| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, 15–21 Webster Street, Liverpool L3 2ET, UK 2 School of Sport and Leisure Management, Sheffield Hallam University, Sheffield, SH10 2BP, UK
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
) in a room maintained at 33°C (active). In a second trial they were passively heated (passive) in a water bath (41.56 ± 1.65°C) until core temperature was equal to the core temperature observed at exhaustion during the active trial. Blood samples were taken from an indwelling venous cannula for the determination of serum prolactin during active heating and at corresponding core temperatures during passive heating. Core temperature was not significantly different between the two methods of heating and averaged 38.81 ± 0.53 and 38.82 ± 0.70°C (data expressed as means ±
S.D.) at exhaustion during active heating and at the end of passive heating, respectively (P > 0.05). Mean arterial blood pressure was significantly lower throughout passive heating (active, 73 ± 9 mmHg; passive, 62 ± 12 mmHg; P < 0.01). Despite the significantly reduced blood pressure responses during passive heating, during both forms of heating the prolactin response was the same (active, 14.9 ± 12.6 ng ml–1; passive, 13.3 ± 9.6 ng ml–1; n.s.). These results suggest that thermoregulatory, i.e. core temperature, and not cardiovascular afferents provide the key stimulus for the release of prolactin, an indirect marker of central fatigue, during exercise in the heat.
(Received 10 June 2005;
accepted after revision 12 September 2005; first published online 12 September 2005)
Corresponding author D. Low: Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, Dallas, Texas, TX 75231, USA. Email: davidlow{at}texashealth.org
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Passive and active (exercise-induced) elevations in core temperature increase central serotonergic activity (Hori & Harada, 1976; Bridge et al. 2003). The central serotonergic and dopaminergic transmitter systems have been implicated in the thermoregulatory control of body temperature and are thought to mediate thermoregulatory heat loss responses such as vasodilatation (Cox et al. 1980; Lee et al. 1985). In addition, alterations in the activity of the central serotonergic and dopaminergic systems can also result in changes in behaviour, including arousal and motor control, that could reduce the motivation to continue exercise, which is evident at fatigue during exercise in hot conditions (Young, 1991; Jacobs & Fornal, 1993; Nielsen et al. 2001). However, the measurement of central serotonergic and dopaminergic activity has practical limitations in humans, so the anterior pituitary hormone prolactin is often used as an indirect marker of central serotonergic and dopaminergic activity, since its release is regulated by the central serotonergic and dopaminergic systems (Freeman et al. 2000; Bridge et al. 2003). Serotonergic neurones in the dorsal raphe nucleus, located in the brainstem, stimulate the secretion of prolactin from serotonergic nerve terminals in the hypothalamus through activation of serotonergic receptors (Van de Kar et al. 1996). Hypothalamic dopaminergic neurones that secrete dopamine into the pituitary portal vessels also tonically inhibit the secretion of prolactin (Van de Kar et al. 1996). Significant increases in prolactin (which peak at the point of exhaustion) are evident during exercise in the heat that leads to an intolerable thermoregulatory strain (Brisson et al. 1989; Pitsiladis et al. 2002). This suggests alterations in central serotonergic and dopaminergic activity, in response to the increased core temperature, that could contribute to the reduced motivation to continue exercise, and subsequently fatigue, in the heat. The prolactin responses at exhaustion were also significantly related to the core temperature responses at exhaustion in these studies, further supporting a link between thermal limits of tolerance and the occurrence of this proposal of central fatigue.
A high ambient temperature increases the cardiovascular strain during exercise, because of the concurrent demands of the active musculature and the cutaneous circulation for blood flow (Gonzalez-Alonso et al. 1995, 1997). A high cardiovascular strain has also been proposed as a possible mediator of fatigue during prolonged exercise in hot conditions (Cheung & Sleivert, 2004). Despite this, the relationship between cardiovascular strain and fatigue during prolonged exercise in hot conditions has not been completely researched. The competition for blood flow between the cutaneous circulation, for heat dissipation, and the active musculature, for substrate delivery and removal of metabolic byproducts, during prolonged exercise in hot conditions threatens the effective regulation of blood pressure (Rowell, 1993). Should blood pressure fall to deleterious levels, cerebral blood flow will decrease and cause syncope (fainting). Reductions in mean arterial blood pressure (Gonzalez-Alonso et al. 1997) and cerebral blood flow (Nybo & Nielsen, 2001b) have been reported during prolonged exercise in hot conditions. The control of blood pressure has also been linked with changes in serotonergic brain activity in the rodent model (Pergola & Alper, 1991, 1992). Marked competition for blood flow between the cutaneous circulation and the active musculature during exercise under hot conditions may result in a reduction of blood pressure to potentially dangerously low levels, and low blood pressure may provide an additional signal, alongside or even instead of core temperature, to induce central fatigue, stop exercise and therefore maintain blood pressure and cerebral blood flow.
Separating the core temperature and blood pressure responses during exercise in hot conditions is difficult to achieve. Active (exercise) and passive methods of heat stress invoke similar thermoregulatory but different cardiovascular responses (Powers et al. 1982). The different cardiovascular responses to active and passive methods of heating with similar rises in core temperature relate to the exercise-induced demand for active skeletal muscle blood flow during active heating. Subsequently, attenuated increases in adrenaline, noradrenaline, heart rate, cardiac output and a lower blood pressure are evident during passive heating (Rowell et al. 1970; Powers et al. 1982; Minson et al. 1998). In addition, during passive heating the core temperature threshold for increases in skin blood flow is lower, and increases in skin blood flow are not attenuated at core temperatures of 
38.0°C, as they are during exercise, which also contributes to a lower blood pressure during passive heating (Kenney & Johnson, 1992). A direct comparison of an active and passive heating challenge and their thermoregulatory, cardiovascular and prolactin responses will therefore permit better insight into the mechanisms underlying changes in prolactin activity, and possibly central serotonergic and dopaminergic activity, relating to central fatigue during exercise under hot conditions. One previous study has examined the prolactin responses to passive and active (bicycle exercise) heating and reported greater increases in prolactin during passive heating (Brisson et al. 1991). In that study, however, no cardiovascular variables were measured, and the subjects were heated for set periods of time and not in relation to target increases in core temperature. Therefore, the aim of this study was to compare the prolactin and blood pressure responses at identical core temperatures during active and passive heat stresses. It is hypothesized that, in comparison to active heating, there will be a greater prolactin response alongside the lower blood pressure response during passive heating, suggesting that peripheral blood flow displacement and an attendant drop in arterial blood pressure stimulates the release of prolactin during exercise in hot conditions.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
After local ethical committee approval, 12 active male subjects gave their written informed consent to participate in this study. Their physical characteristics (means ± 1 S.D.) were: age, 23.9 ± 3.7 years; height, 177.8 ± 4.8 cm; body mass, 75.7 ± 4.4 kg; maximal oxygen uptake (
), 50.0 ± 6.4 ml kg–1 min–1. For the active heating trial, subjects cycled to exhaustion at 60%
at 70–80 cycles min–1 on a semirecumbent cycle ergometer (Kettler Sport, Redditch, Worcestershire, UK) in a room maintained at 33°C and constant humidity (40%). They then conducted (at least 7 days later) a passive heating trial, immersed in a water bath up to the xiphoid process with the arms out until they reached the core temperature at exhaustion in the active heating trial. All procedures were performed according to the Declaration of Helsinki.
Pre-trial phase
Subjects reported to the laboratory and were required to insert a rectal probe (ELLAB, Kings Lynn, Norfolk, UK) 10 cm beyond the anal sphincter. Skin thermisters (ELLAB) were attached to four sites on the right-hand side of the body (anterior thigh, medial calf, chest and anterior forearm) for the determination of weighted mean skin temperature according to Ramanathan (1964). Two laser Doppler flowmetry skin probes (Perimed, Bury St Edmunds, Suffolk, UK) were attached to the anterior side of a forearm for the measurement of forearm skin blood flow. Subjects were also fitted with a heart rate monitor (Polar, Kempele, Finland) for the determination of heart rate using short-range telemetry.
Heating phase
During both active and passive heating trials, heart rate (Polar Accurex Plus, Kempele, Finland), core and skin temperature (ELLAB) were monitored continuously and sampled each minute. Forearm skin blood flow (in volts; Periflux system 5000, Perimed, Jarfalla, Sweden) and blood pressure (in mmHg; (PortaPress Model 2, TPD Biomedical Instrumentation, Amsterdam, The Netherlands) from two digits of the same forearm on which skin blood flow was being measured were also monitored continuously throughout both heating trials and sampled every 20 s. The arm from which skin blood flow and blood pressure were measured was placed at heart level throughout each trial. Forearm cutaneous vascular conductance (CVC) was used as an index of skin blood flow and was calculated by the ratio of forearm skin blood flow to blood pressure (volts mmHg–1). Subjects also provided ratings of thermal discomfort (Toner et al. 1986) during both trials. Data were recorded at 20 min intervals and at exhaustion during the active heating trial. During the passive heating trial, data were recorded at the corresponding core temperatures that were recorded at the 20 min intervals and at exhaustion during the active heating trial. Subjects were passively heated until they reached the same core temperature at exhaustion as in the active heating trial.
Prolactin analysis
An indwelling venous cannula (Becton-Dickinson, Oxford, UK) was inserted in a vein in the antecubital crease or anterior forearm opposite to the forearm where skin blood flow was measured. The cannula was kept patent with 5–10 ml of isotonic saline (Becton-Dickinson) after insertion and after each blood sample. Blood samples were drawn pre-trial, at 20 min intervals and at exhaustion during the active exercise trial. During the passive heating trial, samples were drawn at the corresponding core temperatures recorded at the 20 min intervals and at exhaustion during the active heating trial. Samples were dispensed into serum separation tubes (HMS, Northampton, UK) and were left at room temperature for 1 h before being centrifuged, with the supernatant subsequently being frozen (–20.0°C) for analysis at a later stage. Duplicate haematocrict (Micro haematocrict tubes, L.I.P. Equipment, Bradford, Yorkshire, UK) and haemoglobin samples (Microcuvettes, Hemocue, Angelholm, Sweden) were also collected to calculate changes in plasma volume relative to the baseline sample according to Dill & Costill (1974). Serum prolactin was determined using an enzymeimmunoassay technique (DRG Instruments GmbH, Marburg, Germany) on a fully automated immunoassay system (Triturus, Grifols, Cambridge, UK). All samples were analysed in duplicate in one batch and corrected for changes in plasma volume.
Statistics
Data for all subjects were averaged and are expressed as means ± 1 S.D. Statistical analysis of the thermoregulatory, cardiovascular and prolactin responses at the same core temperatures was carried out using a two-factor (core temperature and condition) repeated measures ANOVA. When significant main effects of each factor(s) and/or an interaction of the two factors were found, multiple comparisons within and between each factor(s) were made according to Atkinson (2002). When the assumption of sphericity was violated, ANOVA results were adjusted using Greenhouse Geisser or Huynh-Feldt values according to Atkinson (2002). An alpha level of 0.05 was taken to indicate statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Thermoregulatory responses
Core temperature increased significantly and in a similar fashion across both trials (F1.36,10.88 = 44.87, P < 0.01; see Fig. 1A). There was no difference in the core temperatures attained at any time point between protocols (F1,8 = 0.73, n.s.). Core temperature averaged 38.81 ± 0.53 and 38.82 ± 0.70°C (range 38.2–39.7°C) at exhaustion during the active heating trial and at the end of the passive heating trial, respectively. Therefore, the remainder of the data were expressed in relation to the core temperatures at the sampling points during the active heating trial and not in relation to time.
|
Cardiovascular responses
The heart rate and stroke volume responses to active and passive heating are displayed in Fig. 2. Heart rate increased significantly with core temperature in both forms of heating (F2.56,12.79 = 111.56, P < 0.01; see Fig. 2A). However, the increase in heart rate was significantly greater during the active heating trial (F2.50,12.52 = 51.44, P < 0.01). Heart rate averaged 109 ± 16 and 167 ± 14 beats min–1 at the end of the passive heating trial and at exhaustion during the active heating trial, respectively (P < 0.01). As a result of technical errors with the blood pressure measurements during two subjects' passive heating trials, statistical analyses of the cardiovascular data were carried out on nine subjects. Both passive and active heating caused stroke volume to decrease significantly with increasing core temperature (F2.70,18.88 = 8.37, P < 0.01; see Fig. 2B). During the active heating trial, after an initial increase at 20 min, stroke volume decreased towards resting baseline levels at exhaustion (F3,21 = 20.68, P < 0.01). During the course of passive heat exposure, stroke volume decreased with progressive increases in core temperature (F1,7 = 53.38, P < 0.01). Stroke volume averaged 79 ± 12 and 105 ± 13 ml at the end of the passive heating trial and at exhaustion during the active heating trial, respectively (P < 0.01).
|
|
|
As a result of errors with blood sampling during two subjects' passive heating trials, statistical analysis of the prolactin data was carried out on nine subjects. Serum prolactin increased significantly during both active and passive heating (F1.05,7.36 = 4.44, P < 0.05; see Fig. 5). There was no difference in the prolactin response between the methods of heating (F1,8 = 0.10, n.s.). The average serum prolactin values at exhaustion during active heating and at the end of the passive heating trial were 26.0 ± 20.3 and 23.1 ± 16.6 ng ml–1 (range 8–85 ng ml–1), respectively. The prolactin and the core temperature responses at the end of both forms of heating were significantly correlated (r2 = 0.870, P < 0.0001, n = 22).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Core and mean skin temperatures and thermal discomfort ratings were not different between the two methods of heating. Increases in heart rate and cardiac output in response to increases in core temperature were significantly attenuated during passive heating. Alongside these similar thermoregulatory responses to passive and active heating, during passive heating skin blood flow was significantly increased and stroke volume and mean arterial blood pressure were significantly reduced. These responses are consistent with previous research that has investigated the cardiovascular responses to active and passive heat stresses (Rowell et al. 1970; Powers et al. 1982; Minson et al. 1998). Despite these altered cardiovascular responses to passive, relative to active, heating the prolactin responses were the same during both methods of heating. The core temperature and prolactin responses at the end of both forms of heating were also significantly correlated (r2 = 0.870, P < 0.0001, n = 22). These results suggest that thermoregulatory afferents, i.e. increases in core temperature, are probably the key stimulus for prolactin release, which is in agreement with previous work (Brisson et al. 1989; Bridge et al. 2003).
The secretion of the anterior pituitary hormone prolactin is regulated by the central serotonergic and dopaminergic systems, and prolactin is therefore often used as an indirect marker of central serotonergic and dopaminergic activity (Freeman et al. 2000; Bridge et al. 2003). Central serotonergic and dopaminergic activity has been shown to increase during passive and active (exercise-induced) elevations in core temperature (Hori & Harada, 1976; Bridge et al. 2003), and alterations in the activity of both of these systems have been implicated in the thermoregulatory control of body temperature, by mediating vasodilatation (Cox et al. 1980; Lee et al. 1985). In addition, central serotonergic and dopaminergic pathways have also been shown to modulate changes in behavioural states, such as arousal and motor control (Young, 1991; Jacobs & Fornal, 1993). In the present study, prolactin significantly increased during both forms of heating and peaked at exhaustion during active heating, consistent with previous data (Pitsiladis et al. 2002; Bridge et al. 2003), suggesting that alterations in the activity of the central serotonergic and dopaminergic systems occur at the same time as when core temperature and thermal discomfort have increased to intolerable levels and when the desire to continue exercise is reduced and fatigue ensues.
A number of mechanisms for a decreased endurance capacity during exercise in the heat have been proposed, including an intolerable thermoregulatory strain, cerebral perturbations, central nervous system disturbances, high cardiovascular strain and altered skeletal muscle function (Febbraio, 2000; Cheung & Sleivert, 2004). Despite an alteration in the initial baseline core temperature or the rate of increase in core temperature during exercise in a hot environment using precooling and prewarming manoeuvres and conducting heat acclimation programmes, studies have shown that fatigue during prolonged exercise in the heat occurs at a similar intolerable thermoregulatory strain (Nielsen et al. 1993; Cheung & McLellan, 1998; Gonzalez-Alonso et al. 1999; Gregson et al. 2002). Increases in core temperature to intolerable levels at exhaustion during exercise in hot conditions occur at the same time as maximal or near-maximal ratings of perceived exertion (Nybo & Nielsen, 2001c), a significantly decreased level of arousal (Nielsen et al. 2001) and a significant reduction of the voluntary activation of a previously exercised muscle (Nybo & Nielsen, 2001a). Other experimental work has shown that increases in prolactin at exhaustion are significantly related to core temperature and ratings of perceived exertion at exhaustion during prolonged exercise in hot conditions (Pitsiladis et al. 2002; Bridge et al. 2003; Low et al. 2005). Collectively, these results support a possible link between alterations in central serotonergic and dopaminergic activity and the attainment of thermal limits of tolerance during prolonged exercise in hot conditions, which could lead to a reduced motivation to continue exercise arising from central command in order to protect against any further potentially damaging increases in core and brain temperature (Nielsen & Nybo, 2003).
Exercise in a hot environment that causes thermoregulatory strain is also accompanied by an increased cardiovascular strain (Rowell, 1993). Decreases in cardiac output and stroke volume alongside decreases in mean arterial pressure and cerebral blood flow are evident during exercise in the heat (Gonzalez-Alonso et al. 1995, 1997; Nybo & Nielsen, 2001b). Should blood pressure and subsequently brain blood flow fall to dangerously low levels, syncope can occur. Therefore, decreases in blood pressure and cerebral blood flow to syncopal levels could provide afferent feedback to the brain to instigate central fatigue in order to terminate exercise. In the rodent model, intercerebroventricular injections of serotonin increase blood pressure (Pergola & Alper, 1991, 1992), suggesting a link between the control of blood pressure and serotonergic brain activity, one of the neurotransmitter systems that has been associated with the onset of central fatigue during exercise in hot conditions. In the present study, active and passive methods of heating invoked similar increases in core temperature to intolerable levels but a significantly lower blood pressure response occurred during passive heating. Despite these differences in the blood pressure response, the prolactin increases were the same during these two forms of heating, which indicates that a high cardiovascular strain and a reduced blood pressure do not contribute to changes in prolactin release and possibly central serotonergic and dopaminergic activity. In support of these findings, baroreflex control of blood pressure is not inhibited during exercise (Mack et al. 1988; Potts et al. 1993) or during hyperthermia per se (Crandall et al. 1999; Crandall, 2000), indicating that blood pressure is effectively regulated during exercise in hot conditions. In addition, the decrease in cerebral blood flow occurring during exercise in hot conditions that leads to an intolerable core temperature (Nybo & Nielsen, 2001b) does not reach a level low enough to cause syncope (Van Lieshout et al. 2003). However, it is important that in the present study and others that have investigated mechanisms of fatigue during prolonged exercise in the heat, owing to methodological considerations, bicycle ergometers rather than upright running postures were used as the exercise mode. An upright running posture compared to a seated bicycle posture will probably invoke a greater orthostatic stress during exercise (Rowell, 1993) and therefore the (in)effective control of blood pressure may possibly play a more important role in fatigue during prolonged exercise in the heat during running. This warrants further investigation.
In a previous study that examined the prolactin responses to 30 min of passive heating and 45 min of activity (bicycle exercise at 65%
in a 41°C environment) Brisson et al. (1991) reported larger increases in prolactin (although no statistical analysis was performed) during passive heating, despite similar increases in rectal temperature (1.6°C). The intensity of exercise, the temperature of the water in which subjects were immersed and the increases in rectal temperature in the study of Brisson et al. (1991) are similar to those in the present study, but the reasons for larger prolactin increases during passive heating in the study of Brisson et al. (1991) compared with the present study are not clear. The prolactin response to exercise in the heat is significantly reduced with facial fanning that reduces mean overall skin temperature but does not change core (rectal) temperature (Brisson et al. 1991; Armada da Silva et al. 2004). In the study of Brisson et al. (1991), subjects were immersed up to the chin, in contrast to the sternum with arms out in the present study, potentially resulting in a greater mean skin temperature and therefore greater prolactin response during the passive, relative to the active, heat stress in the study of Brisson et al. (1991). Another possible reason for the discrepancy is the difference in the components of blood analysed for prolactin in the present study and the study of Brisson et al. (1991; serum versus plasma, respectively).
It has been shown in an animal model that increases in prolactin can be mediated by stress that is induced by exposing the animals to ether or by restraining them (Freeman et al. 2000). Although not performed in this study, to serve as a control condition in the study of Brisson et al. (1989) subjects sat and rested on the cycle ergometer for the same amount of time and under the same conditions as in the active exercise trial with no change in core temperature. In addition, subjects were also immersed in the water bath at a thermoneutral temperature for the same duration as the passive heat stress and no change in core temperature was evident. In both of these control trials no change in prolactin was observed, indicating that being required to be seated on a cycle ergometer or in a water bath, as in the present study, do not per se cause changes in prolactin. In addition, the thermal discomfort ratings at the end of both forms of heating in the present study indicated that the subjects terminated their trials at the point when thermal discomfort was almost maximal.
In conclusion, active (exercise-induced) and passive hyperthermia that invoked identical core temperatures yielded similar prolactin responses. This was despite different cardiovascular responses to the two forms of body heating. These results suggest that increases in core temperature, not alterations in peripheral blood flow and blood pressure, provide the key stimulus for prolactin release, which may be a marker of central serotonergic and dopaminergic activity relating to central fatigue during exercise in hot conditions.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Atkinson G (2002). Analysis of repeated measurements in physical therapy research, multiple comparisons amongst level means and multi-factorial designs. Phys Ther Sport 3, 191–203.
Bridge MW, Weller AS, Rayson M & Jones DA (2003). Responses to exercise in the heat related to measures of hypothalamic serotonergic and dopaminergic function. Eur J Appl Physiol 89, 451–459.[Medline]
Brisson GR, Boisvert P, Peronnet F, Quirion A & Senecal L (1989). Face cooling-induced reduction of plasma prolactin response to exercise as part of an integrated response to thermal stress. Eur J Appl Physiol 58, 816–820.[CrossRef]
Brisson
GR, Peronnet
F, Perrault
H, Boisvert
P, Massicotte
D
&
Gareau
R (1991). Prolactinotrophic effect of endogenous and exogenous heat loads in human adult males. J Appl Physiol
70, 1351–1355.
Bruck K & Olschewski H (1987). Body temperature related factors diminishing the drive to exercise. Can J Physiol Pharm 65, 1274–1280.[Medline]
Cheung
SS
&
McLellan
TM (1998). Heat acclimation, aerobic fitness, and hydration effects on tolerance time during uncompensable heat stress. J Appl Physiol
84, 1731–1739.
Cheung SS & Sleivert GG (2004). Multiple triggers for hyperthermic fatigue and exhaustion. Exerc Sport Sci Rev 32, 100–106.[CrossRef][Medline]
Cox
B, Kerwin
RW, Lee
TF
&
Pycock
CJ (1980). A dopamine-5-hydroxytryptamine link in the hypothalamic pathways which mediate heat loss in the rat. J Physiol
303, 9–21.
Crandall CG (2000). Carotid baroreflex responsiveness in heat-stressed humans. Am J Physiol 279, H1955–H1962.
Crandall CG, Etzel RA & Farr DB (1999). Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans. Am J Physiol 277, H2348–H2352.
Dill
DB
&
Costill
DL (1974). Calculation of percentage changes in volumes of blood, plasma and red cells in dehydration. J Appl Physiol
37, 247–248.
Febbraio M (2000). Does muscle function and metabolism affect exercise performance in the heat? Exer Sport Sci Rev 28, 171–176.[Medline]
Freeman
ME, Kanyicska
B, Lerant
A
&
Nagy
G (2000). Prolactin: structure, function, and regulation of secretion. Physiol Rev
80, 1523–1631.
Galloway SDR & Maughan RJ (1997). Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man. Med Sci Sports Exerc 29, 1240–1249.[Medline]
Gonzalez-Alonso
J, Mora-Rodriguez
R, Below
PR
&
Coyle
EF (1995). Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise. J Appl Physiol
79, 1487–1496.
Gonzalez-Alonso
J, Mora-Rodriguez
R, Below
PR
&
Coyle
EF (1997). Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J Appl Physiol
82, 1229–1236.
Gonzalez-Alonso
J, Teller
C, Andersen
SL, Jensen
FB, Hyldig
T
&
Nielsen
B (1999). Influence of body temperature on the development of fatigue during prolonged exercise in the heat. J Appl Physiol
86, 1032–1039.
Gregson WA, Drust B, Batterham A & Cable NT (2002). The effects of pre-warming on the metabolic and thermoregulatory responses to prolonged submaximal exercise in moderate ambient temperatures. Eur J Appl Physiol 86, 526–533.[CrossRef][Medline]
Hori T & Harada Y (1976). Responses of midbrain raphe neurons to local temperature. Pflugers Arch 364, 205–207.[CrossRef][Medline]
Jacobs BL & Fornal CA (1993). 5-HT and motor control, a hypothesis. Trends Neurosci 16, 346–352.[CrossRef][Medline]
Kenney WL & Johnson JM (1992). Control of skin blood flow during exercise. Med Sci Sports Exerc 24, 303–312.[Medline]
Lee TF, Mora F & Myers RD (1985). Dopamine and thermoregulation: an evaluation with special reference to dopaminergic pathways. Neurosci Biobehav Rev 9, 589–598.[CrossRef][Medline]
Low DA, Cable T, Reilly T & Purvis A (2005). Relationship between exercise hyperprolactinaemia and cardiovascular responses during prolonged exercise in the heat. J Sport Sci 23, 142.
Mack
G, Nose
H
&
Nadel
ER (1988). Role of cardiopulmonary baroreflexes during dynamic exercise. J Appl Physiol
65, 1827–1832.
Minson
CT, Wladkowski
SL, Cardell
AF, Pawelczyk
JA
&
Kenney
WL (1998). Age alters the cardiovascular response to direct passive heating. J Appl Physiol
84, 1323–1332.
Nielsen
B, Hales
JRS, Strange
S, Christensen
NJ, Warberg
J
&
Saltin
B (1993). Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment. J Physiol
460, 467–485.
Nielsen B, Hyldig T, Bidstrup F, Gonzalez-Alonso J & Christoffersen GR (2001). Brain activity and fatigue during prolonged exercise in the heat. Eur J Physiol 442, 41–48.[CrossRef][Medline]
Nielsen B & Nybo L (2003). Cerebral changes during exercise in the heat. Sports Med 33, 1–11.[CrossRef][Medline]
Nybo
L
&
Nielsen
B (2001a). Hyperthermia and central fatigue during prolonged exercise in humans. J Appl Physiol
91, 1055–1060.
Nybo
L
&
Nielsen
B (2001b). Middle cerebral artery blood velocity is reduced with hyperthermia during prolonged exercise in humans. J Physiol
534, 279–286.
Nybo
L
&
Nielsen
B (2001c). Perceived exertion is associated with an altered brain activity during exercise with progressive hyperthermia. J Appl Physiol
91, 2017–2023.
Parkin
JM, Carey
MF, Zhao
S
&
Febbraio
MA (1999). Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise. J Appl Physiol
86, 902–908.
Pergola PE & Alper RH (1991). Vasopressin and autonomic mechanisms mediate cardiovascular actions of central serotonin. Am J Physiol 260, R1188–R1193.
Pergola PE & Alper RH (1992). Effects of central serotonin on autonomic control of heart rate in intact and baroreceptor deficient rats. Brain Res 582, 215–220.[CrossRef][Medline]
Pitsiladis YP, Strachan AT, Davidson I & Maughan RJ (2002). Hyperprolactinaemia during prolonged exercise in the heat: evidence for a centrally mediated component of fatigue in trained cyclists. Exp Physiol 87, 215–226.[Abstract]
Potts JT, Shi X & Raven PB (1993). Carotid baroreflex responsiveness during dynamic exercise in man. Am J Physiol 265, H1928–H1938.
Powers SK, Howley ET & Cox R (1982). A differential catecholamine response during prolonged exercise and passive heating. Med Sci Sports Exerc 14, 435–439.[Medline]
Ramanathan
NL (1964). A new weighting system for mean surface temperature of the human body. J Appl Physiol
19, 531–533.
Rowell LB (1993). Cardiovascular Control. Oxford University Press, New York.
Rowell
LB, Brengelmann
GL, Blackmon
JR
&
Murray
JA (1970). Redistribution of blood flow during sustained high skin temperature in resting man. J Appl Physiol
28, 415–420.
Toner MM, Drolet LL & Pandolf KB (1986). Perceptual and physiological responses during exercise in cool and cold water. Percep Motor Skill 62, 211–220.
Van de Kar LD, Rittenhouse PA, Li Q & Levy AD (1996). Serotonergic regulation of renin and prolactin secretion. Behav Brain Res 73, 203–208.[Medline]
Van Lieshout
JJ, Wieling
W, Karemaker
JM
&
Secher
NH (2003). Syncope, cerebral perfusion, and oxygenation. J Appl Physiol
94, 833–848.
Young SN (1991). Some effects of dietary components (amino acids, carbohydrates, folic acid) on brain serotonin synthesis, mood and behaviour. Can J Physiol Pharm 69, 893–903.[Medline]
This article has been cited by other articles:
|
|
 |
|
  C. R. Abbiss, J. J. Peiffer, J. M. Peake, K. Nosaka, K. Suzuki, D. T. Martin, and P. B. Laursen Effect of carbohydrate ingestion and ambient temperature on muscle fatigue development in endurance-trained male cyclists J Appl Physiol, April 1, 2008; 104(4): 1021 - 1028. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Mundel, S. J. Bunn, P. L. Hooper, and D. A. Jones Human Environmental/Exercise: The effects of face cooling during hyperthermic exercise in man: evidence for an integrated thermal, neuroendocrine and behavioural response Exp Physiol, January 1, 2007; 92(1): 187 - 195. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
P < 0.05 versus baseline; n
= 11 for core temperature, n
= 6 for mean skin temperature and n
= 11 for thermal discomfort rating results. Exh, exhaustion.
