One of the major factors underlying the high aerobic power of endurance-trained athletes is their ability to increase stroke volume during exercise (22). The primary mechanism underlying the greater stroke volumes of the trained appears to be enhanced left ventricular end-diastolic volume (20,24). Thus, one of the major influences of aerobic training on cardiac performance is the enhancement of venous return during exercise.
How trained individuals increase venous return during exercise, however, is undetermined. It is feasible that the increased blood volume accompanying training may be the basis of the greater end-diastolic volumes of trained subjects during exercise (3). For instance, a number of studies have shown that trained males possess greater blood volume compared with untrained subjects (2,5). Importantly, Convertino et al. (4) have demonstrated that with elevated blood volume comes an increase in central venous pressure. Thus, one of the factors underlying the inability of untrained subjects to significantly enhance stroke volume during exercise appears to be their smaller blood volumes that result in a venous return that is insufficient to significantly increase central venous pressure and stroke volume.
The ability of the exercise muscle pumps to effectively return blood to the heart may also contribute to the enhanced stroke volume of the trained subjects (11,25). Every major muscle group in the legs acts as a muscle pump by compressing the veins and forcing blood back to the heart (8,12). Thus, more efficient muscle pumps, or what has been termed the athletes' second heart(23), together with an increased central venous pressure through enhanced blood volume, may be the foundation for the increase in stroke volume of aerobically trained subjects. Therefore, examination of the factors that determine the increase in venous return during aerobic exercise are crucial in explaining how the trained are able to increase stroke volume during aerobic exercise.
Unfortunately, stroke volume increase during exercise is difficult to assess because subjects tend to exhibit a sympathetic response to exercise even at light work loads. The increase in sympathetic activity either through muscular activity or pre-exercise anxiety typically results in elevated heart rates. One method of reducing the autonomic and metabolic response to exercise is passive exercise (19). During passive exercise subjects make no voluntary movement and sit passively while their limbs are moved by an outside agency. If stroke volume during exercise is primarily influenced by venous return, then an enhancement of venous return caused by passive stimulation of the muscle pumps should result in an increase in stroke volume. As aerobically trained individuals typically possess greater blood volume than do the untrained, then it would follow that passive stimulation of their muscle pumps should result in greater venous return and therefore a greater increase in stroke volume.
Although infrequently used, Nobrega et al. (19) have shown that light PCE resulted in increased stroke volume. These authors suggest that the increase in stroke volume may be a result of increased venous return and/or increased myocardial contractility. Whether aerobically trained athletes demonstrate greater stroke volume response to passive exercise compared with the untrained and whether myocardial contractility is increased during passive exercise appears to be undetermined.
Thus, the purposes of the present study were: 1) to examine the cardiac output (CO), stroke volume (SV), myocardial contractility, mean arterial pressure (MAP), total peripheral resistance (TPR), and vagal influence on the heart (HPVts) of subjects during PCE; and 2) to compare the cardiovascular response of endurance-trained with that of untrained subjects during PCE.
Subjects. Twenty trained males (Trained) and 10 fit but untrained controls (Untrained), aged between 18-30 yr, participated in the study with written informed consent in accord with the policy of the American College of Sports Medicine. Criteria for the Trained were participation in a training regimen of at least four training sessions per week for greater than four years and a maximal oxygen uptake (˙VO2peak) of >60 mL·kg-1·min-1. Untrained had no history of aerobic training and a ˙VO2peak of <55 mL·kg-1·min-1.
Procedures. Skinfold measures were taken with calipers at eight sites (abdominal, triceps, suprailiac, midaxillary, thigh, calf, biceps, and subscapular) together with height and body mass. Subjects were then rested in the supine position for 15 min, after which data were collected for 5 min sitting upright. Subjects then sat on a fixed wheel bike that was secured on a treadmill. The rear wheel was fixed so the rotation of the wheels via the treadmill would result in passive movement of the subjects' legs. Subjects' legs were secured to the pedals by toe grips. Subjects sat in an upright position with the left hand (used to collect blood pressure) positioned at heart level. The cycling bouts were performed continuously for 6 min at two intensities (30 and 60 rpm). During passive exercise, CO, SV, and HR were recorded by impedance cardiography (Minnesota Impedance Cardiography, Model 304B) every 25 s. A computer-based system processed and recorded the ECG, basal thoracic impedance (Zo), the first derivative of the pulsatile impedance(dZ·dt-1), and left ventricular ejection time (LVET) which is an index of myocardial contractility. Specialized software using ensemble averaging was used to process the impedance cardiogram (COP, Microtronics Inc., Chapel Hill, NC). SV was determined by the Kubicek equation(10). Blood pressure was recorded by the Finapres system(model Ohmeda 2300, Ohmeda, Madison, WI). TPR was computed according to the equation: TPR (dyne·s·cm-5) = MAP/CO.80.
A flow tube (Morgan, Model AC0980) attached to a face mask was used to monitor breathing rate. Subjects were requested to breathe at a required rate(3 s inhale and 3 s exhale) through breathing instructions from a tape recorder. A signal conditioning transducer (Farnell, Model 142SC01D, Australia) converted the pressure changes occurring in the flow tube to voltage. A physiograph (Humtec, model 100, Australia) and chart recorder(Graphtec Linear-corder, FWR 3701) were used to monitor and record muscular contraction; two EMG electrodes were placed on the right and the left anterior of the quadriceps and a third electrode was placed on the knee joint. During PCE, ECG, EMG, and breathing rate were monitored continuously, and subjects were requested to keep their legs as relaxed as possible. Auditory feedback from an experimenter regarding level of EMG activity was provided throughout PCE to help subjects relax leg muscles. Heart period variability (HPV) was analyzed using a time series method (HPVts) through the Mxedit software package (Delta-Biometrics, Inc, Bethesda, MD). The natural logarithm of the band-passed variance (in ms 2) was calculated and used as high and medium frequency measures of HPVts. These estimates of HPVts appear as a linear scale ranging from 0 (minimal HPVts) to 10 (maximal HPVts) (21).
Peak oxygen consumption was assessed on a separate occasion using a Quinton system (Model Q-Plex I) comprised of a Hans Rudolph (Kansas City, MO) pneumotachograph (Serial No. 187010), a zirconia oxide O2 analyzer, and an infra-red CO2 analyzer. Subjects exercised in the upright position on a stationary electronic ergometer (Excalibur Sport) at a cadence of 70 rpm until volitional exhaustion. The initial load was 30 W for the first 2 min and was increased by 1 W every 2 s thereafter.
Statistical analysis. The design of the study included both between and repeated measures. The between factor was Group (Trained, Untrained) and the repeated measure was Time for each of the measures. When the omnibus F was significant differences between groups for each variable were further examined using one-way ANOVA and New-man-Keulspost-hoc tests. A probability of P < 0.05 was considered significant.
Subject characteristics are shown in Table 1. The Trained group possessed significantly greater ˙VO2peak and was significantly lighter (P < 0.05) than the Untrained.
All subjects reported that they did not consciously contract leg muscles during passive pedal movements. At both intensities EMG activity was consistently less than that observed during actual cycle exercise (seeFig. 1).
Cardiovascular response to PCE for Trained and Untrained. Comparison between groups showed that no cardiovascular response during PCE was significantly different; thus both groups were combined for the remainder of the analysis.
Cardiovascular response to PCE for all subjects combined. During both intensities of PCE, HR, CO, and MAP were significantly greater than upright rest (P < 0.001; Figs. 2 and 3). Averaged over the low intensity, HR increased above baseline values by 7%, CO by 8%, and MAP by 8%. Averaged over the medium intensity, HR increased above baseline values by 10%, CO by 12%, and MAP by 10%. SV and TPR showed no change during PCE (Figs. 2 and 3). LVET was significantly lower (P < 0.001) than upright rest (273 ± 3.78 ms) at the low (263 ± 4.27 ms) and medium (265 ± 4.33 ms) intensities. Vagal influence on the heart, as measured by HPVts, was significantly lower (P < 0.001) than upright rest at both intensities of PCE for frequencies in the high range (0.12-0.40 Hz;Fig. 4). No significant changes occurred for frequencies in the medium range (0.07-0.11 Hz).
The major findings of this study were that none of the cardiovascular responses to PCE of the Trained and Untrained were significantly different. However, the cardiovascular response to both passive exercise intensities for the two groups combined included significantly increased HR, CO, MAP, and cardiac contractility (LVET). Vagal influence on the heart (HPVts) at high frequencies for all subjects combined was significantly decreased throughout PCE.
Cardiovascular response to passive cycle exercise. For the two groups combined, cardiovascular response was significantly influenced by passive exercise. The elevation of HR during PCE supports previous research(18). However, the intensity of passive cycle exercise in this study (18) was much greater than that used in the present study and was similar to cycle sprinting. In contrast, lower intensity PCE, similar to the levels used in the present study, did not result in an increase in HR (19). It is feasible that the differing patterns of HR response to PCE in these studies could have occurred because of the dissimilarity in baselines procedures. In the present study subjects rested for 20 min before PCE. The shorter resting period of the Nobrega et al. (19) study may have resulted in higher resting heart rates and consequently a smaller increase in HR between rest and PCE.
The exercise reflex neural mechanism involves both group III and group IV muscle afferents. Group III muscle afferents appear to be activated primarily by muscle stretch, whereas group IV afferents respond more to chemical changes in the muscle (19). The mechanism underlying the increase of HR during PCE in the present study is likely to be thin myelinated(group III) muscle afferents as blood flow to the passively stretched leg muscles during PCE was unlikely to be restricted(6,15,17,19). During PCE these fibers may provide feedback to the medulla resulting in a withdrawal of vagal tone and an increase in HR (16). Withdrawal of vagal tone was indicated by the significant decrease in HPVts during PCE. HPVts response was most influenced at frequencies between 0.12 and 0.40 Hz. In contrast, HPVts at lower frequencies (0.07-0.11 Hz) was unchanged. The components of HPV at high frequencies are predominantly modulated by the parasympathetic nervous system, whereas medium frequencies appear to be influenced more by the sympathetic system(14). Thus, the unchanged HPVts at lower frequencies indicates a lack of sympathetic influence.
Another possibility underlying the enhancement of HR may be that central command was involved during PCE(7,9,17,19). Benjamin and Peyser(1) have suggested that passive exercise is never purely passive and that there is always a certain degree of positive or negative active work involved. However, in the present study the monitoring of EMG activity showed that little muscle contraction was present. The absence of significant EMG activity suggests that central command may not have contributed in a major way to the HR increase during this form of exercise.
Surprisingly, SV was not significantly increased during the low and medium intensities of PCE. This finding indicates that PCE at low and medium intensities may not be powerful enough to stimulate the muscle pumps. The lack of stimulation of the muscle pumps may have resulted in little increase in venous return, and therefore, little change in SV. Thus, moderate PCE may not sufficiently influence the veins in the exercising muscles.
The increase in myocardial contractility during low and moderate PCE, as indicated by a decrease in LVET, probably reflects the chronotropic effect of HR on systolic time intervals rather than increased beta-adrenergic activity. Thus, as HR increased LVET decreased. An increase in myocardial contractility should result in an increase in stroke volume. As an increase in stroke volume was not evident LVET may be an inappropriate index of myocardial contractility during heart rate increase. The lack of change in the medium frequency component of HPVts supports the notion that beta-adrenergic activity was not increased during PCE.
The MAP and TPR response to PCE were similar to that reported by Nobrega et al. (19). Since TPR was unchanged during light and medium PCE, the significant increase in CO resulted in an increase in both systolic and diastolic blood pressure. Thus, the MAP response to PCE appears to be more similar to the blood pressure response to isometric rather than dynamic exercise and may suggest that during PCE the muscle mechanoreceptors are able to bring about a pressor response(13,19).
The lack of differences in stroke volume response found between the Trained and Untrained groups may underline the important role of the muscle pumps in influencing venous return. Although blood volume was not measured, the high weekly exercise workload of the aerobically trained subjects, coupled with their low resting heart rates and high ˙VO2peak indicate that they were likely to be hypervolemic (3). Thus, despite a possible greater blood volume and potentially more efficient muscle pumps trained subjects' increase in SV during PCE was no larger than that of the untrained. Therefore, it is possible that the increased end-diastolic volume during actual aerobic exercise consistently found in research(24) is only achievable during substantial muscle pump activity. Thus, passively stretching leg muscles during PCE may not provide sufficient increase in venous return to enhance SV. Consequently, moderate passive exercise does not appear to provide a strong enough stimulus to examine the underlying mechanisms of SV increase.
In conclusion, for all subjects combined PCE resulted in an increase of HR which appeared to be caused by decreased vagal influence on the heart. The increase of HR resulted in an increase in CO that led to an increase in MAP. The failure to find an increase in SV suggests that PCE may not have been strong enough to activate the muscle pumps. The lack of stimulation of the muscle pumps may have prevented an enhancement in venous return and therefore an increase in SV could not occur.
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Keywords:©1998The American College of Sports Medicine
STROKE VOLUME; BLOOD PRESSURE; HEART RATE; PERIPHERAL RESISTANCE