Professional Documents
Culture Documents
Paper 10
Paper 10
Paper 10
Abstract. Physical exercise is one of the cornerstones for management and treatment type 2 diabetes mellitus. But
not all people are able to perform physical exercise because of their physical limitation condition. The strategy for
those people in this study is electrical stimulation and passive stretching. The aim of this study is to find out the
effect of electrical stimulation and passive stretching to lowering blood glucose level. 20 subjects is divided into
electrical stimulation and passive stretching group. The provision of electrical stimulation on lower extremities
muscles for 30 minutes for electrical stimulation group (N=10). And other underwent passive stretching for 30
minutes (N=10). The result shows that blood glucose level is decrease from 192.9 ± 10.7087 mg/dL to 165.3 ±
10.527 mg/dL for electrical stimulation intervention group while for the passive stretching group the blood glucose
decrease from 153 ± 12.468 mg/dL to 136.1 ± 12.346 mg/dL. Both electrical stimulation and passive stretching are
effective to lowering blood glucose level and can be proposed for those people restricted to perform exercise .
Keywords: blood glucose, electrical stimulation, exercise, lower extremities, passive stretching
INTRODUCTION
Physical exercise has the main role for the management and treatment for type 2
diabetes mellitus (T2DM) to blood glucose control. In T2DM insulin is present but it does not
function efficiently to stimulate glucose uptake into cells so called insulin resistance [1]. The
contraction muscle doesn’t need insulin to stimulate glucose into cells because the insulin
receptor was increased when muscle activated [2]. This is the main reason for T2DM to
perform physical exercise. T2DM without proper treatment can cause serious long-term
complications such as macro vascular and micro vascular disease. But not all T2DM are able
to perform physical exercise. This is due to a very weak physical condition such as very old
patients, lower limb amputation, disability or bedridden state because of chronic illness.
Therefore the new strategy is needed to blood glucose control for T2DM patients who are
unable to perform physical exercise. The intensity of physical exercise is adjusted to age and
physical fitness of the T2DM patients. But it is quite different to determine the intensity of
physical exercise for those T2DM patients. The treatment management of physical exercise
for elderly patients is choosing the activity that suitable for physic and psychics of elderly
patients. In this study we propose Electrical Stimulation (ES) and passive stretching to blood
glucose control. The aim of this study is to compare electrical stimulation and passive
stretching to blood glucose control.
In our previous study we use ES to replace physical exercise for T2DM. The result
shows that electrical stimulation is able to lower blood glucose level significantly. ES
delivered a low current to muscle through surface electrode that causes muscle contraction.
To produce muscle contraction the signal from electrical stimulation must have the same
characteristic to Central Nervous System. The parameter of ES is adjusted to the aim of the
provision ES to achieve the optimal result and prevent fatigue. The parameters of ES are
consist of frequency, duration, duty cycle, intensity/amplitude, pulse pattern, program
duration and muscle group activated [3]. The parameter of ES has to consider the patients
safety and the aim of the provision ES.
The frequency is determined to the aim of the provision of ES. For clinical
application, the 20 – 50 Hz is commonly used to achieve the optimal result [4, 5]. Pulse
duration influence the muscle contraction. The wider pulse duration the bigger muscle
contraction is produced. If the ES is used to produce muscle contraction in subcutaneous
tissue to secondary tissue the duration must be set wider [6]. The study of variety of duration
width 50, 200, 500 and 1000 µs at 20 Hz frequency at soleus muscle shows that the wider
pulse duration will generate the stronger muscle contraction in plantar flexion [7]. Duty cycle
shows the ration on and off signal from ES device. For clinical application the widely used of
duty cycle is 70%, but the ratio can be changed in accordance with the purpose of the
provision of ES [6]. In this study we use 20 Hz of frequency, 200 µs of pulse duration, 50%
duty cycle. The maximum amplitude and maximum current respectively is 80 V 60 mA. The
exercise program duration in this study is 30 minutes, 3 times a week for 4 week [8]. The
intervention ES will be given to lower extremities muscles.
The other strategy for elderly T2DM patients in this study is passive stretching.
Physical exercise should be adjusted to age and physical fitness condition [9]. Management
exercise for elderly T2DM patients is adjusted to the ability of their physical. Stretching is the
possible alternative for elderly and people with a very weak condition. The study conducted
by Nelson state that stretching for 20-40 minutes every day has the same metabolism to rate
estimated walking exercise 40 meter/minute [10]. Passive stretching is exercise within a
person’s muscle through action performed by an outside source. Passive stretching is able to
perform in seat and lying position. Every stretched position is held for 30 seconds and
repeated for 4 times except for the right and left side stretch movement just 2 times
repetitions [10].
Passive stretching on muscle will increase the adenosine monofosfat kinase (AMPK)
that facilitated glucose transport (GLUT 4). The GLUT4 is main factor to determine the
maximal transportation of glucose to skeletal muscle [11]. Sukamoto in his study state that
kinase β protein is stimulated by perform passive exercise to the glucose uptake [12].
METHODS
The study design was pre-post experimental study. The participants are clinically
diagnosed type 2 diabetes mellitus without complication. The inclusion criteria are men and
women ≥ 55 years old, random blood glucose 100 mg/dL ≤ x ≤ 250 mg/dL, willing to sign
the inform concent. The exclusion criteria are type 2 diabetes mellitus with hypertension,
cardiovascular, had any kind of lower limb contracture. The drop out criteria is participant
who unable to complete the study. Subjects is divided into group A (N=10) underwent 30
minutes electrical stimulation on lower limb muscles and group B (N=10) underwent 30
minutes passive stretching supervised by the therapist. The study was approved by Ethical
Committee from Udayana University No.383/UN.13.2/KEP/2016.
Subjects are informed about the aim and procedures of the study. The blood glucose
samples were determined before and after intervention in both groups. The frequency of
intervention is 30 minutes, 3 times a week for 4 week. The first experimental set up for
electrical stimulation intervention (group A) is the placement of surface electrode on vastus
and harmstring muscles. The electrical stimulation is only on lower extremities. The subjects
sitting relax for 30 minutes while the provision electrical stimulation. For the passive
stretching group (group B) is refer to Nelson [10]: Seated knee flexor (bilateral); Seated knee
flexor-hip adductor (bilateral); Seated shoulder lateral flexor (bilateral); Supine hip flexor-
knee extensor (unilateral). Seated hip external rotators, extensor (unilateral); Seated shoulder
extensors, adductors, retractors (unilateral). Supine knee flexor-plantar flexor (unilateral);
Prone hip flexor (unilateral); Seated shoulder flexors, depressors (bilateral); Seated shoulder
and elbow flexors (unilateral). Every stretch is held for 30 minutes and 4 times repetitions
except the movement on right and left side just 2 repetitions.
The blood sample from both group will be statistical analyzed using pair T-test. The
normal data test using Saphiro-Wilk. Data will express by Mean ± Standard Error.
The normality data test using Saphiro-Wilk for electrical stimulation and passive
stretching group respectively are p = 0.959 and p = 0.569. The p-value > 0.05. It means the
data is normal distribution for both groups. The result for electrical stimulation is shown in
figure 1.
200
*
150
mg/dL
100
50
0
Pre-Exp Post-Exp
Electrical Stimulation
Figure 1. The blood glucose level before and after electrical stimulation intervention
*) significantly different before ES (p<0.001)
The baseline blood glucose level for electrical stimulation is 192.9 ± 10.7087 mg/dL
The subjects in this group underwent electrical stimulation intervention 30 minutes, 3 times a
week for 4 week. The result from statistical analysis shows that the decrement of blood
glucose level to 165.3 ± 10.527 mg/dL. The difference from the baseline to last session is
27.6 mg/dL. This result is significantly decrease from the baseline with t =6.720 and p ≤
0.001.
The baseline blood glucose level in passive stretching group is 153 ± 12.468 mg/dL.
After 4 weeks underwent passive stretching the blood glucose level decrease to 136.1 ±
12.346 mg/dL. The decrement of blood glucose level is significant (t=68.840 , p ≤0.001). The
result of passive stretching intervention is shown at figure 2.
200
*
150
mg/dL
100
50
0
Pre-Exp Post-Exp
Passive Stretching
Figure 2. The blood glucose level before and after Passive stretching intervention *) significantly different
before passive stretching(p<0.001)
CONCLUSIONS
Both electrical stimulation and passive stretching can be used to control blood glucose level
for those sedentary patients because of chronic illness, people who have limitation to perform
exercise and people with a lack of motivation to exercise. The result shows that electrical
stimulation is more effective than passive stretching to lowering blood glucose level.
Exercise is one of cornerstone for diabetes mellitus type 2 management and treatment to
control blood glucose level. This is can reduce a substantial financial saving. T2DM patients
with blood glucose controlled prevent or delay the onset of diabetes mellitus complication.
ACKNOWLEDGEMNTS
The authors thank the subject for participation in this study. And the authors express sincere
thanks to Erry Purnomo for the guidance and motivation to do the research
REFERENCES
1. Bolster, D. R., Kubica, N., Crozier, S. J., Williamson, D. L., Farrell, P. A., Kimball, S.
R., & Jefferson, L. S. (2003). Immediate response of mammalian target of rapamycin
(mTOR)‐mediated signalling following acute resistance exercise in rat skeletal muscle.
The Journal of physiology, 553(1), 213-220.
2. Suyono, Slamet. "Diabetes melitus di Indonesia." Buku ajar ilmu penyakit dalam. Edt
Aru W Sudoyo (2006): 1874-1881.
3. Doucet, B. M., Lam, A., & Griffin, L. (2012). Neuromuscular electrical stimulation for
skeletal muscle function. The Yale journal of biology and medicine, 85(2), 201.
4. de Kroon, J. R., IJzerman, M. J., Chae, J. B., Lankhorst, G. J., & Zilvold, G. (2005).
Relation between stimulation characteristics and clinical outcome in studies using
electrical stimulation to improve motor control of the upper extremity in stroke.
5. Bowman, B. R., & Baker, L. L. (1985). Effects of waveform parameters on comfort
during transcutaneous neuromuscular electrical stimulation. Annals of biomedical
engineering, 13(1), 59-74.
6. Bracciano, A. G., & Bracciano, A. G. (2008). Physical agent modalities: Theory and
application for the occupational therapist. Slack.
7. Lagerquist, O., & Collins, D. F. (2010). Influence of stimulus pulse width on M‐waves,
H‐reflexes, and torque during tetanic low‐intensity neuromuscular stimulation. Muscle
& nerve, 42(6), 886-893.
8. Soewondo, P. (2012). Current practice in the management of type 2 diabetes in
Indonesia: Results from the international diabetes management practices study
(IDMPS). Journal of the Indonesian Medical Association, 61(12).
9. PERKENI, K. P. (2011). Pencegahan Diabetes Melitus Tipe II di Indonesia, Jakarta:
PB.
10. Nelson, A. G., Kokkonen, J., & Arnall, D. A. (2011). Twenty minutes of passive
stretching lowers glucose levels in an at-risk population: an experimental study.
Journal of physiotherapy, 57(3), 173-178.
11. Ritzline, P. D., & Levin, A. Z. (2011). Foot and ankle exercises in patients with
diabetes. Foot and ankle
12. Sakamoto, K., McCarthy, A., Smith, D., Green, K. A., Hardie, D. G., Ashworth, A., &
Alessi, D. R. (2005). Deficiency of LKB1 in skeletal muscle prevents AMPK activation
and glucose uptake during contraction. The EMBO journal, 24(10), 1810-1820.
13. Martin, I. K., Katz, A. B. R. A. M., & Wahren, J. O. H. N. (1995). Splanchnic and
muscle metabolism during exercise in NIDDM patients. American Journal of
Physiology-Endocrinology And Metabolism, 269(3), E583-E590
14. Wojtaszewski, J. F., Higaki, Y., Hirshman, M. F., Michael, M. D., Dufresne, S. D.,
Kahn, C. R., & Goodyear, L. J. (1999). Exercise modulates postreceptor insulin
signaling and glucose transport in muscle-specific insulin receptor knockout mice.
Journal of Clinical Investigation, 104(9), 1257
15. Taniguchi, C. M., Emanuelli, B., & Kahn, C. R. (2006). Critical nodes in signalling
pathways: insights into insulin action. Nature reviews Molecular cell biology, 7(2), 85-
96.
16. Jensen, J., Ruge, T., Lai, Y. C., Svensson, M. K., & Eriksson, J. W. (2011). Effects of
adrenaline on whole-body glucose metabolism and insulin-mediated regulation of
glycogen synthase and PKB phosphorylation in human skeletal muscle. Metabolism,
60(2), 215-226.
17. Aslesen, R., Engebretsen, E. M., Franch, J., & Jensen, J. (2001). Glucose uptake and
metabolic stress in rat muscles stimulated electrically with different protocols. Journal
of Applied Physiology, 91(3), 1237-1244
18. Esbjörnsson-Liljedahl, M., Bodin, K., & Jansson, E. (2002). Smaller muscle ATP
reduction in women than in men by repeated bouts of sprint exercise. Journal of
Applied Physiology, 93(3), 1075-1083.
19. van Loon, L. J., Greenhaff, P. L., Constantin-Teodosiu, D., Saris, W. H., &
Wagenmakers, A. J. (2001). The effects of increasing exercise intensity on muscle fuel
utilisation in humans. The Journal of physiology, 536(Pt 1), 295
20. Iwata, M., Hayakawa, K., Murakami, T., Naruse, K., Kawakami, K., Inoue-Miyazu, M.,
& Suzuki, S. (2007). Uniaxial cyclic stretch-stimulated glucose transport is mediated by
a Ca2+-dependent mechanism in cultured skeletal muscle cells. Pathobiology, 74(3),
159-168.
21. Clinch, N. F. (1968). On the increase in rate of heat production caused by stretch in
frog's skeletal muscle. The Journal of physiology, 196(2), 397-414.
22. Feng, T. P. (1932). The effect of length on the resting metabolism of muscle. The
Journal of physiology, 74(4), 441-454.
23. Hamada, T., Hayashi, T., Kimura, T., Nakao, K., & Moritani, T. (2004). Electrical
stimulation of human lower extremities enhances energy consumption, carbohydrate
oxidation, and whole body glucose uptake. Journal of Applied Physiology, 96(3), 911-
916.
24. Knaflitz, M., Merletti, R., & De Luca, C. J. (1990). Inference of motor unit recruitment
order in voluntary and electrically elicited contractions. Journal of Applied Physiology,
68(4), 1657-1667.
25. Vanderthommen, M., Depresseux, J. C., Dauchat, L., Degueldre, C., Croisier, J. L., &
Crielaard, J. M. (2000). Spatial distribution of blood flow in electrically stimulated
human muscle: a positron emission tomography study. Muscle & nerve, 23(4), 482-489.
26. Greenhaff, P. L., Söderlund, K., Ren, J. M., & Hultman, E. (1993). Energy metabolism
in single human muscle fibres during intermittent contraction with occluded circulation.
The Journal of Physiology, 460(1), 443-453.
27. Rika Wahyuni Arsianti (2010). Adaptif fuzzy reinforcement learning untuk aplikasi
kontrol gerakan knee joint dengan functional electrical stimulation. Pasca Sarjana
National Conference X.
28. Kebaetse, M. B., Turner, A. E., & Binder-Macleod, S. A. (2002). Effects of stimulation
frequencies and patterns on performance of repetitive, nonisometric tasks. Journal of
Applied Physiology, 92(1), 109-116.
29. Subin Solomen, Reagen Shakya, Komal Agrawal, Pravi Aaron, Pradeep S (2015).
Passive stretching versus active stretching on immediate blood glucose in subjects with
type II diabetes mellitus – A pilot study. International Journal of Physical Education,
Sports and Health; 2(1):146-149
30. Ihlemann, J., Ploug, T., & Galbo, H. (2001). Effect of force development on contraction
induced glucose transport in fast twitch rat muscle. Acta Physiologica, 171(4), 439-444.