The adaptation of blood flow and pressure following physical activity
Another element that negatively affects blood pressure during physical activity, above all isometric or high-resistance exercises, is the Valsalva manoeuvre. In fact, the closing of the glottis is exploited in order to block expiration, which from the mechanical point of view causes the movement to stabilize, but from the physiological point of view provokes the increase in intrathoracic pressure.
This situation, as can be guessed, compresses the large venous vessels that guarantee blood flowing back to the heart, making it suffer. To be precise, there are two conflicting elements, which both weigh heavily on the course of pressure values. On one hand the increase in peripheral resistance, and consequently the increase in strain on the left ventricle (due to blood ejection), and therefore the increase in arterial pressure. On the other hand, the venoconstriction caused by the Valsalva manoeuvre lowers the venous pressure and also the blood flow back to the cardiac ventricular area.
Aerobic activity induces a diametrically opposed mechanism, that is even able to improve modest levels of hypertension(10,11) , (values between 140mm/Hg and 150mm/Hg for systolic pressure, 90mm/Hg and 100mm/Hg for diastolic pressure), preventing more acute forms.
This situation is possible thanks to the decrease in peripheral resistance due to stimulating the venous pump (particularly high-performance in the lower limbs), which stimulates blood transit and flow back to the heart, with the consequent drop in blood pressure.
However, it is also due to the elimination of sodium caused by aerobic activity, in a considerably greater degree than anaerobic activity. The loss of sodium causes a decrease in the haematic volume and consequently in hypotension. Not by chance, the blood pressure regulation mechanism exploits the release of aldosterone on a renal level in order to increase sodium absorption and, consequently, to increase blood pressure.
As previously mentioned, blood flow considerably increases in a working muscle, reaching (in elite athletes) even 20/25 times more than in the normal condition, in other words passing from about 3 ml/min for 100 grams of muscle, up to 75-80 ml/min.
The mechanism that determines this increase is due to different factors, mainly metabolic regulation.
The drop in oxygen not only leads to difficulty in muscular work, but also in the contraction of blood vessels, which consequently encounter a vasodilatation process, further assisted by the release of adenosine (the release of adenosine is prominent in hypoxia and great metabolic activity), but also be the freeing of all the elements that contribute to the energetic freeing or are the fruit of the use (aerobic and anaerobic) of ATP (ex. CO2 and lactic acid). More generally, a lower availability of oxygen compared to the demand from muscle causes a release of vasodilating substances(12) .
This release, and a consequent increase in vascular lume, in the hypothesis above particularly involves the resistance vessels, that is those arteries and arterioles, which have walls almost entirely made up of smooth muscular cells and are therefore able to regulate the degree of vessel extension.
As their name suggests, they are greatly involved in regulating blood pressure. Moreover, the relaxation and contraction mechanism of the resistance vessels is also regulated by the entity of forces that act in its extension. In other words, the increase in blood pressure, stimulating extension, starts up an opposing mechanism that leads to vasoconstriction, which is observed in cases in which blood pressure tends to decrease. This mechanism, known as myocenic mechanism, is involved in maintaining a constant blood flow in tissues, also in the change of blood pressure.
Conclusions
In conclusion, it can be asserted that physical activity acts on a vast front of adaptive elements of haematic flow and blood pressure. These elements can be favourably used in the case of aerobic activity, able to bring pressure values back to the best range, preventing hypertension from arising, also if this problem exists, and optimising possible vascular problems such as venous stagnation.
On the other hand, training for maximal strength or hypertrophy training can lead to more or less serious hypertension, depending on the individual’s physical condition and, more generally, they can worsen pre-existing coronary problems.
Also from a vascular point of view, persistent venous compression, typical of such training, blocks venous return and can cause situations typically known as “varicose veins”, worsening, and in more serious cases, leading to problems in the brain, heart, kidneys and eyes.
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Dr. Pierluigi De Pascalis
Founder and training manager of nonsolofitness.it
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(10)Paffenbarger, R.S., Jr., et al.: Physical activity and hypertension: an epidemiological view. Ann. Med., 23:19, 1991
(11)Nelson, L., et al.: Effect of changing levels of physical activity on blood pressure and haemodynamics in essential hypertension. Lancet, 2:473, 1986
(12)Berne R. M.; Levy M. N., Principi di fisiologia, 2a edizione, Casa Editrice Ambrosiana, Milano 1998
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