Weightlifting by A.N. Vorobeyev

Translated by Andrew Charniga


From Weightlifting {Tiiazhelaya Atletika}, Vorobeyev, A.N., FIS, Moscow, 1977

Chapter VI Peculiarities of the weightlifter’s blood circulation

Blood circulation plays an important role in the process of the organism’s accommodation to muscular activities. Of all the organs of the vegetative systems the organ of blood circulation is perhaps the most critical for the life altering changes of adaptation to the external environment (K.M. Bykov, 1954).

Regular training results in alterations of blood circulation which are manifest during work as well as during periods of relative rest. These alterations are connected with the stage of training, the intensity of the loading and the specifics of the type of sport.

Weightlifting has a specific effect on blood circulation. Intense straining, when large weights are lifted, are difficult conditions for blood circulation. These difficult conditions arise from straining while holding the breath; and, coincide with even greater muscle force. Straining and breath holding cause abrupt alterations in the hemodynamics of blood circulation.

There is nothing in the literature concerning the specificity of the adaptation of the cardio – vascular system of the qualified weightlifter. Some of the alterations to the circulatory system of weightlifters has been studied for the most part from the standpoint of the state of conditioning (L.A. Butchenko,1963,  et al).  

Cardio – vascular alterations resulting from regular sport training are found at rest as well in training.

Blood circulation at rest.

Pulse rates.

Pulse rates of the qualified sportsman depend on the type of sport and the level of conditioning. The pule rates of qualified distance runners, skiers, skaters, swimmers and other sportsmen, i.e., endurance athletes is 40 – 50 beats per minute at rest; sometimes 35 beats per minute (Y. K. Zhukov et al).

A bradycardia at rest for endurance athletes is due to the intensification of the para – sympathetic nervous system’s effect on the heart.

Let’s dwell in more detail on the bradycardia of athletes. It is considered an established fact in the scientific literature the slower pulse of trained athletes is due to the increased tonus of the hepatic (?) nerve.

It is common knowledge the vagus center is situated in the cortical stem; there are several cores: sensory, motor and parasympathetic. The dorsal core of the vagus cortex is the source of efferent innervation of the heart (G.E. Samonina et al 1972).

The effect of the vagal nerve on the heart is incontrovertible. Considerable research shows this. But the question arises as to whether the economy of functions of all the activities of the cardio – vascular system originate from the vagus nerve center in isolation from the complex displacements to the body from sport training?

Biological systems are highly reliable. Living things have duplicate organs.   Contemporary skepticism suggests regulation of cardiac functions are carried – out extra – cardio. There are clear indications of this point of view from numerous dissections of animal and human hearts. The heart, devoid extra- cardio regulation is able to fulfill its ‘supercharge’ function. Besides this, the heart is able to adapt to the body’s requirements in response to the character of the activity.  

The accommodative function of the heart including the regulation of extra – cardio mechanisms is carried – out by hormonal factors and the activities of the intra – cardio apparatus.  

G.I. Kositsko, et al., 1968 described the following three factors regulating heart function: 1 – intra – cellular; 2  intra – organ (intra – cardio; 3 – extra – organ (extra – cardio).

Well then, our conceptions of the regulation of cardiac functions should be refined. Bradycardia, hypodynamic myocardia and any alterations in the health of trained sportsmen at rest needs to be connected with significant restructuring of the body and the organs and tissues; primarily at the molecular levels.   

For sportsmen at rest, it is common knowledge, all things being equal, pulse rates, and shock volume are connected with the volume of the heart. The larger the heart volume, the larger the shock volume, the less the heart beats. The anatomical morphological features of the heart are connected with its functions. And, vice versa, its functional inabilities are reflected in its morphological structures.

Considerable research has been conducted in recent years which shows cardiac activity is determined by the exchange of minerals; especially the roles of potassium, sodium and calcium.

Raising the exchange of sodium causes an increase in heart rate; whereas, an increase in potassium lowers heart rate and alters other indices (A. Sent – Derdi, 1959 et al).

On the basis on what has been discussed we can conclude the bradycardia and hypo-dynamic myocardia observed in sportsmen at rest is impossible to explain only as the activities of the sympato – inhibitor and chloro – energetic mechanisms, raising the tonus of the vagus nerve.

A.G. Dembo and M.A. Proyektor (1967) considered bradycardia as a manifestation of conditioning only up to a specific level. They believed special medical research was necessary when heart rates were below 40 beats per minute.

According to M. B. Kazakov’s (1965) data the pulse rates of highly qualified weightlifters under normal exchange conditions is 42 – 70 beats per minute. Pulse rates are even lower for the lifters in the light weight classes. Pulse rate after training days is an average of 59.7±0.45 beats/min; and, 61±0.62 after a rest days.

Our study of our athletes pulse rate in the morning, on an empty stomach and lying in bed fluctuates from 42 to 78 beats per minute or an average of 57 beats (∂±7.07, mx+0.55).

Minute volume of blood flow.

Considerable research shows the minute volume of blood flow to be 3 – 6 liters for a healthy person.

The majority of authors found a lower minute volume of blood circulation at rest for sportsmen in comparison with that of non – sportsmen (V. N. Kuzmin, et al 1955 – 1964; 1935)

We found only one study related to the aforementioned indicator pertaining to weightlifters. They found the minute volume of blood circulation for weightlifters was 6 – 7 liters (I. V. Damansaks, et al 1969).

The minute volume of blood circulation for our subjects, at rest was found to be in the range of 5 – 9.3 l/min; an average of 8.0 ml6.84±0.62 liters; and, a shock volume of blood flow of 65.7 – 116.2 ml, an average of 98.4±8.7 ml; arterial – venous oxygen difference 25.72 – 73.42 ml/L; an average of 45±3.36 ml/L.

The following figures apply to non – weightlifters: minute volume of blood circulation 5.1 – 10 L, an average of 7.36±0.62 L, systolic volume from 68.9 to 138,0 ml, an average of 98.3±9.46 ml; arterial – venous oxygen difference was found in the range of 32.3 to 62.1 ml/L, an average of 46.86±4.7 ml/L (table 32).

If the minute volume of blood circulation and arterial – venous oxygen difference were contrasted between weightlifters and the non – weightlifters; there are no significant differences. The weightlifters had slightly lower minute volume of blood circulation but this difference was not significant (p>0.5).   


Atrio – ventricular conductivity for our group of weightlifter subjects fluctuated in the normal range from 0.13 to 0.18 sec (see table 33). The duration of the QRS complex also fell within the normal ranges of 0.08 – 0.090 sec.

The onset of excitation function of the country’s strongest weightlifters was in the normal range.

The electrical axis of the heart for all of our subjects was normal. There was a constant and definitive tendency for the Wilson altering positions of the electrical position of the heart. For example, the electrical position of the heart was vertical or semi – vertical for 15 men; in between for two and semi – horizontal for two.

Highly qualified weightlifters have a small clockwise tilt in the heart relative to its dorso – ventral axis. We believe this rotation is due to the increased mass of its right ventricle. However, electrical – cardiographic criteria (Sokolov, Lyon, 1949) showed none of the sportsmen exhibited hypertrophy of the right ventricle. The duration of the “internal deflection” of the right ventricle was also normal. All of this data enable us to assert a geometric hypothesis of the heart’s vertical position.   

Three of all the qualified weightlifters were found to have hypertrophy of the left ventricle. This was confirmed with rentgeno-graphic data of the volume of the heart. For instance, T -ca’s duration of “internal deflection” for the left ventricle was found to be in the upper ranges of the norm (0.05 sec).

A clockwise rotation of the heart relative to the vertical usually indicates hypertrophy of the right ventricle. However, the transition to the zone was normal (V3-4) and only two guys were found to have a slight shift to the right (V2).

The T – tooth response to V1 and V6. The so – called TV1>TV6 syndrome was found in two sportsmen. Recently, it is all the more seldom, considered a sign of pathology. Sportsmen with this so – called syndrome were found to have no pathological indications of the heart.

In general all the EKG indicators for our highly qualified subjects were within the average range.

Well then, the majority of EKG indicators of the highly qualified weightlifters were found to be within the range of a healthy person.    

Phase analysis of cardiac activities.   

According to Karpman the activities of the so – called ‘athlete’s heart’ at rest are characterized by the phase syndrome of hypo – dynamic myocardia. But this syndrome is found mainly in endurance athletes.

For weightlifters the work of training is very brief; the actual time of lifting a barbell in training is only 4 – 7 minutes; the hypo – dynamic syndrome is absent. (table 34).

The length of asynchronous contractions fluctuates in the normal range of 0.04 – 0.07 sec or an average 0f 0.058 sec for the majority our weightlifter subjects.

The duration of the phases of isometric tension were also normal for the majority of weightlifters on average 0.049 sec. It exceeded 0.05 sec only for K – ko, T-sa, K- va and V – na.

The duration o the tension period (T) was for the most part normal for the athletes; and average of 0.05 sec.

The duration of the expulsion period (E) was comparable to the given rhythm. We established the following: an accelerated time of blood expulsion at varying degrees of expressiveness were noted in the majority of the weightlifters. The relative significance, in comparison with the mandatory of more than +0.025 sec; was found in three athletes.

The length of mechanical systole (Sm) practically correspond to the ‘usual’ for the majority of our subjects. Only T- sa and K-ko were observed to have longer periods.

The intra – systolic indicators fluctuated within a rather wide range of 74 – 90%; on average 83%. Once again it can said that T – sa was the source of lower indices. He was found to have an elevated myocardia tension index of up to 34% in contrast to the average of 29%. The average intra – systolic indices of all groups of subjects was lower than for non – athletes; but, the myocardia tension index was the reverse being relatively elevated (the index norm is 25%).  

Cardiac electro – mechanical ratios.

It is obvious from table 34 the ratios between the end of T tooth to EKG an the beginning of the second electro – phonogram were normal. None of the weightlifters at rest, manifest the Hegglin phenomena.

Heart Volume.

As has already been mentioned sport specialization is reflected in the function and morphology of the blood circulatory apparatus; first and foremost with respect to the heart.

Endurance athletes (runners, cyclists skiers and others) have hypertrophied hearts (Letunov, 1950, Reindell, 1950; Kuzimina, 1955;   Khruschev, 1966; V. L. Karpman, 1964, 1965; Y.A. Borisov, 1967 et al).

According to Muschoff’s (1958) data, heart volume is an average of 710.3 cm³; whereas it is 922.3 cm³ for sportsmen (cited from S.V. Khruschev and Z. Israel, 1966) based on tele – rentgenogram from two planes: frontal and lateral .

S.V. Khruschev and Z. Israel found an absolute heart volume of 961.9±8.49 cm³ of highly qualified sportsmen; and, 13.58±0.9 cm³ per kilo of body-weight. Weightlifters have an average heart volume.   

Reindell, Roskamn, Muller (1966) also found enlarged hearts in their subjects of which nine were weightlifters. The cyclists, boxers, pentathletes were found to have dilation of the heart.

The heart volumes of our research subjects of qualified athletes were found to be within the normal ranges; characteristic of un – trained people.

There is a definite connection between heart volume and body-weight.

The ratio of heart volume to body-weight (QR, cm³/kg) is conditionally designated the coefficient of Reindell. This coefficient is used extensively to ascertain insignificant individual variations in heart volume as a function of body-weight. According to Y.A. Borisov’s data (1967) the Reindell coefficient for otherwise healthy un – trained people does not exceed 12 cm³/kg. On this basis, a heavyweight such as Zh-ky who has an absolute large heart volume of 1,225 cm³ is connected with the size of his body; since his QR was 8.0 cm³/kg.

We used Nilin’s coefficient, which is the ratio of the heart volume to the surface area of the body to determine individual heart volumes (QN cm³/m²). According to Borisov’s data their norm is 500 cm³/m²).

Presented in table 35 are data of absolute heart volumes of weightlifters and the coefficient values of the relative heart volumes. We found, as is correct, normal heart volumes in highly qualified weightlifters. This indicator did not exceed 875 cm³ for 11 guys; and, for three (3) it was somewhat elevated from 950 – 1225 cm³.

As you can see in table 35, only T- tsa’s QN exceeded the upper ranges of the norm. His heart volume was greater in both absolute and relative terms, according to the electro – cardiographic indices and had hypertrophy of the left ventricle as well.

We found N -va (67 kg bodyweight) had a relatively enlarged heart utilizing the Reindell coefficient. However, the absolute dimensions and volume of his heart according to the Nilin coefficient were practically normal. This indicates the QR readings were insufficiently precise with our subjects who had a smaller body mass. Consequently, in order to obtain a more precise value of heart volume it is necessary to compare the Reindell and Nilin coefficients of absolute volume.

We came to the conclusion the training of even highly qualified weightlifters does not result in enlarged heart in the majority of cases. Heart dimension is physiologically determined only in endurance sportsmen. However, this does not exclude those cases where weightlifters with enlarged hearts have been training with 2 – 3 times larger volumes. But, the results of those sportsmen are not lower than those lifters who execute a relatively smaller loading.

Each instance of a weightlifter’s enlarged heart who trained with a moderate loading in both comparative and absolute values should be subject to medical – pedagogical scrutiny. For instance, as a result of such scrutiny, weightlifter T-sa’s  enlarged heart and elctro-cardiographic displacement was connected with the specifics of his  sport career. T -s competed in track and field for a number of years before switching to weightlifting. We can assume the aforementioned alterations were natural in his case.

Arterial pressure

Arterial pressure of our highly – qualified weightlifters was measured lying; on an empty stomach in the morning.

The range of systolic was from 75 to 155 mm pt. ct or an average of 108 mm pt. ct (σ = ± 12.0, mean standard deviation ±1.0 mm pt. ct., C = 11.0%); the diastolic ranged from 45 to 105 mm pt. ct. or an average of 71 mm pt. ct. mm pt. ct.  (σ = ±8,  mean standard deviation ±.07 mm pt. ct., C = 11.7%). The  mean values for these sportsmen fell within acceptable norms.

The weightlifter’s arterial pressure was found to fluctuate with the time of year. Presented in table 36 are arterial pressure readings for winter and summer. The difference is not happenstance p <0.01.

The difference between diastolic pressure in the summer and winter is an average of 2.5 mm pt.ct. (p <0.05).

In all probability we can assume increased perspiration in the summer plays a role in the elevated systolic arterial pressure of the weightlifter; a significant loss of sodium perhaps alters the ionization equilibrium between sodium and potassium in the blood stream. At any rate, the training loading and the sportsman’s daily regimen are essentially the same.

It must be pointed out, there are numerous references in the literature detailing factors which affect a person’s arterial pressure with changes in the time of year.

People who live in warm climates register lower arterial pressure during the hot periods. Even those with hyper-tonic diseases, stages I and IIA can register slightly lower arterial pressure. Similar situations have been found in central Asia: A.A. Kaplan (1934), I.A. Kassirsky (1935) N.I. Izmailov et al (1949), Z.I. Umidova et al (1961).

It is not possible to separate arterial pressure from the time of year, geographic location and some meteorological factors. Arterial pressure is usually connected with the state of conditioning; as well as the increased tonus of the parasympathetic system in the realms of sport physiology and sport medicine.

Based on our own data it is impossible to ignore time of year in recording the arterial pressure of sportsmen.

For the most part, our observations of weightlifters’ arterial pressure at rest were in the normal ranges. Lower (hypo – tonia) arterial figures were recorded.

Arterial pressure is slightly higher in winter than summer. According to our figures systolic pressures were 113 and 114 mm pt. ct.; diastolic 72 and 70 mm pt ct..

We recorded lower arterial pressures multiple times with our athletes during the period of training for competition in the warm months: 85 – 90 mm pt ct. systolic pressure at rest. Very often hypo-tonia in a weightlifter coincides with lowered work capacity. Physical loading, lifting maximum weights does not provoke a rise of more than 110 – 125 mm pt ct. in systolic pressure. Sportsmen who fatigue quickly in training and don’t feel well with less strength are prone to muscle spasms.

It is common knowledge sportsmen experience hypo-tonia from 1.3 to 3.1 mg loss of the sodium ion. Well then, athletes lose from 1 to 2.5 kg of body-weight from workouts from perspiration. One gram of perspiration contains 1.3 – 3.1 mg of sodium. Consequently as a result of training one can lose up to 1.5 to 5 grams of sodium; which corresponds to 3 – 12 grams of table salt. The potassium ion loss is 3 – 4 times less than the sodium ion.

It has been established with certainty the sodium ion is the crucial factor.  Arterial pressure is principally dependent on sodium levels and some other displacements in the functions of the organism.

Sportsmen with elevated arterial pressure, have hypo-tonia, is rather simple. Following regular use of 20 – 25 grams of table salt a day raises arterial pressure over a period of 2 to 3 days to normal levels. Arterial pressure in response to loading returns to normal; work capacity improves.

At the present time there are many papers which show the roles of sodium and potassium in the regulation of arterial pressure (Reid, Laragh, 1963; Dieter, 1963; Mertz, 1963; S. Fridman, C. Fridman, 1966; C. Hall, O. Hall, 1965; Conn, 1965 and others).

At the present time it has been shown the hormone angiotensin raises arterial pressure only when there is a sufficient serum levels of the sodium ion (Reid, Laragh, 1965).

On the basis of all this data it can be assumed hypo-tonia in healthy sportsmen intensely training cannot possibly be connected only with increased central tonus of the parasympathetic nervous system. Mineral exchange obviously plays an important role here; in particular, some deficit of sodium in the body resulting from training.    

Alterations in Cardio and Hemo-dynamics from Weightlifting and Straining

Functional Indices of the Cardio – vascular System Before Training

Heart rate rhythm. Pulse rates of our subjects, from base conditions adopted as 100%; increase an average of 33% before training. Pulse rate coefficient of variation is 1.2% in the morning; and, 11.8% before training. Such a variability in pulse rates before training can be explained by differences in the forthcoming work. For instance, if one plans to lift maximum weights in the classic exercises pule rates are elevated higher than before the usual workout.

Electro – cardiographic and poly-graphic indices.

It is obvious from the mean data presented in table 37 there are no noticeable peculiarities in the atrio –  ventricular conductivity, electrical systoli and the phasic structures of cardiac activities of the highly qualified weightlifter.

Arterial Pressure.

The arterial pressure of the qualified athlete rises before training; for some rather significantly, up to 150 mm pt. ct.. Systolic arterial pressure rises an average of 10%; diastolic by 6%.

A moderate rise in systolic pressure arterial pressure should be viewed as a favorable factor; indicative of the organism tuning for the training.    

Cardio – vascular activity in weightlifting

Cardiac rhythm.

The pulse quickens an average of 22 beats after the usual warmup; which for our weightlifter subjects lasts 5 – 10 minutes. Heart rates reached up to 140 beats per minute if the sportsman did a high tempo warmup; and, no more than 90 -100 beats per minute if the warmup was of a moderate tempo.

Pulse quickens significantly preceding lifts (recorded over 5 – second intervals) from 7 – 8 beats up to 9 – 12; which works out to be 120 – 140 beats per minute.

Weightlifters rest 2 – 4 minutes between lifts in training. A specific back-round pulse rate of 85 – 106 beats per minute between lifts was established. With significant emotional excitation and short rest intervals (less than 2 minutes) pulse rates rise to 100 and more beats per minute.

The electro-cardiographic data from the period of the press with 60 – 70% of maximum for 4 – 5 repetitions and more; show pulse rates reach 100 – 150; or, an average rate of 132 beats per minute. Two different forms of peaks were observed in pulse rates during work.

Pulse rate quickens during work and continues to quicken after the first 10 – 15 seconds, then stabilizes, i.e., here the reaction is analogous to the Lingrade phenomenon, but in a cardiological variant.

Usually pulse rates are not high when significant weights (more than 80 – 90% of maximum) are lifted. Pulse rate quickens sharply after the exercise is finished. Pulse rates of our sportsmen subjects did not exceed 140 – 150 beats per minute.

The weightlifter’s quickening pulse rate in his approach to a set with a barbell should be considered a conditioned reflex.

 A falling pulse rate when the weightlifter moves from a vertical disposition to the half squat (the starting position) is connected with postural reflexes; the mechanism of which is the drop in hydro – static pressure; as well as rising venous return, increasing the load on the heart “volume” of blood (when the heart receives a rise in blood flow). M.B. Kazakov (1966) observed an analogous circumstance with the alterations of the weightlifter’s pulse.

A drop in pulse rate of 5 – 8 beats per minute for people who lowered their head were recorded V.N. Kolychev and N.A. Noveselov (1966). According to Karpman and others, a lowered disposition of the head increases venous return to the heart and intensifies cardiac activity while reducing rate of cardiac contractions. The authors elucidated a phasic alteration in cardiac activities; the character of which is related to its function during a loading “blood volume”.

When the weightlifter goes from a vertical disposition to an inclined (leaning over) the switch coincides with a rise in venous return to the heart; an intensification and decrease in cardiac contractions. The opposite circumstances are observed when the weightlifter switches from an inclined or horizontal position to a vertical disposition.

The minute volume of blood flow.

According to Lingarde the largest minute blood flow during work is 43 L.; according to Christensen – 37 L. During high power work of 1452 – 1680 kgm/min the oxygen requirement is 3948-3960 ml.

According to Lingarde’s data volume of blood flow during shock work can reach 147 ml; according to Christensen it is 209 ml.     

Lifting weights affected blood flow in our subjects in the following manner: the minute volume averaged 13.34±0.5 L; fluctuating in the range of 10.7 to 20.7 L; shock volume from 55.7 to 143 ml. The smallest  difference in arterio – venous blood oxygen was 19.79 ml/L; the largest was 89 ml/L; and the average was 50.9±3.43 ml/L.

If we take 100% as the initial level at rest; then, we obtain a rise of 95% in minute volume of circulating blood during work for weightlifters; systolic volume actually lags the previous and arterio – venous difference increases by 9%.

From analysis of alterations in minute volume and systolic volumes of circulating blood of non – weightlifters, there are obvious distinctions between theirs and those of weightlifters. So, for those lifting for the first time, the minute volume of circulating blood increases by only 12% during weightlifting; whereas the systolic volume diminishes by 47% to pre – work level.

Consequently, the aterio – venous oxygen difference rises by 13.2% more than for athletes.

The minute and systolic volume of circulating blood and the arterio – venous oxygen differences for our subjects during work is significantly distinct; which is indicated by the standard deviation and coefficient of variations.

The circulatory system of the non – weightlifter is poorly adapted to the difficult conditions of weightlifting and straining. The organism’s rising need for blood is clearly insufficient; whereas, the qualified weightlifter’s volume of circulating blood rises almost two – fold during weightlifting. It is precisely this fact, where we see the special adaptation of the qualified weightlifter’s cardio – vascular system to weightlifting.

EKG Indices during and after lifting weights.  

 A quickening pulse while lifting weights coincides with shortening of the PQ, QT intervals, shifting segments of the PQ and ST below the curve. The P tooth rises, the R tooth falls, the S tooth deepens and the T tooth compresses.

There are clear cut alterations in the T tooth which is in line with the literature.

One can suggest the rising concentration of carbon dioxide gas as well as the concentration of lactic acid during work play significant role in the dynamics of the alterations of the T tooth. The latter has been confirmed experimentally Keul, et al 1966. We found that during heavy muscular work (300 BT) 64% of the energy requirements of the heart are supplied by lactic acid.

A drop in the ST interval during lifting and in an earlier period of restoration can be explained by alterations in coronal hemo-dyanmics. Plas, et al (1956) linked the drop in the ST with coronal insufficiencies and low potassium; whereas, Scherf, et al (1952) with the rising T tooth.

It is common knowledge, the heart’s energy resources are satisfied somewhat by systole. Lifting a big weight coincides with significant strain; which means coronal blood flow is sharply diminished. Therefore, we attribute the typical electrocardiogram alterations of the weightlifter during lifting and an earlier period of restoration from hypoxia; with accumulation of metabolites in the heart muscle; to be a limited flow of energy resources and oxygen.  

Cardiovascular activities after lifting and following training

Cardiac rhythm. The weightlifter’s pulse rate after lifting depends on several factors: the weight of the barbell, the number of lifts, i.e., the amount of work and the functional state.

For many sportsmen the acceleration of pulse rate during rest intervals of less than one minute after lifting is small; since, the initial pulse rate before lifting was larger than during the 3- 4 minute rest intervals, i.e., against the backdrop of a higher pulse rate. Therefore, a less expressive reaction in cardiac rhythm is observed in exercise.  

Despite the restoration of pulse rate after one minute during the usual training regime; this time is insufficient for recuperation of muscular strength and coordination of movement. A rest period of one minute for lifting 90% and above weights is not possible. One can usually lift those weights after resting more than 2 – 3 minutes. It is obvious, a rest period of less than one minute is insufficient for optimal recuperation of the nervous system and skeletal musculature.

Restoration of pulse rate after a single lift in training occurs after 30 – 90 seconds for the trained highly qualified athlete. Pulse rate returns to pre – training levels after 2 – 3 minutes or more after a set of multiple, 2 – 3 repetitions and more.

Minute volume blood circulation.

Research has shown that in the first 30 seconds of the recuperation period after work; minute volume of blood circulation rises and average of 19.77±7 L; and, fluctuates in the range of 9.6 to 19.3 L. Systolic volume increases as well by an average of 119.3±7.1; fluctuating in the range of 88.9 to 155.8 ml.

The minute volume of circulating blood grows even more after work, than pre – work levels reaching 288%; and, in comparison to the work period, increases almost 69%. The systolic volume of circulating blood rises in comparison with pre – work levlesby 19.5%.The aterio – venous oxygen difference after work is in the range of 33.5 to 78.1 ml/L, or an average of 54.0 ml/L. It has restored from an earlier period by 115% form pre – work by 107% from the working period. The minute volume of circulating blood was 137% from rest levels for the non – weightlifters and 113% from the pre – working levels. The arterio – venous difference in these periods were137 and 103%.

All of our subjects clearly expressed the Lindgrade phenomenon for the indices of minute and systolic volume of blood flow and arterio – venous oxygen difference. This can be explained by the fact it is connected with straining and breath holding while lifting weights which makes blood flow difficult. Consequently, there is a re-distribution of blood because of an accumulation in the veins. An intensive loading of “blood volume” takes place after work which causes an intensification of circulation.

Electrocardigraphic and polycardiographic indices after training.

According to our data 10 – 15 minutes of rest after training a quickening of PQ interval was observed for 0.01 seconds (see table 38). The length of the QRS complex is essentially unchanged as is the electrical axis of the heart. The electrical systole quickens.

The electro – mechanical ratios of cardiac activity were found to be within the normal range for all of our subjects after lifting weights. The interval T – II tone is positive before training; on average 0.023±0.004 seconds. After training the TG – II tone drops but the difference between these indices and their levels before training is not reliable. No one exhibited the Heglin phenomena, i.e., the II tone outstripping the EKG end tooth T by 0.04 seconds and more.

Well then, one can conclude that weightlifting training of qualified athletes with an adequate loading effects the electro – cardiographic and poly- cardiographic indicators but not outside established norms.

Arterial pressure.

The arterial pressure of qualified weightlifters usually has normalized over 10 – 15 minutes of rest after training. Quite often pulse pressure lessons after training. Many authors assess this reduction in the shock cardiac volume as a sign of fatigue from the physical loading.

A number of times in training we have observed the phenomena of “tone without end” and the inability to get a arterial pressure with the Korotkov method.

S.P. letunov (1950) considered the “tone without end” phenomena an unfavorable sign.

However, the subjects whom exhibited this phenomena felt good and their work capacity was normal. No connection between condition and aurical arteries was established.

Hnadzo, et al (1955) considered the non – definitiveness of diastolic pressure after muscular loading an artifact. E.A. Porchikov (1967) showed convincingly the “endless tone” phenomena of diastolic pressure was within the range of 60 – 70 mm pt.ct. G.I. Kositsky (1959) the genesis of the “endless tone” as the high systolic energy of the heart. On the other hand, we considered the “endless tone” phenomena as sign of myocardial good work capacity.

The arterial pressure of qualified weightlifters on the day of competition according to our data was found to be in the normal ranges. A rising systolic pressure before training up to 130 – 140 mm pt. ct. and no higher than average is typical; with the diastolic remaining at the previous level; the oscillograph indicator rises. We considered this displacement, tuning for the upcoming work; indicative of a good work capacity.

A sharper displacement of arterial pressure has been observed in some athletes before important competitions. For example, sportsmen have registered the following arterial pressures 30 – 40 minutes prior to international competitions (according to Korotkov):

Arterial pressures of lifter in the 56 – 75 kg group were lower than sportsmen in the 90 and +90 kg group. This is probably due to the higher excitability of the heavier athletes; and, besides the lighter lifters have to lose weight in the sauna (as previously indicated; the larger loss of sodium and its restriction contributes to lower arterial pressure).

Cardiovascular response to straining

All forms of significant muscular effort involve straining. Straining always occurs during static work and is connected with great straining when lifting big weights. Straining is connected with  cessation of breathing and tension of respiratory muscles, raises intra – thoracic and intra – abdominal pressures. Well then, the complex of influences on the various organs and systems of the body resulting from straining cause cessation of breathing, raise intra – thoracic, intra – lung and intra – abdominal pressures.

The majority physiologists characterize the alterations in the activities of the body’s organs and systems during straining on the basis of the experiences of the Italian physiologist Valsalva. Researchers for the most part have focused on the function of blood flow during straining. There is the opinion that breath holding (in the absence of straining) induces some functional alterations to the cardio – vascular system. Perturbative factors connected with breath holding are reduced partial pressure of oxygen and along with it expenditure and elevated partial pressure of carbon gas in the blood and tissues.

Ludin (1963) explained the hemodynamics with the Valsalva test of restricted return of venous blood from the extremities which results in a significant drop in cardio- pluera depot, constriction of pleura vessels and a diminished systolic volume from the left ventricle. This indicates a significant reduction in pressure in the right pre – heart and right ventricles; arterial pressure of the lungs is significantly diminished. Furthermore, systolic pressure drops more than the diastolic; stimulating the pressure receptors of the aortic arch which causes reflexive increase in peripheral resistance. The diameter of the heart increases after straining, the arties dilate and there is a reflexive drop in peripheral resistance.

There is a diminished minute volume of blood flow, the pulse quickens and venous pressure rises during the Valsalva test (Burger, Michael, 1957).

The diameter of the heart decreases during straining. I. Stefan, O. Opyanu and F. Barkin (1959) determined the diameter of the heart diminished by 50% during Valsalva which was connected with the expulsion of lagging blood from its cavities and insufficient inflows. B. S. Hippenreiter (1956) observed a reduction in heart diameter during straining. We recorded the same thing with S.N. Dobronravov with roentgenolgical observations. For the most part this reduction depends on the magnitude and duration of the straining. The diminished diameter of the heart can be explained by the limited venous return due to the rise in intra – thoracic pressure.

The rhythm of cardiac contraction.

Pulse rate increases during straining (B.S. Hippenreiter, 1956; V.V. Vasilyeva, 1957; L.N. Folgelson, 1957; E. .K. Zhukov, 1960; V.L. Karpman, 1965; A.A. Arutsev, 1965, et al).

The increase in pulse during straining is illustrated well by pulse graphic of the subject V – va (figure 40). His initial pulse rate was 72 – 75 beats per minute. The pulse graphic curve increases within the first seconds of straining; indicative of the increased volume; owing to the resistance to the venous blood flow during the drawn out for some time arterial flow; but subsequently, and probably, the diminished arterial flow diminishes because the pulse graphic has a tendency to diminish. Pulse rate rises sharply during straining up to 110 b/min. Pulse rate fluctuations are small during straining, which probably depends on the diminished stroke volume of the heart and the increased tonus of the vessels.   

For a period of 5 – 6 seconds after straining has ceased oscillation of the pulse remains small. But the pulse graphic curve diminishes sharply when straining ceases; consequently, there is no restriction of venous blood. The volume of pre – heart is less in the first seconds after straining the prior to straining.

This is easily explained: venous flow increases, but arterial flow is still restricted. But 5 – 7 seconds after straining has ceased, arterial flow increases sharply, the pulse rate curve rises; while, simultaneously, there is a sharp drop, larger than before straining began, reduction in pulse; which can be explained by irritation of the mechano- receptors of the heart, reflex from the aortic arch and sino – carotid zones.  Bradicardia probably plays a reflexive role with the small vessels of the arch. V.V. Parinym (1941) established a depression effect with the rising pressure in the vessels of the small arch. This is significant as well for the “pooling of blood”. An infrequent pulse and a greater oscillation of pulse was observed for a period 10 – 15 seconds after straining; which is approximately the same time to restore to the initial level of the pre -heart.

The pulse rate of our subjects was practically unchanged after a period of 30 seconds of breath holding in comparison with the period of straining. However, straining at 60 mm pt. ct. 30 seconds increased heart rate by 20%.

Fox, Crawley, Grance and Wood (1966) were able to directly utilize indicator t measure blood flow in the aortic artery during a Valsalva test. They observed this indicator diminished by an average of 35% and rose immediately after ceasing the test by an average of 19% from the initial level. Magnani (1966) observed a brief decrease in blood flow after the Valsalva test.

We studied the speed of blood flow during straining at 400 mm pt. ct.during simple breath holding; utilizing for this v. cubitalis cernokisol magnesium. Speed of blood flow rose for 16 second with breath holding and for 32 seconds of straining.   

Arterial pressure. There exist differing opinions with respect to arterial pressure from straining. According to A.N. krestobnikov, E.K. Zhukov, V. V. Vasliev, it drops. V.S. Hippenreiter noted it initially rose then arterial pressure drops.

V.V. Vasiliev (1957) observed a rise in arterial pressure for those who are trained at straining (weightlifters); whereas for the untrained it was the reverse.  

M.M. Zakin and others (1937, 1940, 1953) observed a rise in arterial pressure from straining.

G.I. Kositsky (1959) studied straining with the Valsalva maneauver and recorded the fist tonus of pre – schoolers of 145 mm pt.ct. After this the subjects were instructed to exhale slowly registering a pressure of 120 mm until the pressure was only 80 mm pt. ct.. G. I. Kositsky considered such drop in ‘sounds’ due to the undulating fluctuations in arterial pressure which is dependent on vessel tonus

It is extraordinarily difficult to determine arterial pressure during straining, especially significant; therefore, some considered it (blood pressure) dropped during straining. The oscillograph method of measuring arterial pressure can be more precise.

Arterial pressure rises in the first period of straining for weightlifters. This is connected with the average systolic and diastolic pressures.

We observed a drop in arterial pressure in untrained women. For subject CH. F. the  value was 125/65 at rest and during straining (at 20 mm pt. ct.) – 97/65; a similar recording we obtained in three out ten subjects.


Straining diminishes blood oxygen levels. T. P. Kovalchuk (1958) conducted various functional tests ; one in particular involved straining with an effort of up to 60 mm pt. ct. and found oxygenation diminished by 25%. Recuperation of arterial blood oxygen concentration returned quickly; but it was slower for poorly trained sportsmen.

A.A. Arytsev (1965) tested oxygenation during straining with an effort of 40 mm pt. ct. and recorded a reduced concentration of blood oxygen which was somewhat less than just breath holding for the same duration. Recuperation of oxygenation after straining occurs quickly. This was also the case with light straining found by Fubre and Legandre in 1955.

We studied this very interesting phenomena with weightlifters. The drop in oxygenation during straining depends on its degree and duration. For example, a well trained weightlifter B- va strained for a period of 30 seconds with an effort of 40 mm pt.ct with no appreciable effect on the concentration of oxygen in the blood. However, straining with an effort of 70 mm pt. ct. reduced oxygenation by 2%.      

For trained athletes, simply holding the breath causes a larger drop in oxygenation than breath holding while straining. In our opinion this fact can be explained. The trained athlete adapts to straining. In al probability, there is already a significant amount of blood in the lungs. The lungs utilize the already present blood depot during the act of straining. The heart ejects a good deal of blood in the initial seconds as blood pressure rises during straining.  Oxygenation cannot diminish until venous rises. In our experience prolonged straining (more than 30 seconds) leads to a more significant drop in oxygenation.

The qualified weightlifter’s adaptive blood circulation apparatus, first and foremost, accommodates to the significant straining characteristic of lifting weights.

The weightlifter’s stabile response to maximum strain is one of the key factors in the adaptation of the cardio – vascular system to regular training in weightlifting.

The stability of weightlifters during maximum straining.

This is one of the important accommodative actions carried out during the process of training with weights.

We studied the ability of highly – qualified weightlifters to exert maximum strain and straining while holding the breath during ¾ maximum straining; under normal barometric conditions at a height of about 2000 meters above sea level. Qualified weightlifters exerted maximum straining, on average of 205 mm pt.ct. at sea level. They exhibited a pressure of 151.5 mm pt. ct. while they were holding their breath for an average of seven seconds. After training for 20 days at a height of 2000 meters above sea level the degree of maximum strain indicator was 233 mm pt.ct. ∂ = ± 12.6 mm or by 13%. They improved their ability to maintain a ¾ maximum strain  by up to 164mm pt. ct. ∂ = ± 11 mm. This despite the time of straining rose to 9 seconds,  ct. ∂ = ± 3.8 seconds, or by 28%.

Considerable research confirms oxygen expiration under rising pressure causes vaso – constriction especially in the cerebral vessels. Therefore, we suggest raising the pressure by increasing the effort of exhalation, including raising the partial pressure of oxygen in the lungs can affect the cerebral vessels. A moderate reduction in the partial pressure of oxygen by exhaling during intense straining can render a favorable effect on cranial blood flow. Otherwise it wold be difficult to explain the 285 rise of the athlete’s stability relative to intense straining under conditions of falling barometric pressure during exhalation.

About the mechanism connected with loss of consciousness associated with lifting maximum weights.

A sportsmen losing consciousness is a not – infrequent occurrence in weightlifting competitions; connected with pressing a maximum weight. This rarely happens in training. The press is performed by first lifting the barbell to the chest; followed by a wait of about 2 seconds for a signal from the referee to begin lifting the barbell from the chest. The barbell must be raised by the muscles of the shoulder girdle; consequently, the movement is executed rather slowly. Typically the athlete holds the breath from beginning until the end of the exercise, i.e., until the arms have fully straightened.

When the barbell is raised very slowly there is a lot of tension and it is at this time the athlete can briefly lose consciousness. Usually the sportsman completes the exercise; but not infrequently, he is unable to fix the barbell; the barbell is dropped and sometimes the sportsman falls. Injury can result. Consciousness returns after 5 – 10 seconds.

This has happened to myself more than once at the national or world championships. Subjectively the sensations are such: during great muscle tension, when the barbell has reached the height of the forehead or slightly higher, small circles of light appear before the eyes, the hall begins revolving; after which one loses consciousness.

For the most part I was able to successfully complete the exercise. Spasmodic contractions of the muscles of the shoulder girdle begin after lowering the barbell to the platform. This state passed after 5 – 10 seconds; but I would stagger from the platform.

Loss of consciousness was a very rare occurrence in training despite the fact the weights were lighter; a milder form.

Why would loss of consciousness occur only in competitions?

The sportsman is affected by the intense emotional atmosphere of competitions. Under such conditions the cerebral cortex needs more oxygen; however, during the press, blood flow to the brain is shunted; restricting the requisite extra oxygen. Furthermore, prior to lifting, especially a maximum weight, athletes significantly speed – up respiratory rate which raises the volume of gases. Many increase depth and frequency of respiration before lifting, i.e., hyperventilate.

According to Henderson, Harrold, Gorvera, purposefully speeding up frequency and depth of breathing negatively impacts blood flow (cited by Schneider, 1930).   

Brown (1963) demonstrated a narrowing of vessels of the cortex during hyperventilation in some basic experiments. Wullenweber (1965) studied the affect of hyperventilation on blood circulation with headache subjects. The author found a reduced cortical blood flow during hyperventilation.  Aizawa et al (1964) recorded a significant reduction cortical blood as a result of hyperventilation on average of 34.5 and 32.2%; which, coincides increased resistance of the vessels corresponding to 45.5 and 30.1%.         

Research on healthy subjects who hyperventilated for a period of 1 hour; experienced 68% reduced blood flow to the cortex compared to initial levels.

Y.R. Sobolevoi’s (1966) research revealed changes in cardiac activities during hyperventilation. Sinusodal rhythm narrowed, arrythmia occurred, blocking the stem of Gisa and  ultimately cardio – vascular insufficiencies developed. Malzarezki (1962) demonstrated unequivocally hyperventilation prior to muscular work does not yield positive effects. It impeded the accommodation of the respiratory organs for the muscular work raising the oxygen debt.

Well then, from this brief review it is obvious that hyperventilation is a factor which aggravates the negative aspects of straining. This has an especially unfavorable effect on the cerebral blood circulation. From our point of view it confirms the subsequent experiences (especially those of Burger, 1923). After a modest hyperventilation (3 – 4 deep exhalations and inhalations which is not possible to even call this hyperventilation) and after a deep inhalation one begins straining with an effort of 100 – 150 mm p. ct., (not a maximum) for a period of 5 – 10 seconds; in almost 100% of cases there is a brief loss of consciousness; and, in some cases a more significant manifestation – with uncontrollable convulsions. Naturally, straining ceases with loss of consciousness; and, after 5 – 10 seconds one regains consciousness.

Exactly the same straining; without a preliminary hyperventilation; does not cause loss of consciousness. I obtained the same results many times in experiments on myself. My straining with an effort of 120 mm pt. ct. is depicted in the oscillograph in figure 41. The second resulting oscillograph was created after a preliminary hyperventilation straining with an effort of 120 mm pt.ct. (figure 42). The straight line in the oscillograph of figure 42 indicates loss of consciousness.   

It is obvious from the oscillograph maximum arterial pressure rises to 200 mm pt. ct. during straining with hyperventilation (the oscillation is larger) which can indicate the tonus of the vessels have diminished. There is no oscillation on the graph at the instant of loss of consciousness. In all probability in this case there is a brief sharp reduction vessel tonus – a collapse.

There is no obvious oscillation after expiration; no sounds can be detected from the brachial artery. A high oscillation returns and sounds can be detected from the brachial arteries when systolic pressure reaches 120 – 110 mm pt. ct..

The nature of our findings can be explained as a complex of factors which are manifest when straining follows hyperventilation. There is a significant decrease in cortical blood flow during hyperventilation the rising oxygen content of the blood effects the cortex vessels, primarily through hypoxia  as well as probably reflexive effects (reflects from the vesicular – motor centers). Straining intensifies this condition to a significantly greater extent by increasing vessicular tonus, reflexively (the mechano- receptors and chemo – receptors).

The unfavorable effects of hyperventilation followed by significant muscular tension under training conditions.

We experimented on myself. I took 3 – 4 deep breaths and exhaled forcefully and attempted to lift a weight slowly. More often than not this procedure resulted in a loss of consciousness.

Our experiment utilizing an arterial oscillograph did not yield an answer as to the mechanism which caused the loss of consciousness. In some cases (see figure 42) we were left with the impression the reason the weightlifter losses consciousness is because the heart stopped beating. In order to confirm this hypothesis and to further research the mechanism of weightlifter’s loss of consciousness we conducted an experiment by modeling loss of consciousness from the method described above. We recorded: electro- cardiogram (EKG) according to Nebu, phono – gram (FKG), spirogram of the temporal artery.    

From the results of this experiment we established that loss of consciousness was not the result of stoppage or even slowing of the heart beat. Figure 43 depicts the activities of the heart following straining, during loss of consciousness (the instant of loss of consciousness is designated by control milli – volts) and the depicted tachycardia during the period it returns. There is an obvious clear cut PQRST complex on the EKG. A clear cut I tone of the heart appears on the FKG. A sharp decrease in the amplitude of the II tone, as well as a sharp rise in the amplitude of the tooth on the T on the EKG. The latter fact is easy to see in figure 45 (the EKG is spread over 10 minutes after loss of consciousness) The initial FKG and EKG are depicted in figure 44.

Consequently neither a – systole nor a sharp bradycardia are cause for loss of consciousness.

The phono – cardiographic data leads to the idea the loss of consciousness was the result of a very sharply diminished cardiac blip. It is appropriate to suggest the fact of a reduction or exhaustive II cardiac tone are changes in myocardial metabolism.

The sphigmo-gram of the temporal artery during straining is depicted in figure 46, during the loss and the regaining of consciousness. A pulse oscillation is absent during loss of consciousness and it returns with the return of consciousness.

The absence of oscillation on the spirogram; can, obviously indicate a sharp reduction in cardiac pulses of blood as well as alterations in vessel tonus immediately after straining has ceased; which cause a sharp hypoxia in the cerebral cortex.  

The unfavorable effect of hyper- ventilation and the after effects of straining and great muscular tension are common not only in weightlifting sport; but, in other forms of man’s endeavors.

For instance, V.A. Averyanov (1975) described a case of an unfavorable consequence of hyper – ventilation on divers; with resulting loss of consciousness. There is considerable data in the literature about loss of consciousness and even death of depth divers whom always hyper – ventilate before immersion in the water (Graig, 1961). Ragman (1973) documented 32 cases of loss of consciousness of climbers. The majority of the cases loss of consciousness occurred when they left the peak, i.e., when the overloading occurred. Research shows many sky divers especially young and inexperienced hyperventilate before exiting the peak which can affect cortical blood flow and prevent loss of consciousness.     

The data we obtained indicates the factors which precipitate of loss of conscious in weightlifting competitions are as follows:

1/ reduced volume of circulation which is connected with a high pulse rate and an insufficient flow of blood to the heart during straining.

2/ hyperventilation;

3/ emotional excitation which increases the requirements of oxygen;

4/ prolonged muscular tension, i.e., slowly lifting the barbell;

5/ forceful muscular contraction; in many cases, or pressure of the chin on the chest which reduces blood flow to the brain;

6/ pressure against the arteries of the neck when the barbell is held on the chest above the clavicles.

By way of conclusion some brief remarks are in order concerning the material of this section on the functional features of the weightlifter’s blood circulation.  

The body’s accommodation to physical loading is a very complex  and distinctive process; in which, all mechanisms regulating homeostasis take part; including the cardio – vascular system. Therefore, it is quite natural there are accommodative alterations to the mechanism of blood circulation which occurs from a person’s muscular work; regulating its execution.

Systematic training in weightlifting is characterized by brief periods of tension and straining. The specificity of this muscular work is reflected in the morpho – functional indicators of blood circulation. At rest the morphology and functioning of the cardio – vascular system of the highly – qualified weightlifter is essentially indistinguishable from an untrained person. The exception being weightlifters tend to have moderate bradycardia and a number display a tendency for hypo – tonia.

There is no connection between heart rate and arterial pressure at rest with training. Weightlifters display a conditioned reflex before workouts to increased heart rate and a rise in systolic blood pressure. Optimal activation of the cardio – vascular system before training usually indicates the athlete is ‘tuning’ for the upcoming work, i.e., a defining of one’s work capacity.     

The adaptive mechanism of blood circulation is specific to weightlifting.  The weightlifter’s minute blood flow in training rises by 2 and three fold; while at the same time this indicator for untrained person rises insignificantly; no more the 60%. There is a clearly expressed rise in pulse rate, minute and systolic volume of blood flow after lifting weights.

Electro -cardiographic data recorded in the early period of restoration of lifting are indicative of the strain on the heart. However, all EKG indicators return to normal after about 2 -3 minutes for the trained weightlifter.

An inadequate response to the training load is reflected in the functional indicators of the cardio – vascular system: a worsening of atri- ventricular  conductivity and potential disruption of rhythm.

In the first minute of the recuperation period after lifting systolic arterial pressure reaches 150 – 180 pt. ct., the average pressure rises; and, the diastolic can rise as the average diminishes.  Normalization of arterial pressure to pre – training range occurs after 1 – 3 minutes of rest after lifting.

With adequate training loads in weightlifting the lifter’s cardio -vascular system adapts; without any pathological manifestations.  

Reports of the USSR Academy of Science

  1. Volume 210, No. 1, 1973

The Intra – Muscular Peripheral Heart

  1. I. Arinchin, G. D. Nedvyetskaya

Translated by Andrew Charniga


It is understood, ever since the time of Harvey, up to the present time; the heart is  the sole motor pumping blood. On the contrary we are of the opinion of the insufficiencies of this viewpoint. We believe a “peripheral arterial heart” exists; not confirmed in physiology clinics, or, otherwise; confirmed in actuality.

General signs have been found from studies indicating extra – cardial factors contribute to blood flow. These include, in particular, the pumping function of the skeletal muscles, or the so – called ‘venous pump’; functioning under the influence of elevated hydrostatic pressure. This is the mechanism for a reduction in the pooling of venous pressure in the lower extremities when a person is standing.

Beginning with I.P. Schchelkovym and V. K. Zadler in 1869, (in the laboratory of K. Ludviga) work in hyper-aemia found extra – cardio factors entirely and fully independent of circulating functions of the heart. In this context, the mechanism of vesical dilation; resulting from the force of blood flow from the cardiac contraction has not been elucidated. A number hypotheses have been put forth to explain this mechanism (7,10, 17, 19). However, they are insufficient to explain this mechanism; consequently we investigated the working of this hyper-aema mechanism further; undercovering new concepts.

Studies of the external (from the aspect of muscle contraction) and internal (from the aspect of blood flow) pressure on vesicular walls (1,6,13,16,20) shows the external pressure (in g/cm) exceeds the intra – vesicular pressures of the venules, capillaries and pre – capillaries; which under static tension would mean the aperture should be closed. However, under these conditions the blood supply to the muscles is even increased ; which was explained by the vibration hypothesis of the hyper-aema of the working skeletal muscles (2,3).

We studied blood flow in a man’s forearm (4) and the isolated gastrocnemius muscles of dogs (5). We established, in our laboratory, an interconnection between blood flow and bioelectricity; especially the vibration sounds of the oscillating muscle fibers; which in turn confirms the vibration hypothesis of the working hyper-aema of the skeletal muscles; which occurs not only under dynamic conditions but static conditions as well.

A new explanation of working hyper- aema from the standpoint of the vibration mechanism; raised a number of questions about its role and significance relative to other mechanisms and hypotheses. We conducted a series of seven studies on an isolated gastrocnemius muscle of a dog keeping the nerves and vessels connected with the organism and the various ends of the vessels.

In the 1st series, the contraction of the arterial inflow empties the thigh veins in the muscles above the  sink  crashing the pressure – gauge; ich the rising the sluggishness of venus pressure  would reach the maximum arterial pressure according to the law of ‘connecting vessels’; but, it does not reach this level; apparently due to the force of the peripheral resistance of the muscular vessels point of blood flow.

When the muscles are stimulated directly or indirectly with the straight – angular electrical stimulation method at varying frequencies from 10 hz, force point from 2 – 3 to 10 long impulses from 0.1 to 300 msec the sluggishness of the venus pressure strives to grow (figure 1, 9), reliably exceeding the maximum arterial pressure (figure 1,8), generated by the heart.

Consequently, the intensification of blood relaxation occurs not only owing to expansion of the vessel circumference, i.e.,  ‘passively’ from the point of view of working hyper aema; but, owing to the inter – organ pumping function of the skeletal muscles.

In the 2nd series both arterial vesicular pressure fell sharply to zero with the simultaneous rise in venus to 70 100 mm/pt.ct. The active intra – organ pump is manifest lacking force  of vis a tergo. {Cardiology: A term referring to the force driving the venous return of peripheral blood, which is supplied by the left ventricle; by the time blood has passed through the capillaries, the blood pressure, or vis-a-tergo, is 15 mm Hg which has a place in the first series.}

In the 3rd (only venous pressure) and 4th series (pressure in both vessels) instead of electro – stimulation we massaged the arm muscles directly all described in the 1st and 2nd series;  where the phenomena was expressed to a larger degree; namely the venous pressure rose to 260 – 300 and higher; however, arterial fell to zero and even reach a negative magnitude uo 5 – 10 mm pt. ct.. This indicates, not only the presence in the working skeletal muscles a super charger; as well as relaxation function.

In the 5th series, a retrograde flow was performed by combining arterial with venous and venous with arterial to a T- shaped glass blood – drip container probably independent of the venous valves stops.

Consequently, the intra – organ pump functions are performed unidirectionally which facilitates the venous valves.

In the 6th (with electro – stimulation) and 7th series (directly massaging the muscle) the experiment was performed with an artificial reserve of  circulating blood (figure 2); here the contraction of skeletal muscle was simulated to unidirectionally circulate fluid; displaying the function of an  independent ‘peripheral heart’. The quantitative characteristics of the ability of skeletal muscle’s circulatory abilities require an independent study.

Our discovery of an intra – organ pumping function of skeletal muscle is not likening it to any known intra – organ pumping function of skeletal or a venous ‘pump’; because it represents a unique mechanism of blood circulation and possesses the following distinguishing characteristics (figure 3).

The ‘venous pump’ functions at the inter – organ level in the large veins with valves and situated between muscles or under them. The ‘venous pump’ increases venous pressure in opposition to hydro – static factors during dynamic muscle work in a standing posture.

The ‘intra – muscular peripheral heart’ functions internally in any posture during dynamic work as well as during static tension. The ‘intra  muscular peripheral heart’ is acting in pre – capillaries, capillaries, venules, and veins, including intra – muscularly elevating venous pressure actively forcing blood from the arteries though the capillaries to the veins.

Figure 1. Schematic of arterial and venous pressure in vessels of an isolated calf muscle of a dog. 1 -gastrocnemius muscle, 2 – thigh artery, 3 – thigh vein, 4 – nerve, 5 – electro – impulsator, 6, 7 – mercury manometers, 8 – depiction of arterial pressure, 9 – depiction of stagnate venous pressure removed from the vein by the contracting muscle, 10, 11 – depiction of the stand, 12 – mark of the zero line, 13 – time line

Figures 2 & 3.

Figure 2. Schematic of blood circulation created for contraction of a dog’s calf muscle. 1 – calf muscle, 2 – thigh artery, 3 – thigh vein, 4 – nerve, 5 – electro –  impulsator

Figure 3. Hemodynamics schematic of the body’s pumps. 1 – heart, 2- venous pump; a – muscle at rest, b – contracting muscle, 3 – the ‘intermuscular peripheral heart’.

Well then, the heart can be conceptualized as the first level of a supercharger of blood circulation; the ‘intermuscular peripheral heart’ as the second level; the venous pump as the third level.

Based on the data obtained we can conclude that according to M.V. Yanovsky (8) the existence of a ‘peripheral heart’; although no acknowledged relative to the arteries; nonetheless prolific. A ‘peripheral hear’ exists, not in the artieries but in the intra – muscular mechanism; the detailed characteristics of which require further study.

Доклады Академии наук СССР 1973. том 210, 1

         удк 612.146.4                                      ФИЗИОЛОГИЯ



(Представлено академиком П. К. Анохиным 30 IX 1972)

От Гарвея ( 11 ) до наших дней принято считать, что единственным двигателем крови является сердце. Имевшие место взгляды о его недостаточности и предсдавления о «периферическом артериальном сердце» ( 8 ) не нашли подтверждения в физиологии и клинике и отнесены к не соответствующим действительности.

 Получили всеобщее признание и стали изучаться экстракардиальные факторы, способствующие кровообращению. К их числу относится, в частности, и насосная функция скелетных мышц или «венозная помпа», действующая в условиях повышения гидростатического давления. Она приводит к снижению застойного венозного давления в нижних конечностях человека при его вертикальном положении ( 9 , , 21).

Открытая И. П. Щелковым и В. К. Задлером в 1869 г. в лаборатории К. Людвига рабочая гиперемия по существующим представлениям не может быть отнесена к категории экстракардиальных факторов потому, что целиком и полностью зависит от нагнетательной функции сердца. При этом механизм расширения просвета сосудов, по которым устремляется усиленный поток крови, нагнетаемой сердцем, до сих пор остается не раскрытым; для объяснения этого механизма создано ряд гипотез 7 10 17 Однако они недостаточны для его исчерпывающего объяснения, а прово, денное нами дальнейшее изучение механизма рабочей гиперемии приводит к новым о ней представлениям.

При изучении соотношения внешнего (со стороны сокращающихся мышц) и внутреннего (со стороны крови) давления на стенки сосудов установлено С, 6 , 13 , 6 ) , что внешнее давление (в г/см 2 ) превышает внутрисосудистое для венул, капилляров и прекапйлляров, просвет которых при статическом напряжении мышц должен закрыться. Однако кровоснабжение мышц в этих условиях даже увеличивается, что было объяснено вибрационной гипотезой рабочей гиперемии скелетных мышц ( 2 , 3 )

 В нашей лаборатории при изучении кровообращения предплечья чело,века ( 4 ) и изолированной икроножной мышцы собаки ( 5 ) установлено наличие взаимосвязи между кровоснабжением и биоэлектрическими, особенно звуковыми и вибрационными колебаниями мышечных волокон, что подтверждает вибрационную гипотезу рабочей гиперемии скелетных мышц, которая осуществляется не только при динамической, но и статической их деятельности.

При новом объяснении рабочей гиперемии с точки зрения вибрационного механизма возник ряд вопросов о его месте и значении среди других механизмов и гипотез. Для их разрешения были проведены 7 серий исследований на изолированной икроножной мышце сббаки с сохранением нервных и сосудистых связей с организмом и различным пережатием сосудов.

В 1-й серии с сохраненным артериальным притоком при пережатии бедренной вены покоящейся мышцы выше канюли ртутного манометра повышение застойного венозного давления должно было достигнуть уровня максимального артериального по >акону сообщающихся сосудов, но оно не достигало этого уровня, по-видимому, в силу периферического сопротивления мышечных сосудов току крови.


При раздражении мышцы прямым или косвенным методом прямоугольными электрическими импульсами с различной частотой от 1 до 400 гц, силой тока от 2—3 до 10 в и длительностью Впјульсов от 0,1 до ЗОО мсек. застойное венозное давление стремительно возрастало (рис. 1, 9) , достоверно превышая максимальное артериальное давление (рис. «1, 8) , развиваемое сердцем. Следовательно, усиление кровоснабжения совершается не только благодаря расширению просвета сосудов, т. е. «пассивно»

Рис. 11. Графическая регистрация артериальпого и венозного давлений в сосудах изолированной икроножной мышды собаки. 1 — икроножная мышца, 2 — бедренная артерия, З— бедренная вена, 4 — седалищный нерв, 5 — электроимпульсатор, 6, 7 — ртутные манометры, 8 — кимограмма артериального давления, 9 — кимограмма застойного венозпого давления при пережатии вены сожращающейся мышцы, 10, 11 — кимограф с приставкой, 12 — отметчик нулевой линии, 13 — отметчик времени

с точки зрения рабочей гиперемии, но и вследствие активной внутриорганной насосной функции скелетных мышц.

Во 2-й серии при одновременном пережатии обоих сосудов и сокращении мышц артериальное давление резко падало вплоть до нуля, а венозное повышалось до 70—100 мм РТ. ст. Активная внутриорганная насосная функция проявлялась при отсутствии сил vis а tergo, которые имели место в первой серии.

В 3-й (при пережатии только вены) и 4-й (при пережатии обоих сосудов) сериях исследований и замене электростимуляции прямым ручным массажем мышцы все описанные в 1-й и 2-й сериях явления были выражены в еще большей степени, а именно венозное давление вырастало до 260—300 и более, а артериальное падало до нуля и даже становилось отрицательным до 5—40 мм РТ. ст. Это указывает на наличие не только нагнетательной, но и присасывающей функции работающих скелетных мышц.

В 5-й серии при ретроградном кровотоке путем соединения артерии. с веной, а вены с артерией Т-образными стеклянными канюлями кровь ток, вероятно в зависимости от венозных клапанов, приостанавливался. Следовательно, внутриорганная насосная функция осуществляется одно, направленно, чему способствуют венозные клапаны.

–В 6-й (при электростимуляции) и в 7-й (при прямом ручном массаже мышцы) сериях исследований с замкнутым искусственным кругом кровообращения (рис. 2) сокращающаяся скелетная мышца оказалась способпой самостоятельно обеспечивать однонаправленную циркуляцию жидко: дти, проявляя функцию самостоятельного «периферического сердца». Количественная характеристика циркуляторной способности скелетной мышцы требует отдельного рассмотрения.

Обнаруженное нами явление внутриорганной насосной функции скелетных мышц не уподобляется общеизвестной внутриорганной насосной функцди скелетных мышц или «венозной помпе» потому, что оно представляет собой самостоятельный механизм кровообращения и имеет следующие отличительные особенности (рис. З) .

«Венозная помпа» функционирует в основном на межорганном уровне в крупных венах, имеющих клапаны и расположенных между мьппцами или под ними. «Венозная помпа» понижает венозное давление, действуя против гидростатического фактора при мышечной динамической работе в вертикальном положении организма.


«Внутримышечное периферическое\сердце» функционирует на внутри-

органном уровне при любых положениях работающего организма как при динамической работе, так и при статйческих напряжениях. «Внутримыщечное периферическое сердце» действует в области прекапилляров, капилляров, венул и вен, заключенных *внутри мышцы, повышая венозное давление и активно перекаџивая кровь •из артерий через капилляры в вены.

Рис. 2. Схема замкнутого круга кровообращения, искусственно созданного для сокращающейся икроножной мышцы собаки. 1 — икроножная мышца, 2 — бедренная артерия, З — бедренная вена, 4 — седалищный хнерв, 5 — электроимпульсатор, 6, 7 — стеклянные ( градуированные трубки, 8, 9, 10 — полиэтиленовые трубки, 11, 12 — Т-образные стеклянные канюли

Рис. З. Схема гемодинамнческих насосов в организме. 1  сердце; 2 — «венозная помпа». а — мышцы в покое,        б — сокращение мышц;       З — «внутримышечное    периферическое сердце»

Рис. 2

Таким образом, сердце можно рассматривать как первый уровень нагнетательной системы кровообращения, «внутримышечное периферическое сердце» — как второй и «венозную помпу» — как третий уровень.

На основании полученных данных можно прийти к заключению, что представления М. В. Яновского ( 8 ) о существовании «периферического

сердца», хотя и не подтвердившиеся по отношению к артериям, оказались плодотворными. «Периферическое сердце» существует, но оно заключено не в артериях, а во внутримышечном механизме, детальная характеристика которого требует дальнейшей разработки.

    Сектор геронтологии                                                      Поступило

    Академии наук БССР                                                        16 х 1972



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Тез. докл. Белорусск. конфер. геронтологов и гериатров, Минск, 1971.

Н а й мит е н к о, Тез. докл. I научн“ой сессии по итогам 1969 г., Минск, (970.

М а нв е лян, Исследования механизмов рабочей гиперемии скелетной мышцы. Автореф. кандидатской диссертации, М., 1968. 7 В. М. Хают ин, XI съезд Всесоюзп. физиол. общ. им. И. П. Павлова, 1, Л., 1970, стр. 264. 8 М. В. Яно в ский, Научная медицина, ЛР2 40, 124 (1922). 9 W. В т а ип е, Das Yenensystem des menschlichen k5rpers, 1, Die 0bersEhenke1vene des Menschen in anatomischer und klinischer Bbziehung, Leipzig, 1873. W. Н. Ga ske11, Л Physi01., З, 48 (1880—1882). W. H arv е у, Exercitation anatomica де •motu cordis et sanguinis in animalibus, Brancofurti, 1628. Т. В. Hich am al., Ат. Heart 7., 37, 1017 (1949).

      Physiol.., 107, 518 (1948).            Но ок er, Ат. 3. Physi01., 28, 54, 235 (1911).•

Н ој ensg ard et al., Acta physiol. scand., 27, 49 (1952). Н. Ma zella, Arch. ind. Physiol., З, 334 (1954). ‘ 17 S. Ме 11 ап der et al., Angiologica, 4, 310 (4967). 18 А. А. P olla ck et al., Ј. Clin. 1nvest., 28, 559 (1949). 19 С. S. Roy, Л G. B rown, 5. Physiol., 2, 323 (1879). 20 О. Sylvest, N. Hvid, Acta rheum. scand., 5, 216 (1959). 21 А. з. Walker et al., Clin. sci., 9, 101 (1950).



From the Textbook Special exercises for Track and Field:

Alabin, V.Gnd Krivnosov, M.P., Trenazhery I Spetsialny Uprazhneniya v Legkoi Atletike, Fizkultury I SportPublishers, Moscow 1982.

Translated by Andrew Charniga

“In their paper “The Intra  Musculature Peripheral Heart,” (1974) N.I. Arinchin and G.D. Nedvatskaya, revealed based on their research, there are essential intramuscular peripheral hearts which assist the “central” heart. The authors corroborated the venous pumps and extra – cardial factors of blood circulation which, along with the central heart, make up the intramuscular heart to perform vital activities; it can function independently and develop appropriate “supercharged” activities which do not take a back seat to the central heart’s pumping functions.

 Indeed, they demonstrated that the pumping function of the peripheral heart can even exceed that of the central heart. They showed that the peripheral heart functions not only at rest, but during work it “pumps” in response to various forms of contraction and stretching. The training of the peripheral heart is of no small significance for facilitating the activities of the central heart.

A natural, logical conclusion can be drawn here; it is necessary to find specific means, exercises and training devices for the skeletal muscles (the intra muscular peripheral heart).”