Consequently, a conditioning program can be defined as "adequate" if it responds to the real needs of the person for whom it is conceived.
This does not mean that the exercise done in aerobic regime is recommended more or less in all gyms, fitness and / or functional recovery centers, or physiology laboratories.
Objectively, this suggestion should be more "considered" than what one might seem to imagine.
In this article we will try to clarify the hemodynamic mechanisms related to aerobic exercise, such as key processes of the adaptive response and the consequent benefits that this type of training confers in the long term.
with regard to joint protection.
The sports or exercise prescription can be very different between a healthy or sick person, depending on the pathology found. In any case, the hemodynamic and cardiorespiratory processes are identical.
It is now known that inactivity is one of the main risk factors for the establishment of cardiovascular diseases: regular aerobic exercises are associated with a greater tolerance to fatigue and an improvement in daily living conditions, as well as an improvement in body composition. All of these changes are brought about by an improved central or cardiac response to exercise.
- for a hemodynamic conditioning to aerobic exercise are:- Heart rate;
- Shot volume;
- Cardiac output;
- Artero-venous difference in O2;
- Blood pressure and blood flow;
- Rate-Pressure;
- Wall Product Stress;
- VO2 max.
The number of cycles, in the unit of time, is called Heart Rate (HR) or Heart Rate (HR) and is expressed in beats per minute (bpm).
HR contributes to increased cardiac work during acute exercise.
Exercise carried out regularly induces a reduction in the demand for O2 to the myocardium both at rest and during exercise, and also induces a reduction in resting HR of about 10 bpm, presumably caused by a conditioning of the Autonomous Nervous System (ANS ).
However, in untrained individuals, HR plays an important role in increasing cardiac work during gradual exercise.
Additionally, maximum heart rate (HRmax) remains unchanged or drops slightly - 3 to 10 bpm - after prolonged aerobic conditioning; this last modification is probably attributable to two adaptive factors: an eccentric cardiac hypertrophy caused by the increase in the thickness of the ventricular cavity and the decrease in sympathetic activity.
neuro-hormonal).
Regular aerobic exercise causes eccentric cardiac hypertrophy, in which the walls of the heart - especially the left ventricle - increase in thickness and move away from the ideal geometric center of the heart chamber, due to the increase in its radius, normally <56 mm.
For example, the diameter in "End-Diastol" (end-diastolic) of the left ventricle in a trained subject can measure up to 55 mm, while in the inactive subject it can also be less than 45 mm.
In the conditioned subject, the ejection fraction - the percentage of blood actually pumped into the circulation, around 70% - is greater than in the sedentary, leading to a decrease in HR - given that the demand for O2 to the myocardium decreases in the sub-maximal exercise .
However, the increased stroke volume caused by chronic training allows predisposed individuals to exercise at a similar absolute work rate but with a lower HR, reducing myocardial O2 demand in sub-maximal exercise.
It should also be noted that the increase in the ejection fraction still increases relatively little, approximately 5-10% during maximal exercise.
to extract and use O2.
Chronic aerobic training induces mitochondrial hyperplasia and capillarization for each muscle fiber and motor unit, therefore this leads to an increased ability to extract and use the circulating O2 in the blood stream.
Thinking in terms of cardiorespiratory fitness, research confirms that AV O2 diff is similar in trained and untrained individuals at sub-maximal levels of exercise, generally <70% HR or 56% VO2 max, while, at higher percentages, AV O2 diff it appears to be higher in trained subjects (155ml / L) rather than in deconditioned ones (135ml / L).
and viceversa.The force that the flow needs to open its way inside the arteries can be expressed in terms of pressure, the same that is impressed on it by the cardiac contraction and which, as seen, also depends on the volume of blood contained within the system. vascular.
However, in addition to the circulating volume, peripheral resistances are also fundamental in determining blood pressure levels.
In fact, blood pressure can be expressed as follows:
- BP mean ≈ CO x Ts Pr
where is it:
- BP mean = mean arterial blood pressure CO = cardiac output
- TsPr = Total systemic Peripheral resistance.
During exercise, systolic pressure increases almost linearly to cardiac work and VO2, and at the same time vasoconstriction occurs in certain areas of the body (eg splanchnic areas) and vasodilation in others (eg skeletal muscle and myocardium).
The primary control of blood pressure is regulated by TsPr adjustments, accompanied by neural mechanisms in the peripheral arteries, by the release of "local" substances called endothelial-derived relaxing factors, and by changes in local chemistry (temperature and hydrogen ions, adenosine and concentration of potassium ions).
With reference to the relationship between cardiac output and TsPr, the studies carried out show that this is inversely proportional, thus explaining why the systolic pressure increases during progressive exercise in apparently healthy individuals due to the "increased magnitude in" cardiac output, which it grows as the TsPr decreases and vice versa.
Furthermore, focusing on steady-state sub-maximal work, we note that conditioned individuals demonstrate substantially similar variations in systolic blood pressure values to untrained individuals.
Relative to VO2 max, systolic blood pressure is lower in trained than in deconditioned, and, in individuals with first degree hypertension, regular aerobic exercise lowers systolic and diastolic blood pressure from 6.0 to 8.0 mmHG at rest. .
by the coronary arteries, which amounts to about three times that consumed by skeletal muscle at rest.As a result, the heart responds by increasing blood flow. In fact, during physical exercise, coronary blood flow can increase from 250 ml / min to 1000 ml / min, therefore 4 times the resting state.
The main factors influencing the demand and consumption of O2 in the myocardium are heart rate, the thickness of the left ventricle and its pre-contraction, and the contractility of the myocardium.
However, except for heart rate, it is very difficult to calculate the other two parameters in most exercise physiology laboratories.
Therefore, starting from this logistical difficulty, many researchers in recent years have tried to overcome this obstacle, scientifically demonstrating that the product between heart rate and systolic pressure is a very specific index for estimating the demand for O2 to the myocardium.
This index is called Rate-Pressure Product (RPP).
So:
- Rate-Pressure Product = HR x Systolic Pressure
Physiologically, during exercise, the RPP increases directly proportional to the increase in HR and to the systolic pressure.
Even after many aerobic workouts, the RPP increases slightly; however, the magnitude of the increase is less comparable to pre-training values, and this increase is attributable to chronic adjustments in heart rate and systolic pressure.
A normal response to exercise results in an RPP of 25,000 or higher.
The importance in the application of this estimation index increases exponentially for subjects with cardiovascular diseases (CAD, angina, coronary stenosis, peripheral arteriopathies, etc.), as it is easy to apply and very high precision.
it is essential for proper planning and prescription of cardiorespiratory fitness.
