Cardiovascular Adjustments to Hot Environments

Environmental heat stress can test the limits of the human cardiovascular system. This pressure system made up of a compliant vascular network and contractile pump (heart) are important components for the regulation of oxygen rich blood, temperature, body fluid balance, and therefore exercise performance (Cheuvront et al., 2010). A complex interplay among physiological systems governs these responses. Increased temperature and humidity affect the cardiovascular response during exercise by diverting a greater fraction of cardiac output to the skin to increase heat removal from body. Sweating for the purpose of evaporative cooling is the primary means of heat loss in a warm environment (Cheuvront et al., 2010). This decreases availability of oxygen rich blood flow to muscles and causes maximal cardiac output, oxygen consumption to be reached at lower workload intensities of exercise (Klabunde, 2005). Blood volume is also affected because of dehydration, which reduces blood volume and venous central pressure and reduces the normal increase in cardiac output. This leads to a fall in arterial pressure and heat exhaustion (Klabunde, 2005). Increase of cutaneous blood flow is controlled by the hypothalamic thermoregulatory centers of the brain. When an increased blood temperature is sensed by thermoreceptors in the hypothalamus, a decrease in sympathetic nerve activity to cutaneous blood vessel occurs, which causes an increase skin blood flow. Also during this time, activation of sympathetic cholinergic nerves to the skin causes sweating by vasodilation of vessels (Klabunde, 2005).

Mechanisms to maintain stroke volume, because of fluid loss, cause an increase in heart rate to maintain pressure (Wilson et al., 2011). Cardiac output increases well above 10 L · min1 during whole body heating. Because stoke volume is importantly maintained, increase in heart rate is the primary mechanism of an increase in stroke volume. Wilson et al. (2011) note that direct effect of temperature on the sinoatrial node and sympathetic and parasympathetic effects on the heart are caused by either baroreflexes (pressure sensors) or global hyperadrenergic (overactive catecholamine) state and regulate heart rate during heat stress. Efferent of the baroreflexes may be involved in increasing heart rate if mean arterial pressure decreases during heat stress. Wilson et al. (2011) also note that heat stress increases noradrenergic signaling and circulating catecholamines. Sweat loss exceeding greater than 3% of total body water causes fatigue due to heat stress on the cardiovascular system, which can cause slowing of self-paced exercise (Cheuvront et al., 2010).

Heart rate has been noted in studies (Coyle and Alonso, 2001, Rowell, 1986) to rise in association with core temperature. The cardiovascular adjustment to heat stress is a phenomenon termed cardiovascular drift, which is characterized as a downward drift in central venous pressure, stroke volume, pulmonary and systemic arterial pressures, and central blood volume, while at the same time a rise in heart rate maintains nearly constant cardiac output by (Rowell, 1986). This drift has that is associated with a small increase in core temperature increases in heart rate at submaximal exercise (Kamon, 1972, Rowell et al. 2004) from local blood temperature receptors in the sinoatrial note and which alter autonomic nervous system (Gorman and Proppe, 1984).

During prolonged exercise in the heat, water may be lost as a result of sweating (3-5%), and when dehydration exceeds 3% of total body water (2% of body mass) then aerobic performance is impaired (Cheuvront et al., 2010, Coyle and Alonzo, 2001). Dehydration can lead to an increase in body core temperature, increased hyperthermia, and plasma volume reduction. This alters cardiovascular and biochemical components in the blood, which reduce VO2max (Cheuvront et al., 2010, Sawka 1985). Research has shown that after 10 minutes of prolonged moderate intensity of 50-75% VO2max in both neutral and warm environments showed a cardiovascular drift (Coyle and Gonzalez-Alonso, 2001). However, there are disagreements in the mechanisms behind the drift. Coyle and Gonzalez-Alonso (2001) note that the drift is due to a decrease in mean arterial pressure associated with dehydration which further increase sympathetic nervous activity and decreases the amount of cutaneous blood flow and increase in heart rate. Ravens and Stevens (1986) also find that cardiovascular drift is due to a progressive increase in cutaneous blood flow as temperature rises.

Cheuvront, S.N., Kenefick, R.W., Montain, S.J., Sawka, M.N. 2010. Mechanisms of aerobic performance impairment with heat stress and dehydration. J. Appl. Physiol. 109: 1989-1995.

Coyle, E.F., and Gonzalez-Alonso, J., 2001. Cardiovascular drift during prolonged exercise: New Perspective., Sport Science Review. 29: 88-92.

Gorman AJ, Proppe DW (1984) Mechanisms producing tachycardia in conscious baboons during environmental heat stress. J Appl Physiol 56: 441-446

Kamon, E. Relationship of physiological strain to change in heart rate during work in heat. Am Ind Hyg Assoc J 33: 701-708, 1972.

Klabunde, R.E. 2005. Cardiovascular Physiology Concepts. Lippincott Williams and Wilkins, MD, 235 pp.

Rowell, L.B. 1986. Human Circulation: Regulation during Physical Stress. New York: Oxford University Press. 72: 223-261.

Rowell, L.B. 2004. Ideas about control of skeletal and cardiac muscle blood flow (1876-2003): cycles of revision and new vision. J. Appl. Physiol. 97:384-392.

Wilson, T.E., Crandall, C.G. 2011. Effects of thermal stress on cardiac function. Exerc. Sci. Rev. 39: 12-17.


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