responsible for the prevailing sympathetic activation and hydro-saline retention in CHF. The activation of cardiopulmonary sympathetic positive-feed back afferents, could be also involved in the characteristic alteration of the vago-sympathetic balance in heart failure. The persistent reduction in heart pump function could lead to the instauration of vicious circles among the various regulatory systems and create an overcompensation condition.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗

On the role of neural mechanisms in the cardiocirculatory inhibitory action of alpha-human atrial natriuretic peptide in the anesthetized rabbit.

The effects induced by alpha-human 28-amino acid residue atrial natriuretic peptide (alpha-hANP) on arterial pressure, heart rate and vascular resistance, measured as hindlimb perfusion pressure (HPP), were examined in anesthetized rabbits. In particular, the involvement of the autonomic nervous system in mediating the cardiocirculatory effects of alpha-hANP was investigated. Intravenous alpha-hANP (8 micrograms/kg, bolus injection) in anesthetized rabbits caused a sustained decrease in atrial pressure, a transient decrease in HPP and no significant changes in heart rate. After sinoaortic denervation, alpha-hANP produced a greater decrease in arterial pressure and in hindlimb vascular resistance and also a consistent decrease in heart rate. Bilateral vagotomy did not significantly alter the cardiocirculatory responses to alpha-hANP in either normal or in sinoaortic denervated rabbits. Intravenous infusion of alpha-hANP (2 micrograms/kg bolus + 0.2 micrograms/kg per min) did not substantially change the baroreflex cardiocirculatory responses to loading and unloading carotid and aortic baroreceptors with bilateral carotid occlusion and phenylephrine or nitroglycerin bolus injection. In addition, alpha-hANP infusion did not modify the cardiovascular reflex responses to chemical stimulation of neural receptors (sensory endings of group III and IV somatic afferents) in the hindlimb muscles which are primarily mediated by sympathetic nerves in the anesthetized rabbit. Pharmacological blockade of the autonomic nervous system with atropine and guanethidine did not reduce the hypotensive and bradycardic effects caused by alpha-hANP in sinoaortic denervated animals. The results indicate that in anesthetized rabbits: (1) alpha-hANP can induce inhibitory cardiocirculatory responses (hypotension, bradycardia, musculocutaneous vasodilation) which are consistently offset by the sinoaortic baroreceptor system; (2) alpha-hANP does not alter the reflex control of arterial pressure and heart rate by arterial baroreceptors and muscle chemosensitive receptors; (3) activation of cardiopulmonary vagally-mediated depressor reflexes does not contribute to the inhibitory cardiovascular action of alpha-hANP; and (4) inhibitory effects on sympathetic activity do not constitute a significant component of the cardiocirculatory action of alpha-hANP.

Anesthesia↗

[A comparison of the parameters used in determining the anaerobic threshold by a computerized analysis of the indices of breath-by-breath gas exchange].

Anaerobic threshold (AT) determination by gas exchange measurements has to date been performed mostly by visual inspection from plots of ventilatory and gas exchange indexes. Owing to its subjective nature, this approach appears to be somehow arbitrary. Moreover, it still remains undetermined which of the commonly used gas exchange indexes is most reliable in detecting the anaerobic threshold. In the present study we have compared the AT values provided by the gas exchange indexes in common use, each one processed by a computerized method, based on a 2-segments linear regression model. A quantitative analysis of their reproducibility has also been performed. By comparison, the same has been done by using the conventional technique based on visual inspection of plots of the same gas exchange indexes, made by 2 independent observers. The aim of the study was to evaluate whether an objective method of AT detection improves the reliability of anaerobic threshold determination by gas exchange measurements. Eight healthy male subjects performed 2 incremental exercise tests at exhaustion with a 2-week interval. Respiratory exchange data were collected on a breath-by-breath basis. The following gas exchange indexes have been employed: V-slope; VE vs VO2; VE/VO2 vs VO2 or time; PetO2 vs VO2 or time. The latter 2 have been examined coupled with the VE/VCO2 and PetCO2 curves, respectively. By employing the computerized method, there were no significant differences in AT detection among the 4 indexes. The best agreement was between V-slope and VE vs VO2 (delta 15.8 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The role of chemosensitive muscle receptors in cardiorespiratory regulation during exercise.

Several possible mechanisms leading to the cardiorespiratory adjustments to muscular exercise can be considered. Activation of the cardiovascular and respiratory centers may result from: (1) direct or reflex action of circulating metabolites (humoral control); (2) cortical influxes (central drive); (3) nervous impulses from receptors in the contracting muscles (peripheral drive). Information presently available focuses most of the interest upon the muscular drive. Our studies on anesthetized animals (rabbits, dogs) have demonstrated that different types of exercise (dynamic and static) produce two different types of adjustments reflexly elicited by activation of sensory endings of somatic afferents in muscles. Dynamic exercise produces a vasodilatory effect with a decrease in blood pressure and heart rate and an increase in breathing frequency; static exercise provokes an increase in blood pressure, heart rate and depth of breathing. These two patterns of adjustments to exercise are also reproducible, in anesthetized animals, by injecting chemical substances into muscular arteries. Injections of bradykinin, K+ ions and acid solutions evoke cardiorespiratory responses analogous to those produced by dynamic contractions; injections of hypertonic NaCl or glucose evoke an excitatory pattern closely similar to that elicited by isometric contractions. These research studies lead to the hypothesis that two functionally distinct types of chemosensitive receptors (K and P) exist in the skeletal muscles which are activated in proportionally different measures during different types of muscular activity, thus evoking coordinated changes in the cardiovascular and respiratory functions. These studies also strongly support the important role of the peripheral reflex mechanism in governing the circulatory and respiratory systems to perfectly match cardiorespiratory changes to the muscular metabolic needs during exercise.

Animals↗