SciELO - Scientific Electronic Library Online

 
vol.6 número2Relação entre a mobilidade da articulação talocrural e a úlcera venosaDerivação com veias de membro superior após trombólise de aneurisma de artéria poplítea: alternativa para salvamento de membro índice de autoresíndice de assuntospesquisa de artigos
Home Pagelista alfabética de periódicos  

Serviços Personalizados

Journal

Artigo

Indicadores

Links relacionados

Compartilhar


Jornal Vascular Brasileiro

versão impressa ISSN 1677-5449versão On-line ISSN 1677-7301

J. vasc. bras. v.6 n.2 Porto Alegre jun. 2007

http://dx.doi.org/10.1590/S1677-54492007000200010 

REVIEW ARTICLE

 

Muscle electrostimulation: alternative of adjuvant treatment to patients with peripheral arterial obstructive disease

 

 

Ana Helena de Oliveira MedeirosI; Sintya Tertuliano ChalegreI; Celina Cordeiro de CarvalhoII

IPhysical therapist. Graduate student in Vascular Physical Therapy, Faculdade Integrada do Recife, Recife, PE, Brazil
IIPhysical therapist. MSc. in Biophysics, Universidade Federal de Pernambuco (UFPE), Recife, PE, Brazil. Professor, Physical Therapy, Faculdade Integrada do Recife, Recife, PE, Brazil. Professor and coordinator, Graduate Program in Vascular Physical Therapy, Faculdade Integrada do Recife, Recife, PE, Brazil

Correspondence

 

 


ABSTRACT

Peripheral arterial disease is included in a group of vascular diseases whose evolution is slow and progressive. This article aimed at performing a literature review to evaluate the benefits of chronic electrostimulation as adjuvant treatment for arteriopathic patients. Based on the literature, we concluded that electrostimulation can generate important changes in the metabolic profile of muscle fibers, switching them from type II to type I, which leads to capillary increase, capillary density and suppression of oxygen. Therefore, this therapeutic resource increases aerobic oxidative capacity and ischemic muscle resistance to fatigue. Thus, electrostimulation is another therapeutic option able to improve these patients' walking ability, reducing expenses related to revascularization surgeries and major complications.

Keywords: Peripheral arterial obstructive disease, electrostimulation, skeletal muscle.


 

 

Introduction

Peripheral arterial disease is a common manifestation of systemic atherosclerosis,1 affecting around 20% of the elderly population and increasing risk of other cardiovascular diseases.2

The most frequent symptom of peripheral arterial occlusive disease (PAOD) is intermittent claudication, which is dependent on the difference between oxygen supply, limited by arteriopathy, and oxygen demand for the muscle involved in walking, which varies according to each patient, according to the degree of muscle ischemia and development of collateral circulation.3,4 It is characterized by pain that occurs when walking or exercising and stops with rest.1

Patients can be classified according to symptom intensity. Half of patients with PAOD is asymptomatic. Among symptomatic patients, approximately 40% have intermittent claudication and 10% have critical ischemia. Of these, 3-8% progress to gangrene and require limb amputation.1

Treatment for these patients, which can be conservative or surgical, aims at mitigating symptoms, concerning intermittent claudication, and reducing disease progression and development of cardiovascular complications.1,3 Among the forms of invasive treatment indicated for patients with critical ischemia, or when there are failures in the conservative treatment, percutaneous transluminal angioplasty and arterial bypass stand out.1,5-7

Despite the fact that change in risk factors and cardiovascular exercises, preferentially supervised by skilled professionals, are extremely important for a good progress of PAOD natural history,3,8 many patients cannot be submitted to physical activity due to major cardiovascular restrictions.9-12 Electrostimulation then appears as an alternative method of treatment able to induce muscle activity. Chronic electrostimulation, even without causing any changes in systemic microvascular permeability,11 increases oxygen offer to ischemic muscles through redistribution of blood flow, resulting in improvement in capillary perfusion and optimization of oxygen consumption.13 Such changes improve walking distance and reduce muscle fatigue in patients with intermittent claudication.12

This study was carried out based on the affirmations above and its main objective was to verify, through a review of the literature, the benefits of chronic muscle electrostimulation as an alternative of associate treatment for patients with PAOD.

 

Methods

Searches were performed in MEDLINE and PubMed databases from 1966 to 1995 and from 1996 to 2005. English and Portuguese were the languages defined for that search, and the descriptors used were electrical stimulation, skeletal muscle, intermittent claudication and ischemia, which resulted in a total of 46 articles. Of these, 33 were included in this study, since they were experimental studies and clinical trials about POAD in the lower limbs associated with muscle electrostimulation.

 

Discussion

Types of fibers

The skeletal muscle is not homogeneous, but composed of different types of muscle fibers, each with their own phenotypes.14 Its histological structure has fast and slow muscle fibers and also fibers with intermediate characteristics. The muscles that have a fast reaction are mostly composed of fast fibers (type II) and a reduced number of slow fibers (type I). On the other hand, those that respond slowly and with long contractions are composed of a majority of slow fibers. Fast muscle fibers have a large amount of glycolytic enzymes, lower number of mitochondria and less extensive blood supply, since the oxidative metabolism has secondary importance.15,16

There are three subgroups of fast fibers that are distinguished by the diversity of their metabolic profile. Type IIA fibers, which have a high oxidative and glycolytic potential and are relatively resistant to fatigue; type IIB fibers, which have a large glycolytic ability and are sensitive to fatigue; and type IIC fibers, which are intermediate between types IIA and IIB.16 On the contrary, slow fibers have a less extensive series of capillary and blood vessel network, and a much higher number of mitochondria to maintain high levels of oxidative metabolism.15,16

The metabolic characteristics of those different types of fibers play a major role in muscle fatigue.14 Chronic electrostimulation in skeletal muscles causes deep changes in the metabolic profile of muscle fibers, converting type II fibers into type I through an increase in mitochondrial volume. It also causes changes in oxidative enzyme activity, associated with reduction in glycolytic enzyme activity.5,17

Studies in fast muscles of rabbits submitted to low frequency chronic stimulation showed that the conversion of muscles that suffer fast fatigue and have fast contraction into fatigue-resistant muscles with slow contraction, occur in the following sequence: type IIB type IIA type I,17,18 therefore stressing that electrostimulation increases the proportion of oxidative fibers and reduces glycolytic fibers.19 In another experimental study, in which the medial gastrocnemius muscle of cats was stimulated with a 20-HZ frequency, there was a higher number of type I fibers and few type IIA fibers after 56 days of stimulation, and only type I fibers after 76 days of stimulation, confirming that increase in oxidative potential was followed by loss in high glycolytic enzyme activity of type II fibers.20

McGuigan et al.,2 in their study performed in patients with symptomatic PAOD and in healthy individuals — control, observed that the percentage of type I fibers in the medial gastrocnemius muscle was significantly small in the individuals with PAOD, compared with the control group. There was significant difference between groups as to percentage of type IIA fibers. Therefore, they concluded that availability of oxygen in muscles of patients with PAOD is not a limiting factor of muscle resistance ability, but composition of type of fiber, which can contribute to an early onset of fatigue during physical activity.

Electrostimulation vs. exercise

Electrostimulation also shows strong effects in capillarization, leading to significant increase in capillary density and perfusion and oxygen supply. These factors contribute to increased oxidative aerobic capacity and resistance to fatigue by chronically stimulated muscles, which brings benefits to patients with PAOD.5,17

Increase in skeletal muscle activity, due to endurance training or by chronic electrostimulation, induces capillary growth.19,21-23 The possible factors responsible for such growth can be metabolic, which are related to hypoxia, situation in which there is a large increase in aerobic potency due to increased oxidative enzyme activity and mitochondria. But these factors can also be mechanical, when they are related to increased blood flow during muscle activity.19,24-26

Hypoxia is known as causing fast induction of endothelial cell mitoses by vascular endothelial growth factor (VEGF), and may stimulate early angiogenesis in chronically stimulated muscles.23,27,28 Electrostimulation of fast muscles in rabbits and rats for more than 2 days corrected PO2 and maintained capillary proliferation, occasionally leading to capillary increase and high VEGF proportion in vessels. It also showed that high levels of capillary VEGF persist with chronic electrostimulation after around 14 days. VEGF can be recruited at early capillary growth, induced by electrostimulation through transient hypoxia. However, whether this contributes to maintaining capillary proliferation in late stages can also be related to other factors. Increased capillary shearing force, due to high blood flow during muscle activity, is a possible factor.28

Increased blood flow may increase capillary shearing force, which can be described as a stimulus to endothelial cell proliferation and, consequently, to capillary growth.19,21,22,28-30 McGuigan et al.2 reported that the degree of capillary angiogenesis should be proportional to the intensity of tissue hypoxia.

Anderson et al.10 observed that chronic electrostimulation of fast muscles experimentally caused effects similar to those of endurance exercises. Opposed to aerobic exercise, in which glycolytic fibers are only recruited during high-intensity exercises,26,30 electrostimulation activates all muscle fibers.28,31 Type II fibers are the first to be recruited, which improves resistance to fatigue earlier.9

Many experimental studies have observed that occurrence of capillary proliferation in endurance training is more evident near oxidative fibers.19,24 In chronically electrostimulated muscles, capillaries start growing near glycolytic fibers innervated by large axons preferentially activated during electrostimulation.19 Therefore, changes described in the metabolism of muscles under chronic electrostimulation are different from changes observed in muscles submitted to endurance training. In this type of treatment, oxidative enzyme activity increases, but capillary density/area ratio remains the same whereas muscle fiber becomes hypertrophic. As a result, oxygen diffusion distance is increased. As to electrostimulated muscles, not only does capillary density duplicate after 28 days, according to Hudlická et al.,32 but fiber diameter is also reduced. Therefore, diffusion distance suffers large reduction, and the muscle can obtain complete advantage of a large increase in blood flow during its contraction, and use oxidative enzyme activity more efficiently.32

Capillarization and oxidative capacity

Many studies17,18,30,32,33 performed in laboratory animals have reported that increase in capillarization and oxidative activity follows different time courses. In general, endurance training induces increased capillarization, which is preceded by an increase in oxidative capacity that can be evaluated by increase in oxidative enzyme activity and in mitochondrial volume density.26,30 In opposition, chronic electric stimulation of fast skeletal muscles, in a frequency similar to that observed during discharges of slow motoneurons, increased capillary supply previous to increase in oxidative capacity.30

In a study in which the anterior tibial muscle of rabbits was submitted to low frequency chronic electrostimulation (10 Hz) for 50 days, whereas increase in intercapillary distance, capillary/fiber proportion and mean capillary area occurred soon after 2 days and progressed with stimulation, increase in mitochondrial enzyme activity became evident after 8 days, in average. Therefore, it was only after that electrostimulation period that the anterior tibial muscle showed properties suggesting that energy supply was no longer glycolytic and increasingly based on oxidative phosphorilation. Increase in capillarization reached its peak in 2-3 weeks of electrostimulation, whereas mitochondrial enzyme activity continued to increase. This different time course indicated that improvement in oxygen supply precedes adaptive increase in aerobic-oxidative potential of energy metabolism.17

Another study of fast skeletal muscles of rabbits (anterior tibial and extensor digitorum longus), electrostimulated at a 10-Hz frequency for 8 hours/day during 2-4 days, reported that increase in capillarization also preceded conversion into type of fiber. Capillary density increased earlier in both muscles after 2 initial days of electrostimulation and became definitive after 4 days. Conversion of fibers was observed in a longer stimulation period.33 Those authors observed that, after electrostimulation prolonged for 28 days, all fibers were converted into oxidative. They also observed, in another study, that capillary proliferation is an early occurrence in chronically electrostimulated muscles, reducing fatigue in fast contraction muscles after a short period of electrostimulation.31,34

Tsang et al.5 reported the need of maintaining the treatment with electrostimulation for long periods, since changes caused by it are temporary. In their studies, they observed that patients with PAOD submitted to electrostimulation of flexor muscles of the ankle for 20 minutes, three times a day, at an 8-Hz frequency for 4 weeks, had improvement in claudication distance, besides increase in performance. However, such changes were not maintained after cessation of stimulation.

High and low frequency electrostimulation

Increase in capillary density in skeletal muscles can be achieved both by low and high frequency electrostimulation. Nevertheless, the difference between the effects of both frequencies seems to be in early stimulation stages.24

At a frequency lower than 20 Hz, the work is more directed to muscle resistance, significantly reducing fatigue. Electrostimulation at 10 Hz provides an increase in oxidative aerobic capacity of type I fibers, leading to an increase in vascularization.16 According to Agne,35 frequencies between 5-10 Hz cause muscle vibration, being useful to activate circulation. A frequency higher than 20 Hz produces tetanic contraction, which makes it essential to plan a rest stage lasting for at least the same time of stimulation.16 Robinson & Snyder-Mackler36 reported a direct relationship between frequency intensity and muscle fatigue due to its contraction.

An study of fast muscles of rabbits (anterior tibial muscles, extensor digitorum longus and fibular muscles), stimulated for 14 days, 8 hours/day, at electrostimulation frequencies between 10 and 40 Hz, showed that there are two types of electrostimulation able to produce different responses in muscle blood flow. Continuous electrostimulation at 10 Hz caused a series of individual contractions and a continuous increase in flow to the stimulated muscle, but was not able to produce sufficiently strong contractions to interrupt that flow, even for a short period. Therefore, perfusion pressure in stimulated muscles was similar to systemic pressure. On the other hand, intermittent electrostimulation with pulse trains (repetitive and continuous sequence of a set of impulses and/or volley of electric impulses35) at 40 Hz proved to be able to interrupt local blood flow during tetanic contraction peak, resulting in a perfusion pressure higher than mean systemic pressure.37

Corroborating that previous study, Hudlická & Tyler24 reported a significant increase in capillary density in muscle groups of rabbits when electrostimulated at a 10-Hz frequency. Such increase, observed with only 4 days of stimulation, doubled after 28 days. However, a similar stimulation, but at an intermittent 40-Hz frequency, did not produce any changes in capillary density after 4 days of electrostimulation, only when prolonged for 28 days, resulting in changes similar to those at 10 Hz. These results led the authors to state that, although chronic electrostimulation with a series of tetanic contractions also results in increased capillary/fiber proportion, this only occurs in late stages.24

 

Final considerations

The literature on PAOD is still quite rare in the sense of dealing with muscle electrostimulation as a whole, and most of the studies are experimental.

Based on the search performed in the databases, we can observe that electrostimulation may be an adjuvant treatment for those patients, playing a major role, since it is a noninvasive therapeutic method that has a low cost (around 1/10 lower than an ergometer). This favors an early increase in capillary bed and consequently a better blood flow condition for the ischemic limb, besides activating all muscle fibers, which brings an early improvement in resistance to fatigue.

Therefore, electrostimulation represents an extra resource in the attempt of avoiding disease progress, improving patients' walking ability, since many of them cannot walk because they also have osteoarticular and muscle problems. Such properties are able to reduce costs in revascularization surgeries and risks of amputation and, above all, they help reintegrate patients back to society, improving their quality of life.

 

References

1. Schainfeld RM. Management of peripheral arterial disease and intermittent claudication. J Am Board Fam Pract. 2001;14:443-50.         [ Links ]

2. McGuigan MR, Bronks R, Newton RU, et al. Muscle fiber characteristics in patients with peripheral arterial disease. Med Sci Sports Exerc. 2001;33:2016-21.         [ Links ]

3. Weitz JI, Byrne J, Clagett GP, et al. Diagnosis and treatment of chronic arterial insufficiency of the lower extremities: a critical review. Circulation. 1996;94:3026-49.         [ Links ]

4. Manfredini F, Mangolini C, Mascoli F, et al. An incremental test to identify the pain threshold speed in patients with intermittent claudication. Circ J. 2002;66:1124-7.         [ Links ]

5. Tsang GM, Green MA, Crow AJ, et al. Chronic muscle stimulation improves ischaemic muscle performance in patients with peripheral vascular disease. Eur J Vasc Surg. 1994;8:419-22.         [ Links ]

6. Walder CE, Errett CJ, Bunting S, et al. Vascular endothelial growth factor augments muscle blood flow and function in a rabbit model of chronic hindlimb ischemia. J Cardiovasc Pharmacol. 1996;27:91-8.         [ Links ]

7. Ristow AV, Cury Filho JM. Aterosclerose obliterante periférica: tratamento cirúrgico das lesões abaixo do ligamento inguinal. In: Maffei FHA, Lastória S, Yoshida WB, Rollo HA. Doenças vasculares periféricas. Rio de Janeiro: MEDSI; 2002. cap. 81. p. 1071-106.         [ Links ]

8. Gey DC, Lesho EP, Manngold J. Management of peripheral arterial disease. Am Fam Physician. 2004;69:525-32.         [ Links ]

9. Hudlicka O, Brown MD, Egginton S, Dawson JM. Effect of long-term electrical stimulation on vascular supply and fatigue in chronically ischemic muscles. J Appl Physiol. 1994;77:1317-24.         [ Links ]

10. Thomas DP, Hudlicka O. Arteriolar reactivity and capillarization in chronically stimulated rat limb skeletal muscles post-MI. J Appl Physiol. 1999;87:2259-65.         [ Links ]

11. Anderson SI, Whatling P, Hudlicka O, Gosling P, Simms M, Brown MD. Chronic transcutaneous electrical stimulation of calf muscles improves functional capacity without inducing systemic inflammation in claudicants. Eur J Vasc Endovasc Surg. 2004;27:201-9.         [ Links ]

12. Kelsall CJ, Brown MD, Kent J, Kloehn M, Hudlicka O. Arteriolar endothelial dysfunction is restored in ischaemic muscles by chronic electrical stimulation. J Vasc Res. 2004;41:241-51.         [ Links ]

13. Presern-Strukelj M, Poredos P. The influence of electrostimulation on the circulation of the remaining leg in patients with one-sided amputation. Angiology. 2002;53:329-35.         [ Links ]

14. Hamilton MT, Booth FW. Skeletal muscle adaptation to exercise: a century of progress. J Appl Physiol. 2000;88:327-31.         [ Links ]

15. Guyton AC, Hall JE. Contração do músculo esquelético. Guyton AC, Hall JE. Tratado de fisiologia médica. Rio de Janeiro: Guanabara Koogan; 2002. cap. 6. p. 63-74.         [ Links ]

16. Salgado ASI. Eletroterapia. In: Salgado ASI. Eletrofisioterapia: manual clínico. Londrina: Midiograf; 1999. cap. 2. p. 69-156.         [ Links ]

17. Skorjanc D, Jaschinski F, Heine G, Pette D. Sequential increases in capillarization and mitochondrial enzymes in low-frequency-stimulated rabbit muscle. Am J Physiol. 1998;274(3 Pt 1):C810-8.         [ Links ]

18. Green HJ, Pette D. Early metabolic adaptations of rabbit fast-twitch muscle to chronic low-frequency stimulation. Eur J Appl Physiol Occup Physiol. 1997;75:418-24.         [ Links ]

19. Hudlicka O, Price S. The role of blood flow and/or muscle hypoxia in capillary growth in chronically stimulated fast muscles. Pflügers Arch. 1990;417:67-72.         [ Links ]

20. Gordon T, Tyreman N, Rafuse VF, Munson JB. Fast-to-slow conversion following chronic low-frequency activation of medial gastrocnemius muscle in cats. I. Muscle and motor unit properties. J Neurophysiol. 1997;77:2585-604.         [ Links ]

21. Hansen-Smith F, Egginton S, Hudlicka O. Growth of arterioles in chronically stimulated adult rat skeletal muscle. Microcirculation. 1998;5:49-59.         [ Links ]

22. Pearce SC, Hudlicka O, Brown MD. Effect of indomethacin on capillary growth and microvasculature in chronically stimulated rat skeletal muscles. J Physiol. 2000;526 Pt 2:435-43.         [ Links ]

23. Milkiewicz M, Hudlicka O, Verhaeg J, Egginton S, Brown MD. Differential expression of Flk-1 and Flt-1 in rat skeletal muscle in response to chronic ischaemia: favourable effect of muscle activity. Clin Sci (Lond). 2003;105:473-82.         [ Links ]

24. Hudlicka O, Tyler KR. The effect of long-term high-frequency stimulation on capillary density and fibre types in rabbit fast muscles. J Physiol. 1984;353:435-45.         [ Links ]

25. Zhou AL, Egginton S, Brown MD, Hudlicka O. Capillary growth in overloaded, hypertrophic adult rat skeletal muscle: an ultrastructural study. Anat Rec. 1998;252:49-63.         [ Links ]

26. Carvalho CC, Moraes SRA, Chalegre ST, Tashiro T. Quantificação de capilares no tecido muscular esquelético em animais com insuficiência arterial periférica induzida submetidos a treinamento de endurance. Acta Cir Bras. 2004;19:487-94.         [ Links ]

27. Sondell M, Lundborg G, Kanje M. Vascular endothelial growth factor has neurotrophic activity and stimulates axonal outgrowth, enhancing cell survival and Schwann cell proliferation in the peripheral nervous system. J Neurosci. 1999;19:5731-40.         [ Links ]

28. Hudlicka O, Milkiewicz M, Cotter MA, Brown MD. Hypoxia and expression of VEGF-A protein in relation to capillary growth in electrically stimulated rat and rabbit skeletal muscles. Exp Physiol. 2002;87:373-81.         [ Links ]

29. Hudlicka O, Brown M, Egginton S. Angiogenesis in skeletal and cardiac muscle. Physiol Rev. 1992;72:369-417.         [ Links ]

30. Egginton S, Hudlicka O. Selective long-term electrical stimulation of fast glycolytic fibres increases capillary supply but not oxidative enzyme activity in rat skeletal muscles. Exp Physiol. 2000;85:567-73.         [ Links ]

31. Egginton S, Hudlicka O. Early changes in performance, blood flow and capillary fine structure in rat fast muscles induced by electrical stimulation. J Physiol. 1999;515(Pt 1):265-75.         [ Links ]

32. Hudlicka O, Brown M, Cotter M, Smith M, Vrbova G. The effect of long-term stimulation of fast muscles on their blood flow, metabolism and ability to withstand fatigue. Pflugers Arch. 1977;369:141-9.         [ Links ]

33. Hudlicka O, Dodd L, Renkin EM, Gray SD. Early changes in fiber profile and capillary density in long-term stimulated muscles. Am J Physiol. 1982;243:H528-35.         [ Links ]

34. Hudlicka O, Graciotti L, Fulgenzi G, et al. The effect of chronic skeletal muscle stimulation on capillary growth in the rat: are sensory nerve fibres involved? J Physiol. 2003;546(Pt 3):813-22.         [ Links ]

35. Agne JE. Eletroestimulação neuromuscular. In: Agne JE. Eletrotermoterapia: teoria e prática. Santa Maria: Pallotti; 2004.         [ Links ]

36. Robinson AJ, Snyder-Mackler L. Estimulação elétrica do músculo: técnicas e aplicações. In: Robinson AJ, Snyder-Mackler L. Eletrofisiologia clínica: eletroterapia e teste eletrofisiológico. Porto Alegre: Artmed; 2001. cap. 4. p. 119-46.         [ Links ]

37. Hudlicka O, Fronek K. Effect of long-term electrical stimulation of rabbit fast muscles on the reactivity of their supplying arteries. J Vasc Res. 1992;29:13-9.         [ Links ]

 

 

Correspondence:
Celina Cordeiro de Carvalho
Rua Rio Tejipió, 183/201, Cordeiro
CEP 50721-640 — Recife, PE, Brazil
Tel.:+55 (81) 3226.4459, +55 (81) 9132.3733
Email: celina@fir.br

Manuscript received April 23, 2006, accepted April 3, 2007.

 

 

This study was based on the final paper for the Graduate Program in Vascular Physical Therapy, Faculdade Integrada do Recife, Recife, PE, Brazil.

Creative Commons License Todo o conteúdo deste periódico, exceto onde está identificado, está licenciado sob uma Licença Creative Commons