477

Journal of Physiology (1991). 442. pp. 477-487 WI'ith 2 figu r es Printed in Great Britain

BREATHING DURING PROLONGED EXERCISE IN HUMANS

BY M. C. KEARON, E. SUMMERS, N. L. JONES, E. J. M. CAMPBELL AND K. J. KILLIAN* From the Ambrose Cardiorespiratory Unit, McMaster University Medical Centre, 1200 Main St West, Hamilton, Ontario, Canada, L8N 3Z5

(Received 22 August 1990) SUMMARY

1. Six normal subjects cycled to endurance or for 60 min at four work rates (WR 1-4): mean of 34% working capacity (93 watts for 60 min); 43% (120 watts for 56 min); 63% (177 watts for 37 min); and 84% (233 watts for 12 min), to determine how breathing pattern and dyspnoea change during prolonged activity. Four to six minutes were allowed to establish steady state and subsequent changes were considered to be endurance related. 2. Dyspnoea (Borg scale, 0-10) increased with the duration of activity at all work rates. 3. Ventilation (VE) did not change at WRI; increased from 44 to 47 1 min-1 at WR2; from 60 to 88 1 min-' at WR3; and from 111 to 132 1 min-' at WR4. Dyspnoea was significantly and independently related to ventilation and duration of activity: dyspnoea = 0-004 VE136 time025 (r = 0-81; partial F 202 and 26 respectively). 4. Inspiratory resistance did not increase at any work rate. Dynamic elastance remained constant during WRI, WR2 and WR3 but increased from 7 4 to 9 1 cmH20 11 during WVR4. 5. Peak inspiratory pressure did not increase, and the increase in VE was accomplished by an increased breathing frequency without change in duty cycle. 6. Duration of activity is an important contributor to dyspnoea independent of changes in respiratory muscle contractile activity. INTRODUCTION

Dyspnoea gradually increases when exercise is continued for long periods. A number of factors may contribute to this increase in respiratory discomfort, including increases in metabolic demands, changes in the mechanical properties of the respiratory system, and reductions in the contractile capacity ('fatigue') of the respiratory muscles (Ekelund, 1967; Henry & Bainton, 1974; Dempsey, Gledhill, Reddan, Forster, Hanson & Claremont, 1977; Martin, Morgan, Zwillich & Weil, 1981; Sharratt, Henke, Aaron, Pegelow & Dempsey, 1987). Before attributing increases in dyspnoea during prolonged activity to respiratory muscle fatigue, the * To whom correspondence should be addressed. NIS 8743

Cl.C KE4RONV AND OTHERS role of these other potentially important contributing factors must first be excluded. The objectives of the present study were to measure the intensity of dyspnoea and each of these factors during prolonged exercise. Mechanical properties of the lungs were measured in terms of dynamic elastance and resistance; respiratory muscle forces were measured in terms of oesophageal pressure; and the metabolic demands of exercise were measured in terms of oxygen uptake and carbon dioxide output. Any increase in dyspnoea unexplained by these factors may represent an increase in breathing effort as a consequence of respiratory muscle fatigue. In this context, fatigue signifies an increase in motor command to achieve the same contractile activity as the duration of exercise increases. 478

METHODS

Subjects Six normal male subjects with a mean age of 34+21 years (S.E.M.) and height of 182+2-1 cm (S.E.MI.) were studied. All had normal pulmonary function with a mean vital capacity (VC) of 6-2+0-27 1 (S.E.M.). had maximum inspiratory pressures of 128+6-8 cmH2O (S.E.M.), were nonsmokers. gave informed consent. and were naive as to the purpose of the study. Apparatus Subjects exercised on an electrically braked cycle ergometer (Siemens Ergomed 740) at a pedalling frequency of 60 r.p.m. Oxygen uptake (V 2), carbon dioxide output (Vco ), ventilation (VE), tidal volume (Vr) and breathing frequency (f) were measured using a calibrated automated universal exercise system (Jones, 1984). Inspiratory flow (V) was measured with a pneumotachometer (Fleisch no. 3) connected to the inspiratory limb of a Hans Rudolph valve (alinear resistance, 09 cmHl20 '1 s-5 at a flow of 1 s-5 and 16 cmH20 1' s-1 at 6 1 s-1). Duty cycle (TI/Ttot) was calculated from the flow tracing. Oesophageal pressure (P.es) was taken as an estimate of pleural pressure (Milic-Emili, Mead, Turner & Glauser. 1964). Respiratory elastance and resistance were calculated as described by MNead & Whittenberger (1953). Rib-cage and abdominal movements were measured using respiratory inductance plethysmography (RIP), calibrated using a combination of the simultaneous equation (Sackner, Nixon. Davis, Atkins & Sackner, 1980) and isovolume methods (Konno & Mead, 1967). All signals were recorded on an eight channel recorder (Hewlett-Packard model 7758). Dyspnoea was measured using the Borg 0-10 scale (Borg. 1980). Procedure Recognizing that metabolic demands increase during prolonged exercise at a constant work rate, and that the resulting changes might make it difficult to detect endurance-specific changes in breathing pattern, we also measured breathing pattern during incremental exercise to allow comparison with prolonged exercise. Incremental exercise. Subjects performed a progressive incremental (15 WV min-') exercise test to maximum work capacity (Wap) (Jones, 1988). Breathing pattern, oesophageal pressure, gas exchange and dyspnoea ratings were recorded at the end of each minute. Endurance exercise. On separate days, four endurance tests were performed at varying work rates: WRI, 93+6-7 W min-1 (S.E.M.); WVR2, 120+8-3 WV min-' (S.E.M.); XVR3, 177+123 W mini1 (S.E.M.); and WR4. 233+ 157 XV min-' (S.E.M.). The actual work rates were selected to correspond to widely differing levels of perceived effort (2 'slight'. 3 'moderate'. 5 'severe', and 7 'very severe') experienced during the initial incremental exercise test. Breathing pattern, oesophageal pressures, gas exchange and dyspnoea ratings were serially measured. Subjects exercised to endurance or 60 min, whichever occurred first.

Analysis of results Mean values for the six subjects were calculated for each work rate (incremental exercise) and for duration (endurance exercise). Linear regression analysis of the variable of interest (e.g. VE) against time (expressed as percentage of time to endurance) was performed to test for the presence

BREATHING DURING PROLONGED EXERCISE

479

of overall changes during prolonged exercise; values at the onset of activity (< 6 min at WRl, WR2 and WR3; < 4 min at WR4) were excluded from the regression, as initial changes were not the focus of the study. Significant increases or decreases with duration were judged to have occurred if the regression slope differed from zero (P < 005). Intersubject variability was controlled for by using dummy variables to identify each subject (Kleinbaum, Kupper & Muller, 1988). Multiple regression analysis with dyspnoea as the dependent variable, the addition of dummy variables to allow for the variability across subjects, inspiratory pressure, ventilation and duration of activity as the contributing variables, was used to verify the independent contribution of time to dyspnoea. Results are given as means+ S.E.M.

RESULTS

Incremental exercise Mean work capacity was 280 + 17-6 W which was 115 + 7-4 % of normal predicted WTap (Jones, Makrides, Hichcock, Chypchar & McCartney, 1985). Vo0 at maximal exercise was 3 57 + 0 335 1 min-' and VPC2 was 3 97 + 0 335 1 min-'. VE, max was 145 + 13-6 1 min-'; VT max was 3-33 + 04194 1;fmax was 43-8 + 3-99 breaths min-'; T1/Ttot was 0 49 + 0-022. Oesophageal pressures (cmH2O) at maximal exercise were: - 29-7 + 2-90 for peak inspiratory pressure; - 15-9 + 3-38 for end-inspiratory pressure; 17-5 + 3-92 for peak expiratory pressure; and 5-3 + 320 for end-expiratory pressure. During exercise, breathing pattern, VE, gas exchange, pleural pressure and the magnitude of dyspnoea were similar to previously reported values in normal subjects (Fig. 1; Grimby, Saltin & Wilhelmsen, 1971; Lind & Hesser, 1984; Jones et al. 1985; Leblanc, Summers, Inman, Jones, Campbell & Killian, 1988). Endurance exercise Work rate 1 (93 W). Between 6 and 60 min, there was a small but significant increase in P0 2 from 1-47 to 1-52 1 min-1; VCO2 decreased from 1-38 to 1-32 1 min-'; and the respiratory exchange ratio (RER) fell from 0 94 to 0-86. VE, f and TI/Ttot did not change significantly. Inspiratory resistance fell from 2-46 to 1P98 cmH2O s 11 and dynamic elastance did not change. Inspiratory and expiratory oesophageal pressures did not change. Dyspnoea increased significantly from 0-6 to 1-5 on the Borg scale (Fig. 2, Table 1). Work rate 2 (120 W). Between 6 and 56 + 4-0 min, Vo0 increased from 1-76 to 1-93 1 min-'; VC02 did not change; RER decreased from 0 93 to 0-84. iF increased from 44-1 to 46-8 1 min-'; VT increased from 1-76 to 1-84 1;f and duty cycle remained constant. Inspiratory resistance and dynamic elastance did not change significantly. Inspiratory oesophageal pressures did not change significantly; peak expiratory oesophageal pressure increased minimally from -0 7 to 1D0 cmH2O. Dyspnoea increased significantly from 1-2 to 2-9. Work rate 3 (177 W). Between 6 and 37+ 6-6 min, Vo increased from 2-35 to 2-84 1 min-'; VC02 increased from 2-28 to 2-61 1 min-'; RER fell from 0 97 to 0-92. VE increased from 60-4 to 87-9 1 min-'; VT fell from 2-69 to 2-55 1; f increased from 23-5 to 34-9 breaths min-1; duty cycle did not change. Inspiratory resistance and dynamic elastance did not change significantly. Inspiratory oesophageal pressures did not change significantly; peak expiratory pressure increased from 3-3 to 9-5 cmH2O. Dyspnoea increased from 2-2 to 4-2.

M. C. KEARON AND OTHERS

480

Work rate 4 (233 W). Between 4 and 12+3-7 min, Vi2 increased from 3-13 to 3-59 l min-1; VC02 did not change significantly during the same period; RER fell from 1t09 to 0-98. VE increased from 100-8 to 131-8 1 min-1; VT fell from 3 30 to 3 05 1; f increased from 31-0 to 44-4 breaths min-1; duty cycle remained constant. Inspiratory 0-64 1-02 0.52 0-83

V02 ( min-)

VC02 ( min-')

1.24 1.01

1.49 1.37

1.92

2.24

2.69

1-80

2.21

2-70

3.57 3.97

160 _ 120

VE(lmin-')

.---I

80

40 0 _ -

VT (I) IR

1-45 17.7 0.40

1-37 19.7 0.39

1,74 20.1 0-41

2.04 21-9 0.44

2-36 2.57 23.6 26.5 0.44 0-47

3.33 43.8 0-49

r 2.02 3.76

2.26 3.77

2-40 4.02

2-28

2-31 3.96

2.25 2.45 3-79 4-64

3.06 6.69

_

(cmH20 S1 1F1) DE

(cmH2O 1-1)

--l-AgEr- 3.rE-

1.54 17-4 0-36

f (min-1)

TV Ttot

Jr--

4*28

20 10 _ Poes (cmH20)

-

Peak exp.

0_t

3

_.

Peak insp.

-20 [ -30 10

Dyspnoea (Borg scale)

Jr-

~

~~

~

~

~

~

~

~

~

_

_

8 6 4 2 _ 1 0.5 05_ 15

45

75

105

165 135 Work rate (W)

195

225

285

255

Fig. 1. Incremental exercise results. Metabolic demand: VP, oxygen uptake; VC02, CO2 output. Ventilatory response: VE, ventilation; VT, tidal volume;f, frequency of breathing; T1/Ttot, duty cycle. IR, inspiratory resistance; DE, dynamic elastance. Pressure response: Poes inspiratory and expiratory esophageal pressures. Sensory response: intensity of dyspnoea estimated using the Borg scale. Solid lines join work rates at which values were available for all six subjects. Broken lines join the last work rate to which all six subjects contributed to the mean of the maximal value for all subjects. Symbols show means + S.E.M.

resistance did not change but dynamic elastance increased from 7-44 to 9'06 cmH2O l-1. Inspiratory pressures did not change significantly; peak expiratory pressure increased from 10-9 to 19-0 cmH2O and end expiratory pressure from 2-4 to 7-1 cmH2O. Dyspnoea increased from 3-3 to 6-3 (Fig. 2, Table 1).

481

BREATHING DURING PROLONGED EXERCISE

Ribcage-abdominal movement Paradoxical ribeage or abdominal movement did not occur during either inspiration or expiration in any subject during either incremental or endurance exercise.

V02 (I min-1) VCO2 (I min-1)

E 1.471.531-48 1.52 1.381.401.33 1-32

3.13 3.32 3.59 3.42 3.46 3.53

2.35 2.55 2.84 2.282.42 2-61

1.761.811-83 1.93 1.631.651-60 1.56

120

VE(I min-)

80 ao

40

1.631.611.67 1.59 24 24 25 24 0.4 0.4 0.4 0.5 2.5 2.2 2.1 2.0 4.9 5.9 5.3 4.5

VT (I) f (min-1) TD(H tot IR (cmH20 S-1 I-1) DE (cmH20 1-1)

PO0 (cmH20)

1*761*811*81 1.84

2.692.442.55 24 31 35

26 26 25 0.4 0.5 0.5

23 0.5

2.1 2.4 2.7 6.1 6.1 6.2

2.8 5.9

2.6 2.9 2-9 6.1 5.7 5.8

I.E-I---i-I

j4i..-.

3.30 3.34 3.05 31 34 44 0.5 0.5 0.5 2.6 2.7 3.1

0.5 0.5 0.5

7.4 8.6 9.1

20 10 0

j-iPeak exp.

-10 -20 -30 10 8

Dyspnoea (Borg scale)

Peak insp.

w'

6

41: 2

05_

0.8

Work rate (W)

[

WR1 I

0

I

L

20

93W |

I*

40

120 W

WR2 |

60

I

0

I

20

I*

40

I

I

L.I

I

20 0 60 Time (min)

WR4 233 W

177 W

WR3 I

I

I

40

I

I

60

0 4 8 12

Fig. 2. Endurance exercise results. Intensity of dyspnoea estimated using the Borg scale, at four different work loads, 93, 120, 177 and 233 watts. Solid lines join time intervals at which values were available for all six subjects. Broken lines join the last data point to which all six subjects contributed to the mean of the endurance value for all subjects. Symbols are means+ S.E.M. See legend to Fig. 1 for definition of symbols.

Dyspnoea Analysis of the contribution of time to the intensity of dyspnoea was complicated by the progressive increase in metabolic demand with duration of activity. This resulted in increases in ventilation at all but the lowest work load. Changes in inspiratory resistance, dynamic elastance, and inspiratory pressure were minor and 16

PHY 442

482

M. C. KEARON AND OTHERS TABLE 1. Changes with endurance exercise Work rate 1 93 ±6&7 W Work rate 2 120 + 8-2 W

Time (min) VT (1) f (min-')

Ttot T,/ VE

Start 6+0 1P76+0-125

384+±2-51

End 60+0 1P59+0-122 24-3+ 200 0-46+0-032 37-7+ 1P88

0-76 0-17 034 0-08

0-43+04017 44-1+2461

1P38+0-071

1P32+0-065

0.002

1P47+00077

1-52+00084

Start 6+0 1P63+0-123 24-2+2-24 0-43+04019

P

End 56+4 1P841+0-158 23-3+2204 0-45+04036

p

46f8+±254

040001 0-14 0-15 0-004

1463+04095

1-56+0-045

0.95

0.0001

1P76+0-087

1P93 + 0075

Breathing during prolonged exercise in humans.

1. Six normal subjects cycled to endurance or for 60 min at four work rates (WR 1-4): mean of 34% working capacity (93 watts for 60 min); 43% (120 wat...
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