The cardiovascular challenge of exercising in the heat

Abstract

Exercise in the heat can pose a severe challenge to human cardiovascular control, and thus the provision of oxygen to exercising muscles and vital organs, because of enhanced thermoregulatory demand for skin blood flow coupled with dehydration and hyperthermia. Cardiovascular strain, typified by reductions in cardiac output, skin and locomotor muscle blood flow and systemic and muscle oxygen delivery accompanies marked dehydration and hyperthermia during prolonged and intense exercise characteristic of many summer Olympic events. This review focuses on how the cardiovascular system is regulated when exercising in the heat and how restrictions in locomotor skeletal muscle and/or skin perfusion might limit athletic performance in hot environments.

Figure 1. Systemic and exercising legs haemodynamics during incremental cycling to exhaustion

Note the attenuation in the rate of rise in blood flow and O₂ delivery to the exercising legs above 50% and the plateau in cardiac output above 90% of (Mortensen et al. 2005). Filled symbols depict the cardiac output, systemic vascular conductance and systemic O₂ delivery for the upper, middle, and lower panels, respectively. Open symbols depict the blood flow, vascular conductance and O₂ delivery to the exercising legs for the respective panels.

Figure 2. Schematic description of the thermoregulatory control of skin blood flow as modified by moderately intense exercise

The relation of skin blood flow to internal temperature is affected, relative to resting conditions, in at least three ways by exercise: a vasoconstrictor response at the onset of dynamic exercise (A), an increase in the internal temperature threshold at which skin blood flow begins to increase (B), and a levelling off, or plateau, in skin blood flow above an internal temperature of 38°C at a level well below maximal (C). Exercise exerts these effects through the vasoconstrictor system for the initial vasoconstriction and through inhibiting the active vasodilator system for the increased threshold and for the plateau. At rest, the plateau only occurs as skin blood flow approaches maximal vasodilatation.

Figure 3. Effects of progressive dehydration and hyperthermia on cardiovascular haemodynamics, metabolism and circulating catecholamines during exhaustive prolonged cycling in the heat

The seven endurance-trained, heat acclimated subjects (VO₂max = 4.9 ± 0.61 min⁻¹) became exhausted after 135 ± 4 min of cycling at 208 ± 21 W in a 35°C, 40–50% relative humidity and 2–3 m s⁻¹ wind speed environment with skin, core and exercising muscle temperatures reaching ∼35, ∼40 and ∼41°C, respectively. (From González-Alonso 2007 with permission, which was redrawn from González-Alonso et al. 1998, 1999). A week after the dehydration trial, the subjects performed a control trial in the heat for the same duration where cardiovascular, metabolic and thermoregulatory haemostasis was maintained throughout exercise by replacing fluid losses with fluid ingestion (data not shown).

Figure 4. Effects of heat stress (A) on leg haemodynamics during maximal cycling compared to control (B) conditions

Time to fatigue while cycling at 356 ± 14 W was diminished in heat stress compared to control (5.5 ± 0.2 versus 7.6 ± 0.2 min, respectively). Note that fatigue in both conditions was preceded by reductions in leg blood flow, O₂ delivery and . Heat stress also reduced from 4.7 ± 0.2 to 4.3 ± 0.2 l min⁻¹ despite equal maximal heart rates. Redrawn from González-Alonso & Calbet (2003).

Figure 5. Effects of heat stress (A) on systemic haemodynamics and cerebral circulation during maximal exercise compared to control (B) conditions

Time to fatigue while cycling at 360 ± 10 W was diminished in heat stress compared to control (5.8 ± 0.2 versus 7.5 ± 0.4 min, respectively). Note that fatigue in both conditions was preceded by reductions in cardiac output, stroke volume, arterial blood pressure and middle cerebral arterial blood velocity. Redrawn from González-Alonso et al. (2004).