The O2 uptake (V˙O2) kinetic response to constant work rate cycling performed below the GET is described by a monoexponential function, where V˙O2 attains a steady-state value after 2–3 min of exercise (22). For work rates performed above the GET but below critical power (i.e., heavy-intensity domain), V˙O2 may only stabilize after 15–20 min, displaying a “slow component” of increasing V˙O2 (V˙O2sc) in the interim. When exercise is performed above critical power (i.e., severe-intensity domain) V˙O2 does not stabilize but instead rises continuously until peak V˙O2 (V˙O2peak) is attained and/or exhaustion ensues (21). It is reported that 80%–90% of the V˙O2sc amplitude is caused by processes within the exercising muscles (30,36), namely, the increasing energetic requirements of fatiguing fibers and the progressive recruitment of additional motor units (13,24,33,38). Thus, the emergence of the V˙O2sc during strenuous exercise reflects a progressive decline in work efficiency and, subsequently, has been implicated in the fatigue process (21). Although intramuscular factors undoubtedly play a major role in the development of the V˙O2sc, factors extrinsic to the locomotor muscles are also known to contribute to its amplitude response, such as the mechanical power of breathing (Pb) (21).
Minute ventilation (V˙E) increases progressively over the V˙O2sc phase during strenuous exercise (9,30,31). Given that both total Pb and respiratory muscle V˙O2 (V˙O2resp) rise disproportionately with increasing V˙E (1,2,16), it follows that the mechanical Pb may influence the development of the V˙O2sc. Indeed, Carra et al. (8) showed that augmenting the Pb causes an approximate 27% increase in the V˙O2sc amplitude, whereas Bailey et al. (5) reported that inspiratory muscle training attenuates the V˙O2sc amplitude and improves tolerance to severe- and maximal-intensity cycling. Moreover, we have recently demonstrated that acute unloading of the Pb (via helium–O2 breathing) causes a reduction in the V˙O2sc amplitude during severe but not heavy work rate cycling (11). This greater energetic contribution from the respiratory muscles to the V˙O2sc may be related to inordinately greater increases in the resistive and elastic Pb during severe-intensity exercise (10). However, to date, no study has provided a direct and systematic assessment and comparison of the resistive and elastic components of Pb in relation to the V˙O2sc amplitude during heavy- and severe-intensity exercise.
The aim of this study was to comprehensively assess the changes in the Pb during heavy and severe cycling transitions, with respect to the V˙O2sc in young, healthy adults. The mechanical work expended by respiratory muscles was determined using the modified Campbell diagram (16), from which the resistive and elastic components of Pb were calculated. On the basis of our previous findings (10,11), it was expected that total Pb would rise to a disproportionately greater extent, relative to the V˙O2sc amplitude during severe cycling trials. Moreover, it was hypothesized that this larger rise in total Pb over the V˙O2sc phase would be explained by relatively greater increases in both the resistive and elastic components of Pb.
METHODS
Participants and ethical approval
Twelve recreational cyclists (24 ± 1 yr, 70.9 ± 3.9 kg, six men and six women) volunteered to participate in this study and provided written informed consent. The participants underwent a preparticipatory health screening to ensure they were physically active nonsmokers with no history of cardiac, pulmonary, or metabolic diseases. The present study conformed to the principles outlined in the Declaration of Helsinki and was approved by the Griffith University Human Research Ethics Committee.
Incremental exercise test
Participants completed an incremental exercise test to volitional exhaustion on an electromagnetically braked cycle ergometer (Lode Excalibur Sport; Lode, Groningen, Netherlands) to determine their gas exchange threshold (GET) and V˙O2peak. The incremental exercise test commenced with 3 min of unloaded cycling, after which the power output was increased by 10–15 W every 30 s (i.e., 20–30 W·min−1) until the participants could no longer continue cycling despite verbal encouragement. A self-selected pedal cadence (85 ± 6 rpm) was maintained by each participant until volitional exhaustion. Cardiac rhythm and HR were monitored using a CM5 electrode configuration (Lohmeier M607; Lohmeier, Munich, Germany). Gas exchange parameters were measured breath by breath (MedGraphics CPX/D; Medical Graphics Corp., St. Paul, MN) and subsequently averaged over 30-s intervals. The O2 and CO2 analyzers were calibrated before each test using room air and a calibration gas (12% O2, 5% CO2, and balanced N2). Participants breathed through a mouthpiece attached to a bidirectional differential pressure pneumotachograph (preVent; Medical Graphics Corp., St. Paul, MN) while wearing a noseclip. The pneumotachograph was calibrated at varying flows (30–360 L·min−1) using a 3-L syringe. Peak exercise values are reported as the average of the two highest 30-s values obtained during the incremental exercise test. The GET was determined using the modified V-slope method (39).
Experimental design
To determine the effect of respiratory muscle power on the amplitude of the V˙O2sc, each participant completed two separate constant work rate cycling bouts at heavy and severe exercise intensities. It is generally accepted that the upper limit of the heavy-intensity domain, i.e., critical power, occurs at a work rate roughly equal to 50% of the difference between the GET and V˙O2peak (i.e., Δ50%)(22). Accordingly, the work rates used for heavy and severe cycling trials in the present study were set to equal Δ25% and Δ60%, respectively. Exercise bouts were separated by at least 48 h, and the order of each test was randomized.
Constant work rate cycling
Each constant work rate test commenced with 5 min of unloaded cycling performed on an electromagnetically braked cycle ergometer (Lode Excalibur Sport V2.0; Lode, Groningen, Netherlands). The predetermined power output was then applied immediately with no previous warning given to the participant. The participants exercised at this work rate for 6 min, followed by a period of active recovery at a low exercise intensity. Participants were instructed to maintain a constant pedal cadence during each test. All participants successfully completed 6 min of exercise at heavy and severe work rates. Gas exchange data during the constant work rate tests were obtained using the same methods as described for the incremental exercise test. Inspiratory capacity (IC) measurements were obtained each minute during constant work rate cycling to characterize dynamic respiratory mechanics (see later portion).
The amplitude of the V˙O2sc
At present, the most sophisticated approach to quantifying the amplitude of the V˙O2sc is via nonlinear least-squares regression, as we and others have done in the past (5,8,11). However, in our study, the multiple IC efforts performed during constant work rate cycling noticeably increased the breath-by-breath variability in gas exchange data; such variability necessarily reduces the statistical confidence in parameter estimates derived from nonlinear regressive techniques, particularly with respect to the time delay parameters (i.e., onset of the V˙O2sc). Furthermore, we could not obtain breath-by-breath measurements of respiratory muscle work because IC efforts were performed at 1-min intervals during cycling trials. If we had chosen to apply nonlinear regressive modeling to gas exchange data, it could not be guaranteed that the time delay of the V˙O2sc (i.e., TD2) would fall precisely on any given 1-min interval of constant work rate exercise. As such, any comparison between the V˙O2sc amplitude and Pb would be made using data obtained over different time epochs. For these reasons, we approximated the V˙O2sc amplitude as the rise in V˙O2 from the third to the sixth minute of constant work rate cycling (23).
Respiratory pressures and lung volumes
Esophageal pressure (Pes) was measured using a latex balloon-tip catheter (Ackrad Laboratories, CooperSurgical, Trumbull, CT) inserted via the nose to a depth approximately 45 cm distal to the nares. The balloon was inflated with 1 mL of air, and the “occlusion” test (7) was performed to ensure correct placement of the catheter (i.e., lower one-third of the esophagus). The balloon-tip catheter was connected to a differential pressure transducer (PX138-005D5V; Omega Engineering, Inc., Stamford, CT) that was calibrated using a water manometer before each test. Pes was recorded continuously during both heavy and severe cycling trials.
Before and immediately after each constant work rate cycling test, participants performed graded vital capacity maneuvers with varying degrees of effort (approximately 20%–100% of maximal effort). In brief, participants inhaled to total lung capacity, followed immediately by maximal expiration to residual lung volume. Participants were instructed to perform this initial expiratory maneuver at 100% of their maximal voluntary effort. Immediately after this effort, participants rapidly inhaled to total lung capacity and, without pause, performed a full exhalation at a slightly lower percentage of maximal expiratory effort. This process was repeated for an additional 6–8 times at progressively lower percentages of effort (roughly 10% decrements). Maximal flow–volume envelopes were then constructed using the maximal flow at each lung volume observed during the graded vital capacity maneuvers. This process minimized thoracic gas compression due to excessive pleural pressures (i.e., underestimation of airflow at a given lung volume) and accounted for possible exercise-induced bronchodilation (15). Parameters of pulmonary function were derived from the maximal flow–volume envelopes obtained at rest before exercise. Participants were also instructed to perform maximal inspiratory maneuvers to determine IC while at rest and 2–3 times toward the end of each minute during constant work rate cycling. The IC maneuver was demonstrated to the participant before each exercise test. Participants were required to practice the maneuver to ensure that satisfactory and repeatable measurements could be obtained. No significant decline in the degree of inspiratory effort during IC maneuvers was observed throughout the constant work rate tests; inspiratory Pes swings were similar to those observed at rest. The volume trace was corrected using the IC ratio method detailed by Dolmage and Goldstein (12) to compensate for signal drift of the pneumotachograph. IC values were used to calculate end-inspiratory lung volume [EILV = VC − (IC − VT)] and end-expiratory lung volume (EELV = VC − IC), where VC represents the largest vital capacity obtained during the multiple, graded vital capacity maneuvers (described earlier), and VT denotes tidal volume. A significantly higher dynamic EELV compared with resting values represented an EELV above functional residual capacity (FRC) (i.e., dynamic hyperinflation), whereas a dynamic EELV significantly lower than resting values denoted an EELV below FRC.
Ventilatory constraint
Global ventilatory constraint was quantified V˙E expressed as a percentage of an individual’s maximal ventilatory capacity (MVC)—the nearer that V˙E encroaches on MVC, the greater is the amount of ventilatory constraint. The method used to calculate MVC was modified from that described by Babb and Rodarte (4). In brief, MVC was calculated from the maximal inspiratory and expiratory flow–volume curves at a given EILV and EELV. The tidal breath was subdivided into 0.01-L increments for n = VT/0.01 number of segments. Each segment was then divided by the corresponding mean expiratory flow rate to yield an expiratory time. The expiratory times of all segments were summed to provide a minimal expiratory time for the breath (TEmin). Similarly, minimal inspiratory time (TImin) was determined by applying the same procedure to the individual’s maximal inspiratory flow–volume envelope. The summation of TEmin and TImin was used to derive a maximal achievable respiratory frequency (fR) (i.e., fRmax = [1/(TEmin + TImin) × 60]). Consequently, fRmax was multiplied by VT to calculate MVC. This method of estimating MVC assumes that an individual can generate maximal flow rates instantaneously at the start of each breath. Therefore, as suggested by Babb and Rodarte (4), the computed TEmin and TImin values were arbitrarily increased by approximately 11% to compensate for inertia of the respiratory system.
Expiratory flow limitation (EFL) was quantified by obtaining the isovolume pressure–flow relation of lungs from each participant before exercise (18,20,28). In brief, pressure, flow, and volume data recorded during the graded vital capacity maneuvers were used to construct isovolume Pes–flow relations at lung volumes corresponding to 15%, 30%, 50%, and 70% of VC. From these data, a range of maximum effective expiratory pressures was identified as a function of lung volume (Pmax,e). EFL was then reported as the percentage of VT where dynamic expiratory pressures met or exceeded Pmax,e during the tidal breath. Inspiratory and expiratory pulmonary resistances (RL,I and RL,E, respectively) were determined by dividing resistive pressure by flow rate at 1.0 L above resting FRC for each breath during exercise (26).
The work and Pb
To use the modified Campbell diagram to calculate the work and Pb, it was necessary to obtain chest wall compliance from our participants. Chest wall compliance was measured at rest using the quasistatic relaxation technique (34). The participants were provided with clear instructions on how to perform the maneuver and were given sufficient time (approximately 30–40 min) to become familiar with relaxing against an occluded airway with the glottis held open at various lung volumes. A pneumatic respiratory valve was used to impose the external occlusion (Series 4260A; Hans Rudolph, Inc., Kansas City, MO). When participants were well practiced, they were instructed to perform three consecutive inhalations to total lung capacity, followed by complete occlusion on the final breath. The participant’s inhaled volume was released in stepwise fashion via rapid actuation of the pneumatic valve. This procedure was repeated 3–5 times. In this manner, Pes values were obtained over a range of lung volumes between total lung capacity and FRC. The elastic recoil pressure of the chest wall (Pcw,el) was taken as the mean Pes after a steady plateau (1–2 s) at each volume decrement during the relaxation maneuver. The slope of the Pcw,el–volume relation above resting FRC described the compliance of the chest wall. All participants performed the relaxation technique while seated on the cycle ergometer.
The components of the work and Pb were quantified using modified Campbell diagrams constructed from flow, pressure, and volume data obtained during constant work rate cycling (Fig. 1). The work of breathing (Wb) is typically reported in units of joules per minute in the wider literature. However, within the context of the present study, we felt that it was important to distinguish between the mechanical work expended by respiratory muscles per breath and that expended per minute. Hence, we refer to these two different quantities as the mechanical “work” and “power” of breathing, respectively (i.e., Wb and Pb).
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FIGURE 1: Example of a modified Campbell diagram (left panel) and exercise flow–volume loop (right panel) from a representative individual. The continuous
solid loop in the left panel represents the
P es–volume relation during inspiration (upward) and expiration (downward) of a representative participant at a V˙
E of 173 L·min
−1 during severe-intensity exercise. A moderate degree of EFL is observed near the end of expiration. The
open circles represent pressure points of zero flow. The slope of the
intersecting line between
open circles (i.e., −
P L,el) equals CL,dyn. The
closed circles denote elastic recoil pressures of the chest wall at points of zero flow.
Fine stippling (
) represents inspiratory resistive work, and coarse stippling (
) denotes expiratory resistive work. The horizontal hatching (
) represents inspiratory elastic work, whereas vertical hatching (
) denotes expiratory elastic work. The
dashed lines demarcate the range of maximum effective expiratory pressures. Note that these component areas of respiratory muscle work were multiplied by
f R to obtain corresponding values for the Pb. The continuous
thin loop on the right panel represents the individual’s maximal flow–volume envelope obtained postexercise. The
thickened loop depicts the exercise tidal flow–volume loop, which corresponds to the
P es–volume displayed in the left panel.
Figure 1 illustrates a Pes–volume loop for a representative male participant during severe-intensity exercise (V˙E, 173 L·min−1, 86% of MVC). A linear segment was fit through points of zero flow representing the dynamic elastic pressure exerted by the lungs in negative sign (i.e., −PL,el). The Pcw,el–volume relation was then positioned according to the participants’ resting end-expiratory Pes at EELV (16,44). The intersection between the lines drawn for the −PL,el–volume and Pcw,el–volume relations represents the lung volume at which “inward” elastic forces of the lung tissue are equal and opposite magnitude to the “outward” recoil of the chest wall, i.e., FRC. The area inside the Pes–volume loop to the left of both −PL,el and Pcw,el (fine stippling) represents the work performed by the respiratory muscles to overcome the resistance of the airways and lung tissues during inspiration (inspiratory resistive Wb). Conversely, the area bound by the Pes–volume loop to the right of both −PL,el and Pcw,el (coarse stippling) represents the work performed by the respiratory muscles to overcome the resistive structures of the lung during expiration (expiratory resistive Wb). The area between −PL,el and Pcw,el above FRC (horizontal hatching) represents the magnitude of work required to inflate the thorax during inspiration in opposition to the elastic properties of the lungs and chest wall (inspiratory elastic Wb). The area between −PL,el and Pcw,el below FRC (vertical hatching) represents the magnitude of respiratory work required to oppose the recoil of the chest wall below relaxation volume during expiration (expiratory elastic Wb). Importantly, when an individual presents with static or dynamic hyperinflation (EELV above FRC), no expiratory elastic work is performed. Negative or eccentric work incurred by respiratory muscles was not quantified. The mentioned components of the Wb (joules, J) were multiplied by fR to yield the corresponding Pb in joules per minute.
Data collection
Analog voltage signals representing fractional O2 and CO2 and respiratory airflow were extracted from the gas exchange system. Fractional O2 and CO2, airflow, and Pes signals were digitized at 100 Hz (NI USB-6009; National Instruments, Austin, TX) and were subsequently analyzed with custom-written software to provide breath-by-breath indices of pulmonary gas exchange and respiratory mechanics. Aberrant breaths were removed by visual inspection, and the 2–3 breaths immediately before and after each IC maneuver were deleted from the data set. All indices of pulmonary gas exchange and dynamic respiratory mechanics were averaged into 10–20 breath bins corresponding to each minute of constant work rate cycling. The magnitude of change in respiratory variables from the third to sixth minute of cycling was divided by the V˙O2sc amplitude of the corresponding work rate. This ratio was used to assess whether the amplitude of change in respiratory variables scaled proportionately (or disproportionately) with the V˙O2sc amplitude between heavy- and severe-intensity domains.
Statistical analyses
Two-way repeated-measures ANOVA were used to assess main effects and/or interactions between exercise time (1–6 min) and work rate (heavy- vs severe-intensity cycling). Pairwise comparisons were assessed after post hoc Bonferroni adjustment. The influence of total Wb on the amplitude of the V˙O2sc was examined using Pearson correlation coefficient for heavy and severe work rates separately. All results are presented as mean ± SEM and were analyzed using SPSS 17.0 (SPSS Inc., Chicago, IL). Statistical analyses were considered significant if P < 0.05.
RESULTS
Pulmonary function and incremental exercise data
All participants displayed normal pulmonary function at rest, with an average peak expiratory flow rate of 8.36 ± 0.53 L·s−1, a forced vital capacity (FVC) of 4.48 ± 0.30 L (115% ± 4% predicted), a forced expiratory volume in 1 s of 3.71 ± 0.26 L (116% ± 4% predicted), and a ratio of forced expiratory volume in 1 s to FVC of 0.84 ± 0.02. The participants were recreationally active, with a mean peak power output of 319 ± 28 W and a V˙O2peak of 44.1 ± 2.0 mL O2·kg−1·min−1. It should be noted that V˙O2peak was not validated by a proceeding bout of supramaximal cycling (32). Thus, V˙O2peak may be slightly underestimated in our participants. The mean power output attained at the GET was 154 ± 17 W (48% ± 2% Wpeak). The average power outputs for the heavy and severe cycling trials were 194 ± 19 W (61% ± 2% Wpeak) and 255 ± 23 W (80% ± 1% Wpeak).
Gas exchange and ventilatory responses to heavy- and severe-intensity cycling
The gas exchange and ventilatory responses to heavy and severe cycling trials are reported in Table 1 and illustrated in Figure 2. V˙O2 was higher during severe than that during heavy cycling trials (P < 0.05). Moreover, the “slow component” rise in V˙O2 between the third and sixth minute of exercise was greater (P < 0.05) during severe (312 ± 36 mL·min−1) compared with that during heavy trials (160 ± 27 mL·min−1). The V˙O2 observed during the sixth minute of the severe cycling trials was not different from the V˙O2peak obtained during the incremental exercise test. The “slow component” increase in V˙E expressed relative to the V˙O2sc amplitude was larger for severe trials (P < 0.05). The progressively increasing V˙E observed at both work rates (heavy and severe) was entirely due to a progressive increase in fR between the third and sixth minute of constant work rate cycling (P < 0.05). To this point, fR increased to a greater extent over the V˙O2sc phase for severe compared with that for heavy cycling trials (P < 0.05).
TABLE 1: Gas exchange and respiratory mechanics during heavy- and severe-intensity cycling trials.
FIGURE 2: Time–course changes in gas exchange and ventilatory parameters during heavy and severe cycling trials. Values represent mean ± SEM. PETCO2, end-tidal partial pressure of CO2; V˙CO2tot, total pulmonary CO2 output; V˙O2tot, total pulmonary O2 uptake. *Significantly different from heavy-intensity cycling trial, P < 0.05. †Significantly different from the third minute of constant work rate cycling, P < 0.001.
The work and Pb during heavy- and severe-intensity cycling
Figure 3 displays the time–course changes in the mechanical work expended by respiratory muscles per breath (i.e., Wb). Total Wb was higher during severe compared with that during heavy cycling trials (P < 0.05). Importantly, the total Wb increased over the V˙O2sc phase for severe work rate transitions only, consequent to increasing amounts of inspiratory and expiratory resistive Wb (P < 0.05). The inspiratory elastic Wb did not change appreciably from the third to the sixth minute of exercise for both work rates. Expiratory elastic Wb was not different between work rates and did not change during constant work rate cycling.
FIGURE 3: Time–course changes in the resistive and elastic components of the Wb during heavy and severe cycling trials. Values represent mean ± SEM. *Significantly different from heavy-intensity cycling trial, P < 0.05. †Significantly different from the third minute of constant work rate cycling, P < 0.001.
The dynamic changes in the components of Pb during cycling trials are illustrated in Figure 4. The total Pb and its subcomponents were higher for severe-intensity exercise (P < 0.05). When expressed relative to the amplitude of the V˙O2sc (Fig. 5), the inspiratory and expiratory resistive Pb and inspiratory elastic Pb together increased to a greater extent over the V˙O2sc phase for severe compared with those for heavy work rate transitions (P < 0.05). We observed no significant relation between the relative rise in total Pb and the relative V˙O2sc amplitude during heavy cycling trials (R2 = 0.04, P = 0.56). Conversely, the relative increase in total respiratory muscle power between the third and sixth minute of severe cycling displayed a strong positive correlation with the relative amplitude of the V˙O2sc (R2 = 0.47, P < 0.01).
FIGURE 4: Time–course changes in the resistive and elastic components of the Pb during heavy and severe cycling trials. Values represent mean ± SEM. *Significantly different from heavy-intensity cycling trial, P < 0.05. †Significantly different from the third minute of constant work rate cycling, P < 0.001.
FIGURE 5: The change in V˙E, fR, and the resistive and elastic components of the Pb between the third and sixth minute of exercise during heavy and severe cycling trials. Values represent mean ± SEM. Note that increases in V˙E, fR, and all displayed components of the Pb are expressed relative to the amplitude of the slow component of O2 uptake. The expiratory elastic Pb is not presented in this figure because its magnitude did not increase significantly between the third and sixth minute of cycling during both heavy and severe cycling trials. *Significantly different from heavy-intensity cycling trial, P < 0.05.
Respiratory mechanics during heavy- and severe-intensity cycling
The changes in parameters of respiratory mechanics during constant work rate cycling are reported in Table 1. V˙E expressed as percentage of MVC, RL,E, and EILV were higher during severe compared with that during heavy cycling trials (P < 0.05). RL,I was higher for severe work rate transitions by the end of the sixth minute of constant work rate cycling (P < 0.05). EELV was similar for both work rates; however, EELV increased over the V˙O2sc phase during severe cycling trials only (P < 0.05). Despite this rise, EELV was lower than resting values by the end of severe cycling trials (P < 0.05). Dynamic lung compliance (CL,dyn) was lower for severe compared with that for heavy trials (P < 0.05). Furthermore, CL,dyn at the end of the severe cycling bouts was significantly lower than resting values (P < 0.05). The degree of EFL was systematically higher (P < 0.05) for severe compared with that for heavy trials at the third minute (2.5% ± 1.1% VT vs 1.0% ± 0.7% VT) and sixth minute (22.1% ± 2.7% VT vs 7.1% ± 6.2% VT) of constant work rate cycling. EFL, V˙E as a percentage of MVC, RL,I, and RL,E significantly increased from the third to the sixth minute of exercise for severe work rates only (P < 0.05), indicating a progressive rise in ventilatory constraint over the V˙O2sc phase.
DISCUSSION
This study is the first to provide a comprehensive and direct analysis of the mechanical Pb in relation to the V˙O2sc. In agreement with our original hypothesis, we found that the “slow component” rise in total Pb is disproportionately greater for severe compared with that for heavy work rate transitions. Moreover, the larger rise in respiratory muscle power is explained by inordinately larger increases in the inspiratory and expiratory resistive Pb, and inspiratory elastic Pb over the V˙O2sc phase during severe cycling trials. In turn, the findings of this study provide further support for the notion that the Pb plays a relatively more important role in the development of the V˙O2sc during severe compared with that during heavy exercise, and that its greater role is attributed to disproportionately larger increases in the resistive and elastic Pb.
It is emphasized here that the total mechanical Pb is not, at least quantitatively or directly, the largest contributor to the V˙O2sc amplitude during strenuous, constant work rate cycling. Most (80%–90%) of the V˙O2sc amplitude is explained by an increasing O2 and/or adenosine triphosphate cost of force production of fatiguing muscle fibers (30,36,43) and the “excess” V˙O2 incurred by progressive recruitment of additional (13,33), primarily type II motor units (24,38). The emergence of an intramuscular V˙O2sc does, however, necessitate that V˙E rises commensurately with V˙O2, lest arterial hypoxemia develop. Certainly, many investigators have reported that V˙E rises continuously over the V˙O2sc phase during strenuous exercise (9,30,31). Given that the total Pb rises exponentially with increasing V˙E (16,25,37), it is elementary that V˙O2resp should contribute to the V˙O2sc amplitude. Moreover, recent data from our laboratory strongly suggest that V˙O2resp constitutes a larger fraction of the V˙O2sc response during severe compared with that during heavy work rate transitions (10,11). Yet, hitherto the present study, it was unclear as to which components of the Pb may conspire to produce a larger “respiratory” contribution to the V˙O2sc during severe-intensity exercise.
The work and Pb during the V˙O2sc
An appreciable “slow component” rise in the inspiratory and expiratory resistive Pb was observed during both heavy and severe cycling trials, the rise being relatively greater in the latter condition. Importantly, however, the factors responsible for the increasing resistive Pb during exercise were notably different for heavy and severe work rates. During heavy cycling trials, the inspiratory and expiratory resistive Pb increased over the V˙O2sc phase primarily because of the emerging tachypnea—the amount of resistive work expended by respiratory muscles per breath (i.e., Wb) did not change during this period of exercise. The observation that the resistive Wb did not change is perhaps not surprising, given that mean tidal flows were both relatively small and increased marginally over the V˙O2sc phase. Furthermore, the degree of ventilatory constraint during exercise at this work rate was trivial, as evidenced by the low percentage of MVC occupied by V˙E and the absence of significant EFL.
In contrast, the “slow component” rise in the inspiratory and expiratory resistive work during severe cycling trials was due, at least in part, to the large increases in mean tidal airflows observed between the third and sixth minute of exercise. Commensurate with these rising flows was a time-dependent increase in pulmonary resistance (i.e., RL,I and RL,E) over the V˙O2sc phase, exacerbating the amount of resistive work expended per breath. The increase in RL,I during severe work rate transitions was probably due to a flow-dependent phenomenon, which may be attributed to the development of turbulent flow within larger-diameter airways (3,29). The increase in RL,E over the V˙O2sc phase, on the other hand, was likely the result of a greater mechanical constraint on breathing during severe cycling trials, namely, the development of EFL. On average, our participants displayed mild-to-moderate flow limitation near end expiration during severe trials, where expiratory pressures could be observed in excess of those required to produce maximal flow (18,28). Under these circumstances, RL,E increases abruptly with rising expiratory pressure and there is a significant “wasting” of respiratory muscle effort, ultimately increasing the resistive work performed during expiration. In light of these findings, we suggest that a higher and progressively increasing resistive load per breath (Fig. 3) and a relatively more pronounced tachypnea (Fig. 5) conspire to produce an inordinately larger rise in the total resistive Pb over the V˙O2sc phase during severe-intensity compared with that during heavy-intensity cycling.
The inspiratory elastic Pb significantly increased over the V˙O2sc phase during both heavy and severe cycling trials (Fig. 4). During both cycling trials, it was evident that most of the “slow component” rise in inspiratory elastic Pb was contributed by the emerging tachypnea and was not due to a time-dependent increase in inspiratory elastic work expended per breath (Fig. 3). This finding is supported by our observation that EILV and CL,dyn did not change significantly from the third to the sixth minute of exercise during both cycling trials. Importantly, EILV and CL,dyn were systematically higher and lower, respectively, during severe cycling trials, describing that inspiratory elastic load per breath was overall greater for severe compared with that for heavy work rate transitions. Not only was inspiratory elastic load higher, but also, the “slow component” rise in fR was relatively larger for severe cycling trials. Consequently, these two factors together mediated a disproportionately greater rise in inspiratory elastic Pb during severe than that during heavy work rate transitions (Fig. 5). Expiratory elastic Pb constituted only a marginal fraction of total Pb and did not significantly increase during the V˙O2sc phase of both cycling trials. For this reason, we suggest that expiratory elastic Pb is not an important contributor to the V˙O2sc amplitude during strenuous exercise.
Implications of our findings
To support our previous observation that V˙O2resp constitutes a higher fraction of the V˙O2sc response during severe cycling transitions (11), total Pb must increase to a relatively greater extent over the V˙O2sc phase during severe-intensity compared with that during heavy-intensity exercise. Consistent with this rationale, our data show that the rise in total Pb from the third to the sixth minute of exercise was approximately 8.7-fold higher for severe than that for heavy cycling transitions when normalized to the amplitude of the V˙O2sc (Fig. 5). The increase in V˙O2resp over the V˙O2sc phase may be known if respiratory muscle efficiency (eresp) and the “heat equivalent” for O2 (α) are given, such that: V˙O2resp = αPb/eresp, where α is kilojoules per liter of O2 (25,27). The energetic contribution of respiratory muscle work to the V˙O2sc amplitude may then be estimated as follows: contribution (%) = 100 (V˙O2resp/V˙O2sc). Unfortunately, published values of eresp vary too greatly (1%–25%) to provide a confident estimate of V˙O2resp in this study (37). Notwithstanding this point, if we assume that eresp is constant and that α does not change appreciably during exercise, the contribution of V˙O2resp to the V˙O2sc should be roughly 8.7 ± 2.6 times higher during severe compared with that during heavy work rate transitions (see document, Supplemental Digital Content, https://links.lww.com/MSS/A364, for detailed explanation). It is more likely, however, that eresp declines when V˙E > 100 L·min−1 (6,42). In this case, the contribution of V˙O2resp to the V˙O2sc is likely to still be greater for severe than those for heavy cycling trials. Although absolute values for V˙O2resp cannot be provided at present, the reasoning outlined above supports our contention that the Pb is a relatively more important contributor to the V˙O2sc during severe compared with that during heavy work rate transitions. Indeed, this conclusion is further supported by our observation that the relative increase in total Pb between the third and sixth minute of constant work rate cycling displayed a strong positive correlation with the V˙O2sc amplitude during severe but not during heavy cycling trials.
It addition to the above, it is possible that the Pb indirectly affects the intramuscular V˙O2sc originating from within the locomotor muscles (11). Fatiguing levels of inspiratory muscle work are known to elicit a reflexive vasoconstriction of blood vessels in the locomotor muscles (40,41). Interestingly, inspiratory muscle fatigue, and the so-called “respiratory steal” of cardiac output, reportedly occurs at work rates >80% Wpeak (17,19,35)—exercise intensities similar to that used here for severe cycling trials. Thus, the high Pb incurred during severe-intensity exercise may compromise O2 delivery to locomotor muscles, which could hasten fatigue in contracting muscle fibers and accelerate the recruitment of additional motor units, further compounding the V˙O2sc.
Methodological considerations
The resistive and elastic components of respiratory muscle work and, subsequently, the Pb were quantified using modified Campbell diagrams. This method of quantifying the Wb and Pb during exercise does not account for the mechanical costs incurred by deformation of the chest wall, flow resistance of chest wall tissues, eccentric (negative) and/or isometric work performed by respiratory muscles, compression of thoracic gas, and the work done on abdominal viscera (14). Accordingly, our values for the Pb may have been underestimated. Had we accounted for these “additional” sources of respiratory muscle work, the differences in the Pb observed between heavy and severe cycling trials would most likely be greater than those reported here. Furthermore, the contribution of V˙O2resp to the V˙O2sc is probably more than 8.7-fold higher during severe compared with that during heavy work rate transitions, as reasoned previously.
It is acknowledged that respiratory muscle power is generally higher at a given V˙E during cycling in females compared with that in males (16). However, we emphasize that sex-based differences in respiratory mechanics did not detract from the importance of our central findings, namely, the “slow component” rise in total Pb is relatively greater for severe compared with that for heavy work rate transitions. Nevertheless, because our data were not separated into groups on the basis of the participants’ sex (because of low participant numbers), we do caution that our findings may only apply to young, recreationally active males and females collectively.
CONCLUSIONS
The findings of this study confirm that total Pb increases commensurately with the V˙O2sc during strenuous, constant work rate cycling. Moreover, this study is the first to report that the “slow component” rise in total Pb is inordinately greater for severe compared with that for heavy work rate transitions. The greater rise in total Pb is consequent to relatively larger increases in the inspiratory and expiratory resistive Pb, and inspiratory elastic Pb over the V˙O2sc phase during severe cycling trials. These findings are consistent with the hypothesis that respiratory muscle power and, by extension, V˙O2resp constitute a larger fraction of the V˙O2sc response during severe-intensity compared with that during heavy-intensity exercise.
The authors thank each participant for their participation in the present study. The authors are also grateful for the guidance and advice provided by Dr. Norman Morris, Dr. Sophie Lalande, and Dr. Manda Keller-Ross during the preparation of this manuscript.
T. J. C. was supported by an Australian Postgraduate Award.
The authors declare no conflicts of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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