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Review
. 2019 Feb;49(Suppl 1):69-85.
doi: 10.1007/s40279-018-1033-y.

Heat, Hydration and the Human Brain, Heart and Skeletal Muscles

Steven J Trangmar  1 , José González-Alonso  2   3
Affiliations
Review

Heat, Hydration and the Human Brain, Heart and Skeletal Muscles

Steven J Trangmar et al. Sports Med. 2019 Feb.

Abstract

People undertaking prolonged vigorous exercise experience substantial bodily fluid losses due to thermoregulatory sweating. If these fluid losses are not replaced, endurance capacity may be impaired in association with a myriad of alterations in physiological function, including hyperthermia, hyperventilation, cardiovascular strain with reductions in brain, skeletal muscle and skin blood perfusion, greater reliance on muscle glycogen and cellular metabolism, alterations in neural activity and, in some conditions, compromised muscle metabolism and aerobic capacity. The physiological strain accompanying progressive exercise-induced dehydration to a level of ~ 4% of body mass loss can be attenuated or even prevented by: (1) ingesting fluids during exercise, (2) exercising in cold environments, and/or (3) working at intensities that require a small fraction of the overall body functional capacity. The impact of dehydration upon physiological function therefore depends on the functional demand evoked by exercise and environmental stress, as cardiac output, limb blood perfusion and muscle metabolism are stable or increase during small muscle mass exercise or resting conditions, but are impaired during whole-body moderate to intense exercise. Progressive dehydration is also associated with an accelerated drop in perfusion and oxygen supply to the human brain during submaximal and maximal endurance exercise. Yet their consequences on aerobic metabolism are greater in the exercising muscles because of the much smaller functional oxygen extraction reserve. This review describes how dehydration differentially impacts physiological function during exercise requiring low compared to high functional demand, with an emphasis on the responses of the human brain, heart and skeletal muscles.

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Conflict of interest statement

José González-Alonso has received funding from the GSSI to undertake fundamental physiological research. The dehydration and hyperthermia studies conducted by José González-Alonso and Steven Trangmar at the Centre for Human Performance, Exercise and Rehabilitation, Brunel University London from 2010 to 2014 were partly supported by a grant from the GSSI.

Figures

Fig. 1
Fig. 1
Effects of dehydration and hyperthermia on aerobic capacity and maximal endurance capacity. Oxygen consumption dynamics were measured during constant load maximal cycling (402 ± 4 W) under control, dehydration (4% body weight loss without hyperthermia), hyperthermia (+ 1 °C and + 6 °C increases in Tes and Tsk, respectively) and combined dehydration and hyperthermia. Note that both combined dehydration and hyperthermia and hyperthermia alone impaired V˙O2max and exercise performance by 16% and 51–53% compared to control, without altering the initial absolute V˙O2 responses. Preventing hyperthermia in dehydrated individuals restored V˙O2max and exercise performance by 65% and 50%, respectively. These data demonstrate that aerobic metabolism and maximal endurance capacity can be drastically compromised in the dehydrated and hyperthermic human. Figure redrawn from data (means ± SE) reported by Nybo et al. [34]. Tes oesophageal temperature, Tsk mean skin temperature, V˙O2 oxygen uptake, V˙O2max maximal aerobic capacity
Fig. 2
Fig. 2
Effects of hyperthermia on respiratory, haematological, regional cardiovascular, metabolic, thermal and regulatory responses to maximal aerobic exercise and maximal endurance capacity. The over-time physiological responses are reported as a percentage of the 0.5-min exercise value, or in the case of the thermal and catecholamine responses, the delta increase in locomotor limb blood temperature and the absolute concentration values, respectively. Thermal strain was higher at the onset of constant load cycling (~ 360 W) in the whole body hyperthermia condition (+ 1 °C and 10 °C higher in Tes and Tsk, respectively), and was associated with significant respiratory, cardiovascular, metabolic and regulatory strain after 3 min of cycling, leading to an accelerated fatigue (5.5 vs. 7.6 min). Note that the reductions in locomotor limb blood flow prior to exhaustion in both conditions led to a reduction in O2 delivery and a depressed exercising limb muscle V˙O2, even though O2 extraction increased. Therefore, the faster fatigue with hyperthermia and dehydration during exercise requiring aerobic capacity seems to be closely coupled with impaired muscle metabolism. Drawn from mean data reported by González-Alonso and Calbet [35] and González-Alonso et al. [107]. VE ventilation, fR respiratory rate, CaO2 arterial oxygen content, BV blood volume, PaO2 arterial oxygen partial pressure, SaO2 arterial oxygen saturation, PaCO2 arterial carbon dioxide partial pressure, a-vO2diffleg arterio-venous oxygen content differences across the leg, V˙O2leg leg oxygen uptake, LBF leg blood flow, O2delleg oxygen delivery to the leg, Tb blood (femoral venous) temperature, NE norepinephrine, E epinephrine, Q˙ cardiac output, a-vO2diffsyst systemic arterio-mixed venous oxygen content differences, HR heart rate, a-vO2diffbrain arterio-mixed venous oxygen content differences across the brain, SV stroke volume, MAP mean arterial pressure, MCA Vmean middle cerebral artery mean blood flow velocity
Fig. 3
Fig. 3
Effects of progressive dehydration and maintenance of euhydration by fluid ingestion on respiratory, hematologic, cardiovascular, metabolic, thermal and regulatory responses to prolonged exercise and submaximal endurance capacity in the heat. The over-time physiological responses are reported as percentage of the 20-min exercise value, or in the case of the thermal responses the delta increase in regional temperature. The physiological responses were not different between trials at this reference time point, as participants’ hydration status was the same. Note, however, that progressive dehydration was associated with significant physiological and perceptual strain preceding exhaustion, as reflected by gradual hyperventilation, haemoconcentration, increased arterial oxygen content, arterial hypocapnia, cardiovascular strain with reductions in brain, contracting skeletal muscle and skin perfusion, cardiac output and perfusion pressure, core and active muscle hyperthermia, alterations in neural activity, increases in perception of effort, but to a large extent maintained exercising limb, brain and systemic aerobic metabolism owing to the corresponding increases in leg, brain and systemic in oxygen extraction. This contrasts with the apparent maintenance of physiological homeostasis and perception of effort during the euhydration trial, in which athletes could have continued cycling for some additional 15–60 min before reaching exhaustion. Drawn from mean data reported by González-Alonso et al. [26, 137]. The cerebral blood flow responses were drawn from data reported by Trangmar et al. [106]. fR respiratory frequency, VE ventilation, PaO2 arterial oxygen tension, PaCO2 arterial carbon dioxide tension, CaO2 arterial oxygen content, SaO2 arterial oxygen saturation, BV blood volume, HR heart rate, SV stroke volume, Q˙ cardiac output, MAP mean arterial pressure, LBF leg blood flow, TPR total peripheral resistance, FBF forearm blood flow, CBF cerebral blood flow, a-vO2diffbrain arterio-venous oxygen content differences across the brain, a-vO2diffsyst systemic arterio-mixed venous oxygen content differences, a-vO2diffleg arterio-venous oxygen content differences across the exercising leg, V˙O2syst systemic oxygen uptake V˙O2leg leg oxygen uptake, Tb blood (femoral) temperature, Tm muscle (vastus lateralis) temperature, Tes oesophageal temperature, NE norepinephrine, E epinephrine
Fig. 4
Fig. 4
Effects of dehydration on cerebral haemodynamics and metabolism. Cerebral haemodynamic and metabolic responses during incremental cycling to exhaustion reported as percent rest reference value. Of note are the declines in cerebral blood flow and oxygen supply at about 60% of maximal aerobic exercise intensity, which are paralleled by proportional increases in oxygen extraction across the brain, such that cerebral aerobic metabolism is maintained. Drawn from mean data reported by Trangmar et al. [108]. CCA common carotid artery blood flow, ICA internal carotid blood flow, PaCO2 arterial carbon dioxide partial pressure, MCA Vmean middle cerebral artery mean blood flow velocity, a-vO2diffbrain differences in oxygen content across the brain, O2supply oxygen delivery to the brain which is the product of cerebral blood flow and arterial oxygen content, CMRO2 cerebral metabolic rate for oxygen
Fig. 5
Fig. 5
Schematic diagram illustrating the effects of dehydration and hyperthermia on physiological function during submaximal exercise, according to Ohm’s law and the Fick principle. Significant dehydration and hyperthermia (i.e., 4–5% body mass loss and 40–41 °C core and muscle temperatures) impair submaximal endurance capacity in athletes. The compromised performance occurs in association with reductions in systemic and regional tissue and organ blood flow, but compensatory physiological adjustments maintain whole-body oxygen uptake. For a full description, see section 6.1. The direction of the arrow indicates the direction of response, whereas its size indicates the magnitude of the response. Q˙ cardiac output, TPR total peripheral resistance, MAP mean arterial pressure, BV blood volume, VR venous return, SNA sympathetic nerve activity, NE circulating noradrenaline concentration, CaO2 arterial oxygen content, CvO2 mixed venous oxygen content, HR heart rate, SV stroke volume, EDV end-diastolic volume, ESV end-systolic volume
Fig. 6
Fig. 6
Schematic diagram highlighting major physiological factors limiting maximal endurance capacity with and without dehydration and hyperthermia. Impaired maximal endurance capacity in dehydrated and hyperthermic athletes (i.e., 4–5% body mass loss and 39–40 °C core and muscle temperatures) is associated with a marked decline in cardiac output (Q˙), a substantial increase in total peripheral resistance (TPR) and a small reduction in mean arterial pressure (MAP), or perfusion pressure. The concomitant reductions in peripheral blood flow and O2 supply lead to suppressed whole body and locomotor limb V˙O2 because the functional oxygen extraction reserve in active skeletal muscle has been exhausted. A lower stroke volume is also the main factor reducing Q˙. Peripheral vasoconstriction is proposed as a major factor reducing venous return, cardiac filling and cardiac stroke volume. The direction of the arrow indicates the direction of response, whereas its size indicates the magnitude of the response. Q˙ cardiac output, TPR total peripheral resistance, MAP mean arterial pressure, BV blood volume, VR venous return, SNA sympathetic nerve activity, NE circulating noradrenaline concentration, CaO2 arterial oxygen content, CvO2 mixed venous oxygen content, HR heart rate, SV stroke volume, EDV end-diastolic volume, ESV end-systolic volume
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