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Physiology Department, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96822
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Fee, Lawrence L., Richard M. Smith, and Michael B. English.
Enhanced ventilatory and exercise performance in athletes with
slight expiratory resistive loading. J. Appl.
Physiol. 83(2): 503-510, 1997.
We determined the
cardiorespiratory and performance effects of slight (1.5-3.0
cmH2O) expiratory resistive
loading (ERL). Twenty-eight highly fit [peak
O2 uptake
(
O2 peak) = 63.6 ± 1.3 ml · kg
1 · min1]
athletes (age = 33.5 ± 1.3 yr) performed paired
O2 peak cycle ergometer tests (control vs. ERL). End-expiratory lung volume was
separately determined in a subset of subjects
(n = 12) at steady-state 75% maximum
power output (POmax) and was
found to increase (0.67 ± 0.29 liter) with ERL. In the
O2 peak
tests, peak expiratory pressure at the mouth, mean inspiratory flow, minute ventilation, and O2 pulse
were greater with ERL at every intensity level (i.e., 75, 80, 85, and
90% POmax). Increased minute ventilation was largely due to a trend toward increased tidal volume
(P < 0.05 at 80%
POmax).
O2 uptake was greater at 90%
POmax with ERL. Increased
O2 pulse with ERL at comparative
workloads suggests that stroke volume was augmented with ERL. Also,
with ERL, athletes attained higher
O2 peak (63.0 ± 1.4 vs. 60.1 ± 1.3 ml · kg1 · min1)
and greater POmax (352.0 ± 9.9 vs. 345.7 ± 9.5 W). We conclude that elevated end-expiratory lung
volume in response to slight ERL during strenuous exercise served to
attenuate both airflow and blood flow limitations, which enhanced
exercise capacity.
expiratory resistance; exercise capacity; airflow limitation; end-expiratory lung volume
INTRODUCTION AIRFLOW LIMITATION (FL) during exercise hyperpnea is
the consequence of portions of the expiratory flow-volume envelope
becoming tangent to the flow-limiting (effort-independent) slope of the maximal expiratory flow-volume (MEFV) curve (18). FL over a significant
portion of the expiratory tidal volume
(VT) has been demonstrated
over the range of intense to maximal exercise, developing at In healthy subjects, EELV has been observed to progressively decrease
by ~0.7 liter during heavy exercise. EELV remains depressed until
exercise becomes intense and then gradually returns to near-resting FRC
at In principle, expiratory resistive loading (ERL) might experimentally
elevate EELV to a volume at which expiratory flow remains entirely
within the MEFV curve (1) and away from the FL experienced at lower
lung volumes (19). One frequently observed consequence of ERL (7, 10,
11, 22) has been increased EELV. Other favorable responses to ERL have
been increased VT and mean
inspiratory flow
(VT/TI)
(11, 14, 24). However, concomitant with the increases in EELV
associated with ERL, typically there have been adverse alterations,
such as compromised
METHODS
83% of
maximal aerobic capacity
(O2 max) in young (mean 25 ± 1 yr) competitive endurance athletes (19). In exceptionally fit older athletes, FL begins to occur at 50-75%
O2 max (18). FL at
lower intensities in fit, older athletes is due to loss of elastic
recoil of the lung (6). FL can compromise minute ventilation
(E) (16),
and it has been speculated that the positive expiratory pleural
pressures (Ppl) attendant to FL may impede venous return (25). One
circumstance that contributes to the development of FL is decrease in
functional residual capacity (FRC) or end-expiratory lung volume (EELV)
with exercise (13). When EELV is lowered, exercise expiratory tidal
flow shifts closer to the MEFV envelope (3), increasing the potential
for FL and reducing the maximal predicted
E
(16). Furthermore, at lung volumes below resting FRC, airway closure in
dependent lung regions adds to maldistribution of inspiratory gas flow
(13).
O2 max (17, 18).
Despite this tendency of EELV to recover to its near-resting FRC
position, a progressively greater portion of the
VT becomes flow limited as
exercise becomes more intense (18, 19).
E (11, 24) and mean expiratory flow
(VT/TE)
(22, 24) and decreased cardiac output (perhaps secondary to reduced
venous return in patients with chronic obstructive pulmonary disease
due to elevated intrathoracic pressures) (23). However, our preliminary
work (5) suggested that the degree of ERL employed in previous studies
may have been too great (5.0-40.0
cmH2O) (7, 10, 11, 14, 22, 24) to
elicit cardiorespiratory benefit. In a prior study, with only slight
reductions in the internal diameter of the expiratory port of the Hans
Rudolph low-resistance three-way valve, we observed mitigated
exercise-induced hypoxemia (EIH) in highly fit, endurance-trained athletes at mild altitude (5). Because our former EIH-ERL study suggested that one of our experimental resistors offered beneficial resistance to expiration during strenuous exercise, we chose to conduct
a sea-level study utilizing the same expiratory flow resistor used at
altitude (5). In the present graded peak aerobic capacity (O2 peak) study, we
measured peak expiratory pressure at the mouth
(PEpeak)
and changes in cardiorespiratory variables in highly fit endurance
athletes. In a companion study, we determined exercise EELV in a
representative subset of athletes (n = 12) with and without the experimental expiratory orifice during heavy,
steady-state exercise at 75% of maximum power output
(POmax).
O2 peak = 63.6 ± 1.3 ml · kg1 · min1).
They were studied with their informed consent, and all procedures were
approved by the Human Experimentation Committee of the University of
Hawaii at Manoa. Selected physical characteristics and lung volumes of
the subjects are given in Table 1. All
paired testing with a given subject was completed within 7 days.
Subjects were asked to refrain from strenuous activity on the day
before testing. All 28 subjects performed paired
O2 peak tests.
Subsequently, EELV at steady-state 75%
POmax was determined in a random
subset of the
O2 peak-tested
subjects (n = 12): 11 men and 1 woman. Their mean age (34.3 ± 2.3 yr),
O2 peak (68.7 ± 1.5 ml · kg1 · min1),
residual volume (1.52 ± 0.11 liters), vital capacity (5.31 ± 0.39 liters), and total lung capacity (7.17 ± 0.26 liters) differed only slightly from the
O2 peak-tested group.
Table 1.
Subject characteristics
Mean ± SE
Range
Age, yr
33.5 ± 1.3
21-51
Height, cm
172.0 ± 1.4
165-192
Weight, kg
70.1 ± 1.5
51.8-80.0
O2peak,
ml · kg1 · min1
63.6 ± 1.3
53.6-78.2
RV, liters
1.45 ± 0.07
1.02-2.47
VC, liters
5.73 ± 0.17
4.78-8.03
TLC, liters
7.21 ± 0.21
5.66-10.35
FVC,* %
111.30 ± 2.42
91-137
FEV1.0,* %
112.10 ± 2.72
89-133
Values are representative of 28 subjects (23 men and 5 women).
O2 peak, peak aerobic
capacity; RV, residual volume; VC, vital capacity; TLC, total lung
capacity; FVC, forced vital capacity; FEV1.0, forced
expiratory volume in 1 s.
*
Percentage of normal predicted values
from Schiller (Schiller derivations based on Knudson, Crapo, and
Morris).
O2 peak series or the
steady-state at 75% POmax series)
began immediately after the transition interval and commenced with the
initial minute at the subject's predetermined, fixed cadence and
chosen PO. Group mean heart rate (HR) at starting PO was 131.0 ± 2.9 (SE) beats/min. Workload was increased by 10 W/min thereafter.
Subjects were asked to keep their cadence within 1-2
revolutions/min (rpm) of the digital, instantaneous rpm readout at all
times, which we strictly monitored along with current wattage.
ERL.
During the control tests, subjects breathed through a three-way
low-resistance valve (model 2700, Hans Rudolph). The three-way valve
was mounted in such a way as to ensure a relatively consistent body
position during the tests. ERL was effected by reducing the internal
diameter of the expiratory port of the three-way valve from 28.6 to
22.2 mm at its juncture with the gas-conducting tubing. Figure
1 regressions are derived from the pooled
data of all subjects during
O2 peak testing and
present the profiles of
PEpeak vs. E in without
(control) and with ERL. The control data were best described by a
first-order polynomial, whereas the ERL data were best described by a
second-order polynomial. In all comparisons within this study the order
of presentation of expiratory orifices was alternated, such that ERL
was presented first in one-half of the subjects, and the subjects were
naive to the intervention. PEpeak was
sampled from a sampling port hose barb in the housing of the three-way
valve. A 0.5-m section of rigid plastic tubing (2 mm ID) connected the
barb to a volumetric pressure transducer (model PT-5A, Grass), which
was linear over 0.0-12.0
cmH2O. Before each test the
transducer was calibrated with a water manometer. The Grass transducer
was interfaced with a strain-gauge coupler (model 2193, Harvard
Apparatus). During all tests,
PEpeak
traces were recorded on a 12-speed chart mover (model 486, Harvard
Apparatus). The chart speed was maintained at 0.025 cm/s, except for
single-breath traces (PE),
which were recorded at 5.0 cm/s.
E) in
control condition (Hans Rudolph valve 2700) and with expiratory
resistive loading (ERL). Data are pooled for all subjects
(n = 28). Confidence level:
P 
0.05. Best-fit lines: control,
1st-order polynomial; ERL, 2nd-order polynomial.
O2 peak testing.
Each subject performed two graded
O2 peak cycle
ergometer tests to exhaustion: one with ERL and one without (control).
In each test, O2 peak
was considered the highest O2
consumption (O2) maintained
for a full minute. The higher of the two
O2 peak values was
used to determine group mean
O2 peak (Table 1). POmax (in W) was considered to be
the higher last full-minute wattage attained in either of the two
O2 peak tests. We did not validate the reproducibility in the
POmax tests. We did, however, randomize the presentation of the orifices (control vs. ERL).
Steady-state testing.
Subjects performed two graded cycle ergometer tests (with and without
ERL) up to a steady state of 75%
POmax, at which point EELV was
determined. The EELV test protocol began just as in the O2 peak tests, except
at 75% POmax the wattage was
manually fixed and maintained for 4 min. With the assumption of steady state (28), metabolic data associated with EELV were collected and
averaged in the 3rd min. At the beginning of the next (4th) minute, we
switched the subject to the closed-circuit He-rebreathing system for 30 s.
EELV determination: He dilution.
EELV was determined by He dilution. Two manual, directional control,
three-way Y-shaped valves (model 2100 C, Collins) were used to switch
from the open-circuit gas-evaluating system to the closed-circuit He
residual volume apparatus (model P-1300, Collins) rebreathing system
with a 13.5-liter spirometer. Before each test the system was purged,
and the He analyzer was calibrated with a known concentration of
He-containing gas (5.0%), purged again, and loaded with 4 liters of
O2 and 0.6 liter of He. During the
rebreathing (30 s), 100% O2 was
infused at a rate that maintained the system volume relatively
constant. The system was scrubbed of
CO2 by barium hydroxide lime, US
Pharmacopoeia (Collins absorbent granules). Final He concentrations
were recorded when further gas mixing elicited no further changes in He
concentration. All volumes were converted to
BTPS.
Measurements.
All tests were conducted under relatively stable environmental
conditions: 20-21°C, 758-765 Torr, and 50-65%
relative humidity. Barometric pressure was ascertained from the
National Weather Service telephone recording, which was updated hourly.
Laboratory temperature and relative humidity were determined from a
thermometer/hygrometer (model 63-844, Micronta). Arterial
O2 saturation
(SaO2) was determined with an ear
oximeter (model OPS-200, Satlite), which was internally self-calibrated
before each exercise test.
SaO2 was measured only in
the
O2 peak
tests. Each subject's ECG and HR were continuously monitored during
exercise testing with the Schiller AT-6 ECG system. Instantaneous
reports of ECG and HR were given on the screen of a monitor (model 710 A, Mitsuba) interfaced with the AT-6 system. Before every exercise test
the ECG monitor was calibrated with the Physio-dyne HR calibrator
(ECG-Cal).
Ventilatory variables were monitored via standard open-circuit
spirometry. Fractional concentrations of expired
O2
(FEO2) and
CO2
(FECO2)
were determined by Ametek analyzers (models S-3A/I and CD-3A,
respectively). Before every test, these analyzers were calibrated with
two reference gases of the following concentrations: 21.03% O2 and
5.02% CO2 or
15.00% O2 and
0.03% CO2.
Inspired ventilation volume
(I) was
determined with a flow transducer (model K520, K. L. Engineering).
These measurements of
FEO2,
FECO2, and I and
those of SaO2 and HR (via Physio-dyne HR
computer/ECG-HR3) were integrated with a CompuAdd 433 (model A000)
computer and monitor (model 51109) that ran the Ametek
O2 uptake system OCM-2 program.
The OCM-2 recorded SaO2, HR, the
respiratory exchange ratio (R),
E, breathing
frequency (f ), VT, duration
of expiration, inspiration, and breathing cycle
(TE,
TI, and
TT, respectively), TI/TT,
VT/TE,
VT/TI,
FEO2,
FECO2,
O2,
CO2 production
(CO2), and
O2 pulse
(O2/HR).
E was
determined from
I and R,
with differences in O2 and
CO2 accounted for and
corrected by the OCM-2 program. All dynamic ventilatory volumes were
converted to BTPS and, along with
SaO2 and HR, were averaged to minute
intervals by the OCM-2.
EELV and resting residual volume measurements were determined by
standard He dilution and reflect allowances for
O2 consumed or added to the
system. CO2 was presumed to be
entirely removed from the system. Vital capacity (VC), forced VC, and
forced expiratory volume in 1 s were determined with the Schiller AT-6
pulmonary function testing equipment. Predicted values were based on a
composite derived by Schiller (manual issue 07.1991) from the work of
Knudson, Crapo, and Morris.
Data analysis.
Because the majority of subjects attained different levels of PO in
each of their O2 peak
tests, POmax was defined to
be the higher full-minute PO of the two
O2 peak tests. The
virtue of this method is that it ensured that every intrasubject
comparison was made at identical PO or wattage levels. It also provided
a criterion for normalizing the data into percentages of
POmax.
Inherent in the fact that if a given subject accomplished two different
POmax levels is that he/she would
have only one set of data at 100%
POmax and that there was no
reference for comparison at that level. Also, in many cases there is no
reference for comparison at 95%
POmax. Therefore, the data were
normalized with reference to POmax
at 75 (heavy exercise), 80, 85, and 90%
POmax (intense exercise) by
interpolation.
Statistics.
All data were analyzed using the SigmaStat program. Repeated measures
analyses of variance were performed on the
O2 peak data, and
where significant differences (P 0.05) between control and treatment (ERL) were indicated, the
Student-Newman-Keuls post hoc test was performed to determine at what
level(s) of POmax there was a
significant (P 0.05) difference.
Steady-state data were analyzed using Bonferroni's pairwise multiple
comparisons to determine whether there were significant
(P 0.05) differences between
control and treatment (ERL).
RESULTS
O2 peak test
series comparisons.
Mean test duration was 13.1 ± 0.73 min. There was slight but
statistically significant EIH in control and ERL tests at 75, 80, 85, and 90% POmax (Fig.
2) compared with resting sea-level SaO2; although
SaO2 with ERL tended to be greater,
there was no significant difference in
SaO2 between control and ERL at rest or at any level of intensity.
PEpeak was
greater (P 0.05) with ERL at every
workload (Table 2).
E with ERL was
greater (P 0.05) at 80, 85, and 90% POmax (Table 2, Fig.
3).
VT was consistently greater with
ERL over the comparison range but significantly greater (P 0.05) only at 80%
POmax, where it was greater by 200 ml (Fig. 4). The increase in
VT with ERL averaged 144 ml from
75 to 90% POmax. This trend
toward increased VT at 80, 85, and 90% POmax in concert with
relatively high f accounted for the increase in E. The
increase of VT in response to
ERL in our study is consistent with the observations of previous
studies (13, 24). From 75 to 90%
POmax, f was unchanged. This
varies from the results of previous investigators who observed
decrements in f with ERL during exercise (11, 14).
VT/TI
was greater (P 0.05) with ERL at every workload (Fig. 5).
VT/TE
tended to be greater with ERL and significantly
(P 0.05) greater at 75%
POmax. HR was consistently lower
(2.0 beats/min) throughout with ERL (Fig.
6) but statistically lower only at 75%
POmax. Relative
O2 was nonsignificantly
higher (3.2
ml · kg1 · min1)
from 75 to 85% POmax with ERL and
significantly greater (P 0.05) with ERL at 90% POmax. The
clear tendencies for elevated O2 and lowered HR produced an
O2 pulse that was significantly greater with ERL at every workload (Fig.
7).
) and without ERL (
). Values
are means ± SE. * Significantly (P 0.05) different from resting
values (with and without ERL).
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E vs.
%POmax with () and without ERL
(control, ). Values are means ± SE;
n = 28. * Significantly
(P 0.05) different from control.
) and without ERL
(). Values are means ± SE; n = 28. * Significantly (P 0.05)
different from control.
) and without
ERL (). Values are means ± SE;
n = 28. * Significantly
(P 0.05) different from control.
) and without ERL (). Values are means ± SE;
n = 28. * Significantly
(P 0.05) different from control.
O2/HR, where
O2 is
O2 consumption) vs.
%POmax with () and without ERL
(). Values are means ± SE; n = 28. * Significantly (P 0.05)
different from control.
Subjects attained 1.8% greater POmax (352.0 ± 9.9 vs. 345.7 ± 9.5 W; Fig. 8) and 4.8% higher
O2 peak (63.0 ± 1.4 vs. 60.1 ± 1.3 ml · kg1 · min1,
both P 0.05) with ERL (Fig.
9).
0.05)
different from control.
O2 peak) with and
without ERL. Values are means ± SE;
n = 28. * Significantly
(P 0.05) different from control.
Steady state at 75% POmax comparisons. Mean test duration was 17.0 ± 0.1 min. Table 3 presents the essential cardiorespiratory data, comparing control with ERL during steady-state exercise at 75% POmax.
E is somewhat
higher than that observed at 75%
POmax in the
O2 peak studies. This disparity can be explained in part by a ventilatory drift (4.96 ± 1.35 and 4.12 ± 1.19 l/min in control and ERL, respectively) that
we observed during the 4 min of cycling leading to steady state.
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0.0
cmH2O are expiratory pressure tracings; values 0.0 cmH2O are
incomplete inspiratory pressure tracings. Max, maximum.
DISCUSSION
In the range of exercise intensity of this study, it is probable that
the athletes experienced various degrees of expiratory FL (19). FL over
a significant portion of expiratory
VT has been demonstrated over
the range of intense to maximal exercise (the range of our study) and,
specifically, developed at ~83% of
O2 max in young (25 ± 1 yr) competitive elite athletes (19). In exceptionally fit older
(69 ± 1 yr) athletes, this occurred at 50-75%
O2 max (18). FL at
lower intensities in fit, older athletes is due to loss of elastic
recoil of the lung (6). With losses in elastic recoil, the static lung
recoil pressure at any given lung volume is lower, so greater effort
(Ppl) is required during expiration (18). In our graded
O2 peak study, we
suspect that slight ERL may have somewhat attenuated the effects of FL
during heavy exercise and effected measurable increases in exercise
performance and in several cardiorespiratory variables; in particular,
we observed increased POmax,
E,
and O2 pulse, which are reported
here for the first time. Also, the increase in
E is contrary
to the findings of all other loaded expiration studies (10, 11, 14, 24)
of which we are aware.
O2 max values have
been <40
ml · kg1 · min1
(8, 22). Healthy subjects in these ranges of aerobic capacity would not
place the ventilatory demand on the pulmonary system, which would
precipitate FL (19). The third factor precluding cardiorespiratory
benefit in response to ERL is that tests have been resting tests or
low-intensity submaximal exercise tests. Such protocols would not
precipitate FL, even in highly fit subjects (19).
Respiratory responses to ERL.
Neither TI nor
TE changed in response to ERL.
Previous investigators have observed an increase in
TI and
TE (24) or no change in
TI or
TE with ERL (7). A prolongation
of TE observed by Goldstein and
co-workers (8) was proportional to the amount of ERL, which ranged from
5.0 to 30.0 cmH2O, far more than
the ERL employed in the present study.
EELV typically increases in response to expiratory loading (7, 8, 11,
22), increasing up to 1.71 ± 0.67 liters in response to extreme ERL
(7). Not unexpectedly, in the steady-state (75%
POmax) comparisons, EELV was
increased with ERL. However, what was surprising, in view of previous
studies employing ERL, was the magnitude of increase in EELV (0.67 ± 0.29 liter) in response to so little increase in
PEpeak (0.4 ± 0.1 cmH2O) with ERL vs. control. Johnson and colleagues (20) observed a consistently slightly
higher EELV (120 ± 10 ml, P < 0.01) with the two-tracer-gas method than with the He-dilution method
employed in this study. This disparity was greatest during heavy
exercise: 158 ± 40 and 209 ± 24 ml with equilibration times of
7 ± 1 and 20 s, respectively. Because this consistently slight and
directional error would have been common to control and ERL trials in
our study, we surmise that the observed differences in EELV with ERL
were not significantly affected by the He method.
PEpeak may
have been a bit lower in steady state than in the graded exercise tests
(which increased 10 W/min), because by the 4th min at 75%
POmax a more comfortable breathing
pattern had been established, with a little less emphasis on the
initial expiratory effort.
The cumulative total resistance of the respiratory system is ~3
cmH2O · l1 · s,
with resistance being somewhat greater during expiration than
inspiration (4). The majority of this resistance is offered by the
upper airways and, in particular, by the glottis (8). Normally, a great
deal of expiratory glottal resistance is progressively lost during
graded exercise in response to increased airflow rates (26). This
phenomenon has been observed during hyperventilation (15) and exercise
hyperpnea (4). In our study the aperture chosen for ERL created
increasingly higher
PEpeak
(Fig. 1), inasmuch as glottal braking presumably diminished with
increasing E
(15).
The ERL presented during the steady-state exercise at 75%
POmax apparently offered
sufficient stimulus to shift EELV upward and away from the FL, which
occurs during heavy to maximal exercise. VT/TE
was unchanged with ERL, in contrast to previous studies in which
reductions in
VT/TE
were observed with ERL (22, 24). Although these larger ERL values (5 and 8 cmH2O, respectively) did
increase EELV, their thwarting effects on expiratory flow probably
contributed to a reduced
E.
The ERL employed here at steady state (1.5 ± 0.2 cmH2O) represents quite modest ERL
compared with that utilized in prior studies (7, 10, 11, 14, 22, 24)
and did not affect
E adversely.
In two of these studies, ERL and
E were
inversely related (10, 24).
Johnson and colleagues (19) suggested that exerting greater effort
earlier in the expiratory phase (when airflow is still effort
dependent) would be one strategy by which to mitigate FL. With ERL,
this strategy appears to be at work, as observed in the sharp rise
in expiratory pressure at the commencement of the expiratory phase
in the single expiratory breath tracings (Fig. 10). Also, there was a
pattern of prolonged elevation (plateau) of
PE with ERL (Fig. 10). This may
have served to distend the airways and may have effectively
prolonged the effort-dependent stage of expiration as well.
O2 peak test series.
In addition to the normal expansion of
VT to a plateau of 50-60%
of VC (30) with graded exercise, there is a further increase in
VT with ERL (14, 24). Throughout
our comparison O2 peak tests, VT was greater and
significantly greater (P 0.05) at 80% POmax with ERL vs. control
(Fig. 4), with little or no change in f with ERL. Further expansion in
VT, after it has reached a plateau, is limited by FL, as described by the descending
profile/envelope of the MEFV curve (3), and is relatively fixed for a
given EELV (12). Because we did observe increases in
VT in response to ERL, we infer
that FL was ameliorated.
Because in these graded
O2 peak tests we
employed the same resistor used in the EELV series, we presumed that
there had been an increase in EELV in response to ERL in the graded
O2 peak series and that
the increased VT (Table 3) was
correspondingly shifted to higher lung volumes. We believe that this
evident increase in VT due to
the probable increase in EELV explains the significantly increased
E at 80, 85, and 90% POmax (Fig. 3). In the
steady-state comparisons, VT was
not significantly greater with ERL. We suspect that at this level of
intensity, i.e., 75% POmax, FL
had not yet become a problem. As mentioned above, in the
O2 peak
tests, VT was significantly
greater.
ERL provokes greater inspiratory effort (10, 11). The increased
end-inspiratory lung volume (Table 3) offers circumstantial evidence of
increased inspiratory effort with ERL. However, opting to do more
inspiratory work appears to be a beneficial trade-off for our athletes.
Although breathing at hyperinflated lung volumes may predispose the
inspiratory muscles to fatigue (3), in our study, it does not appear
that ERL presented any such liability. Fatigability of respiratory
muscles has been shown to be a function of the percentage of
respiratory effort expended vs. the maximal capacity for muscular
effort (29). Our highly trained endurance athletes very likely had
developed superior respiratory muscle strength, so that absolute
increases in respiratory muscle effort would represent smaller
percentages of maximum capacity for muscular effort, making them less
susceptible to respiratory muscle fatigue than less fit subjects (9).
The increase in end-inspiratory lung volume with ERL to 77.9 ± 2.9% VC vs. 66.3 ± 4.2% VC (control) would not appear to have required a great increase in inspiratory effort, since 77.9% VC is
still within the range of optimum compliance (i.e., 20-80% VC),
i.e., within the range in which the elastic work of breathing is at a
minimum (30). With ERL there still remained 1.25 ± 0.17 liters of
inspiratory reserve volume (Table 3). We surmise that the observed
increases in E
associated with ERL were not at the expense of extraordinary
inspiratory effort but rather more probably due to a moderate and
manageable increase in inspiratory effort. Our subjects did not
complain of increased work of breathing with ERL. In fact, anecdotally,
many of the athletes in our study, without solicitation, commented that
"it felt easier" or "I felt stronger this time (or last
time)," unknowingly referring to the ERL test. It is also likely
that the increase in EELV with ERL reduced the energy requirement for
expiration. With ERL, EELV was elevated from 16.7 ± 2.9 to 28.0 ± 3.4% VC and to a more favorable position on the compliance
curve.
There was a nonsignificant increase in
O2 with ERL from 75 to 85%
POmax, which became significant
(P 0.05) at 90%
POmax. A partial explanation for
this elevated O2 during
ERL would be the increased energy requirement to perform increased
inspiratory work. However, the athletes' performances were not
compromised by this increased energy demand, and it would appear that
some fraction of the increased
O2 peak observed with
ERL was delivered to the working skeletal muscle, which produced
(P 0.05) greater POmax (Fig. 9).
Effective Ppl.
When exercising athletes reach FL, Ppl has met or exceeded effective
Ppl (Peff), which is the minimal pressure to drive maximal expiratory
flow, as described by isovolume pressure-volume curves (1). Exceeding
Peff represents a waste of energy and can lead to a decrease in
expiratory flow from dynamic compression of airways (21). However,
during breathing at elevated lung volumes, as the athletes in our study
did with ERL, the Peff is raised (2), and this can move the entire
VT away from the flow-limiting
pressures reached at lower lung volumes (3), thereby enabling the
athlete to exert more effective expiratory pressure. Ordinarily, only a
small fraction of maximum expiratory effort is required to generate maximum expiratory flow (29). In fact, it is estimated that at >40%
of maximal expiratory effort, there is no further effect on expiratory
ventilation (29). At heavy workloads
(E 120 l/min) the cost of breathing increases markedly because of the expiratory work done against FL (17). In our study the
strategy/response to ERL may have been to effectively divert effort
from "wasted" expiratory work, where expiratory Ppl > Peff, to
greater inspiratory activity. With this strategy, FL may have been
prevented and, consequently,
E increased.
Breathing at elevated EELV, in response to ERL, had significant
cardiovascular implications as well. In the graded
O2 peak comparisons,
O2 pulse was greater
(P 0.05) from 75 to 90%
POmax (Fig. 7), yet
SaO2 was only ~1% greater with ERL
(Fig. 1). Because there is little reason to suspect that ERL caused
decreased mixed venous O2 content
and because these comparisons with and without ERL were made at
identical workloads, increased O2
pulse suggests increased stroke volume, probably secondary to augmented
venous return with ERL. Besides the deleterious ventilatory effects of having Ppl exceed Peff, excessive Ppl, which is likely to occur in very
strenuous exercise (3, 18, 19), can impede venous return (25).
Furthermore, elevated EELV, as was observed in our study in response to
ERL, is associated with decreased pulmonary vascular resistance (27).
We suggest that increased stroke volume, in concert with increased
E, very likely
contributed to the increases in
O2 peak and
POmax.
In conclusion, we infer from our findings that increased EELV in
response to slight ERL during strenuous exercise served to attenuate
airflow and blood flow limitations, which otherwise may have been the
product of excessive Ppl developed during active expiration at lower
lung volumes. We further conclude that appropriate ERL during strenuous
exercise can enhance ventilatory and exercise capacity.
ACKNOWLEDGEMENTS
We gratefully acknowledge the technical assistance of Chuck Daniels, Robert and Peggy Dinman, Ron E. Dunn, Jeff Hall, J. M. Hanna, David L. Lally, Charles K. Matsuda, Hurley McBrierty, Ken Mito, and Stephen Wehrman.
FOOTNOTES
Address for reprint requests: L. Fee, 1222 Manu Mele St., Kailua, HI 96734.
Received 16 April 1996; accepted in final form 4 April 1997.
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