HRTP, prolonged ergometer exercise, and single sculling.

The use of the heart rate turn point (HRTP) to set target heart rate (THR) for prolonged rowing ergometer (E) and single scull rowing (R) was evaluated. Ten trained subjects (age 21.3 +/- 4.0 yrs; VO (2max) 4.77 +/- 0.62 l . min-1) performed incremental exercise tests and 30-min prolonged E and R. Expired air and heart rate (HR) were measured continuously. During E and R, blood lactate concentration (La) was measured at rest and after 5, 10, 20, and 30 min. HRTP and V (E)TP (2) were determined as the deflection point of the heart rate performance curve and the second TP in minute ventilation (V. (E)). No significant differences were found for work rate (W), HR, and VO (2) between HRTP and V. (E)TP (2) and they were significantly related (r = 0.94, p < 0.001; r = 0.96, p < 0.001). Mean HR, VO (2), VCO (2), and V. (E) were not significantly different between E and R. La remained at a steady state in both E and R but was slightly higher in E. Tidal volume (V (T)) was found to be lower and breathing rate (BR) was significantly higher in R. HR at HRTP from an incremental rowing ergometer exercise test is valid to establish a THR consistent with constant metabolic training intensity in prolonged ergometer and single scull rowing.

Oral magnesium therapy, exercise heart rate, exercise tolerance, and myocardial function in coronary artery disease patients.

BACKGROUND: Previous studies have demonstrated that in patients with coronary artery disease (CAD) upward deflection of the heart rate (HR) performance curve can be observed and that this upward deflection and the degree of the deflection are correlated with a diminished stress dependent left ventricular function. Magnesium supplementation improves endothelial function, exercise tolerance, and exercise induced chest pain in patients with CAD. PURPOSE: We studied the effects of oral magnesium therapy on exercise dependent HR as related to exercise tolerance and resting myocardial function in patients with CAD. METHODS: In a double blind controlled trial, 53 male patients with stable CAD were randomised to either oral magnesium 15 mmol twice daily (n = 28, age 61+/-9 years, height 171+/-7 cm, body weight 79+/-10 kg, previous myocardial infarction, n = 7) or placebo (n = 25, age 58+/-10 years, height 172+/-6 cm, body weight 79+/-10 kg, previous myocardial infarction, n = 6) for 6 months. Maximal oxygen uptake (VO2max), the degree and direction of the deflection of the HR performance curve described as factor k<0 (upward deflection), and the left ventricular ejection fraction (LVEF) were the outcomes measured. RESULTS: Magnesium therapy for 6 months significantly increased intracellular magnesium levels (32.7+/-2.5 v 35.6+/-2.1 mEq/l, p<0.001) compared to placebo (33.1+/-3.1.9 v 33.8+/-2.0 mEq/l, NS), VO2max (28.3+/-6.2 v 30.6+/-7.1 ml/kg/min, p<0.001; 29.3+/-5.4 v 29.6+/-5.2 ml/kg/min, NS), factor k (-0.298+/-0.242 v -0.208+/-0.260, p<0.05; -0.269+/-0.336 v -0.272+/-0.335, NS), and LVEF (58+/-11 v 67+/-10%, p<0.001; 55+/-11 v 54+/-12%, NS). CONCLUSION: The present study supports the intake of oral magnesium and its favourable effects on exercise tolerance and left ventricular function during rest and exercise in stable CAD patients.

Plasma adiponectin response to sculling exercise at individual anaerobic threshold in college level male rowers.

The purpose of the investigation was to study plasma adiponectin response to a single exercise session in male rowers. Eight college level, single scull rowers (VO2max: 5.01+/-0.43 l.min-1; age: 21.5+/-4.5 yrs; height: 184.9+/-5.0 cm; body mass: 78.5+/-8.4 kg; body fat: 11.8+/-1.2%) participated in this study. Venous blood samples were obtained before, immediately after, and following the first 30 min of recovery of constant load on-water rowing over a distance of 6.5 km (approximately 30 min) at the individual anaerobic threshold (75.2+/-2.9% of VO2max). Adiponectin was unchanged (p>0.05) immediately after the exercise. However, adiponectin was significantly increased above the resting value after the first 30 min of recovery (+14.7%; p<0.05). Similarly, leptin was unchanged immediately after exercise and was significantly decreased after the first 30 min of recovery (-18.2%; p<0.05). Plasma insulin was significantly reduced immediately after exercise and remained significantly lower during the first 30 min of recovery period. Glucose increased with exercise and returned to the pre-exercise level after the first 30 min of recovery. Basal adiponectin was significantly related to VO2max (r=-0.62; p=0.034). However, there was no relationship between basal adiponectin and other measured variables. Similarly, basal leptin demonstrated no relationship with other measured variables. In conclusion, the results of the present study suggest that plasma adiponectin is sensitive in the first 30 min of recovery to the effects of relatively short-term exercise at individual anaerobic threshold when all major muscle parts are involved.

Responses of N-terminal pro-brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) to competitive endurance exercise in recreational athletes.

The present study was designed to investigate whether the stress of a half-marathon race can induce myocardial cell injury or left ventricular dysfunction in moderately trained runners of both gender, as assessed by post-race plasma concentrations of biochemical cardiac-specific markers and by quantitative echocardiographic measurements. We examined 12 male (mean+/-SD); age: 42.8+/-7.3 yr; height: 177.6+/-7.4 cm; body mass: 75.6+/-9.4 kg; BMI: 24.1+/-1.8 and 13 female (mean+/-SD); age: 39.0+/-6.5 yr; height: 164.6+/-6.2 cm; body mass: 58.4+/-9.8 kg; BMI: 21.5+/-3.4 recreational runners, who completed a half-marathon race. Blood samples were collected from each subject before the half-marathon race as well as 20 min and 2 h post-race and cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Quantitative echocardiographic analyses of wall dimensions and ejection fraction were also obtained from 14 of 25 subjects within 1 wk after the race. Both blood markers showed significant changes (p<0.05-0.001) over the time course of the three blood draws. A significant percentage of laboratory analytes analyzed in this study were outside the reference ranges and fulfilled conventional criteria for cardiac muscle damage. However, echocardiography within one week following the competition did not show any evidence that running a half-marathon competition damages the myocardium. Strenuous endurance exercise in middle-aged recreational runners induces a significant elevation of biochemical cardiac-specific markers, which may reflect transient subclinical myocardial damage, but can also reflect a physiological reparative or adaptive process.

%HRmax target heart rate is dependent on heart rate performance curve deflection.

UNLABELLED: The percent of maximal heart rate (%HRmax) model is widely used to determine training intensities in healthy subjects and patients when prescribing training intensities in these groups of subjects. PURPOSE: The aim of the study was to investigate the influence of the time course of the heart rate performance curve (HRPC) on the accuracy of target training heart rate. METHODS: Sixty-two young healthy male subjects performed an incremental cycle ergometer exercise test until voluntary exhaustion. Subjects were then divided into four groups according to the time course of the HRPC. Groups were classified in regular HR response (kHR2 > 0.2), indifferent HR response (0 < kHR2 < 0.2), linear HR response (kHR2 = 0), and inverted HR response (kHR2 < 0). The first and the second lactate turn point (LTP1, LTP2) as well as the heart rate turn point (HRTP) were determined as submaximal markers of performance. Linear regression lines were calculated for HR in the three regions of energy supply defined by LTP1 and LTP2. RESULTS: HR at LTP1 and HRmax was not significantly different between all four groups. HR at LTP2 was dependent on the time course of the HRPC and was significantly lower (P < 0.05) as kHR2 decreased. Power output and blood lactate concentration at LTP1, LTP2 and maximal workload (Pmax) were not significantly different between the groups. CONCLUSION: From our data, we conclude that target training HR detected by means of the %HRmax method may be overestimated in cases where the HR response is not regular, as it was found in many of our subjects.

A physiological profile of tennis match play.

PURPOSE: The aim of this investigation was to examine physiological demands of single match play in tennis. METHODS: 20 players performed 10 matches of 50 min. Respiratory gas exchange measures (RGEM) and heart rates (HR) were measured using two portable systems. Lactate concentration was determined after each game. The average oxygen uptake (VO2) of 270 games was 29.1 +/- 5.6 mL.kg-1.min-1 (51.1 +/- 10.9% of VO2max). Average VO2 for a game ranged from 10.4 to 47.8 mL.kg-1.min-1 (20.4 and 86.8% of VO2max). Average lactate concentration (LA) was 2.07 +/- 0.9 mmol.L-1 (ranging from 0.7 to 5.2 mmol.L-1). Furthermore, we monitored the duration of rallies (DR), the effective playing time (EPT), and the stroke frequency (SF). The average values of 270 games were DR: 6.4 +/- 4.1 s, EPT: 29.3 +/- 12.1%, SF: 42.6 +/- 9.6 shots.min-1. RESULTS: Multiple regression revealed that the DR was the most promising variable for the determination of VO2 in match play (r = 0.54). The body surface area (BSA) and EPT were also entered into the calculation model. In games of two defensive players, VO2 was significantly higher than in games with at least one offensive player. CONCLUSION: Our results suggest that energy demands of tennis matches are significantly influenced by DR. The highest average VO2 of a game of 47.8 mL.kg-1.min-1 may be regarded as a guide to assess endurance capacity required to sustain high-intensity periods of tennis matches compared with average VO2 of 29.1 mL.kg-1.min-1 for the 270 games. Our results suggest that proper conditioning is advisable especially for players who prefer to play from the baseline.

[Amount and intensity of physical exercise in primary prevention]. / Umfänge und Intensität körperlicher Aktivität in der Primärprävention.

Numerous epidemiological studies have demonstrated an inverse relation between physical activity and physical "fitness" on one hand and premature death and the risk of chronic disease on the other hand. However, most of these studies showed crucial methodological and statistical differences, a fact which caused a lack of consensus of dose and intensity of physical activities for "health benefits". The optimal amount of physical activity to decrease mortality is in literature stated to range between 1,000 and 3,500 motoric kcal per week. Only a few data exist concerning the optimal intensity of preventive physical activities. There is some indication that only "vigorous" but not "non-vigorous" physical activities are associated with decreased mortality. Previous investigations suggest that a "threshold-intensity" (e.g. of at least 6 MET of "conditioning physical activity") is needed to produce an adequate preventive effect. On the other hand it has been documented, that "physical fitness" (endurance capacity) is a decisive factor for a decreased mortality. Therefore it may be assumed, that physical activities are only efficient for health benefits, if they also result in increased physical fitness. Following from this assumption the quality and quantity of training in primary prevention has to be adjusted to the individual requirements (performance, age, gender, health) of men.

Change in left atrial and ventricular dimensions during and immediately after exercise.

PURPOSE: The aim of this study was to evaluate differences in the left atrial (LAD), total ventricular end-diastolic (TEDD), end-systolic diameters (TESD), and left ventricular shortening fraction (SF) compared with heart rate (HR) and systolic blood pressure (SBP) during exercise and recovery. METHODS: Healthy young male (N = 15) and female (N = 16) subjects performed an incremental cycle ergometer test in upright position, and three phases of energy supply were defined by means of blood lactate concentration (LA) and respiratory gas exchange variables (I: aerobic; II: aerobic-anaerobic transition; III: anaerobic). Subjects were required to rest their arms on a steering bar and to lean their upper body forward; two dimensional (2-D) echocardiograms were obtained over the left parasternal area at rest (R), at the end of each phase, immediately within 15 s post, and 6 min after exercise (6 min). By using VINGMED's "Anatomical M-Mode," it was possible to extract M-Mode Sweeps from stored 2-D-Loops and perform the M-Mode measurement. RESULTS: In contrast to the significant decrease in TEDD and TESD from III to 15 s up to resting values and the significant increase in SF from III to 15 s, the moderate decrease in HR immediately post exercise (15 s) was not significant. The SBP showed a significantly decrease from III to 15 s; in contrast to TEDD, TESD, and SF, the values at 15 s were comparable with the values at II. For LAD, significant increase during exercise and a decrease during recovery were observed. Sex-specific differences of changes in measured variables could not be found. CONCLUSION: We concluded that post exercise measurement of left ventricular and atrial dimensions or SF were not valid to describe heart function at maximal exercise although immediately post exercise HR was near maximal level.

Comparison of laboratory and "on-court" endurance testing in tennis.

Treadmill testing (TT) commonly used in endurance testing is often not sport-specific. Therefore a field test (FT) for tennis players was developed. The purpose was 1) to compare metabolic and cardiorespiratory response between TT and FT and 2) to assess tennis stroke ratings during FT. In both tests ventilatory variables (VO2, VE, VT, Bf, VE x VO2(-1)), heart rate (HR), and lactate (LA) were measured. For both tests an "individual anaerobic threshold" (IAT) was calculated. The comparison of TT and FT yielded significant differences in cardiorespiratory and metabolic response. LA and VE were significantly higher in TT compared to FT at VO2 of 35, 40, and 45 ml x kg(-1) x min(-1). There were statistical differences between IAT resulting from both tests (TT vs. FT): HR (165+/-16, 175+/-11, p<0.001), VO2 (44.4+/-4.3, 47.8+/-4.8, p<0.05), LA (3.1+/-0.5, 2.5+/-0.4, p < 0.001), VE (97.0+/-15.6, 89.1+/-14.9, p < 0.05), VT (2.66+/-0.34, 2.34+/-0.47, p<0.05), VE/VO2 (27.9+/-3.9, 23.9+/-2.9, p<0.01). High correlation was found between stroke ratings and the national ranking of the players. We concluded that 1) metabolic, ventilatory, and cardiorespiratory demands of TT vs. FT were (semi)sport-specific and significantly different and 2) that the stroke rating in our study was a good predictor for tournament performance (r = 0.94). This type of stroke rating can be implemented in a FT.

Measurement of maximal power output in isokinetic and non-isokinetic cycling. A comparison of two methods.

The main goal of the study was to compare maximal power output and power output at different pedalling frequencies obtained during isokinetic all-out tests with maximal power output obtained during a single all-out sprint (against the same braking force for every subject). Sixty healthy male subjects participated in the study. The ergometer system used in this study has three operating modes: the isokinetic mode (maintaining pedal crank velocity constant at a present level), a revolution dependent mode and a revolution independent mode. In all three operating modes the effective forces are monitored by means of strain gauge. All subjects performed a single all-out sprint against a braking force of 20 Newton and an all-out isokinetic cycling test consisting of ten 10 s bouts of maximal cycling at speeds ranging from 50 rpm to 140 rpm. In both tests, irrespective of which test mode was used, the mean power for a complete crank revolution showed parabolic relationships to crank velocity. For the isokinetic test, the subjects showed a peak power (IsoWpeak) of 15.3+/-1.7 W/kg corresponding to an optimal velocity of 115+/-8.6 rpm. For the force-velocity test NonisoWpeak (the highest power obtained at any time during the test) was 14.4+/-1.9 W/kg and was achieved at a pedalling rate of 127+/-14 rpm. IsoWpeak was significantly higher than NonisoWpeak (p<0.001) but there were no significant differences between NonisoWpeak and IsoWmax (maximal mean power for each full crank revolution) for the revolutions from 90 rpm to 140 rpm. Though, NonisoWpeak and IsoWpeak are significantly different, there was a strong relationship between NonisoWpeak and IsoWpeak (r = 0.7158, p<0.001). There was also a strong relationship between NonisoWpeak and IsoWmax for the revolutions from 50 rpm to 120 rpm (p<0.001) and at 130 rpm (p<0.01).

The heart rate turn point reliability and methodological aspects.

PURPOSE: The aim of the study was to test protocol variations on the heart rate performance curve (HRPC) and the heart rate turn point (HRTP) according to Conconi et al. (1996). Respiratory gas exchange variables were used to define three phases of energy supply (I, II, III). METHODS: Eighteen healthy young male subjects performed 4 tests (T1-T4). T1: initial speed of 6 km x h(-1) followed by increments of 0.6 km x h(-1) every 60 s. Subjects were than randomized for the next three tests. T2: initial speed 5.6 km x h(-1) followed by increments of 0.2 km x h(-1) every 20 s; T3: similar to T2, in the second half of phase III acceleration (S) was increased. T4: like T2, at the beginning of phase III, S was increased. No differences were found in the degree of the deflection of the HRPC expressed as factor kHR between T1 (0.228 +/- 0.225) and T2 (0.248 +/- 0.231) but a significant increase was found in T3 (0.533 +/- 0.248) and T4 (0.770 +/- 0.258). RESULTS: The modifications of the protocol (T3 and T4) systematically influenced the deflection of the HRPC, but kHR was highly reproducible in all tests. Eleven subjects showed degrees of deflection in the HRPC in all tests. There were no significant differences for S, HR, and VO2 at the HRTP. An HRTP was not found in seven subjects in neither T1 or T2; however, in T3 and T4, these seven subjects showed a deflection of HRPC resulting from the protocol. The HRTP was found to be dependent on the start of the acceleration in phase III. In cases with a linear time course in the HRPC in T1 and T2, in T3 an HRTP was found at 15.6 km x h(-1) and in T4 at 13.6 km x h(-1) , respectively. CONCLUSION: The Conconi test protocol with an accelerated increase in S in the final phase of the test has a major influence on the occurrence of the HRTP in cases of near linear HRPC.

[Protection against myocardial ischemia by nisoldipine--an experimental study with valinomycin K-sensitive microelectrodes]. / Myokardiale Ischämieprotektion durch Nisoldipin--eine experimentelle Untersuchung mit Valinomycin-K-sensitiven Mikroelektroden.

It has been shown that dihydropyridines exert a cardioprotective effect during experimental ischemia. This effect is reflected in a reduced K-efflux from the ischemic tissue. Recently we have shown that ischemic K-efflux is largely mediated by ATP-dependent K-channels. Using K-selective microelectrodes we studied the effect of nisoldipine on K-efflux during simulated ischemia (guinea pig papillary muscle immersed in paraffin oil; normal Tyrode solution, HEPES buffered, 100% O2-equilibrated, 37 degrees C). While ischemic K-efflux was Ca-dependent in stimulated preparations, it was independent of extracellular Ca in resting preparations. Our results show that nisoldipine leads to an inhibition of ischemic K-efflux during simulated ischemia. In resting preparations this inhibition is not a direct Ca-antagonistic effect, since withdrawal of extracellular Ca does not inhibit ischemic K-efflux but nisoldipine does. We suggest a direct effect of nisoldipine on the KATP channel which is mainly responsible for ischemic K-loss.

The heart rate performance curve and left ventricular function during exercise in patients after myocardial infarction.

PURPOSE: The aim of the study was to investigate the heart rate turn point (HRTP) in the time course of the heart rate performance curve (HRPC) in patients after myocardial infarction, and the relationship between the HRTP, the left ventricular function, and the second lactate turn point (LTP2). METHODS: We studied the degree and the direction of the HRPC and the left ventricular ejection fraction (LVEF) in 49 male patients 57 +/- 8 d after their first posterior wall infarction (MI). An incremental cycle ergometer test was performed and three phases of energy supply were defined (I: aerobic; II: aerobic-anaerobic transition; III: anaerobic) via blood lactate LA concentration. HRTP and LVEF-turn points (LVEFTP) were assessed by linear turn point analysis. The degree and direction of the deflection of HRPC were described as factor k (k > 0.1: downward deflection; -0.1 < k < 0.1: linear time curse; k < -0.1: upward deflection). The LVEF was determined by RNA. The difference between Pmax and LTP2 was calculated for LVEF (delta LVEF). RESULTS: An HRTP could be found in 44 and a LVEFTP in 47 cases. The HRTP occurred at 85 +/- 17 Watt (W), which correlated (r = 0.95; P < 0.001) with the LTP2 (84 +/- 17 W) and the LVEFTP (84 +/- 17 W, r = 0.93; P < 0.001). From LTP2 to Pmax a significant decrease in LVEF was found. There was a correlation between the percentage of HRmax at the HRTP and k (r = 0.70), as well as delta LVEF (r = 0.56). CONCLUSIONS: To prevent myocardial overloading, it seems to be useful to determine the HRTP, which indicate the workload where LVEF decreases.

First description of recurrent pericardial effusion associated with borrelia burgdorferi infection.

Lyme disease is well known for affecting the myocardium in the form of carditis and dilated cardiomyopathy. Pericardial effusion associated with Lyme disease has not been described as yet. This article demonstrates a case of a female patient, 54 years of age, with Borrelia burgdorferi infection and associated pericardial effusion. Recurrent pericardiocenteses as well as conventional treatment of the condition were without success. Diagnosis of Borrelia infection and subsequent treatment with ceftriaxone led to permanent restitution of the pericardial effusion.

Parasympathetic receptor blockade and the heart rate performance curve.

Parasympathetic receptor blockade and the heart rate performance curve. Med. Sci Sports Sci., Vol. 30. No. 2, pp. 229-233, 1998. The aim of the present study was to investigate the influence of parasympathetic receptor blockade on the heart rate performance curve (HRPC). Twenty healthy male subjects performed a first cycle ergometer test (F), showing a HRPC deflection of varying degree and direction. Subjects then in random order performed two additional cycle ergometer tests, one with atropine (A) and the other with placebo (P). Two lactate turn points (LTP1, and LTP2) were determined by means of linear regression turn point analysis. The degree and direction of the deflection of the HRPC was calculated mathematically as factor kHR (kHR>0 = downsloping of HPRC; kHR<0 = upsloping of HRPC). In comparison with that in F and P, HR in A was significantly higher at rest, LTP1, LTP2, and during recovery, but not at Power(max). An upsloping deflection of the HRPC was seen in only five cases in F and P, whereas in A 10 cases were observed (P < 0.05). In A, kHR was significantly lower than in F and P. A significant correlation for kHR was found among F, P, and A. Independent from parasympathetic receptor blockade and the HR at Power(max), the HR at LTP2 was lower in cases with negative kHR (upsloping). In A as well as in P a significant correlation was observed between kHR and HR at LTP2. The individual time course of HRPC is reproducible and may be independent of parasympathetic activity.

Left ventricular function in response to the transition from aerobic to anaerobic metabolism.

The purpose of this investigation was to study myocardial function at rest, during three phases of energy supply, and during recovery. Radionuclide angiography was performed during the aerobic phase (phase I, rest-first lactate increase), the aerobic-anaerobic transition phase (phase II, first lactate increase-second lactate increase), the anaerobic phase (phase III, second lactate increase-maximal work performance (Pmax)), and during recovery. Thirty-eight male patients (59 +/- 7 d after myocardial infarction) were compared with 19 healthy control subjects and 21 sport students of comparable age. Left ventricular ejection fraction (LVEF) increased from rest to phase I and from phase I to phase II in sports students and control subjects. During phase III, LVEF did not change significantly in sports students, but it decreased significantly in control subjects. This is in contrast to the patients, who showed an increase of LVEF from resting values (47 +/- 3%) to phase I (50 +/- 1%), no change during phase II (51 +/- 2%), and a decrease to resting values (45 +/- 2) during phase III. All subjects showed an increase in stroke volume (SV) during phase I and II, reaching a maximum at phase II. This was evidenced by an improvement of the systolic function with a constant left ventricular end-diastolic volume (EDV) in control subjects and sports students. In contrast, an improved SV in patients was achieved through an increase in EDV and a less distinct increase in the left ventricular end-systolic volume (ESV). Maximal LVEF values were measured during the first 90 s of recovery in all subjects. Values during recovery are not representative of load dependent myocardial function. This increase in LVEF does not cause an increase in cardiac output but is a consequence of changes in the EDV and ESV, which decrease again immediately after the end of exercise performance.

[The extent of diastolic dysfunction and its correlation with subjective impairment of physical capacity in dilated cardiomyopathy]. / Das Ausmass der diastolischen Dysfunktion und dessen Korrelation zur subjektiven Leistungseinschränkung bei dilativer Kardiomyopathie.

OBJECTIVE: To find out whether in patients with dilated cardiomyopathy (DCM) there is a correlation between subjective reduction in physical capacity and the transmitral Doppler profile as a measure of left ventricular (LV) filling. PATIENTS AND METHODS: 30 consecutive patients (24 men, six women; average age 55 +/- 2 years) with chronic primary DCM were examined by Doppler echocardiography to determine possible differences in LV filling pattern, in correlation with subjective impairment of physical capacity graded according to the New York Heart Association (NYHA) classification. RESULTS: Mean LV ejection fraction was 34 +/- 1%. All patients were in sinus rhythm. Eight patients, in NYHA class I had nearly normal LV filling (E wave 79 m/s, A wave 0.76 m/s); 11 patients in class II had impaired relaxation (E wave 0.77 m/s. A wave 0.82 m/s) and 11 in class III/V had a restricted filling pattern (E wave 0.98 m/s. A wave 0.57 m/s). There was a significant difference between class II and class III/IV patients with regard to E wave deceleration time (0.15 and 0.11 s, respectively; P < 0.05), as well as between class I and class III/IV patients (0.18 and 0.11 s, respectively; P < 0.05). The A wave deceleration time was clearly shorter in class III/IV than class II (0.08 s and 0.11 s; P < 0.05) and class I patients (0.08 s and 0.10 s; P < 0.05). CONCLUSIONS: The extent of LV diastolic dysfunction correlated with subjective physical capacity. The more the LV filling pattern had changed from normal towards restricted, the greater the patient's symptoms.

Heart rate performance curve during incremental cycle ergometer exercise in healthy young male subjects.

In 1992 Conconi et al. (20) presented an indirect and noninvasive method for the determination of anaerobic threshold (AnT) in an incremental field test for runners. This noninvasive method for the determination of anaerobic threshold is dependent on the occurrence of a deflection of the heart rate performance curve (HRPC). The aim of our study was to evaluate the degree and direction of the deflection of the HRPC and the relationship of the heart rate threshold (HRT) to the lactate turn point in a group of 227 healthy young subjects (age: 23 +/- 4 yr). The subjects were divided into three groups by means of second degree polynomial fitting (GI: regular deflection, kHR > 0.1; G II: no deflection, 0 < kHR < 0.1; G II: inverse deflection, k < -0.1). No significant differences between the groups were found in the anthropometric data or in the power output and the blood lactate concentration at both the first (LTP1) and second (LTP2) lactate turn points and at maximum performance (Pmax). Using the method of Conconi et al. (20), 85.9% of the subjects showed a "regular" deflection, 6.2% showed no deflection at all, and 7.9% showed even an inverted deflection of the HRPC. An HRT could be obtained in both G I and G III, and power output at HRT was not significantly different in comparison to that at the LTP2. No HRT could be assessed in G II. The heart rate at HRT and the LTP2 were significantly lower in G III compared with G I. The phenomenon of heart rate break point may be attractive in training regulation, but its application is limited because a heart rate deflection cannot be found even in young subjects in some cases.