Autonomic nervous control of heart rate during blood-flow restricted exercise in man

Summary Power spectra of instantaneous heart rate (f _c) allows the estimation of the contribution of sympathetic and parasympathetic control of f _c during steady-state conditions. The present study was designed to examine autonomic control of f _c as influenced by normal dynamic leg exercise and by ischemic leg exercise. Eight subjects performed supine cycle ergometry at 30% of their control peak work rate, with and without blood-flow restriction. Blood-flow restriction was induced by exposing the exercising legs to a supra-atmospheric pressure of 6.7 kPa (leg positive pressure; LPP). The exercise responses of arterial pressure and f _c increased (P<0.05) by LPP exposure. The exaggerated pressor response may be attributed to a chemoreflex drive originating in the ischemic muscles. Exposure to LPP during exercise also produced a significant decrease in parasympathetically mediated high frequency (HF; 0.15-1.00 Hz) fluctuation of f _c, as indicated by a decrease (P<0.05) in percent HF power compared to the control exercise level. During LPP exercise, the sympathetically mediated very low frequency (VLF; 0–0.05 Hz) fluctuation of f _c increased, as indicated by an increase (P<0.05) in percent VLF power above control exercise levels. Both LPP and control exercise conditions decreased (P<0.05) power in all frequency ranges of interest compared to their respective resting conditions. The results suggest that the increase in f _c associated with normal dynamic exercise was mediated predominantly by parasympathetic withdrawal, whereas the exaggerated f _c response during ischemic exercise resulted from a combination of cardiac sympathetic drive and parasympathetic withdrawal. The increase in sympathetic activity is attributable to a muscle chemoreflex drive, which also may have attenuated parasympathetic activity by reciprocal inhibition. Alternatively, augmented central command mediated parasympathetic withdrawal during ischemic exercise.     

Learned control of heart rate during exercise in patients with borderline hypertension

Summary Twelve patients with borderline hypertension [⩽21.33/12.6, ⩾18.6/12.0 kPa (⩽160/ 95; ⩾ 140/90 mm Hg)] participated in an experiment aimed at testing whether they could learn to attenuate heart rate while exercising on a cycle ergometer. Six experimental (E) subjects received beat-to-beat heart-rate feedback and were asked to slow heart rate while exercising; six control (C) subjects received no feedback. Averaged over 5 days (25 training trials) the exercise heart-rate of the E group was 97.8 bt min⁻¹, whereas the C group averaged 107 bt min⁻¹ (P=0.03). Systolic blood pressure was unaffected by feedback training. Generally, changes in rate-pressure product reflected changes in heart-rate. Oxygen consumption was lower in the E than in the C group late in training. We conclude that neurally mediated changes associated with exercise in patients with borderline hypertension can be brought under behavioral control through feedback training.     

Autonomic nervous control of the heart rate during isometric exercise in normal man

The relative contribution of the efferent components of the autonomic nervous system to the regulation of tachycardia induced by isometric exercise was assessed in 23 normal males. The isometric exercise (handgrip) was performed at the maximum intensity tolerated by the individual over a period of 10 s (maximal voluntary contraction — MVC) and at levels equivalent to 75, 50 and 25% of MVC for 20, 40 and 10 s, respectively. The study was performed both under control conditions and after pharmacological blockade with atropine (12 individuals) or propranolol (11 individuals). Under control conditions, the heart rate (HR) responses to isometric effort were dependent on the intensity and duration of the exercise, showing a tendency towards progressive elevation with the maintenance of muscular contraction at the levels studied. The tachycardia evoked by this effort was of considerable magnitude and of rapid onset, especially at the more intense levels of activity. Parasympathetic blockade markedly decreased tachycardia, which manifested itself during the first 10 s of exercise at all levels of intensity, whereas sympathetic blockade markedly modified the HR response after 10 s of effort at the 75 and 50% MVC levels. A slight depression of the tachycardiac response could be observed already after 10 s of maximum effort after propranolol. The present results suggest that the autonomic regulation of these responses is based on a biphasic mechanism, with the initial phase depending on the rapid withdrawal of the parasympathetic influence, followed by a marked sympathetic contribution to the induction of tachycardia after 10 s of isometric contraction or even a little before at maximum exertion.     

Effect of exercise mode on heart rate variability during steady state exercise

This study examined the effect of exercise mode on geometrical, and time and frequency domain measures of heart rate variability (HRV) during steady-state, moderate intensity exercise of the same HR. Seventeen healthy, active male participants volunteered for this study and completed a treadmill determination. One week later, cardiorespiratory, perceptual and HRV measures were recorded during seated rest (15 min) and consecutive bouts (15 min) of steady-state exercise at 50 and 65% of maximal HR. Exercise was performed using either upper body (arm ergometer), lower body (cycle) or whole body (treadmill) modes. Separated by 1 week and in a random order, participants undertook the same procedures with the remaining exercise modes. Cardiorespiratory, perceptual and HRV responses were determined during rest and steady-state exercise and analysed by two-way (mode vs. stage) repeated measures ANOVA and post hoc pairwise comparisons. Apart from a reduced respiratory rate during lower body exercise, whole and lower body exercise resulted in similar cardiorespiratory, perceptual and HRV responses. Compared to whole or lower body exercise, upper body exercise resulted in significantly (P < 0.05) greater measures of HRV particularly those within the very low (0–0.04 Hz) and low (0.04–0.15 Hz) frequency bands, greater rating of perceived exertion and less oxygen consumption. Upper body, moderate intensity exercise resulted in greater HRV compared to whole or lower body exercise with further studies necessary to elucidate the mechanisms and clinical implications for this greater HRV. Part of this work has previously been presented at the 2004 Sports Medicine Australia National Conference, 6–9th October, Alice Springs, Australia.     

Differences in autonomic modulation of heart rate during arm and leg exercise.

Heart rate (HR) is higher during dynamic arm exercise than during leg exercise at equal oxygen consumption levels, but the physiological background for this difference is not completely understood. The vagally mediated beat-to-beat R-R interval fluctuation decreases until the level of approximately 50% of maximal oxygen consumption during an incremental bicycle exercise, but the vagal responses to arm exercise are not well known. Changes in autonomic modulation of HR were compared during arm and leg exercise by measuring beat-to-beat R-R interval variability from a Poincaré plot normalized for the average R-R interval (SD1n), a measure of vagal activity, in 14 healthy male subjects (age 20 +/- 4 years) who performed graded bicycle and arm cranking tests until exhaustion. Seven of the subjects also performed the dynamic arm and leg tests after beta-adrenergic blockade (propranolol 0.2 mg kg-1 i.v.). More rapid reduction occurred in SD1n during the low-intensity level of dynamic arm exercise than during dynamic leg exercise without beta-blockade (e.g. 11 +/- 6 vs. 20 +/- 10 at the oxygen consumption level of 1.2 l min-1; P < 0.001) and with beta-blockade (e.g. 13 +/- 4 vs. 25 +/- 10 at the level of 1.0 l min-1; P < 0.05), and the mean HR was significantly higher during submaximal arm work than during leg work in both cases (e.g. during beta-blockade 81 +/- 12 vs. 74 +/- 6 beats min-1 at the level of 1.0 l min-1; P < 0.05). These data show that dynamic arm exercise results in more rapid withdrawal of vagal outflow than dynamic leg exercise.     

Kinetics of heart rate and catecholamines during exercise in humans

Summary To elucidate the role of factors other than the nervous system in heart rate (f _c) control during exercise, the kinetics off _c and plasma catecholamine concentrations were studied in ten heart transplant recipients during and after 10-min cycle ergometer exercise at 50 W. Thef _c did not increase at the beginning of the exercise for about 60 s. Then in the eight subjects who completed the exercise it increased following an exponential kinetic with a mean time constant of 210 (SEM 22) s. The two other subjects were exhausted after 5 and 8 min of exercise during whichf _c increased linearly. At the cessation of the exercise,f _c remained unchanged for about 50 s and then decreased exponentially with a time constant which was unchanged from that at the beginning of exercise. In the group of eight subjects plasma noradrenaline concentration ([NA]) increased after 30 s to a mean value above resting of 547 (SEM 124) pg · ml^–1, showing a tendency to a plateau, while adrenaline concentration ([A]) did not increase significantly. In the two subjects who became exhausted an almost linear increase in [NA] occurred up to about 1,300 pg · ml^–1 coupled with a significant increase in [A]. During recovery an immediate decrease in [NA] was observed towards resting values. The values of thef _c increase above resting levels determined at the time of blood collection were linearly related with [NA] increments both at the beginning and end of exercise with a similar slope, i.e. about 2.5 beats · min^–1 per 100 pg · ml^–1 of [NA] change. These findings would seem to suggest that in the absence of heart innervation the increase inf _c depends on plasma [NA].     

Influence of intensive cycling training on heart rate variability during rest and exercise.

The current study examined whether changes in heart rate variability (HRV) following intensive cycling training contribute to the mechanism of training-induced bradycardia. Thirteen healthy untrained subjects, ages 18-27 years, underwent recordings of heart rate (HR) and VO2max before and after 8 weeks of cycling, 25-60 min/day, 5 days/week at > 80% maximum HR (HRmax). Heart rate recordings were obtained during supine rest and submaximal exercise and were analysed for the following components of HRV: low frequency (LF, 0.041-0.15 Hz); high frequency (HF, 0.15-0.40 Hz); LF/HF ratio and total power (TP, 0-0.40 Hz). At posttraining, VO2max was significantly increased while HR was significantly reduced at rest and all absolute exercise work rates. Training-induced lower HR was accompanied by significantly greater HF and TP during rest as well as LF, HF, and TP during all absolute exercise work rates. Posttraining HR and the majority of HRV measures were similar to pretraining values at the same relative exercise intensity (% HRmax). These results indicated that 8 weeks of intensive cycling training increased HRV and cardiac vagal modulation during rest and absolute exercise work rates but had little effect during relative exercise work rates. Increased vagal modulation resulting from intensive exercise training may contribute to the mechanism of training-induced bradycardia.     

Heart rate changes with exercise and voluntary heart rate acceleration.

The present study examined the relationship between heart rate (HR) changes accompanying isometric and isotonic exercises and HR changes during attempted voluntary HR acceleration. Substantial cardiac accelerations accompanied both types of exertion, with the isotonic exercise attracting the larger magnitude HR changes. Significant HR increases were also observed during attempted voluntary HR acceleration both with and without feedback; however, feedback prompted larger HR increases than instructions alone. The HR changes accompanying both types of exercise reliably predicted the extent of voluntary HR increase but only for the condition in which feedback was available. This occurred in spite of the absence of observable EMG changes during attempted HR acceleration. Changes in respiration rate during voluntary HR increase were highly correlated with changes in HR. A similar co-variation occurred with the isotonic exercise but was absent with the isometric exercise. The results are discussed in terms of the possible mediational mechanisms underlying voluntary HR acceleration.     

Changes in human heart rate during sleep following daily physical exercise

Summary Four fit, healthy young men (aged 20) volunteered for the experiment. After a 5 day control period, they marched for 6 consecutive days (from 09:00 h to 17:00 h) for 34 km/day at a speed of 6 km/h, with an energy expenditure of 35% of individual max. A recovery period of 5 consecutive days began immediately after the exercise period. Sleep records and electrocardiograms were taken every night during the three periods from 22:00 h to 06:00 h.During the exercise period the night time heart rates increased by about 10%, compared to the previous control condition, and returned to normal during the recovery period.The relation between heart rate changes and sleep stages remained identical throughout the three experimental periods. Three subjects showed an increase in heart rate during paradoxical sleep, compared to the preceding slow wave sleep, while one subject experienced the reverse.The tonic increases in heart rate are discussed in relation to changes in body temperature, sleep patterns, blood composition and hormonal status induced by the physical exercise performed.Supported by grant N 77/1198 from the Direction des Recherches et Etudes Techniques (Délégation Ministérielle pour l'Armement)     

Autonomic blockade does not prevent learned heart rate attenuation during exercise

Each of three monkeys was operantly conditioned to slow its heart, to exercise (lift weights) and to attenuate the tachycardia of exercise by combining these two skills. Each was further tested during beta-adrenergic blockade (atenolol), combined alpha-adrenergic blockade (prazosin) and beta-adrenergic blockade, or cholinergic blockade (methylatropine). During all experiments heart rate, stroke volume, intraarterial blood pressure, O2 consumption, and CO2 production were recorded on a beat-to-beat basis. Each animal was able to attenuate the tachycardia of exercise under each of the drug conditions, indicating that "central command" is not the expression of fixed, cardiovascular and pulmonary reflexes elicited by somato-motor commands, but rather is an adaptive behavior, determined by environmental contingencies and mediated by cardiovascular and pulmonary as well as somato-motor commands. The ability of the animals to perform with greater cardiac efficiency during the combined exercise and heart rate slowing task relative to the exercise-only task was not affected by sympathetic blockade; however, parasympathetic blockade did reduce cardiac efficiency.     

Stable T wave effects during improvement of heart rate control with biofeedback.

Under audiovisual heart rate feedback the differences between attempts to accelerate and decelerate improved with practice. Simultaneously, T wave amplitude was reduced during acceleratory trials and remained constant during deceleratory trials. The T wave difference between acceleratory and deceleratory trials, unlike the heart rate differences, did not improve with trial repetition. It was concluded that the improvement in heart rate control was parasympathetically mediated.     

Spectral analysis of heart rate variability during heat exposure and repeated exercise

This study examined indices of parasympathetic (PNS) and sympathetic (SNS) nerve activity during exposure to heat and/or two successive bouts of exercise. Seven healthy males [age = 27.1 (3.6) years; mean (SD), maximum oxygen consumption (V˙O_{2 max} )= 48.1 (7.6) ml?·?kg^?1?·?min^?1] were assigned to each of four experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber subjects performed exercise on a cycle ergometer (two 30-min bouts at ≈50% V˙O_{2 max} , separated by a 45-min recovery period, (CEx and HEx, respectively) or remained seated (CS and HS, respectively) for 2 h. The R-R intervals of the subjects' ECGs were analyzed for selected near-steady-state time periods [termed Phase I (25–40 min) and Phase II (100–115 min)] according to the method of Yamamoto and Hughson (J Appl Physiol 71:1143–1150, 1991). Total (P_T), low-frequency (P_LF = 0–0.15 Hz) and high-frequency (P_HF = 0.15–0.5 Hz) power spectra were calculated using coarse-graining spectral analysis. Heat exposure alone did not alter autonomic balance or levels of circulating catecholamines significantly. Exercise in both environmental conditions induced a significant decrease in an index of PNS tone (P_HF?:?P_T) [PNS indicator for CS = 0.084 (0.04) vs CEx = 0.023 (0.015) and HS = 0.065 (0.027) vs HEx = 0.015 (0.009)], with an increase in catecholamine concentrations. Although the index of SNS activity (P_LF:P_HF) tended to rise with exercise in both environmental conditions, increments reached levels of significance only during exercise in the heat [SNS indicator for CS = 8.22 (5.58) vs CEx = 34.06 (21.73) and HS = 8.94 (5.49) vs HEx = 54.29 (49.80)]. The relative magnitudes of SNS and PNS indicators did not differ significantly between the first and second bouts of exercise. These results indicate the substantial contribution of vagal withdrawal and catecholamine secretion to the increase in heart rate that occurs during repeated moderate exercise at room temperature and the additional contribution from SNS activity during such exercise in the heat.     

Heart rate variability during cycloergometric exercise or judo wrestling eliciting the same heart rate level

This study compared heart rate variability (HRV) in ten male judokas between two types of exercise eliciting the same near-maximal average heart rate (HR): judo wrestling vs. cycloergometric bout. Beat-to-beat RR intervals were recorded during (1) a 4-min judo randori (wrestling); (2) a 4-min cycloergometric exercise eliciting maximal oxygen consumption (O_2MAX). Time series were analyzed both by short term Fourier transform (STFT) and Poincaré plot (PP). The main results are as follows. First, despite the fact that the same maximal HR was reached during the two exercises, the spectral energy computed from the judo recordings was significantly higher than that recorded from the cycloergometric exercise. Second, according to the PP index of rapid HRV (SD1), the high-frequency spectral energy (HF) was significantly higher during judo than cycloergometric exercise as well. Third, judo spectra show chaotic harmonics in place of the precise HF peak observed during cycloergometric exercise. Fourth, the respective parts of normalized LFn and HFn are not different between the two exercise modes, suggesting that autonomic control during severe exercise cannot depend on the type of exercise. In conclusion, this study shows that it is possible, according to the observed kind of variability from RR time series, to differentiate between two types of effort: steady-state dynamic exercise or conversely exercise made of both isometric and irregular dynamic efforts (wrestling, collective sports, and others).     

Changes in electroencephalogram and heart rate during treadmill exercise in the rat

To explore whether exercise is related to electroencephalogram (EEG) and heart rate changes, continuous EEG power spectral analysis was performed on rats during treadmill exercise. Compared with before exercise, treadmill exercise resulted promptly in a higher mean power frequency and theta (6-10 Hz) power of the EEG, but lower delta (0.5-4 Hz) power of the EEG together with a lower R-R interval of electrocardiogram. Such changes quickly reversed when the treadmill exercise was stopped. We conclude that the cerebral cortex activates along with the autonomic system during running. Our methodology offers an efficient way to study the interaction of cerebral and brain stem functions with exercise in the rat.     

Central and baroreflex control of heart rate during the wake-sleep cycle in rat.

Spontaneous fluctuations in Heart Period (HP) and Mean Arterial Pressure (MAP) make it possible to evaluate baroreceptor-heart rate reflex sensitivity (BRS). 30-s sequences of HP and MAP beat-to-beat values were considered in the different wake-sleep states (Wake, W; Quiet Sleep, QS; Active Sleep, AS) in rats to assess whether 1) BRS changes between states and 2) the different indexes supply consistent BRS measures. BRS indexes were calculated according to validated literature procedures as regression coefficients of HP vs. MAP 1) within all ramps of increasing or decreasing MAP of four beats or more, with HP and MAP changing in the same direction (baroreflex-mediated fluctuations, BRSp), 2) within all such ramps irrespective of the relative direction of HP and MAP changes (baroreflex + non-baroreflex, i.e. non-homeostatic centrally driven, fluctuations, BRSA). HP vs. MAP regression coefficient along the entire 30-s sequence (bHPMAP) was also calculated. RESULTS: BRSp did not change among states, BRSA decreased from QS to W to AS, bHPMAP decreased from QS to W and became negative in AS. CONCLUSIONS: 1) as indicated by BRSp, baroreflex sensitivity is state independent, 2) BRSp to BRS(A) to bHPMAP are increasingly affected by non-baroreflex fluctuations, BRSp being most apt to measure BRS, 3) non-homeostatic MAP and HP fluctuations increase from QS to W and prevail in AS. These potentially harmful fluctuations are normally buffered by baroreflexes: in the case of baroreflex impairment, circulatory risk may arise in conditions like AS, when they prevail.     

Age-related heart rate response to exercise in heart transplant recipients. Functional significance

The heart rate (HR) and O(2) uptake (VO(2)) responses to cycle ergometer exercise and the role of O(2) transport in limiting submaximal and maximal aerobic performance were assessed in 33 heart transplant recipients (HTR) [14 children (P-HTR), 11 young adults (YA-HTR) and 8 middle-age adults (A-HTR)] and in 28 age-matched control subjects (CTL). In 7 P-HTR ("responders") the HR response to the onset of exercise (on-response) was as fast as that of CTL, whereas in all other patients ("non-responders") the HR on-response was typical of the denervated heart. Compared with non-responder P-HTR, responder P-HTR were also characterized by a normal peak HR (177+/- 16 vs. 151+/- 25 beats/min), an equally slow time constant for the VO(2) on-response (tau: 54 +/- 11 vs. 62+/- 13 s) and a similar low (approximately 60% of that of CTL) peak VO(2) (28 +/- 7 vs. 26 +/- 10 ml/kg per min). On the other hand non-responder YA-HTR and A-HTR were characterized by a relatively low peak HR (151 +/- 21 and 144 +/- 29 beats/min, respectively), a slow tau for the on-response (63 +/- 12 and 70 +/- 11 s) and a low peak (28 +/- 7 and 19 +/- 6 ml/kg per min). In conclusion, a sizeable number of paediatric patients (responder P-HTR) may reacquire the normal HR response to exercise, both in terms of kinetics and maximal level. Despite the almost complete recovery of cardiovascular function, and, probably, oxygen delivery, both the kinetics of the VO(2) on-response and the maximal aerobic power of the responder P-HTR were similar to those of non-responder P-HTR. The latter finding is probably attributable to peripheral limitations, due to inborn and/or pharmacological muscle deterioration.     

Body position affects the power spectrum of heart rate variability during dynamic exercise

Summary The power spectrum analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in six men in supine (S) and sitting (C) postures at rest and during steady-state cycle exercise at about 14010, 28%, 45%, 67% of the maximal oxygen consumption (% VO_2max). The total power of RRV decreased exponentially as a function of exercise intensity in a similar way in both postures. Three components were recognized in the power spectra: firstly, a high frequency peak (HF), an expression of respiratory arrhythmia, the central frequency (f _central) of which increased in both S and C from a resting value of about 0.26 Hz to 0.42 Hz at 67% VO_2max; secondly, a low frequency peak (LF) related to arterial pressure control, the f _central of which remained constant at 0.1 Hz in C, whereas in S above 28% VO_2max decreased to 0.07 Hz; and thirdly, a very low frequency component (VLF; less than 0.05 Hz, no f _central). The power of the three components (as a percentage of the total power) depended on the body posture and the metabolic demand. HF% at rest was 30.3 (SEM 6.6) % in S and 5.0 (SEM 0.8) % in C. During exercise HF% decreased by about 30% in S and increased to 19.7 (SEM 5.5) % at 28% VO_2max in C. LF% was lower in S than in C at rest [31.6 (SEM 5.7) % vs 44.9 (SEM 6.4) %; P<0.05], remaining constant up to 28% VO_2max. At the highest intenstities it increased to 54.0 (SEM 15.6) % in S whereas in C it decreased to 8.5 (SEM 1.6) %. VLF represented the remaining power and the change was in the opposite direction to LF. The changes in power spectrum distribution of RRV during exercise depended on the intensity and the body posture. In particular, the LF peak showed opposite trends in S and C tasks, thus suggesting a different readjustment of arterial pressure control mechanisms in relation to the blood distribution and peripheral resistances.