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Biomedical subjects

F Iellamo

Publications and source records attributed to F Iellamo.

At least 19 recordsLinked to original sources

Selective impairment of excitatory pressor responses after prolonged simulated microgravity in humans.

The haemodynamic and autonomic effects of prolonged exposure to simulated microgravity were assessed non-invasively in seven healthy volunteers completing a 42-day -6 degrees head down tilt. Before, during and after head down tilt, subjects were exposed to moderate excitatory stimuli (mental arithmetic and static handgrip) to gauge possible progressive impairment of pressor responses. Before and after head down tilt, subjects were also exposed to orthostatic stress, to assess influences of simulated microgravity on orthostatic defence. Simple haemodynamics (heart rate and systolic arterial blood pressure), linear (i.e., oscillatory) components of beat-by-beat variability, non-linear properties (i.e., corrected conditional entropy (CCE)) of RR interval variability, and baroreflex slope furnished a non-invasive evaluation of autonomic regulatory mechanisms. Pressor responses to mental arithmetic and to handgrip were markedly impaired after 42 days head down tilt, whereas responses in markers of autonomic regulation were not modified. Standing, performed 8 days after head down tilt to limit the risk of syncope, still induced a variable degree of hypotension, with signs of progressively greater sympathetic activation than before head down tilt. Simulated microgravity-induced reduction of pressor responses, in spite of largely maintained autonomic activation, favours the hypothesis of a peripheral impairment of cardiovascular homeostasis. rights reserved.

Autonomic Nervous System↗

Neural mechanisms of cardiovascular regulation during exercise.

This brief review addresses current hypotheses concerning the reflex control of circulation during exercise in humans. In particular, the specific objective of this review is to describe how time and frequency domain analysis of blood pressure and heart rate variability signals permitted to gain new insights onto reflex mechanisms of cardiovascular regulation during exercise, without the need of perturbing the cardiovascular system from the outside, utilizing fully noninvasive approaches and avoiding artificially isolating the influence of the different neural pathways involved in the control of the cardiovascular system. Throughout the article, particular emphasis is given to the complexity and plasticity of the neural control of the circulation during exercise, by presenting data that show how the reflex mechanisms involved in cardiovascular regulation, namely, the arterial baroreflex and the muscle metaboreflex, may be differently modulated in relation to the muscular activity being performed, such as the type of exercise, the intensity of exercise and the size of active muscle masses.

Autonomic Nervous System↗

Positive and negative feedback mechanisms in the neural regulation of cardiovascular function in healthy and spinal cord-injured humans.

BACKGROUND: We tested the hypothesis that in humans, hypertension/tachycardia and hypotension/bradycardia nonbaroreflex sequences that occur within spontaneous arterial pressure (AP) and R-R interval fluctuations are an expression of positive feedback mechanisms neurally regulating the cardiovascular system. METHODS AND RESULTS: We studied 15 spinal cord-injured (SCI) subjects (8 tetraplegics and 7 paraplegics) and 8 healthy subjects. The occurrence of nonbaroreflex (NBseq) and baroreflex (Bseq) sequences, ie, hypertension-bradycardia and hypotension-tachycardia sequences, was assessed during rest and head-up tilt (HUT). The ratio between Bseq and NBseq (B/NB ratio) was also calculated. In resting conditions, the occurrence of NBseq was significantly lower (P:<0.05) in tetraplegics (7.9+/-1.5) than in paraplegics (16.2+/-3.2) and normal subjects (19.0+/-3.5), whereas the occurrence of Bseq was not significantly different between the 3 groups (38.6+/-11.9 versus 45.4+/-6.0 versus 47.0+/-11.9). In tetraplegics, the B/NB ratio showed a marked, significant decrease (from 8.4+/-4.2 to 1.9+/-0.8, P:<0.05) in response to HUT, whereas in normal subjects, it showed a significant increase (from 3.5+/-0.7 to 9.4+/-2.7, P:<0.05). In paraplegics, the B/NB ratio did not change significantly in response to HUT (from 4.5+/-1.6 to 4.8+/-1.1). CONCLUSIONS: Our data suggest that nonbaroreflex sequences occur in humans and might represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation that is able to interact dynamically with feedback mechanisms of baroreflex origin.

Adult↗

Spontaneous baroreflex modulation of heart rate and heart rate variability during orthostatic stress in tetraplegics and healthy subjects.

OBJECTIVE: This study was addressed to investigate the contribution of vagal and sympathetic mechanisms to the genesis of low-frequency (LF) oscillations of RR-interval. DESIGN: To this aim, we utilized the pathophysiological model of tetraplegics, who have intact vagal afferent and efferent pathways of the baroreceptor reflex arc but interrupted medullary-spinal sympathetic pathways. METHODS: We studied nine complete, traumatic, tetraplegics (C4-C7, TET) and 10 normally healthy subjects (NR) at rest and during physiological baroreceptors unloading induced by 70 degrees head-up tilt. Autoregressive power spectral analysis was used to investigate RR-interval and systolic arterial pressure (SAP) variabilities. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. RESULTS: Both at-rest and during-tilt LF and high frequency (HF) components were detected in RR-interval of NR, whereas in TET only the HF component was observed in both conditions (with one exception). Baroreflex sensitivity (BRS) did not significantly differ between TET and NR at rest, and underwent a significant and similar decrease during tilt in both groups, being accompanied in NR by a significant increase in LF relative power. Spectral analysis of SAP provided results similar to RR-interval. Tilt also slowed the centre frequency of the LF components of RR-interval and SAP. CONCLUSIONS: During unperturbed physiological conditions, a change in efferent vagal activity to the heart from baroreflex stimulation by spontaneous arterial pressure changes, is unlikely to contribute on its own to the genesis of LF heart period oscillations in humans who lack the ability to modulate sympathetic nerve traffic to the heart. However, the possibility that a baroreflex modulation of LF oscillations require an intact sympathetic control should be carefully considered.

Adult↗

Neural control of the cardiovascular system during exercise.

The objective of this review was to give an overview on the current knowledge on the neural mechanisms of cardiovascular regulation during exercise. Evidence derived mainly from human studies which supports the contribution of the different control mechanisms, namely the central command, the reflex drive from active muscles and the arterial baroreflex, with the attendant modifications in autonomic nervous system activity, in determining the cardiovascular responses to exercise are discussed, along with some controversial issues and evolving concepts in exercise physiology. In particular, data that show how the various neural mechanisms involved in cardiovascular regulation during exercise are differently modulated by factors related to the muscular activity being performed, such as the type and intensity of exercise and the size of the active muscle masses are presented, stressing the plasticity of the neural network. Finally, clinical implications pertaining to neural cardiovascular regulation and exercise are advanced.

Adaptation, Physiological↗

Effects of aerobic exercise training on 24 hr profile of heart rate variability in female athletes.

BACKGROUND: The aim of this study was to investigate the effects of exercise training on autonomic regulation of heart rate under daily life conditions. METHODS: Twenty-six healthy female athletes (age 24.5 +/- 1.9 yrs) involved in regular physical activity were recruited during a period of yearly rest and randomly assigned to a five-week aerobic exercise training program (n = 13) or to a non-exercise control group (n = 13). MEASURES: Before and after the five-week training, all subjects underwent a bycicle ergometer stress test and a 24-hour dynamic ECG monitoring. Autonomic regulation of heart rate has been investigated by means of both time and frequency domain analyses of heart rate variability (HRV). Spectral analysis of R-R interval variability (autoregressive algorithm) provided markers of sympathetic (low frequency, LF, 0.10 Hz) and parasympathetic (high frequency, HF, 0.25 Hz) modulation of the sinus node. RESULTS: Trained subjects showed a reduced heart rate response to submaximal workload. Before training there was no significant difference between the two groups. After training resting heart rate did not significantly differ between trained and untrained subjects. No significant differences were observed in the different time domain indexes of heart rate variability. The day-night difference in SD and SDRR were significantly less in the trained as compared to the untrained group. Normalized LF and HF components did not significantly differ between trained and untrained subjects, during the awake period. The decrease in the LF and the increase in the HF component during nighttime were significantly less in the trained group. The LF/HF ratio was significantly decreased during the night in the untrained group whereas it was not significantly different from the awake state in the trained group. CONCLUSIONS: These findings of the relative night-time increase in LF and the decrease in the day-night difference in time domain indexes of heart rate variability suggest that, in young female athletes, exercise training is able to induce an increase in the sympathetic modulation of the sinus node which may coexist with signs of relatively reduced, or unaffected, vagal modulation.

Adult↗

Effects of a residential exercise training on baroreflex sensitivity and heart rate variability in patients with coronary artery disease: A randomized, controlled study.

BACKGROUND: Myocardial ischemia and infarction impair baroreflex sensitivity (BRS), which when depressed is predictive of future cardiac events after myocardial infarction (MI). The main objective of this study was to determine whether exercise training improves BRS in patients with coronary artery disease. METHODS AND RESULTS: Ninety-seven male patients with and without a previous MI were recruited after myocardial revascularization surgery and randomized into trained (TR) or untrained (UTR) groups. TR patients underwent a residential exercise program at 85% of maximum heart rate (HRmax) consisting of 2 daily sessions 6 times a week for 2 weeks. Eighty-six patients (45 TR and 41 UTR) completed the study. BRS was assessed at baseline and at the end of the protocol by the spontaneous baroreflex method. The standard deviation of mean R-R interval (RRSD) was also assessed as a measure of heart rate variability. At baseline, there were no significant differences between TR and UTR patients in any variable. In TR patients, BRS increased from 3.0+/-0.3 to 5.3+/-0.7 ms/mm Hg (P:<0.001), RRSD from 18.7+/-1.4 to 23.6+/-1.6 ms (P:<0.01), and R-R interval from 792. 0+/-15.5 to 851.3+/-20.5 ms (P:<0.001). No significant changes occurred in UTR patients. Increases in BRS and RRSD were significant in patients either with or without a previous MI. CONCLUSIONS: Exercise training increases BRS and heart rate variability in patients with coronary artery disease. Improved cardiac autonomic function might add to the other benefits of exercise training in secondary prevention of ischemic heart disease.

Baroreflex↗

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits.

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

Afferent Pathways↗

Effect of 4 hours HD -6 degrees on heart rate variability in symptomatic and non symptomatic subjects.

Orthostatic intolerance is the most serious symptom of cardiovascular deconditioning induced by microgravity exposure. In fact the neural control mechanisms of the cardiovascular system are significantly affected by this condition. Non-invasive measurement of Heart Rate Variability (HRV) have been used as a valuable tool to characterize the ability of neuroendocrine regulatory systems to modulate the cardiovascular function by analyzing the spontaneous fluctuations of arterial pressure and heart period on a beat-to-beat basis. Concerning this, conflicting results have been reported on the heart rate and blood pressure variability responses during exposure to microgravity. These differences seem to be due to different experimental designs used. Moreover, the different behavior of normal subjects in response to orthostatic stress after HD, i.e. Symptomatic (S) or Non Symptomatic (NS), could play some roles in producing these discrepancies. Therefore the aim of the present study was to examine BP and HR variability before and after 4 hours of HD in two groups of normal subjects with and without symptoms of orthostatic intolerance to orthostatic stress.

Adult↗

Muscle metaboreflex contribution to sinus node regulation during static exercise: insights from spectral analysis of heart rate variability.

BACKGROUND: It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. METHODS AND RESULTS: Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. CONCLUSIONS: The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.

Adult↗

Investigating feed-forward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations.

BACKGROUND: Analysis of spontaneous fluctuations in systolic arterial pressure (SAP) and pulse interval (PI) reveals the occurrence of sequences of consecutive beats characterized by SAP and PI changing in the same (+PI/+SAP and -PI/-SAP) or opposite (-PI/+SAP and +PI/-SAP) direction. Although the former reflects baroreflex regulatory mechanisms, the physiological meaning of -PI/+SAP and +PI/-SAP is unclear. We tested the hypothesis that -PI/+SAP and +PI/-SAP "nonbaroreflex" sequences represent a phenomenon modulated by the autonomic nervous system reflecting a feed-forward mechanism of cardiovascular regulation. METHODS AND RESULTS: We studied anesthetized rabbits before and after (1) complete autonomic blockade (guanethidine+propranolol+atropine, n=13; CAB), (2) sympathetic blockade (guanethidine+propranolol, n=15; SB), (3) parasympathetic blockade (atropine, n=16), (4) sinoaortic denervation (n=10; SAD), and (5) controlled respiration (n=10; CR). Nonbaroreflex sequences were defined as >/=3 beats in which SAP and PI of the following beat changed in the opposite direction. CAB reduced the number of nonbaroreflex sequences (19. 1+/-12.3 versus 88.7+/-36.6, P<0.05), as did SB (25.3+/-11.7 versus 84.6+/-23.9, P<0.001) and atropine (11.2+/-6.8 versus 94.1+/-32.4, P<0.05). SB concomitantly increased baroreflex sensitivity (1.18+/-0. 11 versus 0.47+/-0.09 ms/mm Hg, P<0.01). SAD and CR did not significantly affect their occurrence. CONCLUSIONS: These results suggest that nonbaroreflex sequences represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the control of heart period.

Animals↗

Effect of postural changes on cardiovascular responses to static exercise in hypertensive human beings.

OBJECTIVE: In hypertensive patients, exaggerated increases in vascular resistance and arterial blood pressure have been reported on changing posture from supine to upright. In this study we tested the hypothesis that in hypertensive subjects, upright posture induces an increase in the vasoconstrictor and pressor responses to physical exercise. SUBJECTS AND METHODS: We studied 17 males with mild hypertension and 10 sex- and age-matched normotensives. Each performed three bouts of static handgrip at 30% maximum voluntary contraction for 2 min after 10 min of supine rest and, in sequence, after 10 min of sitting and 10 min of standing. Arterial pressure, heart rate and forearm vascular resistance were measured by Finapres and plethysmography, respectively. RESULTS: Exercise posture did not affect the mean arterial pressure and heart rate responses to static handgrip. No significant differences in these responses were observed between the hypertensives and the normotensives in any posture. In the hypertensives (n = 12), forearm vascular resistance did not change significantly from resting values during supine and sitting static handgrip but increased significantly during standing static handgrip. In the normotensives, forearm vascular resistance did not change significantly from resting values during static handgrip in any posture. The forearm vascular resistance response to the standing static handgrip was significantly greater in the hypertensives than the normotensives. The algebraic sum of forearm vascular resistance responses to postural change from sitting to standing plus that induced by sitting static handgrip (i.e. additive reflexes) was significantly less than the forearm vascular resistance response to the standing static handgrip (i.e. combined relexes), indicating a facilitatory interaction between exercise and orthostatic stimuli in hypertensives. In contrast, the algebraic sum of the heart rate responses to postural change from sitting to standing plus that induced by sitting static handgrip was significantly greater than the response to standing static handgrip, indicating an inhibitory interaction. CONCLUSIONS: In hypertensive patients, physiological orthostasis causes an increased vasoconstrictor response to static exercise, but this is opposed by an inhibitory influence on the heart rate response, with the result that the pressor response to static exercise is unaffected by upright posture.

Baroreflex↗

Role of muscular factors in cardiorespiratory responses to static exercise: contribution of reflex mechanisms.

We investigated the effects of muscle mass and contraction intensity on the cardiorespiratory responses to static exercise and on the contribution afforded by muscle metaboreflex and arterial baroreflex mechanisms. Ten subjects performed static handgrip at 30% maximal voluntary contraction (MVC) (SHG-30) and one-leg extension at 15% (SLE-15) and 30% (SLE-30) MVC, followed by postexercise circulatory occlusion (PECO). Mean arterial pressure (MAP) and heart rate (HR) responses were greater during SLE-30 than during SHG-30. The difference in MAP was maintained by PECO, and the part of the pressor response maintained by PECO was greater after SLE-30 than after SHG-30 (88.3 +/- 10.6 and 67.8 +/- 12.7%, respectively, P = 0. 02). There were no differences in MAP and HR responses between SHG-30 and SLE-15 trials. Baroreflex sensitivity was maintained during SHG-30 and SLE-15, whereas it was significantly reduced during SLE-30 and recovered back to the resting level during PECO. Minute ventilation and oxygen uptake increased more during SLE-30 than during both SHG-30 and SLE-15 trials. Minute ventilation remained significantly elevated above rest only during PECO following SLE-30. These data suggest that during static exercise the muscle mass and contraction intensity affect 1) the magnitude of the cardiorespiratory responses, 2) the contribution of muscle metaboreflex to the cardiorespiratory responses, and 3) the arterial baroreflex contribution to HR control.

Adult↗

Effect of aging on responses to autonomic cardiovascular tests.

Cardiovascular deconditioning (CD) and orthostatic intolerance represent some of the major disturbances experienced by astronauts returning on Earth after micro-G exposure. The orthostatic intolerance observed in crew members after space missions has been hypothesized to be related to a disorder of the autonomic control of the cardiovascular system. There is evidence that advanced acing itself may alter the cardiovascular mechanism that underlie the CD. Due to involvement of elderly subjects in space flights it is mandatory to verify how age affects the cardiovascular autonomic neural regulation. In order to assess age-related differences in autonomic cardiovascular regulation our aim is to analyze the cardiovascular responses to 3 different autonomic tests that explore baroreceptor (tilt and deep breathing) and non-baroreceptor (isometric exercise) afferent pathways, in two goups of normal subjects characterized by significant different age.

Adolescent↗

Peripheral vascular changes after short-term simulated microgravity.

Cardiovascular deconditioning and orthostatic intolerance are the main symptoms experienced by astronauts after space flights. Alterations in the cardiovascular neural regulation have been implicated in the genesis of these disorders, but the mechanisms have not been clearly established. Alterations in the reflex control of circulation from the arterial and cardiopulmonary baroreceptive areas have been mainly hypothesized on the basis of long-term simulated microgravity studies. However, symptoms of orthostatic intolerance, and even fainting, are also observed after short-term exposure to simulated micro-G conditions. The possibility does exist that short-term exposure to micro-G conditions could affect the cardiovascular regulation differently from long-term exposure. Previous studies from this laboratory have shown that arterial baroreflex control of heart rate is not altered after 4 hours Head Down (HD) at -6 degrees, whereas it is significantly decreased after 28 days. Again, the role played by possible disturbances of the vasomotor regulation in the genesis of orthostatic intolerance after short term exposure to simulated microgravity has not yet been clarified. The aim of this study was therefore to evaluate peripheral blood flow changes following 2 and 4 h HD -6 degrees in healthy volunteers.

Adult↗

[Spontaneous baroreflex control of heart rate during chronic tandropril therapy].

Differently from other vasodilators, the antihypertensive effect of ACE-inhibitors is not accompanied by an increase in resting heart rate which suggests a modulatory action of these drugs on arterial baroreflex control of heart rate. It is debated whether this modulation involve, an increase in gain (or sensitivity) of baroreflex mechanisms controlling heart rate or is due to a baroreflex control resetting. In this study we investigated the arterial baroreflex control of heart rate both in supine rest and during active standing before and after 7 and 30 days of treatment with a new ACE-inhibitor, trandolapril (2 mg per os oid) in 15 mild hypertensive patients. Baroreflex control of heart rate has been dynamically and non-invasively assessed by analysis of the continuous relationship between beat-to-beat spontaneous fluctuations in systolic blood pressure and pulse interval. By this method, sequences of 3 or more consecutive beats in which systolic blood pressure and pulse interval change in the same direction (either increasing or decreasing) are identified and a linear regression is applied to each individual sequence. The mean individual slope of the systolic blood pressure/pulse interval ratio obtained by averaging all slopes computed within a given period, is calculated and taken as an estimate of the spontaneous baroreflex sensitivity for that period. Trandolapril reduced resting blood pressure significantly (from 147.5 +/- 3.3/95.3 +/- 1.5 to 129.5 +/- 3.7/83.6 +/- 1.6 and 126.6 +/- 3.9/84.5 +/- 1.7 mmHg after 7 e 30 days, respectively) without affecting heart rate. The treatment did not alter baroreflex sensitivity but resulted in an apparent leftward shift of the regression line relating systolic blood pressure to pulse interval along the pressure axis, reflecting the lower prevailing level of arterial pressure. The increases in heart rate and blood pressure induced by standing in control conditions were not significantly modified by trandolapril. Baroreflex sensitivity was significantly reduced by standing both in control conditions and, to the same extent, during treatment. These results suggest that ACE-inhibition does not alter the gain of the integrated baroreflex mechanisms controlling heart rate, but results in a baroreflex resetting that may explain the lack of tachycardia normally observed during antihypertensive therapy with ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗

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↗