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CYCLING PERFORMANCE TIPS

  Last updated: 11/05/20`5

EXERCISE PHYSIOLOGY
THE CARDIOVASCULAR SYSTEM & CONDITIONING

Delivering Oxygen to the Muscle cells



Regular exercise (walking, running, cycling, etc.) stimulates changes in the cardiovascular system, lungs, and muscle cells which improve work capacity - for both endurance and sprint activities. Added health benefits include a decrease in resting heart rate and a lowering of maximal blood pressure with submaximal exercise. These changes can be measured with an exercise program that elicits 60% of your maximum heart rate for 30 minutes, 4 times a week. Understanding the physiology behind this training effect will help you in developing your own training program.

The cardiovascular (heart and blood vessels) and pulmonary (lungs) systems work together to deliver the oxygen necessary for efficient (aerobic) energy metabolism to the exercising muscle. Oxygen is extracted from air in the lungs and then transported in the blood to the cells where it is extracted and utilized. The byproduct of energy production, carbon dioxide, is then transported back to the lungs by the circulating blood and leaves the body in expired air.

CARDIAC OUTPUT

The major reason for an increase in exercise capacity with an aerobic training program is the rise in the maximal cardiac output (amount of blood pumped by the heart per minute). It plays a bigger role in increasing maximal exercise performance than does the increase in oxygen uptake and utilization by the skeletal muscle cells. Since our maximal heart rate does not change, and may even be lower, following exercise training, this increase in cardiac output is the result of a higher stroke volume (amount of blood pumped per heart beat). Cardiac output = stroke volume x heart rate.

The increase in stroke volume is a result of both a hypertrophy (enlargement) of the left ventricle muscle (athlete's heart) as well as an enhancement of the heart's contractile state, probably mediated by the autonomic nervous system.

THE LUNGS

The lungs job is to exchange (extract) oxygen from air drawn into the microscopic air sacs (alveoli) for carbon dioxide, a waste product of metabolism. Normally a half liter of air is drawn into the lungs with each breath (which for the average cyclist is about 3.4 to 4 liters per minute - respiratory rate x air exchanged per breath). A competitive cyclist can exchange an additional 2 liters (6 liters per minute) while the legend Miguel Indurain was reported to have a respiratory capacity of 8 liters per minute. Although our respiratory capacity is relatively fixed (as a result of inherited factors such as body habitus and the size of our thoracic cavity), you can, with practice, increase your lung capacity to some degree.

OXYGEN CONSUMPTION (VO2)

VO2 is the amount (expressed as a volume or V) of oxygen used by the muscles during a specified interval (usually 1 minute) for cell metabolism and energy production. Maximum oxygen consumption (VO2max) is the maximum volume of oxygen that can be used per minute, representing any individual's upper limit of aerobic (or oxygen dependent) metabolism. It can be expressed as an absolute amount (again as a volume per minute) or as a % of each individual's personal maximum (%VO2max).

VO2max. depends on:

Each of these factors improves with aerobic training and results in an increase in VO2max.

The arterio-venous (A-V) O2 difference results from oxygen being delivered and extracted form the blood being delivered to an organ (usually muscle), the arterial concentration, and the blood leaving, the venous concentration. Oxygen extraction) and thus the A-V O2 difference, increases with exertion (almost doubling at maximal exercise versus at rest) as well as with training (increasing for any set level of exertion).

At levels of exertion greater than the VO2 max., the energy needs of the cells outstrip the ability of the cardiovascular system to deliver the oxygen required for aerobic metabolism, and oxygen independent or anaerobic energy production begins. Anaerobic metabolism is not only less efficient (less ATP is formed per gram of muscle glycogen metabolized) resulting in more rapid depletion of muscle glycogen stores, but also results in a build up of lactic acid and other metabolites which impair muscle cell performance (even when adequate glycogen stores remain). The build up of excess lactic acid will be ultimately be eliminated when exercise levels decrease to an aerobic level and adequate oxygen is again available to the muscle cell. The build up of these metabolites (and amount of oxygen which will ultimately be needed to eliminate it) during anaerobic metabolism is responsible for oxygen debt (the period of time required to remove them) and recovery phase that follows anaerobic exercise. The lactic acid produced in the cell during energy production appears to be serve a protective function to prevent the development of excessive acidity, while other acidic compounds are actually responsible for the discomfort and the impairment of muscle cell function.

MEASURES OF CARDIOVASCULAR FITNESS

VO2 max. or maximum oxygen uptake, is considered the gold standard of cardiovascular, pulmonary, and muscle cell fitness. It is usually standardized per body weight and expressed in milliliters of oxygen per kilogram of body weight per minute, and is the maximum amount of oxygen your body (basically your muscles) can utilize. The VO2 max for an elite cyclist can range from 70 to more than 80 ml/kg/minute. It is generally measured on a treadmill or bicycle ergometer at a sports medicine clinic with the appropriate equipment. Exertion at or beyond 100% VO2max can be sustained for a few minutes at most. With training, you will increase your VO2max. as well as the ability to ride for longer periods at any % of your VO2max.

The following all indicate that an individual's VO2max has been reached:

For those of you interested in the mathematical expression of VO2max, it is the product of the arterio-venous oxygen difference (the oxygen content of blood leaving the heart minus that returning to the heart and thus the amount being extracted by the working skeletal muscles) and the maximal cardiac output (the maximal heart rate times the volume of blood pumped per beat). This is called the Fick equation.

Anaerobic Threshold (AT)- also known as lactate threshold (LT), aerobic threshold, onset of blood lactate accumulation (OBLA)

Your body requires adenosine triphosphate or ATP for energy for all cellular activity. This ATP can be produced via 2 different metabolic pathways. The first, the aerobic system, is very efficient and uses oxygen in the ATP production. The other pathway produces ATP less efficiently, is oxygen INdependent, and is called the anaerobic system. Lactic acid is a byproduct of the anaerobic pathway.

Both systems are working at all times, however at low levels of activity almost all the ATP required by the cells is produced via the aerobic system and only a small amount of ATP being produced by the anaerobic system. The small amount of lactic acid being produced as a byproduct is quickly metabolized by the body.

The amount of lactic acid in the blood is the result of the balance between production and removal (by the heart, liver, kidneys, and non working muscles). Although being produced at only a low rate, lactic acid can be measured in the blood even when you are at rest. As you increase your activity, the percentage (and total amount) of ATP energy produced by the anaerobic system increases as does the production of lactic acid. At a certain level of activity the amount of lactic acid produced becomes greater can be removed by the body's metabolism and the blood concentration begins to rise. This level of activity is known as the anaerobic or lactate threshold (AT or LT). The more one's level of exercise exceeds their lactate threshold, the greater the lactic acid buildup (concentration in the blood) , and the greater its negative impact on physical performance. The lactic acid itself does not directly create the slight drop in the blood's pH (from 7.4 to about 7.2) that can be measured and is thought to be the cause of fatigue, labored breathing, and reduced power of muscle contractions experienced at higher intensities of exercise. It is thought that the associated proton (H+) accumulation, coinciding with, but not caused by lactate production, leads to the acidosis which forces the athlete to back off.

LT is typically expressed as a percentage of maximum heart rate (which in turn is thought to reflect VO2max). Although LT occurs at 50 to 60% of MHR in untrained individuals, it rises with training and is between 80 to 85% MHR in trained athletes. The majority of the improvement is felt to be from an improved processing (or removal) of lactic acid although there is almost certainly some decrease in production for a set level of activity as well (see article at the end of this section).

Why is the lactate threshold important? Having a higher lactate threshold means an athlete can perform at a higher intensity for a longer time. The higher the threshold, the faster an athlete can bike (or run) before they reach their exercise limit and are forced to slow down from the lactic acid/acidosis build up. Generally, in two people with the same VO2 max, the one with a higher LT will ride faster in continuous-type endurance events.

The margin by which lactate threshold is exceeded is inversely proportional to the time the athlete is able to sustain that pace. For example, let's say you have a LT of 170 beats per minute. You can sprint with a HR of 180 for a short time, or 185 for even a shorter time, before you become uncomfortable and are forced to slow down. On the other hand you could exercise at your LT of 170 BPM for hour(s). Thus LT defines the pace you can maintain for an endurance event. This suggests an easy way to determine your LT - the average heart rate you can maintain over a 30 minute (about 10 mile) time trial will be a good approximation of your LT.

For a trained athlete, the LT roughly corresponds to Zone 4 (of the 5 heart rate training zones) which is defined as 84-90% of Maximal Heart Rate. This level of cardiovascular activity produces enough lactic acid from anaerobic activity to stimulate improvement in CV and LT status, but not enough to limit the amount of time you can maintain this heart rate. The result is the most efficient heart rate to stimulate maximal improvement in aerobic performance.

Riders with a higher LT are also more efficient in their use of internal glycogen stores. At all levels of activity there are always muscle cells (not entire muscles, but a small number of cells within those muscles) that are relatively deficient in oxygen and thus making ATP inefficiently via anaerobic pathways, producing lactic acid as a result. As the LT is approached, more and more of these inefficient cells are being utilized to power your muscles. Those with an higher LT not only experience less physical deterioration in muscle cell performance for any level of %MHR, but also use less glycogen for ATP production at any level of performance. Thus an improvement in LT will allow the individual to perform at higher intensities for a longer period of time before running out of adequate energy (glycogen) stores.

An individual's LT will improve with training, and cyclists with a higher LT can work at a higher level of energy expenditure for longer periods, defeating opponents of equal (or even greater) physical strength but with lower LTs. That is why interval training, which improves LT, improves endurance performance.

Some of the many factors that affect the rate of lactate accumulation (and thus the intensity of activity at which the LT is reached) include:

For those interested in more detail, I'd recommend the following paper.

A few questions from readers:

  • How do I race based on my LT? This will depend on the duration of the event. For shorter, spring type activities which last minutes at most, you do not generally worry about your LT and lactate levels will often be quite high at the finish. In events of longer duration (30 minutes to 1 hour) you will want to aim for a rate at or just slightly above your LT.
  • Does LT change based on the type of exercise? Yes, the lactate threshold is specific to the exercise task. So if a cyclist moves to rowing, (s)he will fatigue at a lower heart rate initially as rowing employs different muscles, generally less trained. Since these muscles are less trained, the cyclist's rowing LT will be considerably lower. Thus heart rate cannot be used as a guide in "cross training activities". athlete.
  • Can I improve my LT? Yes, training results in a decrease in lactate production for any given exercise intensity. Thus untrained individuals usually reach their LT at about 60% of VO2 max. With training, LT can increase from 60% to above 70% or even higher. And elite athletes have LTs at or above 80% of VO2 max.
  • Concini Test Another method of measuring your AT (and LT) is the Concini test. As a cyclist's efforts increase, their heart rate generally increases in a direct relationship to the energy expended (a linear relationship). But at some point the heart rate begins to level off even as the speed (and energy expenditure) continues to increase. This is the anaerobic threshold, that point at which oxygen cannot reach the muscles fast enough, lactate accumulates, and performance suffers. After an appropriate warm up, using a single gear and a relatively high speed, the rider gradually increases his or her speed by 1 km per hour every 300 meters or so. Heart rate is graphed versus speed, and the break point on the graph is the AT.

    Resting heart rate, your heart rate on awakening in the morning, is a simple but effective indicator of your level of training. It will fall as you train, but then begin to rise again with overtraining.

    Cardiac Stress Testing for asymptomatic coronary artery disease.

    THE SKELETAL MUSCLES

    There are two types of fibers: type I, or slow twitch, and type II or fast twitch. The slow twitch fibers are more energy efficient and use both fats and carbohydrates as an energy source. They are the major muscle fiber in use at 70-80% VO2 max. Fast twitch fibers on the other hand are less efficient, use mainly glycogen as fuel, and are called into action for sprints as the athlete approaches 100% of maximum performance. Although the ratio of slow to fast twitch fibers is generally controlled by genetic (inherited) factors, this ratio does change (often over years) with an ongoing training program.

    Along with these visible changes in the muscle cells, there are microscopic and metabolic changes at the muscle cell level with training. These include an increase in the size and number of the muscle cell mitochondria, an increase in the activity of various metabolic enzymes in the muscle cells, and an increase in the number of capillaries in the muscle that supply blood to the individual muscle cells. The net result is an increase in the amount of oxygen extracted from the blood in a single pass through the muscle (the arterial - venous oxygen difference).

    SUBMAXIMAL EXERCISE

    Endurance training (usually defined as training at less than 60 - 70% VO2max) improves the overall efficiency of the cardiovascular system as reflected in a smaller increase in heart rate for any given exercise intensity, and is also thought to promote a shift towards the use of fat as an energy source (more efficient with 9 Cal per gram versus 4 Cal per gram with carbohydrates). This is supported by the observation of a smaller increase in the plasma free fatty acid levels (indicating enhanced fat oxidation) at these activity levels.

    CHANGES IN EXERCISE PHYSIOLOGY WITH AGE

    Aging results in a progressive decline in the functional capacity of various body systems, and is reflected in a 9 to 10% decrease in maximal aerobic exercise capacity in sedentary individuals. It is well documented, however, that endurance training can attenuate this age related decline to about 5% per decade, and can also improve exercise performance in older men and women. And if you are more than 40, it may be time to consider cardiac stress testing for asymptomatic coronary artery disease.


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