WARBURTON, DARREN E. R.; HAYKOWSKY, MARK J.; QUINNEY, H. ARTHUR; BLACKMORE, DERRICK; TEO, KOON K.; TAYLOR, DYLAN A.; MCGAVOCK, JONATHAN; HUMEN, DENNIS P.
Endurance training results in characteristic improvements in cardiorespiratory function including increased LV performance (e.g., augmented cardiac output (Q̇) and stroke volume (SV)), and maximal aerobic power (V̇O2max) (8,14). Coincident with this improved cardiorespiratory function is a concomitant blood volume (BV) expansion (hypervolemia) (9,10,14). Investigators have reported that a large portion of the enhanced aerobic performance of endurance athletes is directly related to their larger BV (2,8,13,14,28,30,31).
Exercise intensity appears to be the major stimulus for training-induced hypervolemia (2), as significant increases in BV are commonly observed after high-intensity, short-term training (12,22) and significant increases in BV can be achieved after a single bout of high-intensity exercise (6,19). It therefore holds that prolonged interval training may result in greater blood volume expansion than a lower-intensity training program. However, it is unclear what effect more prolonged interval training has on BV in comparison with continuous aerobic training. It is possible that interval training may lead to divergent vascular changes in comparison with continuous training owing to differences in the exercise training stimulation. These differences in training-induced hypervolemia may account for the observed differences in aerobic capacity after continuous and interval training (3,11,20). Owing to the potentially large relationship between vascular volumes and cardiac function (8,14,28,30,31), it is also important to discern what influence the training-induced hypervolemia after interval and continuous training has on left ventricular function. Therefore, the primary purpose of this investigation was to evaluate the effects of continuous and interval aerobic training on BV, myocardial function, and aerobic power. Our hypotheses were as follows: 1) training-induced hypervolemia will account for a significant portion of the improvement in cardiorespiratory performance after interval and continuous aerobic training, and 2) modality-mediated differences in aerobic performance will be related directly to differences in vascular volumes with interval training resulting in larger training-induced hypervolemia.
The protocol was reviewed and approved by the University of Alberta Health Sciences Research Ethics Board, and the investigation was conducted according to the Declaration of Helsinki. All individuals provided written informed consent before starting the investigation. Twenty-five normally active males volunteered for participation in this investigation. One participant was excluded from the investigation, due to a congenital heart defect. Two participants in the interval training group and one in the continuous training group dropped out after week 6, owing to conflicts with their working schedule. One participant was injured (in an unrelated sporting event) after week 9 of continuous training. Baseline characteristics of the 20 male participants who completed the investigation are shown in Table 1.
This investigation was a randomized, controlled design. Participants were stratified (for body mass and aerobic power) and randomly assigned to control, continuous aerobic training, or interval aerobic training conditions. Figure 1 illustrates the time line of vascular volume and cardiorespiratory measurements. The continuous and interval training groups were evaluated for all cardiorespiratory measurements at baseline, and after weeks 6 and 12 of training. Vascular volumes were also assessed at baseline and weeks 1, 3, 6, 9, and 12 (Fig. 1). All measures were taken with a 48-h period of rest (after the last exercise training session). Resting measures were taken in the supine position. The control group was evaluated for all cardiorespiratory and vascular measurements at baseline and at week 12.
FIGURE 1Schematic of...Image Tools
Participants prepared for testing by refraining from physical activity and the consumption of caffeinated beverages 24 h before the test days. Resting measures of BV and the volume-regulatory hormones were measured on test day 1. On the second test day, the participants performed an incremental to maximum cycle ergometer exercise test in the semirecumbent position to assess the cardiorespiratory parameters of interest.
Participants were randomly assigned to either continuous or interval aerobic training. All participants were required to train for 3 d·wk−1 for 12 wk on a Monark cycle ergometer (Model 818, Stockholm, Sweden). Personnel, who were instructed to adjust the work rates according to heart rate, monitored all conditioning days. Participants were instructed to pedal at a constant cadence of 80 rev·min−1 throughout each training day. Each training week consisted of 3 d of continuous or interval training with a period of 24 h of rest between each training day. Each training day began with a standardized 5-min warm-up period, consisting of the participant exercising at 30% of peak power output, followed by the specified training program.
Continuous aerobic training was performed with the work rate set individually at 1% below the participant’s anaerobic threshold (i.e., 64.3 ± 3.7% V̇O2max) for 30–48 min·d−1 based on the pretraining exercise test. The duration of training was 30 min for the first 2 wk of training, 36 min for weeks 3–4, 42 min for weeks 5–6, and 48 min for weeks 7–12.
Each training week consisted of 3 d of interval training using 2-min work:2-min active recovery bouts at 90% and 40% of V̇ O2max, respectively, for a duration that allowed a total work output equivalent to what the participant would have performed if assigned to the continuous training group. Total work output was calculated as a combination of both the high-intensity (i.e., 90% V̇O2max) and low-intensity (i.e., 40% V̇O2max) phases of the workout.
Training Intensity Adjustments
On weeks 6 and 12, participants engaged in 3 d of continuous or interval training (as outlined above) and then repeated the testing done on the pretraining days. Individual workloads were adjusted daily according to a heart rate range to reflect changes in the participants’ fitness. This heart rate range was based on the mean heart rate throughout training from minutes 10 to 30 during the first week of training. A range of ± 5% was calculated, and if the participants fell outside of this range after 10–20 min of training, the resistance setting was adjusted accordingly (± 2.5%) (11). The total work and average power output completed across the 12 wk of training was not significantly different between training groups. The average power output during week 1 was 1.9 ± 0.4 and 1.8 ± 0.5 W·kg−1, respectively, for the continuous and interval training groups, significantly increasing to 2.4 ± 0.4 and 2.2 ± 0.5 W·kg−1, respectively, during the last week of training.
Incremental exercise tests.
The exercise test protocol consisted of incremental to maximum semirecumbent exercise on an electronically braked cycle ergometer (31). The resistance on the ergometer was increased progressively to elicit staged steady-state conditions at predetermined target heart rates (± 5 beats) of 110, 130, and 150 beats·min−1 to maximum heart rate. Participants were instructed to maintain a pedaling cadence of 80 rev·min−1 throughout the incremental test.
Oxygen uptake, anaerobic threshold, heart rate, and blood pressure.
Expired gas and ventilatory parameters were acquired every 20 s using a calibrated metabolic system (Quinton, CA). Anaerobic threshold was determined as the breakpoint in the relationship between minute ventilation and the volume of oxygen consumed over time. The anaerobic threshold was independently determined by two investigators (inter-investigator variability was less than 5%).
During all testing sessions, heart rate was monitored continuously with a 12-lead electrocardiogram. Blood pressure (systolic and diastolic) was determined with a sphygmomanometer and a stethoscope placed on the participant’s right arm, while seated on the cycle ergometer. Mean arterial pressure (MAP) was determined using the formula: diastolic blood pressure + 1/3 pulse pressure (systolic blood pressure-diastolic blood pressure). Measurements were made during rest and at every predetermined stage of exercise during the incremental exercise tests (approximately every 4 min) and immediately upon the cessation of exercise.
Radionuclide ventriculography during incremental exercise.
Radionuclide ventriculography was conducted at rest and during incremental exercise on all test days as previously described (29). Each measurement period was approximately 4 min in duration, with the radionuclide acquisition being taken during the last 2 min of each stage. Quantification of left ventricular ejection fraction and end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated using commercial software. Left ventricular ejection fraction was determined from background corrected counts within the end-diastolic and end-systolic regions of interest. Left ventricular SV was determined as EDV minus ESV, and Q̇ was determined as SV multiplied by heart rate. The systolic blood pressure to ESV (SBP/ESV) ratio was calculated as a surrogate of myocardial contractility (23,32). The systolic blood pressure to end-systolic volume ratio is a noninvasive index used to estimate the slope of the end-systolic pressure-volume relationship. This is thought to be a better surrogate of myocardial contractility than other noninvasive measures (such as ejection fraction) as it is independent of preload and afterload and little affected by heart rate (23). The same experimenter, who was blind to the treatment conditions of the participants, determined the end-diastolic and end-systolic regions of interest. All ventricular volumes were expressed relative to body surface area.
The timing of the blood measurements is illustrated in Figure 1. Hematocrit and hemoglobin concentration were determined in quadruplicate using standard laboratory procedures (microhematocrit and cyanmethemoglobin methods, respectively) as previously described (31). The mean value of the four determinations was reported as the final hematocrit and hemoglobin values. Plasma volume (PV) was determined using Evan’s blue dye (T-1824, New World Trading Corporation, DeBary, FL) in a standard dilution technique (using a 10-min fixed circulation time), and total BV was calculated using hematocrit (31). Red cell volume was calculated as the difference between BV and PV (31). The same experimenter performed all BV measurements to prevent intertester variability.
Angiotensin II, α-atrial natriuretic peptide, and aldosterone were measured using radioimmunoassay kits and 125I-labeling according to standard laboratory procedures and as outlined by the manufacturer of the radioimmunoassay kits. The plasma levels of α-atrial natriuretic peptide and angiotensin II were measured using radioimmunoassay kits supplied by Phoenix Pharmaceuticals (California). The extraction efficiency of known amounts of α-atrial natriuretic peptide or angiotensin II was estimated at 80%. All samples were assayed together. The coefficient of variation for duplicate measures was 4.5% for α-atrial natriuretic peptide and 3.4% for angiotensin II.
The aldosterone assay was performed on unextracted serum according to the Coat-A-Count procedures (Diagnostic Products Corporation, Canadian supplier Intermedico, Markham). The coefficient of variation for duplicate measures of aldosterone was 2.5%. According to the manufacturer’s Coat-A-Count instructions maximal binding is 40% and the detection limit is 16 pg·mL−1.
Descriptive and inferential statistical analyses of all data were conducted using STATISTICATTM. The alpha level of significance was set a priori at 0.05. All measurements subjected to inferential analyses were reported in tabular form as mean and SD of the mean. All data in the figures were reported as mean and SEM. The cardiorespiratory measurements were analyzed using ANOVA. Tukey post hoc comparisons were used to identify differences between means when main effects were observed. Simple linear regression was utilized to establish the relationship(s) between the cardiorespiratory parameters of interest and BV.
The baseline characteristics of the participants are shown in Table 1. All participants were normally active individuals with as reflected by their V̇O2max and relative BV values (Table 1). Analysis of variance of all measures of interest at pretest revealed no significant difference between the continuous training, interval training, and control groups (including all participants) with regard to any measure at baseline. This statistical equivalency remained even after the dropout data was removed from the analysis, indicating that the dropouts occurred in a random fashion.
The control group did not experience a significant change in BV, PV, or red-cell volume from baseline to week 12 (Table 2). The training groups experienced significant increases in BV, and PV beginning at week 1 and continuing throughout training (Table 2). Red cell volume was significantly increased after 6 wk of continuous and interval training.
No significant changes occurred in maximal measures of heart rate, systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, V̇O2, minute ventilation, or power output in the control group (Table 3). No significant differences were seen in the maximal exercise measures of heart rate, systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, or arteriovenous oxygen difference after either continuous or interval training. However, maximal measures of V̇O2, power output, and minute ventilation were significantly increased after 6 and 12 wk of continuous and interval training (Table 3). There were no significant differences between the continuous and interval training groups with respect to the changes in V̇O2max, maximal power output, or maximal minute ventilation (Table 3).
Most indicators of maximal LV function (including Q̇, SV, EDV, peak filling rate, ejection fraction, and the SBP/ESV ratio) did not significantly change in the control group over the 12-wk period (Table 4). However, peak ejection rate during maximal exercise was significantly reduced after the 12-wk period in the control group (Table 4). Continuous and interval training resulted in significant changes in Q̇, SV, EDV, peak ejection rate, and peak filling rate during maximal exercise, but no significant change occurred in ESV, ejection fraction, and the SBP/ ESV ratio (Table 4).
The Q̇, SV, and EDV during maximal exercise were significantly increased after weeks 6 and 12 of interval and continuous training (Table 4). The changes in Q̇ were largely due to the increase in SV, as training resulted in no significant changes in heart rate (Table 3).
Since peak values for Q̇, SV, and EDV can be achieved at a submaximal workload in untrained individuals the changes in the peak values for each of these parameters (irrespective of exercise intensity) were also considered. The peak values for Q̇, SV, and EDV were significantly increased after continuous and interval training. Peak Q̇ was significantly increased after weeks 6 and 12 of continuous (20 ± 21 and 36 ± 37%, respectively) and interval (24 ± 29 and 20 ± 19%, respectively) training. Peak SV was significantly increased after weeks 6 and 12 of continuous (19 ± 23 vs 20 ± 18%, respectively) and interval (21 ± 23 vs 11 ± 18%, respectively) training. End-diastolic volume was significantly increased after weeks 6 and 12 of continuous (17 ± 20 vs 14 ± 16%, respectively) and interval (20 ± 21 vs 11 3 14%, respectively) training. There was no significant difference between the training groups with regards to the changes in peak Q̇, SV, and EDV.
Resting volume-regulatory hormones.
No significant changes in resting concentrations of aldosterone, or α-atrial natriuretic peptide occurred during this investigation despite concomitant increases in vascular volumes (Fig. 2, A–F). However, the resting concentration of angiotensin II increased significantly after week 1 of training and thereafter declined to baseline levels. To evaluate whether the total amount of each hormone was increased after training, each hormone concentration was expressed relative to the changes in PV (Fig. 2, A–F). No significant changes in the total amount of aldosterone, or α-atrial natriuretic peptide occurred during the 12 wk of the investigation (Fig. 2, A–D). The total amount of angiotensin II followed a similar pattern to the resting plasma concentration of angiotensin II, reaching its highest value at week one and then declining from weeks 3 to 12 (Fig. 2, E and F).
FIGURE 2Effects of e...Image Tools
Simple correlation analyses were conducted to evaluate the relationships between vascular volumes and V̇O2max (Fig. 3, A–C). Blood volume, PV, and red cell volume (expressed relative to body mass) were directly associated with V̇O2max (expressed relative to body mass) before training. Changes in the vascular volumes accounted for a significant portion of the variance of the changes in V̇O2max, peak Q̇, SV, and EDV (normalized to body mass) (Fig. 4, A–D).
The primary objectives of this investigation were to evaluate the influence of continuous and interval endurance training on BV, aerobic power, and LV function. The major findings of this investigation are that: a) 12 wk of continuous training and interval training result in similar improvements in vascular volumes, V̇O2max, and exercise LV function; and b) training-induced elevations in vascular volumes are positively associated with increases in V̇O2max, EDV, SV, and Q̇ after continuous and interval training.
Effects of continuous versus interval training on maximal aerobic power.
There is considerable debate as to which training program (continuous vs interval training) will have a greater effect on V̇ O2max (3,4,11,20). Some investigators have revealed that continuous training results in a greater improvement in V̇ O2max in comparison with interval training (24). Others have reported that interval training results in greater improvements in V̇ O2max (11), whereas others have observed no difference between the two methods with regard to V̇O2max (3,4,20). These discrepancies may be related to failure to equate the initial fitness levels of groups, failure to equate total work output between groups, and failure to monitor and change training workloads daily according to improvements in fitness levels. In the present investigation, we controlled for these potential confounding variables by stratifying our participants according to body mass and baseline fitness levels. Also, we equated the total work output between groups throughout training and adjusted the workloads daily according to improvements in fitness. As such, we feel confident that we were able to evaluate accurately the differential effects of continuous versus interval training on V̇O2max.
The findings from the present investigation indicate that continuous and interval training result in similar improvements in V̇O2max after both 6 and 12 wk of training. In the present investigation, the change in V̇O2max after both interval and continuous training were largely related to increased improvements in left ventricular function (i.e., SV and Q̇). Changes in cardiorespiratory function were also directly related to changes in vascular volumes.
Blood volume adaptations to continuous and interval endurance training.
To the best of our knowledge, the present investigation is the first randomized controlled investigation to evaluate the relationship between training-induced hypervolemia and V̇O2max after continuous and interval training. Also, this is the first randomized controlled investigation to compare the adaptations in vascular volumes resulting from continuous and interval training. The present findings reveal that 12 wk of continuous and interval aerobic training result in similar elevations in vascular volumes. The intensity of an aerobic exercise bout used throughout training has been shown to have a large influence on BV expansion (2). The duration of each exercise bout also seems to be an important factor in the training-induced hypervolemia. In the present investigation, the average training intensity (i.e., ~65% of V̇O2max) and duration of each exercise bout, and the total number of exercise bouts were similar between groups. The major difference between the two groups was the training modality (i.e., continuous vs interval exercise). Therefore, an important finding of this investigation is that when the average training stimulus is analogous, continuous and interval training programs will lead to comparable changes in vascular volumes and concomitant changes in cardiorespiratory function.
In the present investigation, the BV expansion throughout the training period occurred as a result of increases in PV and red cell volume, but the majority of changes in total BV were the result of changes in PV. This is a common finding after short- and long-term aerobic training (1,2,21), whereas others have reported no significant change in vascular volumes after short-term training (26). These discrepancies are likely related to differences in the participant sample, experimental protocols, training programs, environmental conditions, and/or the season in which the research was conducted.
Vascular volumes and maximal aerobic power.
We have shown previously (28) that BV explains approximately 56% of the variance in V̇O2max across a wide range of fitness levels. The importance of total hemoglobin in the determination of V̇O2max is well known (9). Recent investigators have revealed that V̇O2max may be increased via augmentation of BV, independent of changes in red blood cells (i.e., hypervolemic anemia) in young untrained individuals (as reviewed by Warburton et al. (28)). Similarly, elevated intravascular volumes have been associated with the higher V̇ O2max in young and older endurance-trained persons (1,8,13,14,27). The findings from the present investigation provide direct support for the hypothesis that the improvement in cardiorespiratory function after endurance training is directly related to the training-induced hypervolemia (8–10,14,28,31).
In the present investigation, PV explained approximately 59% of the variance in V̇O2max at baseline. This is supported by several investigators, who observed a direct relationship between BV and V̇O2max (2,8,14,16,17,31,33) and is contrary to investigations where no significant relationships between V̇ O2max and vascular volumes were found (25). Another important finding was that changes in V̇O2max across all weeks of the training investigation were directly associated with the training-induced hypervolemia (irrespective of training modality). In fact, approximately 47% of the variance in changes in V̇O2max can be explained by training-induced changes in PV.
Adaptations in left ventricular function to continuous and interval training.
In the present investigation, both continuous and interval training resulted in significant improvements in left ventricular diastolic function (e.g., diastolic filling). An enhancement in left ventricular diastolic function after endurance training is a common finding in the literature (8,14). In the present investigation, the increased peak filling rate (i.e., diastolic filling) after continuous and interval training allowed for an improvement in EDV. The improvement in diastolic function occurred with little change in myocardial contractility. Therefore, the primary adaptation (after both continuous and interval training) allowing maximal SV to increase appears to be related to an increased ability to utilize the Frank-Starling mechanism during incremental exercise. This is supported by several investigations, which indicate that the major difference between endurance-trained athletes and their sedentary counterparts is the enhanced capacity of the endurance athletes to utilize the Frank-Starling mechanism (8,14,31). In the present investigation, the enhanced capacity to utilize the Frank-Starling mechanism was (in part) related directly to the training-induced hypervolemia, supporting the findings of other investigators (8,14).
It is also important to note, that there was a nonsignificant reduction in left ventricular function between weeks 6 and 12 of interval training (Table 4). This was largely the result of one participant within the interval training group who exhibited a decline in myocardial performance (during maximal exercise) at week 12 in comparison to week 6.
Several investigators have postulated that elevated intra-vascular volumes will significantly increase V̇O2max, in part, via an increase in SV and Q̇ (8,14,31). Previous investigators have revealed that the elevated BV of endurance-trained individuals is directly associated with an increased EDV, SV, and/or Q̇ in comparison to young and older untrained individuals (8,13,14). Several investigations have also revealed the potential for improvements in SV and Q̇ via acute elevations in vascular volumes (14,28,31). The present investigation extends these previous findings and indicates that endurance training (whether continuous or interval in nature) results in significant improvements in vascular volumes, which are associated directly with an elevated EDV, SV, Q̇, and V̇O2max. It is, however, important to note that approximately 30% of the variance in changes in left ventricular function can be explained by changes in PV. Thus, improvements in left ventricular function after endurance training are not solely the passive result of training-induced hypervolemia.
The findings from the present investigation indicate that training-induced hypervolemia is of great importance for the enhanced cardiore-spiratory function observed after endurance training. Therefore, the maintenance of an elevated BV for prolonged periods of time would be beneficial for aerobic performance. Investigators have consistently shown the ability of endurance-trained individuals to maintain a chronically expanded BV (2,8,14). This is associated with a compensatory attenuation in the volume-regulatory reflex mechanisms (1,5,7).
It is generally believed that endurance training does not significantly change resting concentrations of rennin-angiotensin, aldosterone, vasopressin, or atrial natriuretic peptide. The findings of the present investigation support the contention that endurance training (whether continuous or intermittent in nature) generally does not significantly affect the resting concentrations or the total amount of volume-regulatory hormones. An interesting finding in the present investigation is that week one of training resulted in a significant increase in angiotensin II. However, thereafter angiotensin II returned to baseline values. The transient rise in angiotensin II with no change in aldosterone likely indicates that this early rise in angiotensin II had minimal effect upon the observed training-induced hypervolemia. In fact, the overall changes in the volume-regulatory hormones were small and could not explain the large increases in vascular volumes that occurred throughout training. This however does not negate the potential influence that the release of volume-regulatory hormones during exercise has on the induction of training-induced hypervolemia. Also, other factors, such as increased protein synthesis (specifically plasma albumin) (18), likely play a role in the training-induced hypervolemia.
The maintenance of an elevated EDV and BV over the duration of the training period with minor changes in the resting concentrations of the volume-regulating hormones may also indicate that the pressure mechanisms controlling the volume-regulating hormones (e.g., low pressure cardio-pulmonary baroreceptors) are altered by training as supported by the findings of other investigators (7,15).
A limitation of this investigation is that the measurement of SBP/ESV elastance is only an estimate of the slope of the end-systolic pressure volume relationship. Because SBP/ESV elastance represents only one point within the pressure volume loop, we do not know the true volume intercept (i.e., the unstressed volume). As such, conclusions regarding the effect of training on systolic function must be tempered. Although our findings indicate a large improvement in the capacity for ventricular filling, we also have evidence that the capacity for systolic emptying was enhanced with training (reflected in the changes in peak ejection rate).
Continuous and interval training result in significant improvements in vascular volumes. The increase in BV after continuous and interval aerobic training accounts for approximately 30% of the enhancement in cardiorespiratory function that occurs with training. The improvement in cardiorespiratory function after continuous and interval training is associated with an increased capacity for diastolic filling.
The authors would like to thank Ian McLean, Xenia Cluett, Shirley Shostak, Sue Goruck, Christina Loitz, Margaret Ball-Burnett, and Carrie Hornby for their kind assistance in the experimental procedures, data collection, and/or analyses for this investigation. We would also like to thank Drs. Vicki Harber and Vicki Baracos for the use of laboratory equipment central to the measurement of the volume-regulatory hormones. We would also like to thank Dr. Don McKenzie for his insightful review of our manuscript.
Dr. Warburton was supported by the Killam scholarship during the collection of the data for this investigation and by a Natural Science and Engineering Research Council of Canada postdoctoral fellowship during the preparation of this manuscript.
Dr. Teo is currently with the Division of Cardiology, Faculty of Medicine, McMaster University, Hamilton, Ontario. Dr. Humen is currently with the Division of Cardiology, University of Western Ontario, London, Ontario.
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