Knowing the science will guide you in designing the best training regimen.
From the time the ancient Greek runner Pheidippides ran from Marathon to Athens to announce the Greeks’ victory over Persia in the Battle of Marathon, humans have had a compelling interest in endurance activities. Indeed, humans have repeatedly tried to push the limits of endurance.
From the 50 marathons in 50 days and the 300 miles of nonstop running by Dean Karnazes to the average speed of 25 miles per hour by Lance Armstrong during a 3-week Tour de France—and countless other athletes’ incredible accomplishments—humans’ feats of endurance have been nothing short of remarkable. While only a very few can hold world-record marathon titles, according to www.marathonguide.com more than 400,000 people completed a marathon in the U.S. in 2007. What allows us to do that?
The main cardiovascular factors that influence endurance are cardiac output and blood flow to the muscles. Cardiac output is the volume of blood pumped per minute by the heart’s left ventricle; it is the product of stroke volume and heart rate. Stroke volume is the amount of blood the heart pumps with each contraction of its left ventricle; it is determined by the return of blood back to the heart through the venous circulation (venous return), the heart’s ability to contract quickly and forcefully (contractility), the amount of pressure in the left ventricle (preload) and aorta (afterload), and the size of the left ventricle. The larger the left ventricle, the more blood it can hold; the more blood it can hold, the more blood it can pump. One of the hallmark adaptations to cardiovascular endurance training is an increase in the size of the left ventricle. A large heart is so characteristic of genetically gifted and highly trained endurance athletes that the scientific and medical communities consider it a physiological condition called “athlete’s heart” (Naylor et al. 2008).
Once the blood leaves the heart, its flow to the muscles depends on a number of things:
- the redistribution of blood away from other, less important tissues to the active muscles
- the amount of resistance in the blood vessels
- adequate dilation of blood vessels, which depends on the interplay between the sympathetic and parasympathetic nervous systems and their associated hormones
- oxygen transport capacity of the blood, which is determined by red blood cell volume and the amount of hemoglobin
- the amount of myoglobin, which transports oxygen in the muscles
- the density and volume of capillaries that perfuse the muscle fibers, determining the time available for diffusion into the muscle mitochondria as blood transits the capillary network.
Men have a greater stroke volume and cardiac output than women, meaning men send more blood and oxygen to the muscles, have more hemoglobin in their blood to transport oxygen and as a result have greater cardiovascular endurance.
Once oxygen is delivered to the muscles, they have to use the oxygen to regenerate energy (adenosine triphosphate = ATP) for muscle contraction. The amount of oxygen extracted and used by the muscles is largely dependent on the muscles’ mitochondrial and capillary volumes. The more capillaries that perfuse the muscle fibers, the shorter the diffusion distance for oxygen from the capillaries to the mitochondria, which contain the enzymes involved in aerobic metabolism. The number of mitochondrial enzymes is also an important determinant of endurance, since enzymes, through their catalyzing effect on chemical reactions, control the rate at which ATP is produced.
Together, the cardiac output and the amount of oxygen extracted and used by the muscles determine aerobic power (VO2max), the maximum volume of oxygen that your muscles can consume per minute. VO2max is considered the best single indicator of a person’s aerobic fitness. Since it was first measured in humans in the 1920s, it has become one of the most often measured physiological variables in exercise physiology. In 1930, David Dill and his colleagues were among the first physiologists to suggest that there are marked differences in the amount of oxygen different people use when running at the same speeds and that these differences in “economy” of oxygen use could be a major factor explaining differences in endurance performance (Dill, Talbot & Edwards 1930). Economy is the volume of oxygen (VO2) you use at submaximum exercise intensities.
Aerobic economy is an important indicator of endurance and is influenced by biomechanics, the proportion of slow-twitch muscle fibers, mitochondrial density and body weight. For example, if two clients have the same VO2max, yet client A uses 70% of VO2max and client B uses 80% while exercising at a specific intensity, the exercise feels easier for client A because that client is more economical. Therefore, client A can exercise at a higher intensity before feeling the same amount of fatigue as client B.
Endurance is influenced by a number of metabolic factors, including the removal of lactate and the buffering of metabolic acidosis. At low exercise intensities, lactate is removed from the muscles as quickly as it is produced. At higher intensities, there is a greater reliance on anaerobic glycolysis for the production of ATP, and aerobic metabolism (Krebs cycle and electron transport chain) can’t keep up with the production of pyruvate from glycolysis. So pyruvate is converted into lactate, and lactate removal starts lagging behind lactate production, causing lactate to accumulate. Concomitant with lactate accumulation is the accumulation of hydrogen ions in muscles and blood, causing metabolic acidosis and the development of fatigue. The lactate threshold (LT) is the highest exercise intensity above which lactate production begins to exceed its removal, with blood lactate concentration beginning to increase exponentially.
The LT demarcates the transition between exercise that is almost purely aerobic and exercise that includes significant oxygen-independent (anaerobic) metabolism. (All exercise intensities have an anaerobic contribution, although that contribution is negligible when a person is exercising below the LT.) Thus, the LT is an important determinant of endurance, since it represents the highest intensity attainable without a significant anaerobic contribution to the activity (and thus the development of metabolic acidosis). The LT indicates the highest exercise intensity that an individual can sustain for long periods of time.
The ability to metabolize fat also influences endurance, since the muscles’ preferred fuel—carbohydrate—is limited, providing enough energy for only about 100 minutes of marathon running (Newsholme 1981). By contrast, fat stores are virtually unlimited in humans; a 145-pound person with 18% body fat has enough fat to fuel about 5 days of marathon running (Newsholme 1981) or about 1,000 miles of walking (Coyle 2000). At low exercise intensities, some of carbohydrate’s metabolic responsibility for ATP regeneration is relieved by fat, in the form of free fatty acids in the blood and intramuscular triglycerides. But even with the contribution of fat oxidation helping to delay the depletion of glycogen, moderate-intensity exercise (70%–75% VO2max) can be sustained for only 2–3 hours (Coyle et al. 1986).
While women are at a definite cardiovascular disadvantage to men, they seem to have a greater capacity to metabolize fat and conserve glycogen (Tarnopolsky 1998), which may give them an advantage for very long endurance activities. Indeed, in 2002 and 2003, Pam Reed beat all the men at the 135-mile Badwater Ultramarathon.
There are a number of steps that lead to muscle contraction and force production. Briefly, in response to the central nervous system’s signal to a motor neuron, acetylcholine is released at the neuromuscular junction, causing the muscle membrane to depolarize. The ensuing action potential propagates deep into the muscle to the sarcoplasmic reticulum, from where calcium ions diffuse to the area of the contractile proteins actin and myosin. Once calcium causes the normally hidden binding sites on actin to be exposed to myosin, the two proteins combine. Finally, an ATP molecule contained inside the myosin is broken down, allowing the muscle to contract. For force production to continue, and for clients to maintain exercise intensity, the central nervous system has to increase the number of motor units recruited and increase the frequency of motor unit stimulation.
Endurance training stimulates many physiological, biochemical and molecular adaptations, including a greater storage of fuel (glycogen) in the muscles; an increase in intramuscular fat use; an increase in the number of red blood cells and hemoglobin, which improves blood vessels’ oxygen-carrying capability; a greater capillary network for a more rapid diffusion of oxygen into the muscles; and, through the complex activation of gene expression, an increase in mitochondrial density and the number of aerobic enzymes, which results in greater aerobic metabolic capacity.
High-intensity training (>90% VO2max) using long intervals (3–5 minutes) provides the greatest cardiovascular load, because clients repeatedly reach and sustain their maximum stroke volume, cardiac output and VO2max during the work periods. Long intervals are the most potent stimulus for improving VO2max (Billat 2001; Midgley, McNaughton & Jones 2007). However, short intervals (≤1 minute) can also improve VO2max, as long as the intervals are performed at a high intensity and with short, active recovery periods to keep VO2 elevated throughout the workout (see the sidebar “Methods for Improving Endurance”). While initial improvements in VO2max can come from increasing the volume of training, the need for intensity (for improved VO2max) increases as the client becomes more trained.
A large volume of endurance training may be the simplest way to increase the muscular factors associated with endurance (mitochondrial and capillary density and enzyme activity). Interval training has also been shown to increase aerobic enzyme activity (Talanian et al. 2007).
Exercising at the LT raises it to a higher intensity and percentage of VO2max, making a previously anaerobic intensity now high-aerobic. LT training can be done as a continuous workout or as intervals performed at LT intensity with short rest periods. LT intensity is about 75%–80% of heart rate maximum (HRmax). For clients who already have great endurance, LT intensity corresponds to about 85%–90% HRmax. The intensity should feel “comfortably hard.”
To increase fat use, clients should increase the volume of aerobic exercise and include a prolonged weekly workout. A large volume of endurance training enhances fat oxidation by increasing skeletal muscle mitochondrial content and respiratory capacity, allowing for the sparing of muscle glycogen (Holloszy & Coyle 1984).
In addition to increasing mitochondrial and capillary density, a large volume of endurance training may have a neuromuscular benefit. It is possible that, just as repetition of the walking movement changes a toddler’s walk from jerky to smooth, repetition of a specific muscular movement has an underrecognized neural component. Through countless repetitions, motor unit recruitment patterns, all of the steps involved in muscle contraction and perhaps even the relationship between breathing and limb movement are optimized to minimize oxygen cost and improve economy.
Power training can also target neuromuscular factors and aerobic economy. Studies have shown that both explosive strength training with heavy weights and plyometric training improve economy in endurance athletes (Hoff, Helgerud & Wisløff 2002; Jung 2003; Paavolainen et al. 1999; Spurrs, Murphy & Watsford 2003; Turner, Owings & Schwane 2003). When strength training, clients should use a very high intensity and very few repetitions to focus on neural adaptation rather than muscle hypertrophy (which would decrease economy by adding muscle mass).
Understanding the science of endurance will help fitness professionals in their work with clients. And if those clients train long enough, they’ll surely have enough endurance even to chase Pheidippides.