ISSN 0362-1197, Human Physiology, 2006, Vol. 32, No. 5, pp. 609–614. © Pleiades Publishing, Inc., 2006.

Original Russian Text © D.V. Popov, D.V. Swirkun, A.I. Netreba, O.S. Tarasova, A.B. Prostova, I.M. Larina, A.S. Borovik, O.L. Vinogradova, 2006, published in Fiziologiya Che-
loveka, 2006, Vol. 32, No. 5, pp. 121–127.

Hormonal Adaptation Determines the Increase

in Muscle Mass and Strength during Low-Intensity
Strength Training without Relaxation
D. V. Popov, D. V. Swirkun, A. I. Netreba, O. S. Tarasova, A. B. Prostova,
I. M. Larina, A. S. Borovik, and O. L. Vinogradova
Institute of Biomedical Problems, Russian Academy of Sciences, Moscow, 123007 Russia
Received December 12, 2005

Abstract—The study was designed to test the hypothesis that, during strength training, a restricted blood sup-
ply to the working muscles stimulates the secretion of anabolic hormones and an increase in the muscle mass
and strength can be achieved with significantly lower training loads. During eight weeks, three times a week,
18 young, physically active males trained their leg extensor muscles. Nine subjects (group I) worked at 80% of
the maximal voluntary contraction (MVC), whereas the rest (group II) performed their exercise without relax-
ation and at a lower load (50% MVC). The total training load in group II was significantly lower than in group
I (77 ± 5 vs. 157 ± 7 kJ, respectively). The eight-week training of both groups significantly increased the mean
maximum strength (by 35 and 21% in groups I and II, respectively) and volume (by 17 and 9%, respectively)
of the muscles trained (however, the differences between the groups with respect to these changes were nonsig-
nificant). Group I displayed a higher increase in the blood level of creatine phosphokinase than group II, while
group II showed a greater increase in the blood concentration of lactate. In contrast to group I, group II dis-
played a significant increase in the blood concentrations of growth hormone, insulin-like growth factor 1 (IGF-1),
and cortisol. Hence, the suggestion that the secretion of metabolic hormones is triggered by a metabolic, rather
than mechanical, stimulus from working muscles seems plausible.
DOI: 10.1134/S0362119706050161

INTRODUCTION McCall et al. that the increase in the blood concentra-

tion of growth hormone (GH) is related to the activity
Strength training, aimed at increasing the strength of muscle Ia afferent receptors [4]. In addition, intense
of muscles, leads to the hypertrophy of muscle fibers, strength training, accompanied by a rather high muscle
which is expressed as an increase in the mass of the tension, is also associated with intense synthesis of
muscle trained. Furthermore, this training can rear- autocrine insulin-like growth factor 1 (IGF-1) [5]. On
range the entire regulatory scheme of the locomotor the other hand, it should be taken into consideration
system [1–3]. At least two factors may be involved in that increased concentrations of anabolic hormones are
the development of this hypertrophy. First, it may be frequently explained by certain metabolic changes in
induced by a direct mechanical influence exerted upon the working muscles [1, 6, 7]. For example, controlled
the working muscles. In this case, higher external ischemia of the extremities was shown to potentiate the
loads should produce stronger effects. On the other hormonal response during strength [8] and aerobic
hand, it may be induced by some products of tissue exercises [9, 10].
metabolism abundant in working muscles. Therefore,
it seems reasonable to suppose that a restricted blood This study was designed to test the hypothesis that,
supply to a muscle during its training should intensify during strength training, a restricted blood supply to the
the training effect even at a rather low intensity of working muscles stimulates the secretion of anabolic
mechanical activity. hormones and, therefore, an increase in the muscle
mass and strength can be achieved with significantly
It should be noted that both mechanical activity and lower training loads. Usually, to restrict the blood sup-
metabolic factors can initiate muscle hypertrophy ply to working extremities, some sort of occlusion cuffs
either by direct action on muscle fibers or indirectly, are used [8, 11–13] or an increased pressure is applied
through induced secretion of anabolic hormones. to the lower half of the body placed into a pressure
Which of these two factors (i.e., mechanical or meta- chamber [9, 10, 14], which is extremely inconvenient
bolic) is more important for triggering the hormonal for training. Therefore, to restrict the blood supply to
response to the activity of the muscles? To answer this working muscles, we decided to use low-intensity exer-
question, we should take into account the opinion of cise with incomplete relaxation [15, 16].

609
610 POPOV et al.

Table 1. Volumes of muscles and maximal voluntary contraction before and after eight weeks of strength training
Group I Group II
Parameter (classic strength training) (strength training without relaxation)
before after before after
Volume of the m. quadriceps femoris, cm3 2155 ± 1175 2467 ± 147* 2209 ± 113 2320 ± 75*
Volume of the m. gluteus maximus, cm3 907 ± 57 1064 ± 64* 859 ± 48 979 ± 51*
MVC displayed in exercise, N 410 ± 18 553 ± 29* 397 ± 29* 481 ± 28*
* Significantly different from the pretraining value, p < 0.05.

METHODS many). To avoid aberrations caused by the redistribu-

tion of internal fluids, the subjects remained recumbent
The study was performed with 18 young, physically for 15 min before each MR scan. The results are pre-
active males (age, 21 ± 2 years; body weight, 75 ± 3 kg; sented as the muscle volumes averaged for both legs.
body height, 1.81 ± 0.10 m). All subjects gave their
informed consent before taking part in the study. The Tests for lactate, GH, IGF-1, testosterone, and corti-
study was approved and supervised by the Ethics Com- sol were performed in blood samples taken at weeks 2
mission of the Institute of Biomedical Problems (the and 7 of the training course, 2 h after a standard break-
commission is subordinate to the National Committee fast, immediately before and after the developing exer-
on Biomedical Ethics of the Russian Academy of Sci- cise. Blood samples for creatine phosphokinase (CPK)
ences). and its myocardial isozyme (CPK MB) were taken
before and 18 h after exercise. The level of CPK muscle
During eight weeks, three times a week, these sub- isozyme (CPK MM, released from striated muscle
jects trained the extensor muscles of their knee and hip fibers) was calculated as the difference between the
joints with an exercise machine for leg presses. Nine total CPK activity and the activity of its MB isozyme.
subjects (group I) were trained according to the classic Concentrations of hormones and enzymes were deter-
scheme of strength exercise; the rest (group II) per- mined with the use of DSL test systems (United States).
formed low-intensity exercise without relaxation (their
muscles remained strained throughout the exercise In this paper, all data are presented as mean ± stan-
because they did not move the working platform of the dard error of the mean. The significance of differences
machine to its highest and lowest positions). was determined with the Wilcoxon and Mann–Whitney
tests at p = 0.05. Interrelations between variables were
The weekly schedule of the classic training cycle described with Pearson correlation coefficients.
(group I) consisted of three exercise sessions. The first,
high-load, session (on Monday) was a developing one.
Two toning-up sessions (on Wednesday and Friday) RESULTS
were significantly lower in volume. The developing Eight-week strength training significantly increased
session consisted of seven bouts with 10-min pauses for the strength (by 35 and 21% in groups I and II, respec-
recovery. Each bout was performed at 80% of the max- tively) and volumes of the quadriceps (15 and 6%) and
imal voluntary contraction (MVC; determined before gluteus maximus (18 and 13%) muscles (Table 1).
and after each training cycle) to exhaustion (6–12 repe- However, these data showed no significant differences
titions, 50–60 min). A toning-up session consisted of between the groups. Nevertheless, the total work per-
three bouts with the same pauses. formed during the eight-week training course was sig-
Similarly, three sessions were included in the nificantly lower in group II (77 ± 5 vs. 157 ± 7 kJ in
weekly schedule of the low-intensity training without group I, Fig. 1).
relaxation (group II). The developing session (on Mon- At the beginning of the training course (week 2), an
day) consisted of four sets of three bouts at a load of exercise session increased the blood lactate concentra-
50% MVC. Each 50- to 60-s bout was performed to tion by 6.2 mmol/l (group I) and 10.8 mmol/l (group
exhaustion; the pauses between bouts and between sets II); by the end of the course (week 7), this between-
were 30 s and 10 min, respectively. Toning-up sessions group difference became weaker (Fig. 2).
(on Wednesday and Friday) consisted of single sets. During week 2, group I displayed a 59% greater
The volumes of the quadriceps muscle (m. quadri- postexercise increase in the activity of CPK MM than
ceps femoris) and gluteus maximus muscle (m. gluteus group II (258 ± 69 vs. 152 ± 38 IU/l, respectively).
maximus) were calculated from magnetic resonance However, by the end of the training course, a low-inten-
(MR) spin echo cross-sectional scans (at 1.5 T and 17- sity exercise session (group II) produced a significantly
mm intervals between scans) performed at the Myasni- lesser increase in the activity of this isozyme (65 ± 6
kov Institute of Clinical Cardiology (Moscow) by IU/l; p < 0.05); in contrast, group I displayed only a
means of a Magnetom 63SP apparatus (Siemens, Ger- nonsignificant decrease (Fig. 2). In other words, by the

HUMAN PHYSIOLOGY Vol. 32 No. 5 2006

 HORMONAL ADAPTATION DETERMINES THE INCREASE IN MUSCLE MASS 611

Work, kJ mmol/l
30 15
(a)
25
‡ *
20 *
* 10
15 * * * *
*
10
b
5 5

0
1 2 3 4 5 6 7 8
Training time, weeks
0
‡ b ‡ b
Fig. 1. Time course of the work performed in (a) group I IU/l
(trained according to the classic scheme at a load of 80% (b)
MVC) and (b) group II (trained without relaxation at a load
of 50% MVC). Asterisks indicate significant between- 300
group differences (p < 0.05).

end of the training course, the classic training session 200

(group I) resulted in a 129% higher increase in the
activity of CPK MM than a low-intensity exercise ses-
sion (group II).
100 *
Both at the beginning (week 2) and the end (week 7)
of the training courses, exercise sessions resulted in an
increased secretion of GH. This increase was more pro-
nounced in group II (Table 2). Especially important is 0
‡ b ‡ b
the fact that such a strong GH response persisted Week 2 Week 7
throughout the entire training course. Note that only in
this group was the postsession increase in the blood Fig. 2. Training-induced increases in the concentration of
IGF-1 level significant at weeks 2 and 7, whereas in (a) lactate and (b) activity of creatine phosphokinase muscle
group I it did not change at all (Table 2). The postses- isozyme at the beginning (week 2) and the end (week 7)
sion changes in the concentrations of GH and IGF-1 observed in (a) group I (trained according to the classic
recorded at week 2 showed a rather good correlation scheme at a load of 80% MVC) and (b) group II (trained
without relaxation at a load of 50% MVC). Asterisks indi-
(r = 0.88, p < 0.05). cate significant differences from the concentrations
A significant end-of-the-course (week 7) postexer- detected in the same group at week 2 (p < 0.05).
cise increase in the total testosterone level was
observed only in group I (Table 2).
A significant increase in the blood level of cortisol This fact allows us to conclude that the training scheme
after the exercise was observed only in group II with incomplete relaxation has a rather high hyper-
(throughout the training course, Table 2). By the end of trophic potential.
the course, this group displayed a significant decrease These results can be explained by the assumption
in the testosterone/cortisol ratio, whereas group I dis- that the two training schemes produced different
played only a weak (nonsignificant) trend toward a changes in the blood concentrations of lactate and CPK
decrease in this ratio. MM. Lactate is the end product of anaerobic glycolysis.
Because the work performed during strength exercise
(at 40- to 60-s maximum loads) is supplied with energy
DISCUSSION predominantly through the anaerobic pathway, the
Many researchers have shown that strength training blood lactate level can serve as an indicator of the met-
performed at external loads below 60% MVC does not abolic rates in the working muscles. As expected, a
increase the MVC [11, 17]. In this study, however, we restriction of the blood supply was accompanied by a
observed a significant increase in muscle mass and significant increase in the blood lactate concentration.
strength achieved via low-intensity (50% MVC) At the beginning of the training course (week 2), an
strength training performed without relaxation. These exercise session increased this concentration to 6.2 and
changes were somewhat lower than in the group trained 10.8 mmol/l (in groups I and II, respectively) (Fig. 2).
according to the classic scheme of strength training (at By the end of the course, the difference between the
80% MVC) but did not differ significantly from them. groups became lower. Hence, in spite of the lower vol-

HUMAN PHYSIOLOGY Vol. 32 No. 5 2006

612 POPOV et al.

Table 2. Biochemical parameters of the blood at the beginning (week 2) and the end (week 7) of the training course before
and after training sessions in groups I and II
Group I (classic strength training)
Parameter 2 week 7 week
before after before after
Growth hormone, ng/ml 0.22 ± 0.02 3.47 ± 0.76* 0.20 ± 0.05 6.30 ± 2.82*
Insulin-like growth factor 1, ng/ml 277 ± 39 259 ± 29 276 ± 27 266 ± 30
Testosterone, ng/ml 4.0 ± 0.7 4.1 ± 0.8 3.5 ± 0.5 4.0 ± 0.6*
Cortisol, ng/ml 195 ± 19 259 ± 37 253 ± 22 341 ± 53
Testosterone/cortisol 0.021 ± 0.006 0.014 ± 0.002
Group II (strength training without relaxation)
Parameter 2 week 7 week
before after before after
Growth hormone, ng/ml 0.27 ± 0.03 9.09 ± 1.37* 0.20 ± 0.03 8.29 ± 1.41*
Insulin-like growth factor 1, ng/ml 320 ± 50 350 ± 47* 304 ± 17 372 ± 30*
Testosterone, ng/ml 2.8 ± 0.3 3.4 ± 0.6 2.3 ± 0.5 2.5 ± 0.6
Cortisol, ng/ml 154 ± 18 264 ± 29* 187 ± 14 358 ± 30*
Testosterone/cortisol 0.024 ± 0.006 0.013 ± 0.003**
*Significantly different from the preexercise value, p < 0.05
**Significantly different from the preexercise value recorded at week 2, p < 0.05.

ume of work performed in the training with incomplete Hence, the changes in the blood levels of lactate and
relaxation, the corresponding postexercise blood con- CPK MM observed for the two training schemes indi-
centrations of lactate were higher than its concentra- cate that the classic scheme is associated with greater
tions after the classic training. damage to muscle fibers, manifested through a higher
blood level of this CPK isozyme. On the other hand, the
The presence of muscle CPK in the blood indirectly exercise performed with incomplete relaxation is asso-
reflects the load-dependent damage to cell membranes ciated with a higher rate of glycolysis, which leads to
in the working muscles. For example, any eccentric higher blood concentrations of lactate. This means that
exercise produces higher blood levels of CPK than any the classic training scheme predominantly produces a
concentric exercise [18–20]. At week 2 of our study, its mechanically dependent stimulus that can trigger ana-
increase was higher in group I (Fig. 2), which, most bolic processes in muscle fibers, whereas the training
probably, is related to the higher training load than in scheme with incomplete relaxation is associated with
group II, training at a low intensity without relaxation larger metabolic changes. Any explanation of the
(80 vs. 50% MVC, respectively). Occlusion of the hypertrophic response observed in the latter case (if the
working extremity during low-intensity training does restriction of the blood supply to the working muscles
not increase the postexercise blood level of CPK MM can be regarded as the main feature of this scheme)
[8]. By the end of the training course (week 7), the dif- should necessarily involve the results of occlusion tests.
ference between the groups in the postexercise concen- For example, MR images showed that four weeks of
trations of CPK MM became even greater because of its aerobic bicycle ergometer training (45-min sessions at
significant decrease in group II, which was not accom- a load of approximately 20% MVC performed four
panied by any significant changes in group I (Fig. 2). times a week at an additional pressure of 50 mm Hg
The lower postexercise increase observed at week 7 applied to the lower half of the body) increased the
agrees very well with the fact that, in response to a stan- cross-sectional area (CSA) of a working muscle (pre-
dard load, trained subjects displayed a much lower dominantly, type I and IIB fibers) [9, 14]. The authors
increase in the concentrations of CPK MM than their explain this hypertrophy by higher levels of contractile
untrained counterparts did [21]. A remarkable reduc- proteins and glycogen accompanied by hyperhydration.
tion in its increase after exercise was observed in the Similar results were obtained during eight-week
course of eccentric training, which can be explained by ischemic (with a cuff pressure of 200 mm Hg) low-
weaker damage to membranes (a consequence of adap- intensity strength training (twice a week, four sets of
tation of muscles to high loads) [22]. exercise at 50% MVC) of elite rugby players [11]. In

HUMAN PHYSIOLOGY Vol. 32 No. 5 2006

 HORMONAL ADAPTATION DETERMINES THE INCREASE IN MUSCLE MASS 613

this case, the dynamic strength of the knee extensor muscle ischemia, is caused by stronger effects of meta-
muscles and their CSAs increased by 14 and 15%, bolic stimuli in the muscle during its training with
respectively. Like the accompanying changes in the incomplete relaxation necessarily associated with a
electromyographic activity, these phenomena are restricted blood flow. The eight-week strength training
explained by a corresponding increase in the contractile performed according to the classic scheme or to the
protein content. scheme with incomplete relaxation resulted in rather
An increased secretion of GH and IGF-1 may be similar gains in muscle strength and volume. Our data
responsible for these effects. We found that the postex- allow us to attribute the positive effect of the low-inten-
ercise blood concentration of GH was higher in group sity training performed without relaxation to metaboli-
II, although the mechanical effects exerted on the mus- cally stimulated secretion of anabolic hormones; the
cle fibers were significantly lower than in the classic mechanism of this phenomenon requires further, more
scheme (Table 2). A similar increase in the concentra- detailed analysis.
tion of GH was observed earlier during aerobic and
strength exercises performed with controlled occlusion ACKNOWLEDGMENTS
of veins [8, 10]. The authors of these papers attributed
this effect to the activation of group III and IV afferents We are grateful to O.I. Belichenko, B.E. Sinitsyn,
caused by the local intramuscular accumulation of and D.V. Ustyuzhanin (Myasnikov Institute of Clinical
some physiologically active metabolites that took place Cardiology).
under the restricted blood supply (a phenomenon This work was supported by the Ministry of Science
known as a metabolic reflex). and Education of the Russian Federation (contract no.
IGF-1 is the main mediator of the anabolic effects of 02.467.11.3001 of March 30, 2005) and the Russian
GH. It is secreted both systemically (by GH-stimulated Foundation for Basic Research (project no. 06-04-
liver cells) and in the autocrine way (by skeletal muscle 49699-a).
fibers during their high contractile activity) [5]. For
example, intense synthesis of IGF-1 takes place in mus- REFERENCES
cles after heavy strength training with a rather high
mechanical tension [5]. Similarly, we detected 1. Kraemer, W.J., Patton, J.F., Gordon, S.E., et al., Compat-
increased blood concentrations of IGF-1 only after the ibility of High-Intensity Strength and Endurance Train-
ing on Hormonal and Skeletal Muscle Adaptations,
exercise performed with incomplete relaxation. In con- J. Appl. Physiol., 1995, vol. 78, no. 3, p. 976.
trast, the classic strength training performed with much
higher mechanical loads caused no significant changes 2. Ahtiainen, J.P., Pakarinen, A., Alen, M., et al., Muscle
Hypertrophy, Hormonal Adaptations and Strength
in its concentration. It should be noted that the postex- Development during Strength Training in Strength-
ercise increase in the IGF-1 concentration observed in Trained and Untrained Men, Eur. J. Appl. Physiol., 2003,
the subjects trained with incomplete relaxation coin- vol. 89, no. 6, p. 555.
cided with a higher secretion of GH (Table 2). The sig- 3. Hakkinen, K., Alen, M., Kraemer, W.J., et al., Neuro-
nificant correlation (r = 0.88) between the postexercise muscular Adaptations during Concurrent Strength and
increases in the concentrations of GH and IGF-1 Endurance Training versus Strength Training, Eur. J.
observed during week 2 of the training course allows Appl. Physiol., 2003, vol. 89, no. 1, p. 42.
us to conclude that the increased concentration of 4. McCall, G., Grindeland, R., Roy, R., and Edgerton, V.
IGF-1 resulted from the metabolic increase in the Muscle Afferent Activity Modulates Bioassayable
secretion of GH. Growth Hormone in Human Plasma, J. Appl. Physiol.,
Remarkably, the low-intensity strength training 2000, vol. 89, p. 1137.
stimulated not only the secretion of anabolic hormones 5. Goldspink, G., Mechanical Signals, IGF-1 Gene Splic-
but also the secretion of cortisol. Table 2 shows that, by ing, and Muscle Adaptation, Physiology, (Bethesda)
the end of the training course, group II displayed a sig- 2005, vol. 20, p. 232.
nificant decrease in the testosterone/cortisol ratio com- 6. Gordon, S.E. Kraemer, W.J., Vos. N.H., et al., Effect of
pared to its level during week 2; a similar (although Acid–Base Balance on the Growth Hormone Response
nonsignificant) trend toward a decrease was observed to Acute High-Intensity Cycle Exercise, J. Appl. Phys-
iol., 1994, vol. 76, no. 2, p. 821.
in group I. This indicates that the physiological cost of
this training load is rather high [23]. 7. Lu, S.S., Lau, C.P., Tung, Y.F., et al., Lactate and the
Effects of Exercise on Testosterone Secretion: Evidence
for the Involvement of a cAMP-Mediated Mechanism,
CONCLUSIONS Med. Sci. Sports Exerc., 1997, vol. 29, no. 8, p. 1048.
8. Takarada, Y., Nakamura, Y, Aruga, S., et al., Rapid
This work provides the first evidence that low-inten- Increase in Plasma Growth Hormone after Low-Inten-
sity exercise (at 50% MVC) without relaxation leads to sity Resistance Exercise with Vascular Occlusion,
greater secretion of anabolic hormones than the more J. Appl. Physiol., 2000, vol. 88, no. 1, p. 61.
intensive classic strength exercise (80% MVC). Pre- 9. Sundberg, C.J., Exercise and Training during Graded
sumably, this phenomenon, like the effect produced by Leg Ischemia in Healthy Men with Special Reference to

HUMAN PHYSIOLOGY Vol. 32 No. 5 2006

614 POPOV et al.

Effects on Skeletal Muscle, Acta Physiol. Scand. Suppl., 17. Dons, B., Bollerup, K., Bonde-Petersen, F., and Hancke,
1994, vol. 615, p. 1. S., The Effect of Weight-Lifting Exercise Related to
10. Viru, M., Jansson, E., Viru, A., and Sundberg, C.J., Muscle Fiber Composition and Muscle Cross-Sectional
Effect of Restricted Blood Flow on Exercise-Induced Area in Humans, Eur. J. Appl. Physiol. Occup. Physiol.,
Hormone Changes in Healthy Men, Eur. J. Appl. Phys- 1979, vol. 40, no. 2, p. 95.
iol. Occup. Physiol., 1998, vol. 77, no. 6, p. 517. 18. Cerney, F.G. and Haralambie, G., Exercise-Induced Loss
11. Takarada, Y., Sato, Y., and Ishii, N., Effects of Resistance of Muscles Enzymes, in Knuttgen, H.G., Vogel, J.A., and
Exercise Combined with Vascular Occlusion on Muscle Poortmans, J., Eds., Biochemistry of Exercise, Cham-
Function in Athletes, Eur. J. Appl. Physiol., 2002, paign (IL): Human Kinetics, 1983, vol. 13, p. 441.
vol. 86, no. 4, p. 308. 19. Newham, D.J., McPhail, G., Mills, K.R., and Edwards,
12. Burgomaster, K.A., Moore, D.R., Schofield, L.M., et al., R.H., Ultrastructural Changes after Concentric and
Resistance Training with Vascular Occlusion: Metabolic Eccentric Contractions of Human Muscle, J. Neurol.
Adaptations in Human Muscle, Med. Sci. Sports Exerc., Sci., 1983, vol. 61, no. 1, p. 109.
2003, vol. 35, no. 7, p. 1203.
20. Newham, D.J., Jones, D.A., and Edwards, R.H., Plasma
13. Moore, D.R., Burgomaster, K.A., Schofield, L.M., et al., Creatine Kinase Changes after Eccentric and Concentric
Neuromuscular Adaptations in Human Muscle Follow- Contractions, Muscle Nerve, 1986, vol. 9, no. 1, p. 59.
ing Low Intensity Resistance Training with Vascular
Occlusion, Eur. J. Appl. Physiol., 2004, vol. 92, nos. 4– 21. Evans, W.J., Meredith, C.N., Cannon, J.G., et al., Meta-
5, p. 399. bolic Changes Following Eccentric Exercise in Trained
14. Nygren, A.T., Sundberg, C.J., Goransson, H., et al., and Untrained Men, J. Appl. Physiol., 1986, vol. 61,
Effects of Dynamic Ischaemic Training on Human Skel- no. 5, p. 1864.
etal Muscle Dimensions, Eur. J. Appl. Physiol., 2000, 22. Newham, D.J., Jones, D.A., and Clarkson, P.M.,
vol. 82, nos. 1–2, p. 137. Repeated High-Force Eccentric Exercise: Effects on
15. Seluyanov, V.N., Podgotovka beguna na srednie distan- Muscle Pain and Damage, J. Appl. Physiol., 1987,
tsii (Training of a Middle-Distance Runner), Moscow: vol. 63, no. 4, p. 1381.
SportAkademPress, 2001. 23. Hakkinen, K., Pakarinen, A., Alen, M., et al., Relation-
16. Netreba, A., Popov, D., Vdovina, A., et al. Physiological ships between Training Volume, Physical Performance
Effects of Low-Intensity Strength Training without Capacity, and Serum Hormone Concentrations during
Relaxation, in 10th Annual Congress of the ECSS. Book Prolonged Training in Elite Weight Lifters, Int. J. Sports
of Abstracts, Belgrade, Serbia, 2005, p. 397. Med., 1987, vol. 8, suppl. 1, p. 61.

HUMAN PHYSIOLOGY Vol. 32 No. 5 2006