2. According to the World Health Organization
(WHO), 366 million people are projected to have
a form of diabetes by the year 2030.
Increased incidence among VA population
Nearly 4.5% of the world’s population
◦ Prevalence: M > F
◦ Greatest increase in people >65 y.o.
(Wild S, et al. 2004)
3. Cade (2008) notes that:
“As physical therapists increasingly become
first-line providers of treatment for
musculoskeletal and movement disorders in
people with diabetes, it will be important for
clinicians to be keenly aware of the
underlying vascular deficits in their treatment
programs, even if [diabetes] was not the
reason for referral.”
4. Impairment of glucose metabolism in which
glucose is underutilized and blood glucose
levels become abnormally elevated
(hyperglycemia)
Complications: stroke, CVD, genitourinary
dysfunction, neuropathy, diabetic coma,
retinopathy, nephropathy, atherosclerosis,
decreased wound healing/infection,
osteoporosis (Goodman, 2004)
6. Usually diagnosed in childhood (under 20
years).
The body makes little or no insulin, and daily
injections of insulin are required to sustain
life. Without proper daily management,
medical emergencies can arise.
These patients are prone to ketoacidosis and
disorders associated with hyperglycemia.
They comprise ~5-10% of all cases of
diabetes mellitus. (Cade, 2008; Goodman,
2004)
7. Makes up 90% or more of all cases of
diabetes mellitus and historically occurs in
adulthood (over 40 years).
The pancreas does not make enough insulin
for normal blood glucose levels, often
because the body does not respond well to
the insulin.
Continuum with Metabolic Syndrome and
Obesity
8. S & S of Type 1
Diabetes:
Increased thirst
Increased urination
Weight loss in spite
of increased appetite
Fatigue
Nausea
Vomiting
S & S of Type 2
Diabetes:
Increased thirst
Increased urination
Increased appetite
Fatigue
Blurred vision
Slow-healing
infections
Impotence in men
9. ◦ Insulin not present at all, or in sufficient amounts
◦ Glucose collects in bloodstream and can’t enter
cells
OR
◦ Insulin present but cell wall/transport proteins
resistant to its action
◦ Glucose collects in bloodstream and can’t enter
cells
ALL cells in the body require insulin for
glucose to enter the cell, except:
◦ Central nervous system tissue
◦ Working (exercising) muscle tissue
10. Increases GLUT-4 transporters at cell
membrane
◦ Increases transport of glucose into cell
◦ Does NOT require insulin during this time
(temporary; follows exercise)
◦ DOES need some insulin in the system
Over time, increases sensitivity of cells to
insulin (helpful in Type II DM)
Changes composition of lipids in bloodstream
(Gulve, 2008)
11. Check blood glucose BEFORE AND AFTER
exercise
◦ Per Goodman: 100-150 mg/dL before
◦ Per Gulve: >/= 110 mg/dL after
Do NOT exercise if BGL is:
◦ < 100 mg/dL
◦ > 250-300 mg/dL
Optimal timing for exercise is 2-3 hours after
meal (between peaks of fast-acting and slower-
acting components of insulin) (Goodman 2004)
Low to moderate intensity is best to prevent
abrupt changes in BGL (Gulve 2008)
12. Gibson, et al. (2013) found that predictors for
acute glucose response to exercise included:
◦ Pre-exercise glucose
◦ % age adjusted max HR
◦ Duration of exercise
◦ Minutes since eating
◦ Hgb A1c
◦ Age
13. Aerobic Exercise: 150 min a week, spread
over at least 3 days each week
◦ “aerobic activity alone cannot deliver the full
benefits of exercise to individuals with Type 2
DM”
Resistance Exercise (strength training): 2 to 3
times a week
◦ highly effective adjunct for weight loss
◦ only type of exercise offering some protection
against sarcopenia and decreasing muscle
strength/physical function occurring with age
(agrees with findings by Gulve, 2008)
14. Exercise helps improve insulin sensitivity (DMII)
Exercise counteracts several negative outcomes
of the disease process
◦ Atherosclerosis (change in lipid concentrations)
◦ Cardiovascular disease (improved CV function)
◦ Poor wound healing (boosting immune system)
◦ Neuropathy (increased VO2)
Exercise can improve weight-control efforts
(DMII)
Timing of insulin and/or meds may be the
most important self-controlled factor to tight
glycemic control
15. Cade, TW. Diabetes-related microvascular and macrovascular
diseases in the physical therapy setting. Phys Ther.
2008;88(11):1322-1335. doi:10.2522/ptj.20080008
Gibson BS, Colberg SR, Poirier P, et al. Development and
validation of a predictive model of acute glucose response to
exercise in individuals with type 2 diabetes. Diabetology & Metab
Synd. 2013;5(33):1-9.
Goodman CC, Fuller KS, Boissonnault WG. Pathophysiology:
implications for the physical therapist. 2003;2nd ed. pp. 350-1.
Gulve, EA. Exercise and glycemic control in diabetes: benefits,
challenges, and adjustments to pharmacotherapy. Phys Ther.
2008;88(11):1297-1321. doi:10.2522/ptj.20080114
Wild S, Roglic, G, Green A, Sicree R, King H. Global prevalence of
diabetes estimates for the year 2000 and projections for 2030.
Diabetes Care. 2004;27(5):1047-1053.
doi:10.2337/diacare.27.5.1047