Heart rate recovery after exercise: relations to heart rate variability and complexity

Physical exercise is associated with parasympathetic withdrawal and increased sympathetic activity resulting in heart rate increase. The rate of post-exercise cardiodeceleration is used as an index of cardiac vagal reactivation. Analysis of heart rate variability (HRV) and complexity can provide useful information about autonomic control of the cardiovascular system. The aim of the present study was to ascertain the association between heart rate decrease after exercise and HRV parameters. Heart rate was monitored in 17 healthy male subjects (mean age: 20 years) during the pre-exercise phase (25 min supine, 5 min standing), during exercise (8 min of the step test with an ascending frequency corresponding to 70% of individual maximal power output) and during the recovery phase (30 min supine). HRV analysis in the time and frequency domains and evaluation of a newly developed complexity measure - sample entropy - were performed on selected segments of heart rate time series. During recovery, heart rate decreased gradually but did not attain pre-exercise values within 30 min after exercise. On the other hand, HRV gradually increased, but did not regain rest values during the study period. Heart rate complexity was slightly reduced after exercise and attained rest values after 30-min recovery. The rate of cardiodeceleration did not correlate with pre-exercise HRV parameters, but positively correlated with HRV measures and sample entropy obtained from the early phases of recovery. In conclusion, the cardiodeceleration rate is independent of HRV measures during the rest period but it is related to early post-exercise recovery HRV measures, confirming a parasympathetic contribution to this phase.

Heat storage rate and acute fatigue in rats

Thermal environmental stress can anticipate acute fatigue during exercise at a fixed intensity (%VO2max). Controversy exists about whether this anticipation is caused by the absolute internal temperature (Tint, ºC), by the heat storage rate (HSR, cal/min) or by both mechanisms. The aim of the present study was to study acute fatigue (total exercise time, TET) during thermal stress by determining Tint and HSR from abdominal temperature. Thermal environmental stress was controlled in an environmental chamber and determined as wet bulb globe temperature (ºC), with three environmental temperatures being studied: cold (18ºC), thermoneutral (23.1ºC) or hot (29.4ºC). Six untrained male Wistar rats weighing 260-360 g were used. The animals were submitted to exercise at the same time of day in the three environments and at two treadmill velocities (21 and 24 m/min) until exhaustion. After implantation of a temperature sensor and treadmill adaptation, the animals were submitted to a Latin square experimental design using a 2 x 3 factorial scheme (velocity and environment), with the level of significance set at P<0.05. The results showed that the higher the velocity and the ambient temperature, the lower was the TET, with these two factors being independent. This result indicated that fatigue was independently affected by both the increase in exercise intensity and the thermal environmental stress. Fatigue developed at different Tint and HSR showed the best inverse relationship with TET. We conclude that HSR was the main anticipating factor of fatigue.

Effect of acute nitric oxide synthase inhibition in the modulation of heart rate in rats

Acute nitric oxide synthase inhibition with N G-nitro-L-arginine methyl ester (L-NAME) on chronotropic and pressor responses was studied in anesthetized intact rats and rats submitted to partial and complete autonomic blockade. Blood pressure and heart rate were monitored intra-arterially. Intravenous L-NAME injection (7.5 mg/kg) elicited the same hypertensive response in intact rats and in rats with partial (ganglionic and parasympathetic blockade) and complete autonomic blockade (38 ± 3, 55 ± 6, 54 ± 5, 45 ± 5 mmHg, respectively; N = 9, P = NS). L-NAME-induced bradycardia at the time when blood pressure reached the peak plateau was similar in intact rats and in rats with partial autonomic blockade (43 ± 8, 38 ± 5, 46 ± 6 bpm, respectively; N = 9, P = NS). Rats with combined autonomic blockade showed a tachycardic response to L-NAME (10 ± 3 bpm, P<0.05 vs intact animals, N = 9). Increasing doses of L-NAME (5.0, 7.5 and 10 mg/kg, N = 9) caused a similar increase in blood pressure (45 ± 5, 38 ± 3, 44 ± 9 mmHg, respectively; P = NS) and heart rate (31 ± 4, 34 ± 3, 35 ± 4 bpm, respectively; P = NS). Addition of L-NAME (500 µM) to isolated atria from rats killed by cervical dislocation and rats previously subjected to complete autonomic blockade did not affect spontaneous beating or contractile strength (N = 9). In vivo results showed that L-NAME promoted a tachycardic response in rats with complete autonomic blockade, whereas the in vitro experiments showed no effect on intrinsic heart rate, suggesting that humoral mechanisms may be involved in the L-NAME-induced cardiac response.

Role of nitric oxide of the median preoptic nucleus (MnPO) in the alterations of salivary flow, arterial pressure and heart rate induced by injection of pilocarpine into the MnPO and intraperitoneally

We investigated the effect of L-NAME, a nitric oxide (NO) inhibitor and sodium nitroprusside (SNP), an NO-donating agent, on pilocarpine-induced alterations in salivary flow, mean arterial blood pressure (MAP) and heart rate (HR) in rats. Male Holtzman rats (250-300 g) were implanted with a stainless steel cannula directly into the median preoptic nucleus (MnPO). Pilocarpine (10, 20, 40, 80, 160 µg) injected into the MnPO induced an increase in salivary secretion (P<0.01). Pilocarpine (1, 2, 4, 8, 16 mg/kg) ip also increased salivary secretion (P<0.01). Injection of L-NAME (40 µg) into the MnPO prior to pilocarpine (10, 20, 40, 80, 160 µg) injected into the MnPO or ip (1, 2, 4, 8, 16 mg/kg) increased salivary secretion (P<0.01). SNP (30 µg) injected into the MnPO or ip prior to pilocarpine attenuated salivary secretion (P<0.01). Pilocarpine (40 µg) injection into the MnPO increased MAP and decreased HR (P<0.01). Pilocarpine (4 mg/kg body weight) ip produced a decrease in MAP and an increase in HR (P<0.01). Injection of L-NAME (40 µg) into the MnPO prior to pilocarpine potentiated the increase in MAP and reduced HR (P<0.01). SNP (30 µg) injected into the MnPO prior to pilocarpine attenuated (100%) the effect of pilocarpine on MAP, with no effect on HR. Administration of L-NAME (40 µg) into the MnPO potentiated the effect of pilocarpine injected ip. SNP (30 µg) injected into the MnPO attenuated the effect of ip pilocarpine on MAP and HR. The present study suggests that in the rat MnPO 1) NO is important for the effects of pilocarpine on salivary flow, and 2) pilocarpine interferes with blood pressure and HR (side effects of pilocarpine), that is attenuated by NO.

Heart rate variability in athletes and nonathletes at rest and during head-up tilt

The purpose of the present study was to determine if autonomic heart rate modulation, indicated by heart rate variability (HRV), differs during supine rest and head-up tilt (HUT) when sedentary and endurance-trained cyclists are compared. Eleven sedentary young men (S) and 10 trained cyclists (C) were studied. The volunteers were submitted to a dynamic ECG Holter to calculate HRV at rest and during a 70º HUT. The major aerobic capacity of athletes was expressed by higher values of at anaerobic threshold and peak conditions (P < 0.05). At rest the athletes had lower heart rates (P < 0.05) and higher values in the time domain of HRV compared with controls (SD of normal RR interval, SDNN, medians): 59.1 ms (S) vs 89.9 ms (C), P < 0.05. During tilt athletes also had higher values in the time domain of HRV compared with controls (SDNN, medians): 55.7 ms (S) vs 69.7 ms (C), P < 0.05. No differences in power spectral components of HRV at rest or during HUT were detected between groups. Based on the analysis of data by the frequency domain method, we conclude that in athletes the resting bradycardia seems to be much more related to changes in intrinsic mechanisms than to modifications in autonomic control. Also, HUT caused comparable changes in sympathetic and parasympathetic modulation of the sinus node in both groups.

Identification of anaerobic threshold using heart rate response during dynamic exercise

The objective of the present study was to characterize the heart rate (HR) patterns of healthy males using the autoregressive integrated moving average (ARIMA) model over a power range assumed to correspond to the anaerobic threshold (AT) during discontinuous dynamic exercise tests (DDET). Nine young (22.3 ± 1.57 years) and 9 middle-aged (MA) volunteers (43.2 ± 3.53 years) performed three DDET on a cycle ergometer. Protocol I: DDET in steps with progressive power increases of 10 W; protocol II: DDET using the same power values as protocol 1, but applied randomly; protocol III: continuous dynamic exercise protocol with ventilatory and metabolic measurements (10 W/min ramp power), for the measurement of ventilatory AT. HR was recorded and stored beat-to-beat during DDET, and analyzed using the ARIMA (protocols I and II). The DDET experiments showed that the median physical exercise workloads at which AT occurred were similar for protocols I and II, i.e., AT occurred between 75 W (116 bpm) and 85 W (116 bpm) for the young group and between 60 W (96 bpm) and 75 W (107 bpm) for group MA in protocols I and II, respectively; in two MA volunteers the ventilatory AT occurred at 90 W (108 bpm) and 95 W (111 bpm). This corresponded to the same power values of the positive trend in HR responses. The change in HR response using ARIMA models at submaximal dynamic exercise powers proved to be a promising approach for detecting AT in normal volunteers.

A semi-automatic computerized method to measure baroreflex-mediated heart rate responses that reduces interobserver variability

Arterial baroreflex sensitivity estimated by pharmacological impulse stimuli depends on intrinsic signal variability and usually a subjective choice of blood pressure (BP) and heart rate (HR) values. We propose a semi-automatic method to estimate cardiovascular reflex sensitivity to bolus infusions of phenylephrine and nitroprusside. Beat-to-beat BP and HR time series for male Wistar rats (N = 13) were obtained from the digitized signal (sample frequency = 2 kHz) and analyzed by the proposed method (PRM) developed in Matlab language. In the PRM, time series were low-pass filtered with zero-phase distortion (3rd order Butterworth used in the forward and reverse direction) and presented graphically, and parameters were selected interactively. Differences between basal mean values and peak BP (deltaBP) and HR (deltaHR) values after drug infusions were used to calculate baroreflex sensitivity indexes, defined as the deltaHR/deltaBP ratio. The PRM was compared to the method traditionally (TDM) employed by seven independent observers using files for reflex bradycardia (N = 43) and tachycardia (N = 61). Agreement was assessed by Bland and Altman plots. Dispersion among users, measured as the standard deviation, was higher for TDM for reflex bradycardia (0.60 ± 0.46 vs 0.21 ± 0.26 bpm/mmHg for PRM, P < 0.001) and tachycardia (0.83 ± 0.62 vs 0.28 ± 0.28 bpm/mmHg for PRM, P < 0.001). The advantage of the present method is related to its objectivity, since the routine automatically calculates the desired parameters according to previous software instructions. This is an objective, robust and easy-to-use tool for cardiovascular reflex studies.

Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine

Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 ± 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5% pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 ± 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 ± 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 ± 1.4; pilocarpine = 2.7 ± 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.

Loss of resting bradycardia with detraining is associated with intrinsic heart rate changes

The mechanisms underlying the loss of resting bradycardia with detraining were studied in rats. The relative contribution of autonomic and non-autonomic mechanisms was studied in 26 male Wistar rats (180-220 g) randomly assigned to four groups: sedentary (S, N = 6), trained (T, N = 8), detrained for 1 week (D1, N = 6), and detrained for 2 weeks (D2, N = 6). T, D1 and D2 were treadmill trained 5 days/week for 60 min with a gradual increase towards 50% peak VO2. After the last training session, D1 and D2 were detrained for 1 and 2 weeks, respectively. The effect of the autonomic nervous system in causing training-induced resting bradycardia and in restoring heart rate (HR) to pre-exercise training level (PET) with detraining was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. T rats significantly increased peak VO2 by 15 or 23.5% when compared to PET and S rats, respectively. Detraining reduced peak VO2 in both D1 and D2 rats by 22% compared to T rats, indicating loss of aerobic capacity. Resting HR was significantly lower in T and D1 rats than in S rats (313 ± 6.67 and 321 ± 6.01 vs 342 ± 12.2 bpm) and was associated with a significantly decreased intrinsic HR (368 ± 6.1 and 362 ± 7.3 vs 390 ± 8 bpm). Two weeks of detraining reversed the resting HR near PET (335 ± 6.01 bpm) due to an increased intrinsic HR in D2 rats compared with T and D1 rats (376 ± 8.8 bpm). The present study provides the first evidence of intrinsic HR-mediated loss of resting bradycardia with detraining in rats.

Effects of age and physical activity on the autonomic control of heart rate in healthy men

The effects of the aging process and an active life-style on the autonomic control of heart rate (HR) were investigated in nine young sedentary (YS, 23 ± 2.4 years), 16 young active (YA, 22 ± 2.1 years), 8 older sedentary (OS, 63 ± 2.4 years) and 8 older active (OA, 61 ± 1.1 years) healthy men. Electrocardiogram was continuously recorded for 15 min at rest and for 4 min in the deep breathing test, with a breath rate of 5 to 6 cycles/min in the supine position. Resting HR and RR intervals were analyzed by time (RMSSD index) and frequency domain methods. The power spectral components are reported in normalized units (nu) at low (LF) and high (HF) frequency, and as the LF/HF ratio. The deep breathing test was analyzed by the respiratory sinus arrhythmia indices: expiration/inspiration ratio (E/I) and inspiration-expiration difference (deltaIE). The active groups had lower HR and higher RMSSD index than the sedentary groups (life-style condition: sedentary vs active, P < 0.05). The older groups showed lower HFnu, higher LFnu and higher LF/HF ratio than the young groups (aging effect: young vs older, P < 0.05). The OS group had a lower E/I ratio (1.16) and deltaIE (9.7 bpm) than the other groups studied (YS: 1.38, 22.4 bpm; YA: 1.40, 21.3 bpm; OA: 1.38, 18.5 bpm). The interaction between aging and life-style effects had a P < 0.05. These results suggest that aging reduces HR variability. However, regular physical activity positively affects vagal activity on the heart and consequently attenuates the effects of aging in the autonomic control of HR.

The decreased oxygen uptake during progressive exercise in ischemia-induced heart failure is due to reduced cardiac output rate

We tested the hypothesis that the inability to increase cardiac output during exercise would explain the decreased rate of oxygen uptake (VO2) in recent onset, ischemia-induced heart failure rats. Nine normal control rats and 6 rats with ischemic heart failure were studied. Myocardial infarction was induced by coronary ligation. VO2 was measured during a ramp protocol test on a treadmill using a metabolic mask. Cardiac output was measured with a flow probe placed around the ascending aorta. Left ventricular end-diastolic pressure was higher in ischemic heart failure rats compared with normal control rats (17 ± 0.4 vs 8 ± 0.8 mmHg, P = 0.0001). Resting cardiac index (CI) tended to be lower in ischemic heart failure rats (P = 0.07). Resting heart rate (HR) and stroke volume index (SVI) did not differ significantly between ischemic heart failure rats and normal control rats. Peak VO2 was lower in ischemic heart failure rats (73.72 ± 7.37 vs 109.02 ± 27.87 mL min-1 kg-1, P = 0.005). The VO2 and CI responses during exercise were significantly lower in ischemic heart failure rats than in normal control rats. The temporal response of SVI, but not of HR, was significantly lower in ischemic heart failure rats than in normal control rats. Peak CI, HR, and SVI were lower in ischemic heart failure rats. The reduction in VO2 response during incremental exercise in an ischemic model of heart failure is due to the decreased cardiac output response, largely caused by depressed stroke volume kinetics.

Role of the cardiac nerve in the effect of a novel innocuous stimulus on the heart rate of Megalobulimus mogianensis

The effects of a brief jet of water delivered to the anterior portion of body-head on the heart rate of Megalobulimus mogianensis were determined in a group of intact snails (N = 8), previously prepared for electrocardiogram recording. The heart rate was significantly increased following stimulation. Nevertheless, with repetition of the stimulus there was a significant decrease in the magnitude of the heart rate variation and in the time for the basal heart rate to recover (first stimulus, 7.4 ± 1.2 bpm and 15.5 ± 1.8 min; second stimulus, 4.8 ± 1.0 bpm and 10.6 ± 1.5 min; third stimulus, 5.0 ± 0.3 bpm and 11.1 ± 1.8 min), indicating that this behavioral response undergoes early habituation. To determine the role of the cardiac nerve in mediating the heart rate alterations induced by the jet of water two other groups were tested: denervated animals (N = 8) and sham-operated control animals (N = 8). Although the innocuous stimulus caused the heart rate to increase significantly in both experimental groups, the mean increase in heart rate in denervated animals (3.2 ± 0.4 bpm) was 41% of the value obtained in sham-operated animals (7.8 ± 1.5 bpm), indicating that the cardiac nerve is responsible for 59% of the cardioacceleration induced by the innocuous stimulus. The increase in heart rate observed in denervated animals may be due to an increase in venous return promoted by the intense muscular activity associated with the retraction-protraction of the anterior part of the body induced by the jet of water.

Luteal phase of the menstrual cycle increases sweating rate during exercise

The present study evaluated whether the luteal phase elevation of body temperature would be offset during exercise by increased sweating, when women are normally hydrated. Eleven women performed 60 min of cycling exercise at 60% of their maximal work load at 32ºC and 80% relative air humidity. Each subject participated in two identical experimental sessions: one during the follicular phase (between days 5 and 8) and the other during the luteal phase (between days 22 and 25). Women with serum progesterone >3 ng/mL, in the luteal phase were classified as group 1 (N = 4), whereas the others were classified as group 2 (N = 7). Post-exercise urine volume (213 ± 80 vs 309 ± 113 mL) and specific urine gravity (1.008 ± 0.003 vs 1.006 ± 0.002) changed (P < 0.05) during the luteal phase compared to the follicular phase in group 1. No menstrual cycle dependence was observed for these parameters in group 2. Sweat rate was higher (P < 0.05) in the luteal (3.10 ± 0.81 g m-2 min-1) than in the follicular phase (2.80 ± 0.64 g m-2 min-1) only in group 1. During exercise, no differences related to menstrual cycle phases were seen in rectal temperature, heart rate, rate of perceived exertion, mean skin temperature, and pre- and post-exercise body weight. Women exercising in a warm and humid environment with water intake seem to be able to adapt to the luteal phase increase of basal body temperature through reduced urinary volume and increased sweating rate.

Autonomic modulation of heart rate of young and postmenopausal women undergoing estrogen therapy

The aim of the present study was to determine whether estrogen therapy (ET) reduces alterations of the autonomic control of heart rate (HR) due to hypoestrogenism and aging. Thirteen young (24 ± 2.6 years), 10 postmenopausal (53 ± 4.6 years) undergoing ET (PM-ET), and 14 postmenopausal (56 ± 2.6 years) women not undergoing ET (PM) were studied. ET consisted of 0.625 mg/day conjugated equine estrogen. HR was recorded continuously for 8 min at rest in the supine and sitting positions. HR variability (HRV) was analyzed by time (SDNN and rMSSD indices) and frequency domain methods. Power spectral components are reported as normalized units (nu) at low (LF) and high (HF) frequencies, and as LF/HF ratio. Intergroup comparisons: SDNN index was higher in young (median: supine, 47 ms; sitting, 42 ms) than in PM-ET (33; 29 ms) and PM (31; 29 ms) women (P < 0.05). PM showed lower HFnu, higher LFnu and higher LF/HF ratio (supine: 44, 56, 1.29; sitting: 38, 62, 1.60) than the young group in the supine position (61, 39, 0.63) and the PM-ET group in the sitting position (57, 43, 0.75; P < 0.05). Intragroup comparisons: HR was lower in the supine than in the sitting position for all groups (P < 0.05). The HRV decrease from the supine to the sitting position was significant only in the young group. These results suggest that HRV decreases during aging. ET seems to attenuate this process, promoting a reduction in sympathetic activity on the heart and contributing to the cardioprotective effect of estrogen hormones.

Antibodies to citrullinated peptides are not associated with the rate of joint destruction in patients with a well-established diagnosis of rheumatoid arthritis

Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis (RA) and represent a significant risk factor for undifferentiated polyarthritis. This prognostic ability may be related to the very diagnostic performance of these autoantibodies, since RA is a more erosive disease than other forms of arthritis. The present study evaluated an association of antibodies to citrullinated peptides and the rate of joint destruction in patients with a well-established diagnosis of RA. Seventy-one patients with RA were evaluated in 1994 and again in 2002 (functional class, joint count, Health Assessment Questionnaire score, hands X-ray). Autoantibodies (rheumatoid factor (RF), anti-perinuclear factor, anti-cyclic citrullinated peptide (CCP) antibodies) and Sharp's index were analyzed blindly. Delta Sharp was calculated as the difference in Sharp's index obtained in 1994 and 2002. During the follow-up the Health Assessment Questionnaire score increased from 0.91 ± 0.74 to 1.39 ± 0.72 (P < 0.001). Similarly, the number of swollen joints increased from 4.6 ± 5.71 to 6.4 ± 4.1 (P = 0.002). The frequency of autoantibodies and anti-CCP titer remained stable; however, serum RF concentration increased from 202.8 ± 357.6 to 416.6 ± 636.5 IU/mL (P = 0.003). Sharp's index increased from 56.7 ± 62.1 to 92.4 ± 80.9 (P < 0.001). No correlation was observed between Delta Sharp and the presence of RF, anti-perinuclear factor, and anti-CCP antibodies at baseline. Antibodies to citrullinated epitopes are specific and early markers for the diagnosis of RA but do not seem to be associated with the rate of joint destruction in patients with a well-established diagnosis of RA.