Rui Wen Lim is a 2nd year Biological Sciences student at Imperial College London.
Franzi König-Paratore is a Sociologist at St Giles Medical, Berlin.
Steven Walker is Director at St Giles Medical, London and Berlin.
‘Dear weather, stop showing off. We know you’re hot!’ – Unknown
Climate change needs no introduction. It is the hot (quite literally) topic in the news, talked about so much that we have almost become desensitised to it. It is a disastrous but hazy concept, far away, safely contained in newspapers and scientists’ minds, in the Arctic and in the future. We can just stay inside. But we can’t. Many of us across Europe and beyond experienced record temperatures this summer and realised that staying indoors provides little relief. We feel tired, develop brain fog, have an increased risk of cardiovascular failure, and cannot stop sweating. What exactly is the heat doing to our cells and vital organs?
As mammals, our bodies are constantly held in an optimum homeostatic state. When the external temperature rises relative to our internal environment, more tasks are required to be completed by the brain for homeostasis. The Global Workspace Theory (GWT), proposed by Bernard J Baars, provides a good model for better understanding the operation of the brain.
Think of the brain as an office workspace with limited resources. Heat stress brings additional tasks into the workspace. As a result, energy and resources in the brain are redistributed to maintain homeostasis, leaving fewer resources for other tasks and cognitive functions, causing fatigue and confusion.1 One of these new tasks is losing heat via the bloodstream. The brain sends electrical signals to the heart to increase the force and rate of pumping. An increase in surrounding temperature above 21°C can as much as double cardiac output. As the blood circulates throughout the body, we lose heat by radiation through the skin.
“Think of the brain as an office workspace with limited resources. Heat stress brings additional tasks into the workspace.”
In hot weather, the temperature gradient between the skin and the surrounding air decreases, making heat loss by radiation less effective. To counter this, heat loss by sweating becomes more important for homeostasis. The extra work of pumping blood more quickly and forcefully puts a strain on the heart, increasing the risk of heart failure and potential death. Under heat stress, the circulatory system struggles to ensure sufficient blood is sent to the skin for heat dissipation as well as to maintain sufficient flow through the heart and lungs.
This is especially important during exercise in hot weather when increased blood flow to the skin reduces the volume of blood available to the lungs, reducing their contractility and thus ability to take up oxygen. A fall in cardiopulmonary circulation also leads to reduced cardiac output and venous return. Less oxygen reaches cells resulting in a decrease in metabolic efficiency. Available blood volume is further decreased by peripheral vasodilation and fluid loss through sweat.2
Sweat glands are activated when thermosensitive neurones in the brain detect an increase in body temperature, triggering the secretion of sweat: a combination of water and electrolytes that evaporate to cool the body. However, in a humid environment, sweating is not sufficiently effective to cool us down. Because the usual water potential gradient between the skin and the air is reduced, less sweat evaporates. Instead, it can get trapped inside skin pores and leak to surrounding tissues, ultimately causing a heat rash.3 With the sweat mechanism inhibited, the risk of heat stroke increases. Affected individuals may feel nauseous, lose consciousness, and, untreated, can even die.
“Under heat stress, the circulatory system struggles to ensure sufficient blood is sent to the skin for heat dissipation … “
On a cellular level, GWT may explain why in a hot environment our bodies channel resources away from growth-related functions to stress-related processes. A new priority under heat stress is the reparation of misfolded proteins. In cells, proteins are constantly synthesised by the folding of polypeptide chains into highly specific functional formations. Under heat stress, the bonds between amino acids in the polypeptide chains weaken, freeing them up to form ‘incorrect’ bonds with other amino acids.4
This can lead to the synthesis of a dysfunctional protein. Sometimes, separate polypeptide chains can form bonds with each other, resulting in toxic accumulations that predispose individuals to diseases such as cancer.5 The key players in protein reparation are heat shock proteins; when temperatures are high, the expression of genes encoding these proteins is switched on to increase their abundance. They bind to the misfolded proteins and rearrange them into their correct configuration.
If the cell is overwhelmed and there are too many misfolded or unfolded proteins, heat shock proteins will also chaperone the dysfunctional proteins (such as the toxic aggregates) to the proteasome where they will be metabolised.6 However, heat shock proteins aren’t the only important elements in a cellular heat shock response (HSR).
“… in the future, our bodies will need to cope both on a cellular and an organic level with future heatwaves.”
A study on moss cells found that the cell membrane is extremely sensitive to temperature changes and even a slight temperature rise can initiate the HSR. This is because calcium ions were found to be involved in triggering the HSR pathway, and heat increases membrane fluidity, allowing for the influx of extracellular calcium into the cell cytoplasm. Because the HSR in plants is similar to that in other species, it is likely that for humans, the cell membrane plays a big role in heat detection and kickstarts the pathway to mitigating heat stress.7
Many of us are already struggling with increased temperatures. It is likely that in the future, our bodies will need to cope both on a cellular and an organic level with future heatwaves. Adapting our clothing and modern amenities, such as air conditioning and the way we build our houses, can only do so much. Could it be that humans might evolve to better cope with the heat?
Animals, for example, have adapted to survive. Reptiles and birds excrete moisture-free uric acid (which is toxic to humans) to conserve water, and camels use their fur as shade.8 While news reports continue to create awareness about the effects of climate change on the environment and our animal neighbours, it is equally important to shed light on how protracted heat can affect humans as well as recognise the many gaps in our knowledge.
So, to answer the title question, we are struggling to take the heat and we need to do something about it.
Glossary:
- Cardiopulmonary circulation: the circulation of blood between the heart and the lungs
- Heat shock response: a cell stress response that increases the abundance of chaperones (heat shock proteins) to defend against heat-induced damage to the cell
- Homeostasis: the maintenance of the body’s internal conditions at an optimum state
- Metabolism: the total amount of biochemical reactions
- Peripheral vasodilation: the dilation of blood vessels that branch out from arteries and veins (arterioles and venules)
- Polypeptide chain: a chain of amino acids that will fold to make a protein
- Venous return: the flow of blood through veins back to the heart
References:
1. Gaoua N. Cognitive function in hot environments: a question of methodology. Scand J Med Sci Sports 2010; 20 Suppl 3: 60–70.
2. Sawka MN, Wenger CB, Young AJ, Pandolf KB. Physiological responses to exercise in the heat. In: Marriott BM. Ed. Nutritional needs in hot environments: applications for military personnel in field operations. Washington, DC: National Academies Press, 1993.
3. Starkman E. What is Heat Rash? 2022. https://www.webmd.com/skin-problems-and-treatments/understanding-heat-rash-basics (accessed 12 Sep 2022).
4. Bouchama A, Aziz MA, Al Mahri S, et al. A model of exposure to extreme environmental heat uncovers the human transcriptome to heat stress. Sci Rep 2017; 7(1): 9429.
5. Cuervo AM, Wong E. Chaperone-mediated autophagy: roles in disease and aging. Cell Res 2014; 24(1): 92–104.
6. Stetler RA, Gan Y, Zhang W, et al. Heat shock proteins: cellular and molecular mechanisms in the CNS. Prog Neurobiol 2010; 92(2): 184–211.
7. Hofmann NR. The plasma membrane as first responder to heat stress. Plant Cell 2009; 21(9): 2544.
8. Jones V. Animal adaptations to hot climates. 2019. https://sciencing.com/animal-adaptations-hot-climates-8586200.html (accessed 12 Sep 2022).
Featured photo by Scott Goodwill on Unsplash
