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Fitness Science Vol 2--Cardiovascular and Musculoskeletal Adaptations to Exercise Training

The first diary in this series discussed the body's stress response reflex, and how that stimulus initiated physical changes leading to improved fitness. In this diary, changes to the cardiovascular and musculosketal systems in response to exercise training will be described in greater detail. The goals are to provide more information for those who are interested and give some practical tips on applying this information to your workout routine.

To summarize, physical adaptations to exercise can be grouped into two categories: central and peripheral. As a rule, central changes are short-term and peripheral changes are long-term.

Cardiovascular System
The role of the cardiovascular system is to deliver energy to living tissues. It includes the heart, the lungs, the vascular system, the enzymes and cellular structures necessary for metabolism, and the central nervous system. The system is set up to extract oxygen from ambient air and deliver that oxygen to specific muscle cells to generate adenosine triphosphate (ATP) aerobically.

The circulatory system is a 2-loop system: the right side of the heart pumps blood to the lungs where it is oxygenated and returns to the left side of the heart. The left side of the heart then pumps blood to the rest of the body.

The amount of blood that the left ventricle can pump with each heart rate is called stroke volume. The volume of blood pumped each minute is called cardiac output, which is stroke volume x number of heartbeats. The average cardiac output for a person at rest is 5 liters/minute. Resting cardiac output is the same for trained and untrained individuals--the difference is that trained individuals have a larger stroke volume, therefore resting heart rate is less.

In the capillaries, oxygen is extracted from arterial blood and used to produce energy. The amount of oxygen extracted is referred to as the a-v O2 Difference. As the cells become metabolically more active during aerobic exercise, oxygen consumption increases dramatically.

Oxygen consumption is the way that we measure the intensity of aerobic exercise. The term for oxygen consumption is VO2. Because of differences in body size, aerobic intensity is measured in milliliters of oxygen per kilogram of body weight per minute, or ml/kg/min.

VO2 is determined by two factors: a-v O2 difference and cardiac output. Since a-v O2 difference becomes maxed out at submaximal effort, aerobic capacity is ultimately determined by cardiac output.

From a resting value of 5 liters/min, cardiac output increases during maximum exercise to 20-22 l/min for untrained individuals to 40 l/min for elite athletes. Given that we only have 5 liters of blood supply, that means that during exercise we must circulate our entire blood supply 4-10 times per minute. The demands of exercise not only dramatically increase the need for cardiac output, but also the need to deliver blood to the working muscles. We have a tremendous vascular capacity, much greater than our blood supply. Therefore, the ability to divert blood flow from less-essential areas like the liver and kidneys to working muscles is an important training adaptation. At rest, blood flow to the kidneys and liver represents almost 50% of cardiac output (2.45 l/min), with 20% going to the muscles. During moderate exercise, flow to the liver/kidneys decreases both in relative and actual amounts (3% of total, 1.2 l/min), while blood flow to muscles increases to 71% of total output or 12.5 l/min.

Here is a list of cardiovascular adaptations to exercise:

Central/Short term
Increased stroke volume
Increased plasma volume
Increased maximum ventilation
Increased amount of O2 extracted from inspired air
Improved blood shunting
Improved recruitment of muscle fibers (mechanical efficiency)

Peripheral/Long Term
Increase in a-v O2 difference
Increase in enzymes and cellular structures (e.g. mitochondria) needed for ATP production
Increased capillary density in working muscles
Increased ability to clear lactic acid
Increased stroke volume

Stroke volume is listed twice because there is an initial increase due to the increase in plasma volume and there can also be long-term moderate thickening of the left ventricular wall in response to high-volume aerobic training.

Improvements in lung function with exercise are modest, primarily because a healthy person has a substantial lung capacity to begin with. In the absence of pulmonary disease, lung function is not a limiting factor in exercise performance. Even at maximal effort, we do not utilize our entire lung capacity. Maximum aerobic effort is determined by maximum cardiac output.

The central nervous system (CNS) plays in important role in exercise training. As mentioned earlier, the CNS determines the shunting of blood flow to the working muscles. The CNS is also involved in mechanical efficiency, i.e. the recruitment of muscles to perform a given activity like walking or running.

Some central adaptations/improvements can start to take place in 2-4 workout sessions, but are generally considered to begin to occur in 2-6 weeks. Peripheral adaptations can take 6-12 months.

Musculoskeletal system
In terms of fitness training, the musculoskeletal system is designed to generate force and apply that force through the levers of the limbs. This involves the muscles themselves, connective tissues such as tendons and ligaments, multiple hormones, enzymes and proteins, and, again, the central nervous system.

Muscle cells (often called muscle fibers) are long, cylindrical cells about the diameter of a human hair, and often running the length of the muscle itself. Muscle fibers are grouped into larger bundles surrounded by connective tissue. The connective tissue ultimately forms a muscle sheath which is continuous with the tendons that attach the muscle to the bone.

Motor neurons (nerve cells) innervate muscle cells. A muscle fiber is attached to only one motor neuron, but one motor neuron controls many muscle fibers.

The interior of the muscle fiber consists of hundreds of thousands of myofibrils. Myofibrils contain the apparatus that contracts the muscle cell, a series of filaments that slide inward when activated, causing the muscle to contract.

The maximum force capacity of a muscle is believed to be related to the cross sectional area of the muscle--the larger the cross-sectional area, the more potential for applying force. The amount of "strength" generated by a muscle group is also affected by the intensity of stimulation, number of muscle fibers recruited, and the frequency and coordination of muscle fiber stimulations.

Skeletal muscle fibers are commonly grouped into 2 classes based on morphological and specific physiological characteristics--slow twitch (Type I) and fast-twitch (Type II). Fast-twitch fibers are subdivided into Type IIA and Type IIB. Type I fibers develop force slowly and have a longer twitch time; they also have more oxidative capacity. Type II fibers develop force more rapidly with a faster twitch time. The distinction of IIA and IIB is based on a relative difference in oxidative capacity--IIA can increase oxidative capability in response to training (although not to the extent of a Type I fiber) whereas IIB fibers are more "anaerobic" and do not change with endurance training.

The number and type of muscle fibers is genetically deterimined. Strength training does not increase the number of muscle fibers and endurance training results in only modest adaptations in Type IIB fibers. Elite sprinters have a genetically high percentage of Type IIB fibers; elite marathoners a high percentage of Type I. The rest of us are decidedly average ;-)

Here are the musculoskeletal adpatations to exercise:

Central/short term
Increased recruitment of muscle fibers
Inreased mechanical efficiency
Amount of sythesis and storage of hormones

Peripheral/long term
Increased muscle size (hypertrophy)
Increased volume of proteins and cellular structures involved in muscle contraction
Increased strength of connective tissue
Cellular adaptations to more effectively utilize hormones

When starting a strength-training program, virtually all of the initial increases in strength are due to neuromuscular facilitation. The body learns to recruit muscle fibers more efficiently, in greater numbers, and with improved coordination. The average person has a large unused muscle capacity, so there is a tremendous ability to "use what you have" before you ever need to "make more". Often, muscle hypertrophy does not occur until strength levels have increased at least 100% (not that difficult for an untrained person to achieve).

The amount of hypertrophy one can achieve is dependent on genetic factors (muscle fiber amount and type) and volume of training. Just lifting heavier weights will not make you look like Ahnauld in his younger days--you need to do a substantial volume of work as well (and, like most elite athletes, champion body builders are born with particular body types, so chances are, even if you train like Arnold, you still won't look like Arnold.)

Hypertrophy is also dependent on hormones. Women do not have the same levels of testosterone as men, so they will not get as large. Women should not shy away from heavier weights out of a fear of "looking like a bodybuilder".

Again, short-term adaptations can take place in 2-6 weeks. Long-term depends more on type and volume of training, but, while you can see improved tone and definition in 6-weeks, substantial increases in size will probably take 3-9 months.

Practical ConsiderationsFirst of all, this is more proof that exercise benefits can be realized in a relatively short period of time. Someone who is not currently exercising should not think it takes weeks and months or a superhuman effort to see improvement. It doesn't.

It also means that those who want to train seriously should realize that, after the initial improvement, further gains will come more slowly--but they will continue for an extended time.

For those with busy schedules, it is important to understand that improvements are lost in roughly the same amount of time they were gained. And, it is easier to maintain than it is to gain. So, if you are faced with a busy stretch of work or family issues, 1 or 2 quality workout sessions per week can be enough to help you maintain, and with a short layoff, you can quickly get back to form.

This holds true for illness and injury, but with one difference. After a longer layoff, you can get back into things relatively quickly, but you probably will have lost some long-term improvements.

The other caveat about returning from extended injury or illness is that your "central" abilities will improve faster than your musculoskeletal system can handle. In other words, your perceived fitness level will return faster than your tendons' and ligaments' ability to handle the physical strain of movements. So don't ramp up the volume too quickly.

Core Training
In the strength training part of the diary, I dealt with the adaptations that occur with weight lifting. I did not address core training. Core training involves primarily muscle fiber recruitment and coordination, as opposed to muscle hypertrophy. I will address core training more in the diary on "Specificity of Training".

Other Issues
There are two other issues I want to address that don't fit the topic as closely, but I couldn't figure out where else to put them, and they are topics that are frequently misunderstood.

Heart Rate Training
Monitoring heart rate can be an important tool for making sure you are exercising efficiently and a motivator as well. However, heart rate response to exercise tends to be oversimplified and it is important to know some things to get the most out of this method.

First of all, heart rate is only an indirect measuring tool. As stated earlier, the intensity of aerobic exercise is based on cardiac output and oxygen consumption. It is not practical to measure oxygen consumption. However, in most cases there is a linear relationship between heart rate and VO2, and measuring heart rate is VERY practical and convenient, so we can use heart rate to gauge aerobic intensity. However, I must repeat that increased heart rate per se does not always mean aerobic activity is taking place.

During aerobic exercise, heart rate increases as a part of increased cardiac output. During strength training, heart rate can increase, but it is due to pressure changes in the intrathoracic cavity, NOT because of increased cardiac output. Therefore, just because heart rate increases during strength training, that does not mean you can perform strength training and aerobic training simultaneously.

The biggest challenge in using heart rate monitoring to measure aerobic intensity is the variation of maximum heart rates and heart rate response to exercise in the general population. All heart rate guidelines use a percentage of maximal heart rate (HRmax) as the measurement of intensity. Measuring HRmax directly requires you to take a maximal exercise test--a REAL maximal exercise test, not a doctor's stress test. That can be risky, expensive, and is definitely not a pleasurable experience. Most people use a formula to estimate HRmax. The problem is that, within the normal population distribution, the SEE for all HRmax calculations is 10-12 beats per minute. That means that fully 1/3 or the population has a true HRmax that is 10-30 beats/min above or below the calculated HRmax. That's a significant variation. (And that does not include medication effects).

In my experience I have had numerous clients become confused and distressed when they first put on their heart rate monitors and saw a response substantially different that what the "guidelines" predicted. In extreme cases, I was contacted by younger runners who had actually stopped running because they were afraid they were damaging their hearts.

Another factor affects HR response to exercise and that is cardiovascular drift. That simply refers to the fact that heart rate tends to drift upward during the length of an exercise session, even when intensity is kept constant. The likely reasons are increased body core temperature and loss of plasma volume through perspiration. I have noticed a 20 beat/min increase over the course of a 30-40 min run on a treadmill, with no change in speed. If you are doing a programmed workout based on a target heart rate goal, the exercise machine will actually start to decrease your intensity when this occurs, thus lowering the quality of the workout.

The thing to do with a new heart rate monitor is to put it on and be a passive observer for the first few sessions. Do your usual routine and see what happens. Compare your heart rate response to your rate of perceived exertion--if it feels easy, it probably is, regardless of  the heart rate. Once you have determined your individual response, you can then use the HR monitor to guide your workouts. But keep it simple. I have seen programs that get very detailed about different heart rate "zones"--I think those plans are devised mainly to make it seem more complicated so that you will "need" the paid expertise of the author/presenter.There are three basic "training zones": easy, medium, and hard. It doesn't have to be any more complicated than that. 

Also keep in mind that exercise heart rate can be affected by illness or stress. Always compare your heart rate to you overall feelings of exertion and guide your efforts accordingly.

Lactic Acid
This is just a personal thing with me. Lactic acid is often described as a "waste product" that "builds up in the muscles" and is responsible for muscle soreness. None of these are true.

Lactic acid is formed during exercise metabolism and increased levels of lactic acid contribute to fatigue. But lactic acid is not a "waste product"--it is a dynamic substrate that can traverse a number of different metabolic pathways. It can be used directly as fuel by cardiac muscle tissue, it can be used as an oxidizeable substrate for aerobic metabolism or it can be incorporated into amino acids and proteins.

Actually both trained athletes and untrained individuals produce the same amounts of lactic acid at any given relative intensity. The difference is that trained athletes can clear lactic acid more efficiently.

And lactic acid has nothing to do with delayed onset muscle soreness (DOMS). DOMS is most likely caused by microtrauma-related edema and is especially related to eccentric muscle contractions.


2 votes + -


Celestia wrote 66 months ago:
Thanks for writing this Azdak! This is chock full of really useful information that I will be referring back to frequently. Thanks!
Anonymous wrote 15 months ago:
a lot of bad information given, central and peripheral changes are wrong. The differences between these two body adaptations are that central changes are related to the heart, lung, blood and liver when the peripheral changes are related to muscular change/adaptation not short and long term changes.
Anonymous wrote 13 months ago:
fanks azdak! di was v helpfl and mde me get a distinction on ma btec sport THANKS :) xoxox
Anonymous wrote 13 months ago:
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Anonymous wrote 2 months ago:

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