Insulin Resistance and Resisted Exercise Post Burn
Phase: NA
Conditions: Insulin Resistance
Sponsor: Cairo University

 
 
 
 
 
 
Resisted Exercise and Insulin Resistance 
Post Burn 
 
Documented date : 21/1/2024 
 
 
 
 
 
 
 
 
 
 
 
 
 

 
 
 
 
 
 
Resisted Exercise and Insulin Resistance Post Burn 
 
 
 
By  
Mahmoud Saeed Abdel Aziz Gobara 
Bachelor degree of physical therapy (2016) 
 
 
Submitted for partial fulfillment for requirement of master degree of physical 
Therapy for surgery  
Faculty of Physical Therapy 
Cairo University  
2023 
 
 
 
 
 
 

 
 
 
 
 
 
 
Supervisors 
 
Prof. Dr. Hesham Galal Mahran 
Professor of Physical Therapy Department of Surgery 
Faculty of Physical Therapy 
 Cairo University  
 
 
Dr. Abdallah Ahmed Amin  
Lecturer of plastic and reconstructive surgery  
Faculty of medicine 
Al-Menoufia University 
 
Dr. Amany Refaat Mohammed Abdel Wahid 
Lecturer of Physical Therapy Department of Surgery  
Faculty of Physical Therapy 
 Cairo University  

 
 
 
 
Chapter 1 
Introduction 
 
A burn injury represents the fourth most common type of trauma globally, 
though it is associated with the most devastating consequences. Severe burn injuries, 
encompassing 20% of the total body surface area (TBSA) in adults, present a unique 
challenge compared with other forms of trauma given the magnitude and persistence 
of systemic deregulation. Indeed, an extensive inflammatory response develops 
immediately following a severe burn to promote wound healing. This period, known 
as the “ebb” phase, is comparable with a fight-or-flight response and lasts for the 
first 72–96 h post injury (Lippi et al, 2010). 
Despite a considerable decrease in the incidence of burns in the developed 
world, they remain one of the commonest forms of injury and account for a 
significant proportion of trauma cases in hospital emergencies worldwide. In the 
United States, up to 1.2 million people experience burn injuries each year, while 
there are 2 million fires reported. Most cases (75%) are mild and are treated on an 
out-patient basis. Severe burns, however, continue to cause devastating morbidity 
and significant mortality. 
Emphasis in research on burn pathophysiology has shifted considerably over 
the last few decades. Hypovolemic shock, followed by wound infection, accounted 
for the majority of deaths from burns in the early part of this period. Consequently, 

they were the main areas of burns research in the period leading up to the 1980s. 
Wound treatment, healing and scar problems were also prominent areas in the 
published literature at that time. The direct outcome of this earlier work was that 
various strategies to prevent hypovolemic shock were developed and incorporated 
into clinical practice. These involved phased fluid/colloid replacement regimens 
(P.I. Jewo et al, 2015). 
  
Following an initial sympathetic-mediated shock of a severe injury, the ebb 
phase is accompanied by a depression in the metabolic rate and reduced tissue 
perfusion. Thereafter, the systemic inflammatory response becomes uncontrolled 
and is further exacerbated by tissue and organ dysfunction, which drives the patient 
into a hyper metabolic state—a “flow” phase, which persists after wound healing 
and may last up to 36mo after initial injury (Culnan et al, 2018) . 
  
Hyper metabolism is a classic yet highly complex and multifactorial challenge 
to overcome in patients with severe burns. The chronic increase of circulating stress 
mediators, such as catecholamines and glucocorticoids, drives a multiorgan hyper 
catabolic response resulting in lipolysis, glycogenolysis, and proteolysis leading to 
an insulin-resistant and lipotoxic state, which only worsens the hyper metabolic 
response in a futile cycle (Knuth et al, 2021). 
If hyper metabolism cannot be curbed, the patient may succumb to sepsis 
and/or multi organ failure. Targeting skeletal muscle is central to mitigating hyper 
metabolism, as proteins and amino acids serve as a major fuel source following a 
severe burn. Mechanistically, this results from a substantial increase in muscle 
protein breakdown that grossly exceeds the rate of muscle protein synthesis 
(Hollenberg et al, 2004). 

The enormous energy demand, measured by resting energy expenditure, is a 
typical finding in burn patients, with the increase in metabolism (hypermetabolism) 
dependent on the size of burn. In patients with a TBSA of less than 10%, resting 
energy expenditure remains at physiological levels, but for TBSA in excess of 40%, 
this rate is twice as high during acute admission. Having reached the maximum 
value, the resting metabolic rate in severely burned patients gradually declines, 
amounting to 150%, 140%, 120% and 110% of baseline at the time of burn wound 
healing, 6, 9 and 12 months after thermal injury, respectively (Wojciech Żwierełło 
et al, 2023). 
Moreover, burn-induced muscle catabolism places a significant burden on the 
recovery process, as a 10%–30% loss impairs immune responses and delays wound 
healing, thereby increasing the risk of infection, and a 40% loss becomes fatal. 
Despite a mountainous effort to prevent muscle catabolism and wasting, we have yet 
to provide a safe and effective solution. Therefore, a better understanding of the 
pathophysiology and consequences of burn-induced skeletal muscle wasting is 
pivotal to alleviating hyper metabolism and reducing morbidity and mortality 
patients with severe burns (Rowan et al, 2015). 
Hence, extensive burn injury produce clinical syndromes characterized in part 
by “insulin resistance, it is unclear if these insulin resistant states are identical. To 
test if the maximal biological effectiveness of insulin is altered in burned patients 
(Cree et al, 2007). 
 
The aim of our study is to assess the effect of resisted exercise on insulin 
resistance provide an overview of all procedures needed and current knowledge with 

regard to HOMA IR test to evaluate the progression of insulin resistance post burn 
cases (Hwang et al, 2016). 
Severe burns cause a profound pathophysiological stress response and a 
radically increased metabolic rate that can persist for years after injury. Trauma and 
sepsis also result in hyper metabolism, although to a much lesser degree and for a 
significantly shorter duration .Immediately after severe injury, patients have a period 
of decreased metabolism and reduced tissue perfusion known as the “ebb” phase. 
Soon after, they enter the phase of hyper metabolic rates and hyper dynamic 
circulation, referred to as the “flow” state. This hyper metabolic state reflects an 
increase in whole-body oxygen consumption, and a patient is usually considered 
hyper metabolic when resting energy expenditure (REE) is more than 10% above 
normal. In the acute post burn injury phase, patients with a burn that covers greater 
than 40% of total body surface area (TBSA) have a REE between 40 and 100% 
above normal (Audra Clark et al,2017). 
 
Statement of the problem 
Does resisted exercise affect insulin resistance post burn? 
Purpose of the study  
This study aims to  
The main objective of the present study is to assess the effect of the resisted 
exercise on insulin resistance post burn. 
Significance of the study: 
1- Insulin resistance is a major problem post-burn which may led to serious 
complications. 

2- The lack of knowledge and information in the published studies about the effect 
of resisted exercise on improving insulin resistance post-burn. 
3- This study will be carried out to investigate the effectiveness of resisted exercise 
in improving insulin resistance in post-burned patients. 
 
The hyper metabolic response to injury is characterized by increased blood 
pressure and heart rate, peripheral insulin resistance, and increased protein and lipid 
catabolism, which lead to increased resting energy expenditure, increased body 
temperature, total body protein loss, muscle wasting, and stimulated synthesis of 
acute-phase proteins. These responses occur in all trauma, surgical, or critically ill 
patients, but the magnitude with which they occur and their duration are particularly 
severe and sustained for burn patients (Gerd G Gauglitz et al, 2022). 
 
Delimitation 
This study will be delimited in the following aspects: 
Subjects 
Sixty eight patients with insulin resistance post burn will participate in this study, 
they will be selected from government hospitals (general and insurance). 
Will be randomly divided into two equal groups (group A, group B). 
Their ages range from 18-35 years. 
 
Equipment and tools: 
Measurement: 

Insulin resistance homeostasis model assessment [HOMA IR test]. 
 
Null hypothesis 
There will be no effect for resisted exercise on insulin resistance post burn. 
 
Basic assumption 
It will be assumed that: 
- All patients will be evaluated in the same way. 
- All patients will be cooperative and follow instructions during the 
assessment procedures. 
- The results obtained from this study will be of value in the physical therapy 
field. 
 
Definition of terms: 
The following terms will be defined and explained for a clear understanding of the 
terminology used in this study: 
Insulin resistance 
Insulin resistance is defined as the decreased tissue response to insulin-mediated 
cellular actions and is the inverse of insulin sensitivity. The term “insulin resistance,” 
as generally applied, refers to whole-body reduced glucose uptake in response to 
physiological insulin levels and its consequent effects on glucose and insulin 
metabolism. Euglycemic hyperinsulinemic clamp studies have shown that insulin 
resistance is determined primarily by the response of skeletal muscle, with over 75% 
of infused glucose taken up by muscle and only 2–3% by adipose tissue (Claire 

Levy-Marchal et al, 2010). 
 
 
 
 
Chapter II 
Literature review 
 
Burns affect nearly 300 million patients annually worldwide, with an 
associated substantial mortality. In the USA half a million Americans per year get 
burned, with approximately 40,000 requiring hospitalization. Thermal injuries 
induce systemic bimolecular changes with profound physiological alterations, such 
as increased muscle and bone catabolism, hepatic steatosis, higher susceptibility to 
infections, multiple organ dysfunction, insulin resistance and sepsis. The hyper 
metabolic response, a profound increase in metabolic demand reflected by an 
elevated resting energy expenditure (REE), is the primary contributor to 
aforementioned complications, and can persist for up to 3 years after a severe burn.  
The metabolic changes following burns are not dissimilar to other traumas but 
very different in terms of their extent and persistence; characterized primarily by an 
‘ebb’ phase within 48 h where metabolism, cardiac output and oxygen consumption 
are all decreased. This is typically followed by a ‘flow’ phase at around 120 h post-
burn, where these variables gradually increase and plateau. For instance, the acute 
response allows vital organs to conserve energy, and mild to moderate 
hyperglycemia provides fuel for the brain and immune system after trauma. Burn 

injuries, however, stand out in their intensity and duration. The chronic persistence 
of the hyper metabolic response, which appears to be driven by catecholamine, stress 
hormones, and pro-inflammatory cytokines, far surpasses the ability of the patient 
to respond, and physiological exhaustion ensues. Augmented rates of glycolysis, 
lipolysis and proteolysis induce a loss of lean and total body mass which 
subsequently causes immune dysfunction, decreased wound healing and severe 
infections. Left untreated, the amalgamation of these systemic injuries leads to organ 
dysfunction, sepsis and death (Christopher Auger et al, 2017). 
Insulin resistance can be linked to diabetes, hypertension, dyslipidemia, 
cardiovascular disease and other abnormalities. These abnormalities constitute the 
insulin resistance syndrome. Because resistance usually develops long before these 
diseases appear, identifying and treating insulin-resistant patients has potentially 
great preventive value. Insulin resistance should be suspected in patients with a 
history of diabetes in first-degree relatives; patients with a personal history of 
gestational diabetes, polycystic ovary syndrome or impaired glucose tolerance; and 
obese patients, particularly those with abdominal obesity. Present treatment consists 
of sensible lifestyle changes, including weight loss to attain healthy body weight, 30 
minutes of accumulated moderate-intensity physical activity per day and increased 
dietary fiber intake. Pharmacotherapy is not currently recommended for patients 
with isolated insulin resistance (G Rao, 2001). 
The hypermetabolic response to severe burn trauma is associated with 
increased energy expenditure and energy substrate release from protein and fat 
stores. After burn, protein is catabolized, which leads to a loss of lean body mass 
and muscle wasting (Hart, David W., et al, 2000). 
Clinical features of Insulin resistance 

Severe insulin resistance syndromes show variable metabolic traits and 
diverse clinical manifestations. Along with skin tags, acanthosis nigricans, a velvety 
hyperpigmented thickening of the skin, is an early sign and a common cutaneous 
manifestation of severe insulin resistance. Among women, ovarian dysfunction and 
hyperandrogenism are also common features. Hirsutism, polycystic ovaries, 
menstrual irregularities, or oligomenorrhea usually constitute the primary clinical 
manifestation in affected females. Hyperinsulinemia, in particular the synergy of 
insulin and gonadotropins, is implicated in the pathogenesis of polycystic ovary 
syndrome and ovarian hyperandrogenism. Other clinical features observed in some 
of the severe insulin resistance syndromes include dyslipidemia, namely 
hypertriglyceridemia; nonalcoholic fatty liver disease; adipose tissue loss; abnormal 
adipose topography; abnormal musculature; acromegaloid features; and other 
growth disorders (Angeliki M. Angelidi et al, 2021).  
Conditions Associated with Insulin Resistance: 
Though the development of type 2 diabetes is the most obvious and direct 
consequence of insulin resistance and β (beta)-cell stress that proceeds unchecked, 
there are myriad other associations that healthcare providers should be aware of and 
screen for as indicated. Like insulin resistance, many of these conditions are more 
commonly seen in adulthood, but can certainly affect the pediatric population. Many 
of these disease associations and syndromes are not entirely surprising, given the 
multi organ effects of insulin even beyond glucose homeostatic mechanisms. 
Resistance to insulin-mediated control of circulating fatty acids may predispose to 
worsening dyslipidemia, a well-known risk factor for cardiovascular disease. 
Insulin, in addition, increases androgen synthesis and simultaneously decreases liver 
production of sex hormone-binding globulin, thus providing a mechanism for the 
reproductive disruption seen in PCOS. Consequently, insulin resistance itself is 

associated with many well-known diseases and syndromes that incorporate other 
organ and system effects of insulin (Melinda E. Chen et al, 2019). 
 
 
 
Model assessments of insulin resistance: 
Homeostasis Assessment Model (HOMA). The Homeostasis Assessment 
Model is a mathematical model which allows values for insulin sensitivity and β-
cell function (expressed as a percentage of normal) to be obtained if simultaneous 
fasting plasma glucose and fasting insulin/C-peptide concentrations are known. 
Since insulin secretion is pulsatile, the optimal sample should be the mean of three 
results at 5-min intervals (0, 5, and 10-min samples). However, many researchers 
have used single basal samples for epidemiological studies. HOMA modelling is an 
appropriate method for assessing change in insulin resistance with time in 
individuals. 
HOMA has proved be a robust method for assessing insulin resistance in 
groups of patients over long periods of time because the sampling is simple, and the 
result is available without complex computing as soon as fasting glucose and insulin 
values are available. 
Estimates of insulin resistance from HOMA correlate well with estimates 
from the euglycaemic clamp (Rs = 0.88, P < 0.0001, Rs = 0.85, P < 0.0001). 
Although the coefficient of variation (CV) for HOMA was initially reported as 31%. 
A potential source of confusion is that of terminology, which has sometimes 
allocated normal insulin resistance as 1 or 100%. Sensitivity has always been 

described in percentage terms from 100% as the median norm. However, scales of 
percentages raise their own problems, since statements describing a percentage 
change can be ambiguous—a change on the scale from 50% to 60% is a 10% change 
in units but a 20% relative change (T. M. Wallace, D. R. Matthews, 2002). 
 
The changes in patient metabolism following a major burn may be seen for 
more than 12 months after the initial injury. The ensuing period of 
hypermetabolism and catabolism post-burn leads to impaired immune function, 
decreased wound healing, erosion of lean body mass, and hinders rehabilitative 
efforts delaying reintegration into normal society. The typical changes in 
metabolism are the development of a hyperdynamic circulation, increased body 
temperature, increased protein catabolism with peripheral protein wasting, 
increased lipolysis leading to fatty infiltration of the liver, increased glycolysis and 
insulin resistance. These changes are responsible for much of the morbidity and 
mortality seen with such an injury and as such are important targets for available 
treatments including: early excision and grafting; aggressive treatment of burn, 
early commencement of high protein, high carbohydrate enteral feeding, elevation 
of the immediate environmental temperature to 31.5°C (±0.7°C); and early 
institution of an aerobic and resistive exercise program. Several 
pharmacotherapeutic options are also available to further reduce erosion of lean 
body mass (W. B. Norbury et al, 2006). 
Since rehabilitation exercise training (RET) is considered the cornerstone of 
treating post burn patients, it has been proven that it has a great effect on restoring 
lean body mass, glucose, insulin resistance and protein metabolism. due to 
improvements in acute burn care over the last few decades, most patients with 
severe burns (up to 90% of the total body surface) survive. However, the metabolic 

and cardiovascular complications that accompany a severe burn can persist for up 
to three years post injury. Accordingly, there is now a greater appreciation of the 
need for strategies that can hasten recovery and reduce long-term morbidity post 
burn. RET (including resistance exercise and aerobic exercise) is a vital maneuver 
to restore normal body metabolism and glucose sensitivity in burn survivors. Given 
that RET is a safe and efficacious treatment that restores function and reduces post 
burn morbidity, the purpose is that a long-term exercise prescription plan should be 
considered for all patients with severe burns (Alen Palackic et al, 2021). 
 
 
 
 
 
 
 
 
 
 
 
Chapter III 
Subject, Materials and Methods 

In this part of the study, the materials and methods will be presented under the 
following headings: subjects, equipment, procedures of the study and the statistical 
procedures. 
Sample size 
Sample size calculations will be performed using G*Power statistical software 
(version 3.1.9.2, Franz Faul, University Kiel, Germany) and will be revealed that the 
appropriate sample size for this study is N=68 patients, will be divided into two 
groups each consist of 34 patients, using the following assumptions: alpha level = 
0.05, power = 0.90, effect size (Cohen’s d) = 0.80, and two-tailed test. 
Subjects  
          sixty-eight patients, who have upper limb, upper chest and upper back burn.  
Their ages will be ranged from 18-35 year old. Only patients around (20% - 40%) 
of total body surface area (TBSA) burned. The participants will be selected from 
government hospitals (General and insurance hospitals) and randomly distributed 
into 2 equal groups (group A, group B). 
Design of the study: 
In this study, the patients will be randomly assigned into two equal groups (34 
patients for each group). 
 
 
 
1.1(a) Group A: (Study group) 

This group includes 34 patients who have insulin resistance and who will 
receive resistance exercise and routine medical treatment. The patients will receive 
3 sessions per week for 12 weeks, time of the session is 03 minutes. 
1.1(b) Group B: (Control group) 
This group includes 34 patients who have insulin resistance and who will 
receive routine medical treatment.  
1.2 Criteria for Patients selection. 
The criteria for patients selection are classified into two various criteria: 
1.2 (a) Inclusion criteria 
-  Patients ranged from 18-35 years of age. 
- Patients has waist hip ratio around 0.8 in female and 0.95 in male. 
- Patient has body mass index (BMI around 25 kg/m2) (J Obes Weight Loss Ther 
,2015). 
- Patients has second degree thermal burn injury (superficial and deep partial 
thickness). 
- Patients with around (20% - 40%) of total body surface area (TBSA) burned. 
- Patients who are able to follow verbal commands. 
- Patients will have upper limb, upper chest and upper back burn. 
- Patients with normal hemoglobin A1C (5.6 %). 
- Patients should take diet rich protein, omega 3 and should have good sleep. 
- Patients passed two months post severe burns (Melanie G. Cree et al, 2008). 
1.2 (b) Exclusion criteria 

- Potential participants were excluded if they reported a leg amputation, anoxic 
brain injury, psychological disorders, quadriplegia, or severe behavior or cognitive 
disorders history of heart disease, stroke, diabetes mellitus, or any condition that 
would prevent them from engaging in an exercise study. 
- Patients with liver disease, pancreatic disease or any disease affects metabolism. 
- If they were already engaging in 2 or more planned exercise sessions per week. 
- Patients with any medication to lower glucose levels. Blood pressure and 
medications to lower lipid levels (Lance E. Davidson et al, 2009). 
2. Equipment and Tools: 
Equipment in this study will be divided into two main categories; therapeutic 
and measuring equipment. 
2.1. Therapeutic Equipment: 
Resisted exercise program will be done by using: 
1- Sand bags. 
 
 
2-Elastic bands. 

 
 
3- Resistance machines. 
 
 
 
2.2. Measuring Equipment: 

The following tools are used to assess the insulin resistance: 
 -HOMA-IR analysis will be used to assess insulin resistance by taking  
    Blood sample using sterile syringe 5 cm (Pilar Gayoso-Diz et al, 2013).  
3. Procedures of the study: 
The procedures of this study are classified into the following: 
3.1 Measurement Procedures:  
In this phase HOMA-IR analysis measurements: 
All measurements will be taken before the treatment program, 6 weeks after 
the beginning of treatment program and 12 weeks after the beginning of the 
treatment program. 
 
 
Assessment of insulin resistance: 
 By doing HOMA-IR analysis. 
 Participants were asked to fast for nine hours prior to coming in for blood 
testing. To maximize the validity of the glucose and insulin results, before 
the blood sample, participants filled out a fasting survey that asked specific 
questions addressing the last time they had consumed food or liquids. 
Included in the questionnaire were questions specific to the ingestion of less 
commonly thought of foods such as breathe mints, gum, tea, alcohol, or 
supplements to ensure that the participants were following the fasting 
protocol. Blood samples of 89-92 mL were collected (McKayla J. Niemann 
et al, 2020). 

  HOMA-IR test was performed for both groups before the treatment 
program, after the 6 weeks of the treatment program and after 12 weeks of 
the treatment program to evaluate the progression of insulin resistance in 
both groups. 
 
Scoring  
The HOMA-IR is defined as [fasting glucose (mmol/L) × fasting insulin 
(μmol/L)/22.5] or [fasting glucose (mg/dL) × fasting insulin (μmol/L)/405]. 
The HOMA score of <1.9 was considered as indicator of “Insulin sensitivity”; 1.9 
to 2.9 as indicator of “Low IR” and >2.9 as indicator of Significant IR (Haamid 
Bashir et al, 2022). 
 
3.2 Therapeutic procedures: 
Procedures for the exercise program: 
- Resisted exercise will be done for patients with upper back, upper chest and upper 
limb burn. 
- Resisted exercise will target muscle groups of lower limb. 
- Resisted exercise will be done by using sand bags, elastic bands and resisted 
machines. 
-Three-Repetition Maximum Test 
The first and second sessions of actual training will be spent with patients being 
tested for a three repetition maximum to establish training loads that will be used 

during the training period. The exercises will be performed included leg press, leg 
extension and leg curl. After an instruction period on correct exercise technique the 
patient will perform a warm-up to become familiar with the movement. Next, the 
weight will be progressively increased to which the patient can successfully perform 
four repetitions with correct technique. If four repetitions will be performed with 
correct technique a one minutes rest will be given and the weight will be increased. 
This will be repeated until the patient can perform three repetitions, with the fourth 
repetition not volitionally possible with correct technique, and the test will be 
terminated. The amount of weight lifted from the successful lift will be recorded as 
the individuals three repetition maximum. From this information, the basic 3 sets of 
8-12 repetitions RM’s were established. 
Resisted Exercise Training Program 
Rehabilitative exercise training will be performed as previously described. All 
exercises will be performed using free weights, elastic bands and variable-resistance 
machines. Modifications to exercises will be made when appropriate depending on 
the patient injury characteristics. The load will be gradually increased from 50-60% 
of 3RM at the beginning of the program up to 80-85% of 3RM (repetitions 
maximum) at the end of the program. All exercise sessions will be preceded by a 5-
minute warm-up at <50% VO2peak. No strength training activities will be permitted 
outside the supervised training session; however, both groups will be encouraged to 
maintain normal daily activities (Justin P. Hardee et al, 2014). 
 
4- Statistical procedures: 

 In this study, the mean, the standard deviation and the standard error will be 
calculated for all the patients (2 groups of the study) after the detected time of 
the study. 
 The mean and the standard deviation will be used as a primary source of 
connecting facts about each parameter to measure central tendency. 
 Repeated measure ANOVA test will be used to compare variables within each 
group to detect the level of significance in each group. 
 Unpaired t-test to compare the variable between groups to detect significance 
level between two groups (comparison). 
 The statistical package for social science (SPSS) will be utilized for data 
analysis and the level of significance set at 0.05 levels. 
 
 
 
 
 
 
 
 
 
 
 
Reference 

1- Lippi, G., Ippolito, L., & Cervellin, G. (2010): “Disseminated intravascular 
coagulation in burn injury” In Seminars in thrombosis and hemostasis (Vol. 36, 
No. 04, pp. 429-436). © Thieme Medical Publishers. 
2- Jewo, P. I., & Fadeyibi, I. O. (2015): “Progress in burns research: a review of 
advances in burn pathophysiology” Annals of Burns and Fire Disasters, 28(2), 105. 
3- Culnan, D., Voigt, C., Capek, K. D., Muthumalaiappan, K., & Herndon, D. 
(2018): “Significance of the hormonal, adrenal, and sympathetic responses to burn 
injury” In Total burn care (pp. 248-258). Elsevier. 
4-Knuth, C. M., Auger, C., & Jeschke, M. G. (2021): “Burn-induced 
hypermetabolism and skeletal muscle dysfunction” American Journal of 
Physiology-Cell Physiology, 321(7), C58-C71. 
5- Hollenberg, S. M., Ahrens, T. S., Annane, D., Astiz, M. E., Chalfin, D. B., 
Dasta, J. F., ... & Zanotti-Cavazzoni, S. (2004): “Practice parameters for 
hemodynamic support of sepsis in adult patients”: 2004 update. Critical Care 
Medicine, 32(9), 1928-1948. 
6-Żwierełło, W., Piorun, K., Skórka-Majewicz, M., Maruszewska, A., 
Antoniewski, J., & Gutowska, I. (2023): “Burns: classification, pathophysiology, 
and treatment: a review” International journal of molecular sciences, 24(4), 3749.  
7- Rowan, M. P., Cancio, L. C., Elster, E. A., Burmeister, D. M., Rose, L. F., 
Natesan, S., ... & Chung, K. K. (2015): “ Burn wound Healing and Treatment: 
review and advancements” Critical care, 19, 1-12. 
8- Cree, M. G., Aarsland, A., Herndon, D. N., & Wolfe, R. R. (2007): “Role of 
fat metabolism in burn Trauma-induced skeletal muscle insulin resistance” Critical 
care medicine, 35(9), S476-S483. 
9- Hwang, C. L., Yoo, J. K., Kim, H. K., Hwang, M. H., Handberg, E. M., 
Petersen, J. W., & Christou, D. D. (2016): “Novel all-extremity high-intensity 
interval training improves adults” Experimental gerontology, 82, 112-119. 

10- Clark, A., Imran, J., Madni, T., & Wolf, S. E. (2017): “Nutrition and 
metabolism in burn patients” Burns & trauma, 5. 
10- Gerd G Gauglitz, Felicia N Williams (2022): “Hypermetabolic response to 
moderate-to-severe burn injury and management”. 
11- Levy-Marchal, C., Arslanian, S., Cutfield, W., Sinaiko, A., Druet, C., 
Marcovecchio, M. L., ... & ESPE-LWPES-ISPAD-APPES-APEG-SLEP-
JSPE, and the insulin resistance in children consensus conference group. 
(2010): “Insulin resistance in children: consensus, perspective, and future 
directions. The Journal of Clinical Endocrinology & Metabolism”, 95(12), 5189-
5198. 
12- Auger, C., Samadi, O., & Jeschke, M. G. (2017): “The biochemical 
alterations underlying post-burn hypermetabolism. Biochimica et Biophysica Acta 
(BBA)-Molecular Basis of Disease”, 1863(10), 2633-2644. 
13- Rao, G. (2001): “Insulin resistance syndrome. American Family Physician”, 
63(6), 1159-1164. 
14- Hart, D. W., Wolf, S. E., Chinkes, D. L., Gore, D. C., Mlcak, R. P., 
Beauford, R. B., ... & Herndon, D. N. (2000): “Determinants of skeletal muscle 
catabolism after severe burn” Annals of surgery, 232(4), 455. 
15- Angelidi, A. M., Filippaios, A., & Mantzoros, C. S. (2021): “Severe insulin 
resistance syndromes” The Journal of Clinical Investigation, 131(4). 
61- Chen, M. E., & Hannon, T. S. (2020): “Clinical Manifestations of Insulin 
Resistance in Youth” Insulin Resistance: Childhood Precursors of Adult Disease, 
3-17.    . 
61- Wallace, T. M., & Matthews, D. R. (2002): “The assessment of insulin 
resistance in man” Diabetic medicine, 19(7), 527-534. 

-
61  Norbury, W. B., Jeschke, M. G., & Herndon, D. N. (2006): “Metabolic 
changes following major burn injury: how to improve outcome”. In Intensive Care 
Medicine: Annual Update 2006 (pp. 514-524). Springer New York. 
61- Palackic, A., Suman, O. E., Porter, C., Murton, A. J., Crandall, C. G., & 
Rivas, E. (2021): “ Rehabilitative exercise training for burn injury”. Sports 
Medicine, 51(12), 2469-2482. 
20- Keshel, T. E., & Coker, R. H. (2015): “Exercise training and insulin 
resistance: a current review” Journal of obesity & weight loss therapy, 5(0 5). 
21- Cree, M. G., Fram, R. Y., Barr, D., Chinkes, D., Wolfe, R. R., & Herndon, 
D. N. (2009): “Insulin resistance, secretion and breakdown are increased 9 months 
following severe burn injury” Burns, 35(1), 63-69. 
22- Davidson, L. E., Hudson, R., Kilpatrick, K., Kuk, J. L., McMillan, K., 
Janiszewski, P. M., ... & Ross, R. (2009): “ Effects of exercise modality on 
insulin resistance and functional limitation in older adults: a randomized controlled 
trial” Archives of internal medicine, 169(2), 122-131. 
23- Gayoso-Diz, P., Otero-González, A., Rodriguez-Alvarez, M. X., Gude, F., 
García, F., De Francisco, A., & Quintela, A. G. (2013): “Insulin resistance 
(HOMA-IR) cut-off values and the metabolic syndrome in a general adult 
population: effect of gender and age: EPIRCE cross-sectional study” BMC 
endocrine disorders, 13(1), 1-10. 
24- Bashir, H., Majid, S., Khan, M. S., Bhat, M. H., Hamid, R., Ashraf, R., & 
Faiz, S. (2022): “Inter-relationship of Pro-and Anti-inflammatory Biomarkers with 
the development of Type 2 Diabetes Mellitus”. Heliyon, 8(11). 
25- Niemann, M. J., Tucker, L. A., Bailey, B. W., & Davidson, L. E. (2020): 
“Strength training and insulin resistance: the mediating role of body 
composition” Journal of Diabetes Research, 2020. 
26- Hardee, J. P., Porter, C., Sidossis, L. S., Børsheim, E., Carson, J. A., 
Herndon, D. N., & Suman, O. E. (2014): “Early rehabilitative exercise training in 
the recovery from pediatric burn” Medicine And Science In Sports And Exercise, 
46(9), 1710.