Adaptations to aerobic training – part I

Improvements in endurance that accompany regular(daily, every other day, etc.) aerobic training, such as running, cycling, or swimming, result from multiple adaptations to the training stimulus. Some adaptations occur within the muscles themselves, promoting more efficient transport and utilization of oxygen and fuel substrates. Still other important changes occur in the cardiovascular system, improving circulation to and within the muscles. Pulmonary adaptations occur to a lesser extent.

Aerobic training, or cardiorespiratory endurance training, improves central and peripheral blood flow and enhances the capacity of the muscle fibers to generate greater amounts of adenosine triphosphate(ATP).

Endurance: Muscular versus cardiorespiratory

Endurance is a term that refers to two separate but related concepts: muscular endurance and cardiorespiratory endurance. Each makes a unique contribution to athletic performance, and each differs in its importance to different athletes.

For sprinters, endurance is the quality that allows them to sustain a high speed over the full distance of, for example, a 100 or 200m race. This component of fitness is termed muscular endurance, the ability of a single muscle or muscle group to sustain high-intensity, repetitive, or static exercise. This type of endurance is also exemplified by the weightlifter doing multiple repetitions, the boxer, and the wrestler. The exercise or activity can be rhythmic and repetitive in nature, such as multiple repetitions of the bench press for the weightlifter and jabbing for the boxer. Or the activity can be more static, such as a sustained muscle action when a wrestler attempts to pin an opponent to the mat. In either case, the resulting fatique is confined to a specific muscle group, and the activity duration is usually no more than 1 to 2 min. Muscular endurance is highly related to muscular strength and to anaerobic power development.

While muscular endurance is specific to individual muscles or muscle groups, cardiorespiratory endurance relates to the entire body’s ability to sustain prolonged, dynamic exercise using large muscle groups. This type of endurance is used by the cyclist, distance runner, or endurance swimmer who completes long distances at a fairly fast pace. Cardiorespiratory endurance is related to the development of the cardiovascular and respiratory systems’ ability to maintain oxygen delivery to working muscles during prolonged bouts of exercise, as well as the muscles’ ability to utilize energy aerobically. This is why the terms cardiorespiratory endurance and aerobic endurance are sometimes used synonymously.

Evaluating cardiorespiratory endurance capacity

To study training effects on endurance, there needs to be an objective, repeatable means of measuring an individual’s cardiorespiratory endurance capacity. In that way, the exercise scientist, coach, or athlete can monitor improvements as physiological adaptations occur during the training program.

Maximal endurance capacity: VO₂max or aerobic power

Most exercise scientists regard VO₂max, sometimes called maximal aerobic power or maximal aerobic capacity, as the best objective laboratory measure of maximal cardiorespiratory endurance. VO₂max is defined as the highest rate of oxygen consumption attainable during maximal or exhaustive exercise. VO₂max is defined as the highest rate of oxygen consumption attainable during maximal or exhaustive exercise. VO₂max as defined by the Fick equation is dictated by maximal cardiac output(delivery of oxygen and blood flow to working muscles) and the maximal(a-ṽ)O₂ difference(the ability of the active muscles to extract and use the oxygen). As exercise intensity increases, oxygen consumption eventually either plateaus or decreases slightly, even with further increases in workload, indicating that a truly maximal VO₂ has been achieved.

With endurance training, more oxygen can be delivered to, and consumed by, active muscles than in an untrained state. Previously untrained subjects demonstrate average increases in VO₂max of 15% to 20% after a 20-week training program. These improvements allow individuals to perform endurance activities at a higher intensity, improving their performance potential. Figure below illustrates the increase of VO₂max after 12 months of aerobic training in a previously untrained individual. In this example, VO₂max increased by about 30%. Note that the VO₂ “cost” of running at a certain submaximal intensity did not change but that higher running speeds could be attained after training.

Submaximal endurance capacity

In addition to increasing maximal endurance capacity, endurance training increases submaximal endurance capacity, which is much more difficult to evaluate. Steady-state submaximal heart rate at the same exercise intensity measured before and after training is one physiological variable that can be used to objectively quantify the effect of training. Additionally, exercise scientists have used performance measures to quantify submaximal endurance capacity. For example, one test used to determine submaximal endurance capacity is the average peak absolute power output a person can maintain over a fixed period of time on a cycle ergometer. For running, the average peak speed of velocity a person can maintain during a fixed period of time would be similar type of test. Generally, these tests will last 30 min to an hour.

Submaximal endurance capacity is more closely related to actual competitive endurance performance than VO₂max, and is likely determined by both the person’s VO₂max and the threshold for his or her onset of blood lactic acid accumulation(OBLA) – that point at which lactate begins to appear at a disproportionate rate in the blood. With endurance training, submaximal endurance capacity increases.

Cardiovascular adaptations to training

Numerous cardiovascular adaptations occur in response to exercise training, including changes in the following cardiovascular variables:

• Heart size
• Stroke volume
• Heart rate
• Cardiac output
• Blood flow
• Blood pressure
• Blood volume.

To understand completely, it is very important to review how these components relate to oxygen transport.

Oxygen transport system

Cardiorespiratory endurance is related to the cardiovascular and respiratory systems’  ability to deliver sufficient oxygen to meet the needs of metabolically active tissues.

The ability of the cardiovascular and respiratory systems to deliver oxygen to active tissues is defined by Fick equation. The Fick equation states that systemic oxygen consumption is determined by both the delivery of oxygen(cardiac output) via blood flow and the amount of oxygen extracted by the tissues, the (a-ṽ)O₂ difference. The product of cardiac output and the (a-ṽ)O₂ difference determines the rate of which oxygen is being consumed:

VO₂ = stroke volume x heart rate x (a-ṽ)O₂ diff.

The oxygen demand of exercising muscles increases with increasing exercise intensity. Aerobic endurance depends on the cardiorespiratory system’s ability to deliver sufficient oxygen to these active tissues to meet their heightened demands for oxygen for oxidative metabolism. As maximal levels of exercise are achieved, heart size, blood flow, blood pressure, and blood volume can all potentially limit the maximal ability to transport oxygen. Endurance training elicits numerous changes in these components of the oxygen transport system that enable it to function more effectively.

Heart size

As an adaptation to the increased work demand, heart mass and volume increase with training. Cardiac muscle, like skeletal muscle, undergoes morphological adaptations as a result of chronic endurance training. At one time, cardiac hypertrophy induced by exercise – “athlete’s heart”, as it was called – caused some concern because experts incorrectly believed that enlargement of the heart always reflected a pathological state, as sometimes occurs with severe hypertension. Training-induced cardiac hypertrophy is now recognized as a normal adaptation to chronic endurance training.

The left ventricle, does the most work and thus undergoes the greatest adaptation in response to endurance training. The extent and location of heart size adaptations depend on the type of exercise training performed. For example, during resistance training, the left ventricle must contract against increased afterload from the systemic circulation. It was postulated to overcome this high afterload, the heart muscle compensated by increasing left ventricular wall thickness, thereby increasing its contractility. Blood pressure during resistance training can exceed 480/350 mmHg. This presents a considerable resistance that must be overcome by the left ventricle. Thus, the increase in its muscle mass is in direct response to repeated exposure to the increased afterload with resistance training.

With endurance training, left ventricular chamber size increases. This allows for increased left ventricular filling and consequently an increase in stroke volume. The increase in left ventricular dimensions is largely attributable to a training-induced increase in plasma volume that increases left ventricular end-diastolic volume(increased preload). In concert with this, a decrease in heart rate at rest caused by increased parasympathetic tone, and during exercise at the same rate of work, allows a longer diastolic filling period. The increases in plasma volume and diastolic filling time increase left ventricular chamber size at the end of diastole.

It was originally hypothesized that this increase in left ventricular dimensions was the only change in the left ventricle caused by endurance training. Additional research has revealed that myocardial wall thickness also increases with endurance training, rather than just with resistance training. Using magnetic resonance imaging, Milliken and colleagues found that highly trained endurance athletes(competitive cross-country skiers, endurance cyclists, and long-distance runners) had greater left ventricular masses than did non-endurance-trained control subjects. Left ventricular mass was highly correlated with VO₂max or aerobic power.

Fagard conducted the most extensive review of the existing research literature in 1996, focusing on long-distance runners(135 athletes and 173 controls), cyclists(69 athletes and 65 controls), and strength athletes(178 athletes, including weight- and powerlifters, bodybuilders, wrestlers, throwers, and bobsledders, and 105 controls). For each group, the athletes were matched by age and body size with a group of sedentary control subjects. For each group of runners, cyclists, and strength athletes, the internal diameter of the left ventricle(LVID, an index of chamber size) and the total left ventricular mass(LVM) were greater in the athletes compared with their age- and sized-matched controls(figure below). Thus, data from this large cross-sectional study support the hypothesis that both left ventricular chamber size and wall thickness increase with endurance training.

Most studies of the heart size changes with training have been cross-sectional, comparing trained individuals with sedentary, untrained individuals. We can learn much from cross-sectional studies, but they do not provide us with the same information that we could get from studying a group of untrained people who train for months or years, focusing on their changes from the untrained to the trained state. Certainly a portion of the differences that we see in figure above us can be attributed to genetics, not training. However, a number of studies have followed individuals from an untrained state to a trained state to an untrained state. These studies have reported increases in heart size with training and decreases with detraining. So, training does bring about changes, but they are likely not as large as the differences we see in the figure above us.

Stroke volume

As a result of endurance training, stroke volume increases. Stroke volume at rest is substantially higher after an endurance training program than it is before training. This endurance training-induced increase is also seen at a given submaximal exercise intensity and at maximal exercise. This increase is illustrated in figure below, which shows the changes in stroke volume of a subject who exercised at increasing intensities up to maximal intensity before and after a six-month aerobic endurance training program. Typical values for stroke volume at rest and during maximal exercise in untrained, trained, and highly trained athletes are listed in the table below. The wide variation in stroke volume values for any given cell within this table is largely attributable to differences in body size. Absolute stroke volume at rest and during exercise is not merely a function of a person’s state of training but also reflects differences in body size. Larger people typically have larger hearts and a greater blood volume, and thus higher stroke volumes – an important point when one is comparing stroke volumes of different people.

Stroke volumes(SV) for different states of training
Subjects	SVrest(ml/beat)	SVmax(ml/beat)
Untrained	50-70	80-110
Trained	70-90	110-150
Highly trained	90-110	150- >220

After aerobic training, the left ventricle fills more completely during diastole than it does in an untrained state. Plasma volume expands with training, which allows for more blood to enter the ventricle during diastole, increasing end-diastolic volume(EDV). The heart rate of a trained heart is also lower at rest and at the same absolute exercise intensity than that of an untrained heart, allowing more time for the increased diastolic filling. More blood entering the ventricle increases the stretch on the ventricular walls; by the Frank-Starling mechanism, this results in an increase in force of contraction.

The thickness of the posterior and septal walls of the left ventricle also increases slightly with endurance training. Increased ventricular muscle mass results in increased contractile force, in turn causing end-systolic volume to decrease. More blood is forced out of the heart, leaving less blood in the left ventricle after systole.

The decrease in end-systolic volume is augmented by the decrease in peripheral resistance that occurs with training. Increased contractility resulting from an increase in left ventricular thickness and greater diastolic filling(Frank-Starling mechanism), coupled with the reduction in systemic peripheral resistance, increases the ejection fraction[equal to (EDV-ESV)/EDV] in the trained heart. More blood enters the left ventricle, and a greater percentage of what enters is forced out with each concentration, resulting in an increase in stroke volume.

Adaptatioins in stroke volume during endurance training are illustrated by a study in which older men endurance trained for one year. Their cardiovascular function was evaluated before and after training. The subjects performed running, treadmill, and cycle ergometer exercise for 1h each day, four days per week. They exercised at intensities of 60% to 80% pf VO₂max, with brief bouts of exercise exceeding 90% of VO₂max. End-diastolic volume increased at rest and throughout submaximal exercise. The ejection fraction increased, which was associated with a decreased end-systolic volume, suggesting increased contractility of the left ventricle. VO₂max increased by 23%, indicating a substantial improvement in endurance.

It is clear that central stroke volume adaptations occur with endurance training, but there are also peripheral adaptations that contribute to the increase in VO₂max, at least in middle-aged exercisers. This was demonstrated in a unique longitudinal study involving both exercise training and a bed rest deconditioning model. Five 20-year-old men were tested(baseline values), placed on bed rest for 20 days(deconditioning), and then trained for 60 days, starting immediately at the conclusion of bed rest. These same five men were restudied 30 years later at the age of 50; they were tested at baseline in a relatively sedentary state and after six months of endurance training. The average percentage increases in VO₂max were similar for the subjects at age 20(18%) and at age 50(14%). However, the increase in VO2max at age 20 was explained by increases in both maximal cardiac output and maximal(a-ṽ)O2 difference; at age 50, the increase was explained primarily by an increase in(a-ṽ)O2 difference, while maximal cardiac output was unchanged. Maximal stroke volume was increased after training at both age 20 and age 50 but to a lesser degree at age 50(+16ml/beat at age 20 vs. +8ml/beat at age 50).