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Human core temperature increase as a stimulus to breathing during moderate exercise
HUMAN
CORE TEMPERATURE INCREASE AS A STIMULUS BREATHING DURING MODERATE EXERCISE
TO
JOHN G. HENRY and CEDRIC R. BAINTON Deparfments of Anesthesia and Physiology, University qf California. School of Medicine. San Francisco, California 94143, U.S.A.
Abstract.
Core
temperature study under change
temperature
increase
as a ventilatory
in body
temperature
might
Since heat loss mechanisms
exert
mistaken
the true
magnitude
In three
male
moderate
exercise
(A core
induced
within
22 min during
l/min)
between
men and
from 37.2 to 38.5 “C. fro, was constant. (mean
increase
expired
Plop
&S.E. for 17 studies): (mm
Hg) decreased
t-test (P >0.05).
moderate
exercise,
response
a 0.9 “C increase
3 mph treadmill
the three
exercise
During
The authors
(l/min)
None
because
by circulating suits. 0.6kO.4,
Lumbar
skin
workers
temperature
(37.3
and
that core temperature
to
system. may have was
not
38.2 “C) was
air, (75 “C, 30% humidity skin temperature
rise, the following
of these differences
to the hyperpnea
previous
temperature
core temperature
conclude
does not contribute
in core
their exercise
ventilation
0.3kO.2.
via the thermoregulatory
by a falling skin temperature,
of a thermoventilatory
subjects,
300-500
during
during
an effect on ventilation
can be inhibited
assessed.
by paired
stimulus
0.5 “C, oxygen consumption i 1.5 l/min) has been re-evaluated in man in the present conditions which prevent a decrease in skin temperature. The authors considered that a
frequency/min were shown increase
of exercise
factors
at
increased increased
0.110.1.
Mid-
to be significant
in man, as observed
via the thermoregulatory
or any other system. Control
of breathing
Exercise hyperpnea
Core temperature
Skin temperature
Grodins (19%) and Cotes (1955) have suggested that core temperature increase might explain the increase in breathing during moderate exercise (i.e. oxygen consumption less than 1.5 I/min in man and core temperature increase of 0.5 “C). At rest, ventilation begins to increase when core temperature exceeds normal by 1 “C (Barltrop, 1954; Bazett and Haldane, 1921; Haldane, 1905; Landis et al., 1926). During moderate exercise the lesser change in core temperature could be an effective stimulus to breathing only if exercise enhanced the sensitivity of the system responsible for the thermoventilatory response. Dejours et al. (1958) explored this possibility. However, they detected no effect on ventilation in subjects during Accepted
forpublication 17 April 1974. 183
184
J. G. HENRY AND C. R. BAINTON
exercise after deliberately raising their core temperature 0.6 C. Thus they concluded that the increase in core temperature as it occurs during moderate exercise does not constitute a stimulus to breathing. In the present study we postulate that the thermoventilatory response in man might be mediated via the thermoregulatory system. a system known to be enhanced in sensitivity during exercise and skin warming and inhibited by skin cooling (van Beaumont and Bullard, 1963). We were attracted to this hypothesis by our observations in the dog (Bainton and Mitchell, 197 I) where ventilation (i.e. panting) is a clear thermoregulatory response. We were startled to observe the prompt onset of panting at the start of exercise in the dog with no change in core temperature, i.e. enhanced sensitivity and the equally prompt inhibition of panting after instituting skin cooling. Hammel (1968) has proposed a theoretical basis for unders~nding these findings. He describes the thermoregulatory system as demonstrating proportional control, with a variable set point. Heat loss (vasodilation, panting, and sweating) and heat conservation (vasoconstriction and shivering) are initiated in response to actual core temperature differing from a “set” hypothalamic temperature after a threshold difference (actual minus “set”) in temperature has been achieved. Setpoint temperature in the system is variable. Exercise depresses the set point and has the effect of reducing the threshold for heat loss. The set point is also affected by skin temperature: hot skin reduces the set point just as exercise does, whereas cold skin elevates it. Such a control system appears to be independent of absolute core temperature, since thermoregulatory responses can be initiated promptly without any change in core tem,perature. We speculated that an analogous situation to that of the dog might exist in man and since skin cooling can occur with the onset of exercise in man (Nielsen and Nielsen, 1965) and since Dejours et al. (1958) did not measure skin temperature, that they might have missed the thermoventilatory response of moderate exercise in man if there was an inadvertant fall in skin temperature. The purpose of the experiments reported here was to re-examine the effect of a change in human core temperature on ventilation during excercise conditions which would permit no fall in skin temperature. Such conditions were achieved without discomfort to the subjects by circulating hot, moist gas with a high flow rate between each subject and his exercise suit. This, in fact, produced conditions of constantly elevating skin temperature--.-a state which, if anything, should accentuate the heat loss response to core temperature change. We also adopted additional improvements over earlier investigations as follows: (1) We evaluated the effect of core temperature increase on ventilation by inducing a rise in core temperature during sfabk exercise. Previous investigators (Dejours et cd., 1958; Whipp and Wasserman, 1970) examined ventilation during brief episodes of exercise (46 min) superimposed upon an increase or decrease of core temperature attained at rest. In man, even in the course of moderate activity, the transition from rest to exercise can be accompanied by alterations in several
CORE TEMPERATURE INCREASE AND EXERCISE ‘jE IN MAN
185
variables. For example, levels of blood lactate (Harris et af., t968) can rise and reach stability o&y L&Y 20 min of constant exercise. As we have already noted (Nielsen and Nielsen, 1965) skin temperature is particularly vulnerable to change in the initial period of exercise. (2) We changed the core temperature in a minimal amount of time. We have found that ventilation can vary when measured at intervals of 1 hr or more from day to day, despite the maintenance of a constant treadmill speed and grade, as well as uniform room temperature. Earlier investigators have limited their observations of ventilation to reporting the separate values obtained before and after core temperature change R.v lf4 min (Dejours trt ttf., 1958) or on different days (Whipp and Wasserman, 1970).
The three sub.jects investigated in this study were a technician and the two authors. All were fit, weighed 140, 170 and 165 lb, respectively, and were 29, 29 and 3X years old, They ran on a treadmill (Quinton Instrument Company, Seattle, Washington) at a level consistent with moderate exercise (%‘o, less than 1.5 l/min STPD). Prior to each run a manifold was strapped comfortably to the abdomen (fig. 1, left) for air delivery. Next they wore vinyl suits (Sears Roebuck, Inc.) sealed at the neck
Fig. 1. Left: Nanifald strapped to abdomen for air delivery. The apparatus is constructed of light plywood and padded with-foam rubber. Air delivered to the manifold is deflected up across the chest and down over the upper thighs. The foam rubber padding was extended to protect skirt areas in the direct line of air flow. Deliberate air leaks were created at wrists and ankles (Z-in diameter rubber tube) as illustrated. Right: Subject fully suited and ru@ng on treadmill with air delivery tube in place. The mouthpiece and vent&tory tubing are supported by a iight helmet.
186
J. G. HENRY
AND C. R. BAINTON
and around the air-intake manifold to prevent unwanted continuous surface flow of air, outflow ports were created
air leakage. For a at wrists and ankles
by strapping tubes (8 in long, 2 in in diameter) at these points with one end protruding from the vinyl suit in each case. Down jackets and pants (Eddie Bauer,
Seattle)
were worn
over the vinyl to prevent
heat loss. The suit, although
bulky, did not affect the ability to run and afforded complete comfort during the delivery of hot air (fig. 1, right). Air was delivered to the manifold through 3 ft of flexible tubing, 6 in in diameter, containing a heavy spiral wire to prevent collapse and attached to the treadmill handrails so that a minimal weight of the apparatus was supported by the subjects. While running, they were forced to adjust their positions on the treadmill in relation to the expansion limits of the delivery tube, but this was accomplished with ease. A wooden valve was attached to the other end of the flexible tube. consisting of inflow ports of hot air and room temperature air as well as a common exit to the flexible air-delivery tube. A manually operated flap valve allowed the subjects to switch quickly from 22 “C air to hot air. An air conditioner delivered 22 -‘C air at 2000 l/min. Hot, moist air was produced in a heat generator constructed of a box of light bulbs, a boiling kettle, and a vacuum-cleaner blower. A rheostat controlled the blower speed with flows of up to 500 l/min. By adjusting the number of light bulbs turned on and the air flow, 75 “C air at 30% humidity could be produced. Ventilatory measurements were obtained using a circle system comprising the following items: a mouthpiece (see fig. 1) attached at each end to 5-ft sections of 1.5-in tubing (Collins Equipment Co., Boston), a CO, absorber with inspiratory and expiratory valves, a wedge spirometer (Med Sciences Electronics, St. Louis), a unidirectional circulating fan to reduce valve resistance and a water-cooled coil of copper tubing which maintained inspired gas at 22 “C. The mouthpiece and connecting tubes were supported by a light helmet to maintain a comfortable mouth fit. Connecting tubes were draped over the shoulder, cinched around the waist with a strap to avoid flapping, and then directed to the side over the handrail to keep them from hindering steady running. Oxygen was added to the system through a flow-meter. All studies were conducted with only oxygen added. Alveolar Pco, (PA,,,) was recorded by continuous sampling from the mouthpiece through an infrared analyzer (Beckman LB-l). The sample tube was heated to prevent water-droplet accumulation. In addition, CO,-calibrating gases were saturated with water vapour at a temperature equal to the subject’s. During exercise, the relationship of P&o2 to Pa,-oZ is altered from that at rest. In the dog, . mid-expiration PA,-c, is very nearly equal to P+o, in the arterial blood (Bainton and Mitchell, 1971). Wasserman et al. (1967) reported similar findings in man. For this reason, PA,-~, as reported in these studies refers to mid-rxpirution PA,-~~. Oxygen consumption was measured as volume loss from the circle system when it was completely closed, i.e. with no outward leaks nor gas input. The following temperatures were measured with thermistors (Yellow Springs
~~str~~rne~t Co., Y&low Springs, Ohio): upper abdomen under the f~~m-~b~r pad, Iumbar skin of back under one layer of adhesive tape, i~~ow gas at the level of the delivery manifold, inspired air and index tinger outside the vinyl suit and insulated from ambient air by several layers of gauze. This finger temperature was used to indicate vasodilation, i,e. as a ~~~~~l~reg~la~~ry response. Tympanic membrane tem~rature was measured with a thermoco~F~e (Leeds and ~ortbrup f Ndrth Wales, Pe~~sy~v~nia~and this value was used as the index of core tem~er~tnre. (Ben-zinger, t959).
A total of 17 separate experiments ~rn~~~yi~g our three subjects were ~~rnpl~t~d, All studies began at least 3 hr after a light breakfast. Fully dressed in their exercise suits with air manifold, temperature probes and ventilatvry app~r~tns in place, they commenced exercise. For the next 51 min (the mean of all studies), ~._‘_._.--_.-.c._.-.---~ 7.5 !7’.-’
Fig. 2, Time course of change in indicated temperatwes Occurringafter the onset of surface heating applied to subjects during exercise ( 3 mph, 07; grade) was maintained constant for 51 min, a 20.&n control period, and 31 min o? heating. Temperatures represent the mean values for preheating, ~antrai and two mean points in time aRer the in~tjat~o~ of heating (identified as heating periods i and 2). Tk m~asu~m~nts are cannected by broken lines to assist identification d specific t~m~ratures. Note that during the initiaf 9 min of h&in& skin t~m~~ratur~s rapidly a~~r~~h~ cow temperatures, and LY)F~ temperature did not. change. During snhscqnent 22 min of heatin& skin and COWtemperatures wars a~~r~x~rnat~~~equal and ascended top&r.
188
J. G. HENRY AND C. R. BAINTW-4
exercise was maintained constant at 3 mph, 05; grade. During the first 20 min. 22 “C air was circulated in the suit. This period was used to establish stable exercise conditions and to obtain control ventilatory measurements. Heating of the suit was then initiated, and was continued for a mean of 31 mm until core temperature had increased by 0.9 “C. Exercise and heating were then terminated, the subject was allowed to cool, and then, in five instances, a second identical experiment was performed. In no case were more than two studies per day conducted.
P AC% fnnl
50~.
m
40..
36-
L/min
30
frrk
Fig. 3. Time course of change in cure tempxzrature, Pbz and 9~ during heating whiie running at 3 mph. Lines connect individual points for I7 studies in three subjects.
CORE TEMPERATURE INCREASE AND EXERCISE YE IN MAN
389
Results The time-course for temperature change during surface heating was uniform in all subjects; therefore temperatures are presented as the mean response for the group in fig, 2. Temperature changes during heating are divided into two distinct periods as defined in fig. 2. Although intermediate temperatures are not presented, at no time did skin temperature fall during the period of rising core temperature. Note also that the index-finger temperature increased as soon as surface heating was initiated, indicating vasodilation at a site outside the suit. Therefore, it is evident that the thermoregulatory system had been stimulated to activate a heatlosing response. The effect of changing core temperature from a mean of 37.3 “C to 38.2 “C on Tiin and PkoL is illustrated in fig. 3, Mean oxygen consumption (po,) was 1.20 l/min STPDand mean frequency 18.6 at the start of surface heating. In order to identify small changes which might occur under these conditions the difference in VE, P&o:, f and iror were compared between the control period and the two heating periods defined in fig. 2. These measurements are presented in table 1. Although ?E increased and P& o2 decreased progressively from control levels throughout the heating periods, these differences were small and became significant only when comparing the control with the final heating period. More important, during the period of core temperature rise? the period of greatest interest to us, changes in VE and P&o, were not significant by paired t-test analysis (P > 0.05). TABLE 1 Difference in Comparisons
VE,
P&o,, f and oo, between control and heating periods I and 2 ALE
(ljmin
BTPS)
@AC02
4
(mm
(/mW
%d
Heating period 1 - control Heating period 2 - heating period 1 Heating period 2 - control
+ 0.9 f 0.4”
-0.7*0.3*
+ 0.3 f 0.2
+ 0.04 * 0.02
Experimental periods are defined in fig. 2. Values are presented as 15 difference -&SE. for 17 experiments. n for each subject was: 6, 6 and 5. * P < 0.05 paired t-test analysis.
Discussion
Although it is intruding to consider that the thermoventi~atory response in man is thermoregulatory in origin, this theory obviously does not apply to the small
190
J. G. HENRY AND C. R. BAINTON
changes in core temperature during moderate exercise. Our results indicate that under experimental conditions loss (i.e. exercise and increasing the skin temperature), response
to heat
loss is indeed
activated
(finger
which accentuate heat with evidence that a
temperature
or
vasodilation
increase), the additional factor of a change in core temperature had no significant effect of ventilation. These studies therefore confirm the work of Dejours et ~11. (1958) and those of Whipp and Wasserman (1970). Except for skin temperature determinations, our studies were similar to those of Dejours et ~11.(1958). Under their experimental conditions (exercise performed at a room temperature of 37 C with 60% humidity), it is unlikely that skin temperatures would fall unless high air flows were directed over the skin of the subjects, thereby increasing evaporative heat loss. Thus we conclude that the increment of 0.5 “C in human core temperature as observed during moderate exercise does not constitute a stimulus to ventilation via the thermoregulatory system, nor by any other known mechanism. Acknowledgements This study was supported in part by the U.S. Public Health Service Grants GM 05881 and GM 00063, and Training Grant GM 15571. Dr. Bainton is the recipient of Career Development Award GM 42350-4. References Bainton,
C. R. and R. A. Mitchell
(1971).
Effect of skin cooling
on exercise
ventilation
in the awake
J. Appl. Physiol. 30: 370-377.
dog Barltrop.
D. (1954).
The relation
between
body
temperature
and
respiration.
J. Physiol.
(Londort)
J. Physiol.
(London)
125: 19p20P Bazett,
H. C. and J. B. S. Haldane
(1921).
Some effects of hot baths
in man.
55: iv-v. Benzinger,
T. H. (1969).
Heat
regulation:
homeostasis
of cerebral
temperature
in man.
Physiol.
Reo.
49: 671-759. Cotes.
J. E. (1955).
normal Dejours,
subject
The role of body breathing
P., A. Teillac,
mod&r&e dans
F. Girard
la regulation
temperature
in controlling
J. Physiol. (Lundon)
oxygen. and
A. Lacaisse
de la ventilation
ventilation
during
exercise
in one
129: 554-563.
(1958).
Etude
du role de I’hyperthermie
de I’exercice musculaire
chez l’homme.
centrale
Rev. Franc.
Etudes Clin. Eiol. 3: 7755761. Grodins,
F. S. (1950).
Analysis
of factors
concerned
in regulation
of breathing
in exercise.
Physiol.
Rec. 30: 220-239. Haldane,
J. S. (1905). The influence
Hammel,
H. T. (1968). Regulation
Harris,
P.. M. Bateman,
servations
of high air temperatures. of internal
T. J. Bayley,
on the course
J. Hyg. 5: 494-513.
body temperature.
K. W. Donald,
of the metabolic
events
Ann. Rec. Physiol. 30: 641-710.
J. Gloster accompanying
and
T. Whitehead
mild exercise.
(1968).
Quart.
Ob-
J. Exptl.
Physiol. 53 : 4364. Landis,
E. M., W. L. Long,
of baths
on man.
J. W. Dunn,
111. Effect of hot
C. L. Jackson baths
and U. Meyer (1926).
on respiration.
blood
and
Studies urine.
on the effects
Am. J.
Physiol.
76: 35-48. Nielsen, B. and M. Nielsen Sand. 64: 314-322.
(1965).
On the regulation
of sweat
secretion
in exercise.
Acta Physiol.
CORE TEMPERATURE Van
Beaumont,
W. and
R. W. Bullard
INCREASE (1963).
191
AND EXERCISE irE IN MAN
Sweating:
its rapid
response
to muscular
work.
Science 141: 643646. Wasserman, during Whipp,
K., A. L. Van Kessel and G. G. Burton
B. J. and
exercise.
(1967).
Interaction
of physiological
mechanisms
exercise. J. Appl. Physiol. 22: 71-85. K. Wasserman
(1970).
Respir. Physiol. 8: 3544360.
Effect of body
temperature
on the ventilatory
response
to
CORE TEMPERATURE INCREASE AS A STIMULUS BREATHING DURING MODERATE EXERCISE
TO
JOHN G. HENRY and CEDRIC R. BAINTON Deparfments of Anesthesia and Physiology, University qf California. School of Medicine. San Francisco, California 94143, U.S.A.
Abstract.
Core
temperature study under change
temperature
increase
as a ventilatory
in body
temperature
might
Since heat loss mechanisms
exert
mistaken
the true
magnitude
In three
male
moderate
exercise
(A core
induced
within
22 min during
l/min)
between
men and
from 37.2 to 38.5 “C. fro, was constant. (mean
increase
expired
Plop
&S.E. for 17 studies): (mm
Hg) decreased
t-test (P >0.05).
moderate
exercise,
response
a 0.9 “C increase
3 mph treadmill
the three
exercise
During
The authors
(l/min)
None
because
by circulating suits. 0.6kO.4,
Lumbar
skin
workers
temperature
(37.3
and
that core temperature
to
system. may have was
not
38.2 “C) was
air, (75 “C, 30% humidity skin temperature
rise, the following
of these differences
to the hyperpnea
previous
temperature
core temperature
conclude
does not contribute
in core
their exercise
ventilation
0.3kO.2.
via the thermoregulatory
by a falling skin temperature,
of a thermoventilatory
subjects,
300-500
during
during
an effect on ventilation
can be inhibited
assessed.
by paired
stimulus
0.5 “C, oxygen consumption i 1.5 l/min) has been re-evaluated in man in the present conditions which prevent a decrease in skin temperature. The authors considered that a
frequency/min were shown increase
of exercise
factors
at
increased increased
0.110.1.
Mid-
to be significant
in man, as observed
via the thermoregulatory
or any other system. Control
of breathing
Exercise hyperpnea
Core temperature
Skin temperature
Grodins (19%) and Cotes (1955) have suggested that core temperature increase might explain the increase in breathing during moderate exercise (i.e. oxygen consumption less than 1.5 I/min in man and core temperature increase of 0.5 “C). At rest, ventilation begins to increase when core temperature exceeds normal by 1 “C (Barltrop, 1954; Bazett and Haldane, 1921; Haldane, 1905; Landis et al., 1926). During moderate exercise the lesser change in core temperature could be an effective stimulus to breathing only if exercise enhanced the sensitivity of the system responsible for the thermoventilatory response. Dejours et al. (1958) explored this possibility. However, they detected no effect on ventilation in subjects during Accepted
forpublication 17 April 1974. 183
184
J. G. HENRY AND C. R. BAINTON
exercise after deliberately raising their core temperature 0.6 C. Thus they concluded that the increase in core temperature as it occurs during moderate exercise does not constitute a stimulus to breathing. In the present study we postulate that the thermoventilatory response in man might be mediated via the thermoregulatory system. a system known to be enhanced in sensitivity during exercise and skin warming and inhibited by skin cooling (van Beaumont and Bullard, 1963). We were attracted to this hypothesis by our observations in the dog (Bainton and Mitchell, 197 I) where ventilation (i.e. panting) is a clear thermoregulatory response. We were startled to observe the prompt onset of panting at the start of exercise in the dog with no change in core temperature, i.e. enhanced sensitivity and the equally prompt inhibition of panting after instituting skin cooling. Hammel (1968) has proposed a theoretical basis for unders~nding these findings. He describes the thermoregulatory system as demonstrating proportional control, with a variable set point. Heat loss (vasodilation, panting, and sweating) and heat conservation (vasoconstriction and shivering) are initiated in response to actual core temperature differing from a “set” hypothalamic temperature after a threshold difference (actual minus “set”) in temperature has been achieved. Setpoint temperature in the system is variable. Exercise depresses the set point and has the effect of reducing the threshold for heat loss. The set point is also affected by skin temperature: hot skin reduces the set point just as exercise does, whereas cold skin elevates it. Such a control system appears to be independent of absolute core temperature, since thermoregulatory responses can be initiated promptly without any change in core tem,perature. We speculated that an analogous situation to that of the dog might exist in man and since skin cooling can occur with the onset of exercise in man (Nielsen and Nielsen, 1965) and since Dejours et al. (1958) did not measure skin temperature, that they might have missed the thermoventilatory response of moderate exercise in man if there was an inadvertant fall in skin temperature. The purpose of the experiments reported here was to re-examine the effect of a change in human core temperature on ventilation during excercise conditions which would permit no fall in skin temperature. Such conditions were achieved without discomfort to the subjects by circulating hot, moist gas with a high flow rate between each subject and his exercise suit. This, in fact, produced conditions of constantly elevating skin temperature--.-a state which, if anything, should accentuate the heat loss response to core temperature change. We also adopted additional improvements over earlier investigations as follows: (1) We evaluated the effect of core temperature increase on ventilation by inducing a rise in core temperature during sfabk exercise. Previous investigators (Dejours et cd., 1958; Whipp and Wasserman, 1970) examined ventilation during brief episodes of exercise (46 min) superimposed upon an increase or decrease of core temperature attained at rest. In man, even in the course of moderate activity, the transition from rest to exercise can be accompanied by alterations in several
CORE TEMPERATURE INCREASE AND EXERCISE ‘jE IN MAN
185
variables. For example, levels of blood lactate (Harris et af., t968) can rise and reach stability o&y L&Y 20 min of constant exercise. As we have already noted (Nielsen and Nielsen, 1965) skin temperature is particularly vulnerable to change in the initial period of exercise. (2) We changed the core temperature in a minimal amount of time. We have found that ventilation can vary when measured at intervals of 1 hr or more from day to day, despite the maintenance of a constant treadmill speed and grade, as well as uniform room temperature. Earlier investigators have limited their observations of ventilation to reporting the separate values obtained before and after core temperature change R.v lf4 min (Dejours trt ttf., 1958) or on different days (Whipp and Wasserman, 1970).
The three sub.jects investigated in this study were a technician and the two authors. All were fit, weighed 140, 170 and 165 lb, respectively, and were 29, 29 and 3X years old, They ran on a treadmill (Quinton Instrument Company, Seattle, Washington) at a level consistent with moderate exercise (%‘o, less than 1.5 l/min STPD). Prior to each run a manifold was strapped comfortably to the abdomen (fig. 1, left) for air delivery. Next they wore vinyl suits (Sears Roebuck, Inc.) sealed at the neck
Fig. 1. Left: Nanifald strapped to abdomen for air delivery. The apparatus is constructed of light plywood and padded with-foam rubber. Air delivered to the manifold is deflected up across the chest and down over the upper thighs. The foam rubber padding was extended to protect skirt areas in the direct line of air flow. Deliberate air leaks were created at wrists and ankles (Z-in diameter rubber tube) as illustrated. Right: Subject fully suited and ru@ng on treadmill with air delivery tube in place. The mouthpiece and vent&tory tubing are supported by a iight helmet.
186
J. G. HENRY
AND C. R. BAINTON
and around the air-intake manifold to prevent unwanted continuous surface flow of air, outflow ports were created
air leakage. For a at wrists and ankles
by strapping tubes (8 in long, 2 in in diameter) at these points with one end protruding from the vinyl suit in each case. Down jackets and pants (Eddie Bauer,
Seattle)
were worn
over the vinyl to prevent
heat loss. The suit, although
bulky, did not affect the ability to run and afforded complete comfort during the delivery of hot air (fig. 1, right). Air was delivered to the manifold through 3 ft of flexible tubing, 6 in in diameter, containing a heavy spiral wire to prevent collapse and attached to the treadmill handrails so that a minimal weight of the apparatus was supported by the subjects. While running, they were forced to adjust their positions on the treadmill in relation to the expansion limits of the delivery tube, but this was accomplished with ease. A wooden valve was attached to the other end of the flexible tube. consisting of inflow ports of hot air and room temperature air as well as a common exit to the flexible air-delivery tube. A manually operated flap valve allowed the subjects to switch quickly from 22 “C air to hot air. An air conditioner delivered 22 -‘C air at 2000 l/min. Hot, moist air was produced in a heat generator constructed of a box of light bulbs, a boiling kettle, and a vacuum-cleaner blower. A rheostat controlled the blower speed with flows of up to 500 l/min. By adjusting the number of light bulbs turned on and the air flow, 75 “C air at 30% humidity could be produced. Ventilatory measurements were obtained using a circle system comprising the following items: a mouthpiece (see fig. 1) attached at each end to 5-ft sections of 1.5-in tubing (Collins Equipment Co., Boston), a CO, absorber with inspiratory and expiratory valves, a wedge spirometer (Med Sciences Electronics, St. Louis), a unidirectional circulating fan to reduce valve resistance and a water-cooled coil of copper tubing which maintained inspired gas at 22 “C. The mouthpiece and connecting tubes were supported by a light helmet to maintain a comfortable mouth fit. Connecting tubes were draped over the shoulder, cinched around the waist with a strap to avoid flapping, and then directed to the side over the handrail to keep them from hindering steady running. Oxygen was added to the system through a flow-meter. All studies were conducted with only oxygen added. Alveolar Pco, (PA,,,) was recorded by continuous sampling from the mouthpiece through an infrared analyzer (Beckman LB-l). The sample tube was heated to prevent water-droplet accumulation. In addition, CO,-calibrating gases were saturated with water vapour at a temperature equal to the subject’s. During exercise, the relationship of P&o2 to Pa,-oZ is altered from that at rest. In the dog, . mid-expiration PA,-c, is very nearly equal to P+o, in the arterial blood (Bainton and Mitchell, 1971). Wasserman et al. (1967) reported similar findings in man. For this reason, PA,-~, as reported in these studies refers to mid-rxpirution PA,-~~. Oxygen consumption was measured as volume loss from the circle system when it was completely closed, i.e. with no outward leaks nor gas input. The following temperatures were measured with thermistors (Yellow Springs
~~str~~rne~t Co., Y&low Springs, Ohio): upper abdomen under the f~~m-~b~r pad, Iumbar skin of back under one layer of adhesive tape, i~~ow gas at the level of the delivery manifold, inspired air and index tinger outside the vinyl suit and insulated from ambient air by several layers of gauze. This finger temperature was used to indicate vasodilation, i,e. as a ~~~~~l~reg~la~~ry response. Tympanic membrane tem~rature was measured with a thermoco~F~e (Leeds and ~ortbrup f Ndrth Wales, Pe~~sy~v~nia~and this value was used as the index of core tem~er~tnre. (Ben-zinger, t959).
A total of 17 separate experiments ~rn~~~yi~g our three subjects were ~~rnpl~t~d, All studies began at least 3 hr after a light breakfast. Fully dressed in their exercise suits with air manifold, temperature probes and ventilatvry app~r~tns in place, they commenced exercise. For the next 51 min (the mean of all studies), ~._‘_._.--_.-.c._.-.---~ 7.5 !7’.-’
Fig. 2, Time course of change in indicated temperatwes Occurringafter the onset of surface heating applied to subjects during exercise ( 3 mph, 07; grade) was maintained constant for 51 min, a 20.&n control period, and 31 min o? heating. Temperatures represent the mean values for preheating, ~antrai and two mean points in time aRer the in~tjat~o~ of heating (identified as heating periods i and 2). Tk m~asu~m~nts are cannected by broken lines to assist identification d specific t~m~ratures. Note that during the initiaf 9 min of h&in& skin t~m~~ratur~s rapidly a~~r~~h~ cow temperatures, and LY)F~ temperature did not. change. During snhscqnent 22 min of heatin& skin and COWtemperatures wars a~~r~x~rnat~~~equal and ascended top&r.
188
J. G. HENRY AND C. R. BAINTW-4
exercise was maintained constant at 3 mph, 05; grade. During the first 20 min. 22 “C air was circulated in the suit. This period was used to establish stable exercise conditions and to obtain control ventilatory measurements. Heating of the suit was then initiated, and was continued for a mean of 31 mm until core temperature had increased by 0.9 “C. Exercise and heating were then terminated, the subject was allowed to cool, and then, in five instances, a second identical experiment was performed. In no case were more than two studies per day conducted.
P AC% fnnl
50~.
m
40..
36-
L/min
30
frrk
Fig. 3. Time course of change in cure tempxzrature, Pbz and 9~ during heating whiie running at 3 mph. Lines connect individual points for I7 studies in three subjects.
CORE TEMPERATURE INCREASE AND EXERCISE YE IN MAN
389
Results The time-course for temperature change during surface heating was uniform in all subjects; therefore temperatures are presented as the mean response for the group in fig, 2. Temperature changes during heating are divided into two distinct periods as defined in fig. 2. Although intermediate temperatures are not presented, at no time did skin temperature fall during the period of rising core temperature. Note also that the index-finger temperature increased as soon as surface heating was initiated, indicating vasodilation at a site outside the suit. Therefore, it is evident that the thermoregulatory system had been stimulated to activate a heatlosing response. The effect of changing core temperature from a mean of 37.3 “C to 38.2 “C on Tiin and PkoL is illustrated in fig. 3, Mean oxygen consumption (po,) was 1.20 l/min STPDand mean frequency 18.6 at the start of surface heating. In order to identify small changes which might occur under these conditions the difference in VE, P&o:, f and iror were compared between the control period and the two heating periods defined in fig. 2. These measurements are presented in table 1. Although ?E increased and P& o2 decreased progressively from control levels throughout the heating periods, these differences were small and became significant only when comparing the control with the final heating period. More important, during the period of core temperature rise? the period of greatest interest to us, changes in VE and P&o, were not significant by paired t-test analysis (P > 0.05). TABLE 1 Difference in Comparisons
VE,
P&o,, f and oo, between control and heating periods I and 2 ALE
(ljmin
BTPS)
@AC02
4
(mm
(/mW
%d
Heating period 1 - control Heating period 2 - heating period 1 Heating period 2 - control
+ 0.9 f 0.4”
-0.7*0.3*
+ 0.3 f 0.2
+ 0.04 * 0.02
Experimental periods are defined in fig. 2. Values are presented as 15 difference -&SE. for 17 experiments. n for each subject was: 6, 6 and 5. * P < 0.05 paired t-test analysis.
Discussion
Although it is intruding to consider that the thermoventi~atory response in man is thermoregulatory in origin, this theory obviously does not apply to the small
190
J. G. HENRY AND C. R. BAINTON
changes in core temperature during moderate exercise. Our results indicate that under experimental conditions loss (i.e. exercise and increasing the skin temperature), response
to heat
loss is indeed
activated
(finger
which accentuate heat with evidence that a
temperature
or
vasodilation
increase), the additional factor of a change in core temperature had no significant effect of ventilation. These studies therefore confirm the work of Dejours et ~11. (1958) and those of Whipp and Wasserman (1970). Except for skin temperature determinations, our studies were similar to those of Dejours et ~11.(1958). Under their experimental conditions (exercise performed at a room temperature of 37 C with 60% humidity), it is unlikely that skin temperatures would fall unless high air flows were directed over the skin of the subjects, thereby increasing evaporative heat loss. Thus we conclude that the increment of 0.5 “C in human core temperature as observed during moderate exercise does not constitute a stimulus to ventilation via the thermoregulatory system, nor by any other known mechanism. Acknowledgements This study was supported in part by the U.S. Public Health Service Grants GM 05881 and GM 00063, and Training Grant GM 15571. Dr. Bainton is the recipient of Career Development Award GM 42350-4. References Bainton,
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