If you put motor oil in your car which is too viscous, the only things you may notice is reduced torque and horsepower and decreased gas mileage. Fuel efficiency may decrease by only 1%, but that adds up over the life of the vehicle. The decreased fuel efficiency seen with higher viscosity motor oil is due to the extra energy necessary to pump a thicker fluid through the engine. In very cold weather, oil which is too viscous could prevent your car from even starting, a mechanical equivalent of cardiac arrest.
If your blood viscosity is too high, you also may not notice anything. Although you may not be aware of it, increased blood viscosity decreases tissue perfusion. Decreased delivery of oxygen and glucose to skeletal muscle will decrease the muscle’s power output, decreasing athletic performance. Chronically decreased glucose delivery and utilization by skeletal muscle may be one of the basic defects in the metabolic syndrome, resulting in hyperglycemia.
Decreased oxygen delivery to the heart muscle leads to chest pain or angina pectoris. With increased blood viscosity, the heart works harder to pump the thicker blood, which increases the oxygen and energy requirements of the heart. At the same time, the thicker blood decreases perfusion of the heart, decreasing oxygen delivery, leading to ischemia and chest pain. Indeed, therapeutic phlebotomy, which reduces blood viscosity, was used to treat angina pectoris at the renowned Charity Hospital in New Orleans as late as the 1960’s.1
High-viscosity oil increases engine wear, which occurs mostly at start-up. For this reason, engine oils with viscosity ratings as low as 0W-30 are used in automotive racing to prevent engine wear. Similarly, increased blood viscosity increases wear and tear on our arteries. In a recent paper, my colleagues and I pointed out
that increased blood viscosity increases tension on arterial walls by directly increasing blood pressure. This increased tension accelerates the fatigue and ultimate failure of the elastic elements in the arterial wall.2
Each pulse reversibly deforms the elastic elements in an artery. Like any material, cyclical deformation eventually results in mechanical fatigue and failure of elastic elements, causing progressive arterial stiffening. In a forthcoming paper, my colleagues and I argue that failure of the elastic elements in the aorta limits lifespan. In general, mammals have an allotment of 1 x 109 heartbeats in a lifespan. We believe this is because failure of the elastic elements in an artery and arterial stiffening lead to thrombosis and atherosclerosis, the leading causes of death worldwide. Those who over exercise use up their allotment of heartbeats prematurely, resulting in premature cardiovascular mortality.3
Is there a human equivalent to elevated oil viscosity preventing an automobile engine from starting? The closest example would be the sudden cardiac death of dozens of elite cyclists who doped using erythropoiesis stimulating agents. In the 1980’and 1990’s, it is estimated that perhaps as many as 80 cyclists died, “their doped-up blood coagulated to stone.”4 It is quite possible that increased blood viscosity, perhaps worsened by dehydration during competition, could decrease myocardial perfusion, oxygen delivery, leading to arrhythmia and death.