It is well known that the increase in heart rate (HR) during incremental exercise is mediated by both a decrease in parasympathetic activity and in an increase in sympathetic stimulation. Brooke et al. (1) and Brooke and Hamley (2) demonstrated that the majority of racing cyclists showed a nonlinear HR response to an incremental cycle ergometer test. These authors reported that in most cases the heart rate performance curve (HRPC) was S-shaped with a long linear portion in the middle. They further report that during maximal workload tests the HR response is linear up to approximately 70% of maximal performance with a distinctly more leveled-off response in HR for the duration of the test. Conconi et al.(4,5) used the deflection of the HRPC near maximal HR to determine a HR deflection point and found a significant relationship between this HR deflection point and the lactate threshold. Several authors confirmed a high correlation between the HR deflection point and the lactate threshold (6,12,21) and between the HR deflection point and the ventilatory threshold(3,27). The method of HR deflection point determination has been criticized in a number of papers(9,15,16,25) because this leveling off of the HRPC could not be detected in all subjects. In a group of 227 healthy young male subjects, Hofmann et al. (13) found a leveling off of the HRPC in 85.9% of cases, a linear HR response in 6.2% of cases, and an upward deflection of HRPC curve in 7.9% of all subjects. Similar results have been reported by Kara et al. (14), although without a linear time course description of the HRPC.
In earlier studies we found significant difference in the HRPC despite no statistically significant differences in peripheral blood catecholamine concentration (19), suggesting that the deflection in the HRPC is not dependant upon sympathetic drive. Heck et al.(10) described the variation in HR performance possibly as a normal physiologic response to maximal exercise test. A physiological explanation of the deflection of the HRPC is still missing.
The present study was designed to investigate the influence of parasympathetic receptor blockade in a group of healthy subjects and to evaluate the individual differences in HR and HRPC response during incremental exercise test.
The study was approved by the ethics committee, and a signed written consent was obtained before all testing.
After a first cycle ergometer test (F), a group of 20 healthy male subjects, age 24 ± 3 yr, height 181 ± 7 cm, body mass 74± 6 kg, with differences in HRPC deflections, performed two additional randomly ordered ergometer tests: one with 2.5 mg of atropine (A) and one with a placebo of 2.5 mL 0.9% NaCl (P). Subjects had no clinical evidence of cardiovascular disease, were taking no medication, and did not consume caffeine within 24 h before the tests. Atropine and placebo were given by intravenous injection. There was an interval of 7 d between experiments. Subjects performed all tests in an upright position using an electromagnetically braked cycle ergometer (Jäger, Germany). A modified test method (13) based on the “Conconi test”(5) was employed. The exercise intensity in all three tests was increased by 20 W every minute from an initial level of 40 W until voluntary exhaustion. Capillary blood (20 μL) for lactic acid concentration(LA) measurements was collected from the hyperaemized ear lobe at rest, during the last 10 s of each increment, at the end of each exercise test, and after 3 min and 6 min of recovery time. LA was measured by a fully enzymatic photometric method in whole blood by immediate deproteinization with perchloric acid (Test Combination Lactate for Sports Medicine, Boehringer Mannheim GmbH, Germany).
According to Skinner and McLellan (24) and Morton et al. (17), LA performance curves were used to determine three phases of energy supply. Two lactate turn points (LTP1 and LTP2) were defined. LTP1 was defined as the point where the LA level began to increase systematically above resting values, which is comparable to the lactate threshold and the anaerobic threshold according to Wassermann et al. (26). LTP2 was defined as the second abrupt increase of LA, the so-called “lactate turn point” according to Davis et al. (6). Both LTP1 and LTP2 were analyzed as previously described(13,19,20). LTP1 was determined exclusively between the first LA value and 75% of the maximal performance(Powermax); LTP2 was determined exclusively between predetermined LTP1 and the LA value at Powermax. A computer-aided iterative calculation of the point of intersection of two regression lines with minimal standard deviation of the two straight lines was used to determine both lactate turn points in the section between the LA value at the end of the first workload level and 75% of Powermax(LTP1), and between predetermined LTP1 and Powermax(LTP2) (Fig. 1). The LA values were determined as a function of work performance, with scaling of performance values to a value of Powermax. The two lactate turn points separated three phases of energy supply: phase I from rest to LTP1, phase II from LTP1 to LTP2, and phase III from LTP2 to Powermax.
The HR was recorded continuously for 5 s (Sporttester PE 4000, Polar Electro, Kempele, Finland). The direction and degree of HRPC deflection was calculated by second degree polynomial equation of the HRPC between LTP1 and Powermax, satisfying the conditions of least error squares. From the function thus found, the slopes of the tangents k1HR and k2HR at the points of LTP1 and Powermax, were calculated, as well as the differences of angels represented by the following equation: kHR = (k1HR - k2HR) · (1 + k1HR·k2HR)-1. A downward deflection of HRPC described a factor kHR > 0 and an upward deflection as a factor kHR < 0. Figure 1 shows the principle of this determination for a single subject with positive kHR with and without parasympathetic receptor blockade; Figure 2 represents the HRPC for a single subject with negative kHR.
Statistics. The results are expressed as means ± SD. The data were analyzed using repeated measures ANOVA to determine differences among the three tests. Post-hoc comparisons were made employing the last significant differences test. The difference in the number of downward and upward deflections between A and P were calculated with the Chi square-test. Linear regression analysis was used to describe the relationship between heart rate response (kHR) in the first cycle ergometer test(F), and the cycle ergometer test with placebo (P), and between the cycle ergometer test with atropine (A) and P test. Linear regression analysis was used to describe the relationship between kHR and HR at LTP2 in A and P. The results obtained include the correlation coefficient r and the statistical significance was accepted of P < 0.05.
Mean (±SD) values of HR, systolic blood pressure (SBP), and LA at rest, LTP1, LTP2, Powermax, 3 min and 6 min of recovery, are listed with and without atropine in Table 1. In A, the HR was significantly higher than in F and P at rest [F (2,38) = 45.08; P< 0.001, LTP1] [F (2,38) = 13.40; P < 0.001] LTP2 [F (2,38) = 4.38; P < 0.05], and after 3 min [F(2,38) =48.30; P < 0.001] and 6 min [F (2,38) = 53.82;P < 0.001] of recovery. There was no significant difference among all tests for HR at Powermax. SBP was significantly lower in A than in F and P at LTP1 [F (2.38) = 18.86; P < 0.001], LTP2[F (2,38) = 6.58; P < 0.01] and Powermax [F (2,38) = 6.71;P < 0.01]. Work performance at all submaximal and maximal workload levels as well as LA at rest, LTP1, LTP2, Powermax, and during recovery were similar in all tests. No significant differences were found between F and P.
The degree of the deflection of the HRPC represented by factor kHR was significantly (P < 0.001) lower in A (-0.045 ± 0,303, range -1.033/0.483) than in P (0.255 ± 0.308, range -0.557/0.784). There were significant differences in kHR between A and F but not between P and F. An upward deflection of the HRPC with a negative value of factor kHR was observed in only five subjects in P; however, in A it was observed in 10 subjects. The number of upward deflections (negative kHR) in A (10 subjects) was significantly higher (P < 0.05) then in P (five subjects). A significant correlation between P and A as well as between P and F was found for the factor kHR(Fig. 3). The greater the degree of negative deflection(upward shift), the lower the absolute HR at LTP2 and vice versa. Similar occurrence of the HRPC was observed during the administration of parasympathetic blockade. The parasympathetic blockade elevated the absolute HR at LTP2 and shifted the HRPC upwards without affecting the correlation between absolute HR and kHR(Figs. 4 and 5).
In general, young and healthy subjects show an S-shaped HRPC with a more level HRPC under anaerobic conditions in phase III(1,2). In rare cases an increase of the HR response(upward deflection) was found (Fig. 2). Our results indicate that HRPC and HR regulation is an individual and reproducible characteristic under normal circumstances as well as under parasympathetic receptor blockade. Robinson et al. (23) and Ekblom et al.(7) have shown that the autonomic nervous system increases the HR at all submaximal workload levels. Additionally, this investigation showed that parasympathetic receptor blockade reduced the downward deflection(less deflection) of the HRPC in subjects who had previously more pronounced downsloping of the HRPC in P test. Subjects with linear HRPC responded with an upward deflection of the HRPC under parasympathetic receptor blockade. Subjects with an upward deflection in HRPC (negative kHR) responded with a greater upward shift of the HRPC under parasympathetic receptor blockade. We interpret these results to indicate that the downward deflection of the HRPC observed in most (85.9%) people (13) is dependent upon parasympathetic control of HR retained even at very high exercise intensities. Our investigation is in agreement with Robinson et al.(23) and Ekblom et al. (7) that parasympathetic receptor blockade increases the exercise HR response at submaximal work. Regardless of the shape of the HRPC from LTP1 to Powermax, the HRPC in our study always shifted upward under parasympathetic receptor blockade condition. Thus, the characteristic of the individual HRPC observed in the P test is generally retained. An accurate determination of a heart rate deflection point according to Conconi et al.(4,5) depends on the degree of kHR(13) and as kHR was reduced under parasympathetic receptor blockade, any calculation of the HR deflection point was considered unreasonable and, therefore, was not performed.
The influence of the parasympathetic activity on both the degree and the direction of the deflection of the HRPC was investigated using the time course of HRPC in healthy male subjects with a deflection of HRPC of varying degree and direction under parasympathetic blockade via intravenous injection of atropine. A single dose of 2.5 mg atropine is sufficient to induce a complete blockade for at least 1 h (8). Similar to previous results(7,8,22,23), atropine caused an increase of heart rate at rest and during submaximal exercise.
The regulation of HR under exercise conditions is achieved by a decreasing parasympathetic activity at lower workloads as well as increasing sympathetic drive at higher workload levels (22). However, the autonomic nervous system is probably not the only mechanism involved in increasing the heart rate during intense exercise. The increase in HR during maximal exertion after sympathetic and parasympathetic double blockade may be a result, at least in part, to nonautonomic influences(23) and intrinsic HR regulation(7).
In a previous study (19) we could not find a significant correlation between individual HRPC response and individual time courses of plasma epinephrine or norepinephrine. Our results suggest that during phase III of energy supply (24) the individual response of load dependent HR and possibly altered left ventricular function(11,18) may result from a different individual intrinsic HR regulation. This exercise-dependent HR response is a reproducible individual characteristic. It is possible that the endurance-trained subjects with greater heart volumes measured at rest produce different HRPC observed during phase III (LTP2 to Powermax). We postulate that those subjects with physiologically greater heart volumes at rest will exhibit a flattening of the HR increase in a effort to defend diastolic filling time and, thus, EDV and SV during heavy exertion. In subjects with smaller hearts or other limitations to maintenance of SV (patients), the cardiac output may best be defended by increases in HR. The systematic decrease in maximal HR in response to training support this concept. Additional investigations in highly endurance-trained individuals and in patients with compromised ventricular function may provide additional information regarding the mechanical events at maximal and near-maximal performance of left ventricular function, heart rate response, and the intrinsic function of the damaged heart which may aid in diagnosis and prognosis of myocardial health. Myocardial double blockade may further elucidate this assumption in case the HRPC reflects the intrinsic HR regulation.
The authors wish to thank Mag. A. Daxböck for his assistance in writing the manuscript.
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Keywords:©1998The American College of Sports Medicine
CYCLE ERGOMETRY; HEART RATE CONFIGURATION; ATROPINE