Volume 11 Number 4, 1998, Pages 231-237
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Exercise Precautions and Recommendations for Patients With Autonomic Neuropathy
Ann L. Albright, PhD, RD
Physical activity has the potential to yield several health benefits for people with diabetes. These benefits can include improvements in glucose control,1-3 insulin sensitivity,4-6 lipid profile,7,8 blood pressure,9,10 coagulation properties,11 body composition,12,13 and psychological well-being.14,15
Nearly everyone with diabetes can derive some benefit from an exercise program, although not all benefits will be realized by each person with diabetes. Both health care professionals and patients with diabetes need to remember this when determining the components of an exercise program. When chronic complications of diabetes develop, the benefits and risks of exercise must be carefully considered to maximize the benefits and assure safety.16 This is especially true when evaluating the use of exercise in diabetes complicated by autonomic neuropathy.
In considering the benefits and risks of exercise for those with chronic complications of diabetes, attention must also be given to the effects of not participating in some level of physical activity. Known as disuse syndrome, the deleterious effects of an imbalance between rest and physical activity include decreased physical work capacity, muscle atrophy, negative nitrogen and protein balance, cardiovascular deconditioning, pulmonary restrictions, and depression.17 The consequences of disuse combined with the complications of diabetes are likely to lead to more disability than the diabetes complications alone. Since physical activity can prevent or reverse disuse syndrome, serious consideration must be given to the use of exercise in all people with diabetes, including those with autonomic neuropathy.
Diabetic autonomic neuropathy can strike any system of the body (e.g., cardiovascular, respiratory, neuroendocrine, gastrointestinal, genitourinary, sudomotor, or ocular), since the autonomic nervous system regulates all involuntary functions in the body. Many of these systems are integral to the ability to perform exercise. The possible risks from autonomic neuropathy on the bodys response to exercise and resulting safety considerations are discussed below. Table 1 provides a summary of the effects of autonomic neuropathy on exercise risk.18
EFFECTS OF AUTONOMIC NEUROPATHY ON EXERCISE RESPONSE Cardiovascular
It is generally considered that parasympathetic dysfunction precedes sympathetic loss. However, more sensitive tests have revealed that there may be pervasive but uneven areas of sympathetic denervation of the heart, which otherwise appears normal, and these findings indicate significant risk for premature death.20,21
Patients with CAN have higher resting heart rates and lower maximal heart rates during exercise than diabetic patients without autonomic neuropathy.22 The lower maximal heart rate achieved during exercise makes the use of heart rate to gauge exercise intensity inappropriate for many of these patients.
Unexplained sudden death not associated with myocardial infarction, in which the heart becomes unresponsive to nerve impulses (cardiac denervation syndrome), has been reported in diabetic patients with CAN.23,24 A variety of potential mechanisms have been proposed to explain sudden death, but an exact understanding of this occurrence remains speculative.
Prolonged QT intervals corrected for heart rate (QTc) have been found in diabetic patients with autonomic neuropathy.24,25 A prolonged QTc is an indicator of increased risk for sudden death. Lengthening of QT/QTc intervals over time is associated with deterioration of autonomic function.
Some investigators have suggested that the electrocardiographic evaluation of QT/QTc interval should be conducted to evaluate autonomic neuropathy in that this evaluation may provide some information about the risk of sudden death.18 It should be noted, however, that inter-observer variability with regard to the measurement of QT interval and QT dispersion is high.26 Thus, although this noninvasive method for identifying patients who may be at an increased risk of life-threatening ventricular arrhythmias is promising, one should be aware of difficulties with regard to QT measurements.
Ventricular function. Abnormal left ventricular responses to exercise have been observed in patients with CAN.27,28 Zola and associates found depressed left ventricular systolic function in the absence of ischemic heart disease in approximately one-third of patients with autonomic neuropathy.22,29 Reduced mean ejection fractions at rest and with maximal exercise have also been reported.30 Abnormal diastolic function has been found in patients with more severe CAN.31 This finding was correlated with a reduction in catecholamine levels and postural hypotension, indicating sympathetic involvement with cardiac diastolic dysfunction.31 These potential ventricular function abnormalities indicate the importance of prescribing exercise at low to moderate intensities in this patient population.
Blood pressure. Blood pressure response with posture change and during exercise is abnormal in those with CAN. Postural hypotension, often defined as a drop in systolic blood pressure of >2030 mmHg or a drop in diastolic blood pressure of >10 mmHg upon standing, may be seen.
Postural hypotension is caused by the failure of reflex vasoconstriction in the splanchnic area and the subcutaneous tissues, and its extent is related to the severity of baroreflex dysfunction.32 As a result of this vasoconstrictive dysfunction, the blood pressure response to exercise does not increase to expected levels in these patients. A lower mean systolic blood pressure response at comparable relative exercise workloads in patients with autonomic neuropathy compared to diabetic subjects without this complication has been reported.19,22 Zola and Vinik, however, also found that subjects occasionally have severely exaggerated increases in blood pressure.3
The symptoms of postural hypotension may occur with eating or within a few minutes of taking insulin. The effect of insulin may be the result of direct action on the peripheral blood vessels, causing vasodilation.34 The insulin-induced hypotension is often worse in the morning and improves later in the day.18 This must be taken into consideration when determining the timing of exercise in relation to meals and insulin injections. Exercise may need to be deferred to later in the day, and insulin should not be injected just before exercise, regardless of the location of the injection.
Postural hypotension symptoms are similar to those of hypoglycemia and may be mistaken for a drop in blood glucose, even though they are due to a drop in blood pressure. Patients should be alerted to the potential confusion in these symptoms and instructed to check blood glucose before treating for hypoglycemia.
Sobotka and associates reported that five of eight patients with diabetic autonomic neuropathy lost their ventilatory drive and ventilatory response to hypoxemic conditions at rest.35 They concluded that the respiratory dysfunction in these patients resulted from the failure of initiation of respiratory drive under conditions of hypoxia and that the defect was either in the carotid body or in the parasympathetic afferents. No significant difference in the ventilatory response to transient hypoxia with exercise between diabetic subjects with and without autonomic neuropathy was found by Calverly and associates.36
During exercise, additional input from other sources, such as catecholamines or local chemical changes in muscles, may compensate.37 Tantucci and associates found that diabetic subjects with autonomic neuropathy had an excessively increased respiratory rate and alveolar ventilation with stressful exercise (>90% maximum predicted heart rate or symptom-limited).38 A progressively higher inspiratory activity was proposed to be involved with the greater ventilatory response to exercise. The suggested mechanism was reduced neural inhibitory modulation from sympathetic afferents and/or increased CO2 chemosensitivity. This finding emphasizes the need to be cautious about exercise intensity.
Abnormal Neuroendocrine Response
A blunted response of catecholamines and other glucoregulatory hormones to exercise has been reported in those with autonomic neuropathy, but with no effect on blood glucose values.39 The specific importance of this abnormal neuroendocrine response on exercise or post-exercise metabolism is unclear, but it may be a contributing factor to exercise intolerance.
Liquids are preferred over solids to prevent or treat hypoglycemia in patients with gastroparesis, since the rate of liquid emptying remains within the normal range for most of these patients.40 Individuals using diabetes medications that can cause hypoglycemia should keep liquids containing carbohydrate available during and after exercise.
It is vital for patients with hypoglycemia unawareness to frequently check their blood glucose to prevent episodes of unconsciousness. Frequent monitoring of blood glucose is especially important when participating in physical activity, since reductions in blood glucose can occur up to several hours after the conclusion of exercise.
Sweating and Cutaneous Blood Flow Disturbances
Both sweating disturbances and compromised cutaneous blood flow in the lower limbs underscore the need to provide appropriate foot care information to these patients before they begin an exercise program. Patients must use properly fitting shoes and routinely examine their feet before and after exercise. It is also extremely important that patients stay adequately hydrated and do not exercise in extreme temperatures.
Tests that evaluate the cardiovascular reflexes are most often used because of their noninvasive nature and the importance of identifying the potentially serious cardiovascular problems resulting from autonomic neuropathy. The reader is referred to pages 224 and 227 for discussions of autonomic testing.
Exercise Capacity and Evaluation for the Presence of Coronary Artery Disease
The exercise test should begin at an intensity significantly below the expected peak or symptom-limited capacity. The test should gradually increase in 2- or 3-minute stages with a suggested duration of 10 ± 2 minutes.49 Indications for terminating the test should be carefully observed. Test results should be the basis for determining duration and intensity of the exercise program.
CAD is a major concern in patients with diabetes, and it is important that those with autonomic neuropathy also be screened carefully for this. Symptoms of angina are not reliable indicators of CAD in those with autonomic neuropathy, since these patients have a higher frequency of silent myocardial ischemia and infarction. Exercise thallium scintigraphy is the preferred screening for CAD in those with diabetic autonomic neuropathy.29,50
The need to carefully assess patients should not serve as a deterrent for recommending safe exercise for those with autonomic neuropathy, particularly if a patient expresses an interest in physical activity.
Exercise recommendations for those with complications of diabetes are based primarily on test results from acute bouts of exercise and on clinical judgement, with primary attention given to safetynot on the results of specific training studies in these diabetic populations. Therefore, exercise guidelines are considered approximate, and modifications must be made for each patient. A conservative approach to exercise is recommended for those with autonomic neuropathy.
The exercise prescription must address recommendations on intensity, type, duration, frequency, and rate of progression of physical activity based on the findings of careful evaluation. In addition, patients must be given information on safety precautions and symptoms to be aware of if discernible ones do develop. It may be most appropriate for those with CAN to participate in exercise programs supervised by people trained in cardiac care who have an adequate understanding of diabetes.18
Instead, careful attention should be given to a patients subjective feelings of intensity using the Rating of Perceived Exertion (RPE) scale (Table 2). The exercise intensity is prescribed according to the numerical values associated with corresponding adjectives subjectively describing intensity. Vinik recommends that patients strive to reach a moderate-range RPE (~3) gradually over 24 weeks.18 It is important that health care professionals clearly explain the RPE scale and emphasize its reliance on patients subjective feelings. Exercise should be terminated if a patient is unable to continue talking or, if pedaling, to maintain a consistent pedaling frequency.51
Activities that should be encouraged in this population are stationary cycling, semi-recumbent cycling, and water exercises.51 Water activities and semi-recumbent cycling are especially beneficial for those with orthostatic hypotension, since the pressure of water surrounding the body and the semi-recumbent posture, respectively, help maintain blood pressure. Sitting in a chair doing light resistance exercises (e.g., lifting light weights or using an elastic exercise band) may help maintain or increase muscle strength.
Activities that should be avoided are those that cause rapid changes in body position (e.g., certain calisthenics) or that cause rapid and significant changes in heart rate and blood pressure (e.g., high-intensity running or lifting heavy weights).
The intensity and duration of physical activity may be modest in many of these patients. If even a small amount of physical activity can be done each day, it will allow patients to derive some of the benefits of physical activity more safely. It is more likely the activity will become a habit if participation occurs on a daily basis. In addition, daily activity will lessen the difficulty of balancing insulin dosages and food intake with physical activity in those taking insulin. Daily physical activity should be attempted, but it is important to remind patients that when days are missed, they should begin again as soon as possible and not feel defeated.
Rate of Progression
PREVENTION OF HYPERGLYCEMIA AND HYPOGLYCEMIA
A mismatch between insulin levels and blood glucose may be especially common in patients with gastroparesis. Exercise should be planned around gastric delivery of nutrients in order to try to maximize the acute glucose-lowering effects of exercise.
Because of the risk of hypoglycemia unawareness in patients with autonomic neuropathy, patients must receive careful instruction about the frequency and timing of SMBG, insulin action (peak and duration), and the importance of trying to avoid exercise at the peak of insulin action or before the stomach has delivered its contents (if gastroparesis is also present). Patients should be instructed on how to treat hypoglycemia, and significant others should be trained in the use of glucagon. A set time for participating in physical activity may be helpful in reducing the adjustments that need to be made to avoid hypo- and hyperglycemia.
MAINTENANCE OF THE EXERCISE PROGRAM
The Ease of Access Index asks the question, "How easily can I engage in my activity of choice where I live?" Many times, people select activities that they initially feel they can accomplish, but when examined in more depth, they find that they may have ignored, rationalized, or just not been aware of factors that may serve as barriers to long-term adherence to an exercise plan. To determine the ease of access for a given activity, patients should be asked to consider the following questions:
If the selected exercise activity is reasonably accessible, then an assessment of the ease of performance should be conducted. The Ease of Performance Index assesses of how suitable the activity is in terms of personal physical attributes and lifestyle. Patients should be asked to consider the following questions:
The use of these two indices will hopefully help patients and health care professionals to consider in advance issues that often undermine long-term participation in physical activity.
Other factors that may assist patients in maintaining a physical activity program include the following:54
Autonomic neuropathy may affect several systems that are necessary for the bodys adjustment to exercise, particularly the cardiovascular system. Careful testing to evaluate autonomic function and to determine exercise capacity and the presence of CAD are extremely important. The need for careful evaluation before starting an exercise program should not prevent participation in physical activity. Working with patients to develop an appropriate exercise plan will yield a program with the greatest capability of maximizing the benefits.
1Lampman RM, Schteingart DE: Effects of exercise training on glucose control, lipid metabolism, and insulin sensitivity in hypertriglyceridemia and non-insulin dependent diabetes mellitus. Med Sci Sports Exercise 23:703-12, 1991.
2Reitman JA, Vasquez B, Klimes I, Nagulusparan M: Improvement of glucose homeostasis after exercise training in non-insulin-dependent diabetes. Diabetes Care 7:734-41, 1984.
3Schneider SH, Amorosa LF, Khachadurian AK, Ruderman NB: Studies on the mechanism of improved glucose control during regular exercise in type 2 (non-insulin-dependent) diabetes. Diabetologia 26:325-60, 1984.
4Horton ES: Exercise and physical training: effects on insulin sensitivity and glucose metabolism. Diabetes Metab Rev 2:1-17, 1986.
5Koivisto VA, Yki-Jarvinen H, DeFronzo RA: Physical training and insulin sensitivity. Diabetes Metab Rev 1:445-81, 1986.
6Mayer-Davis EJ, DAgostino R, Karta AJ, Haffner SM, Rewers MJ, Saad M, Bergman RN: Intensity and amount of physical activity in relation to insulin sensitivity. JAMA 279:669-74, 1998.
7Kohl HW, Gordon NF, Villegas JA, Blair SN: Cardiorespiratory fitness, glycemic status, and mortality risk in men. Diabetes Care 15:185-92, 1992.
8Ruderman NB, Ganda OP, Johansen K: The effect of physical training on glucose tolerance and plasma lipids in maturity-onset diabetes. Diabetes 28(Suppl 1):89-92, 1979.
9Krotkiewski M, Lonnroth P, Mandroukas K, Wroblewski Z, Rebuffe-Scrive G, Holm: The effects of physical training on insulin secretion and effectiveness and on glucose metabolism in obesity and type 2 (non insulin dependent) diabetes mellitus. Diabetologia 28:881-90, 1985.
10Schneider SH, Khachadurian AK, Amorosa LF, Clemow L, Ruderman NB: Ten-year experience with an exercise-based outpatient lifestyle modification program in the treatment of diabetes mellitus. Diabetes Care 15(Suppl 4):1800-10, 1992.
11Schneider SH: Long-term exercise programs. In The Health Professionals Guide to Diabetes and Exercise. Ruderman N, Devlin JT, Eds. Alexandria, Va., American Diabetes Association, 1995, p. 125-32.
12Klem ML, Wing RR, McGuire MT, Seagle HM, Hill JO: A descriptive study of individuals successful at long-term maintenance for substantial weight loss. Am J Clin Nutr 66:239-46, 1997.
13Wing RR: Behavioral strategies for weight reduction in obese type 2 diabetic patients. Diabetes Care 12:139-44, 1989.
14Lustman P, Carney R, Amado H: Acute stress and metabolism in diabetes. Diabetes Care 4:658-59, 1981.
15Vasterling JJ, Sementilli ME, Burish TG: The role of aerobic exercise in reducing stress in diabetic patients. Diabetes Educ 14:197-201, 1988.
16Devlin JT, Ruderman N: Diabetes and exercise: the risk-benefit profile. In The Health Professionals Guide to Diabetes and Exercise. Ruderman N, Devlin JT, Eds. Alexandria, Va., American Diabetes Association, 1995, p. 3-4.
17Valbona C: Bodily responses to immobilization. In Krusen Handbook of Physical Medicine and Rehabilitation, 3rd ed. Kottke FJ, Stillwell GK, Lehman JF, Eds. Philadelphia, Pa., WB Saunders, 1982, p. 963-75.
18Vinik AI: Neuropathy. In The Health Professionals Guide to Diabetes and Exercise. Ruderman N, Devlin JT, Eds. Alexandria, Va., American Diabetes Association, 1995, p. 183-97.
19Hilsted J, Galbo H, Christensen NJ: Impaired cardiovascular responses to graded exercise in diabetic autonomic neuropathy. Diabetes 28:313-19, 1979.
20Sisson JC, Wieland DM, Sherman P, Mangner TJ, Tobes MC, Jacques JR: Metaiodobenzylguanidine as an index of the adrenergic nervous system integrity and function. J Nucl Med 28:1620-24, 1987.
21Sisson JC, Shapiro B, Meyers L, Mallette S, Mangner TJ, Wieland DM, Glowniak JV, Sherman P, Beierwaltes WH: Metaiodobenzylguanidine to map scintigraphically the adrenergic nervous system in man. J Nucl Med 28:1625-36, 1987.
22Kahn JK, Zola B, Juni J, Vinik A: Decreased exercise heart rate and blood pressure response in diabetic subjects with cardiac autonomic neuropathy. Diabetes Care 9:389-94, 1986.
23Kahn JK, Sisson JC, Vinik AI: Prediction of sudden cardiac death in diabetic autonomic neuropathy. J Nucl Med 29:1605-06, 1988.
24Ewing DJ, Boland O, Neilson JM, Cho CG, Clarke BF: Autonomic neuropathy, QT interval lengthening, and unexpected deaths in male diabetic patients. Diabetologia 34:182-85, 1991.
25Kahn JK, Sisson JC, Vinik AI: QT interval prolongation and sudden cardiac death in diabetic autonomic neuropathy. J Clin Endocrinol Metab 64:751-54, 1987.
26Hill JA, Friedman PL: Measurement of QT interval and QT dispersion. Lancet 349:894-95, 1997.
27Mildenberger RR, Bar-Shlomo B, Druck MN: Clinically unrecognized ventricular dysfunction in young diabetic patients. J Am Coll Cardiol 4:234-38, 1984.
28Vered Z, Battler A, Sega P: Exercise-induced left ventricular dysfunction in young men with asymptomatic diabetes mellitus (diabetic cardiomyopathy). Am J Cardiol 54:633-37, 1984.
29Zola B, Kahn J, Juni J, Vinik AI: Abnormal cardiac function in diabetics with autonomic neuropathy in the absence of ischemic heart disease. J Clin Endocrinol Metab 63:208-14, 1986.
30Scognamiglio R, Fasoli G, Ferri M, Nistri S, Miorelli M, Egloff C, Buja G, Fedele D, Dalla-Volta S: Myocardial dysfunction and abnormal left ventricle exercise response in autonomic diabetic patients. Clin Cardiol 18:276-82, 1995.
31Kahn JK, Zola B, Juni JE, Vinik AI: Radionuclide assessment of left ventricular diastolic filling in diabetes mellitus with and without cardiac autonomic neuropathy. J Am Coll Cardiol 7:1303-309, 1986.
32Ewing J, Clarke BF: Diabetic autonomic neuropathy: present insights and future prospects. Diabetes Care 9:648-65, 1986.
33Zola BE, Vinik AI: Effects of autonomic neuropathy associated with diabetes mellitus on cardiovascular function. Curr Sci 3:33-41, 1992.
34Takata S, Yamamoto M, Yagi S, Noto Y, Ikeda T, Hattori N: Peripheral circulatory effects of insulin in diabetes. Angiology 36:110-15, 1985.
35Sobotka PA, Liss HP, Vinik AI: Impaired hypoxic ventilatory drive in diabetic patients with autonomic neuropathy. J Clin Endocrinol Metab 62:658-63, 1986.
36Calverly PMA, Ewing DJ, Campbell IW, Wraith PK, Brash HM, Clarke BF, Flenley DC: Preservation of the hypoxic drive to breathing in diabetic autonomic neuropathy. Clin Sci 63:17-22, 1982.
37Flenley DC, Warren PM: Ventilatory response to O2 and CO2 during exercise. Annu Rev Physiol 43:415-26, 1983.
38Tantucci C, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Scionti L, Sorbini CA: Ventilatory response to exercise in diabetic subjects with autonomic neuropathy. J Appl Physiol 81:1978-86, 1996.
39Hilsted J, Galbo H, Christensen NJ: Impaired responses of catecholamines, growth hormone, and cortisol to graded exercise in diabetic autonomic neuropathy. Diabetes 29:257-62, 1980.
40Barnett JL, Vinik AI: Gastrointestinal disturbances. In Therapy for Diabetes Mellitus and Related Disorders. Lebovitz HE, Ed. Alexandria, Va., American Diabetes Association, 1994, p. 288-96.
41Stansberry KB, Hill M, McNitt PM, Bhatt BH: Cutaneous blood flow reactivity and neuropathy. Abstract. Diabetes 43(Suppl 1):107A, 1994.
42Vinik A, Mitchell B: Clinical aspects of diabetic neuropathies. Diabetes Metab Rev 4:223-53, 1988.
43Fraser D, Campbell I, Ewing D: Peripheral and autonomic nerve function in newly diagnosed diabetes mellitus. Diabetes 26:546-50, 1977.
44Young R, Ewing D, Clarke B: Nerve function and metabolic control in teenage diabetics. Diabetes 32:142-47, 1983.
45Pfeifer MA, Weinberg CR, Cook DL, Reenen A, Halter JB, Ensinck JW, Porte D: Autonomic neural dysfunction in recently diagnosed diabetic subjects. Diabetes Care 7:447-53, 1984.
46McDaid EA, Monaghan B, Parker AI, Hayes JR, Allen JA: Peripheral autonomic impairment in patients newly diagnosed with type 2 diabetes. Diabetes Care 17:1422-27, 1994.
47Albright AL: Diabetes. In ACSMs Exercise Management for Persons with Chronic Diseases and Disabilities. Durstine JL, Ed. Champaign, Ill., Human Kinetics, 1997, p. 94-100.
48American Diabetes Association: Position statement: Diabetes mellitus and exercise. Diabetes Care 21(Suppl 1):S40-44, 1998.
49Franklin BA: Myocardial infarction. In ACSMs Exercise Management for Persons with Chronic Diseases and Disabilities. Durstine JL, Ed. Champaign, Ill., Human Kinetics, 1997, p. 19-25.
50Kahn JK, Vinik AI: Exercise training in the diabetic patient. Med Interne 9:117-25, 1988.
51Graham C, Lasko-McCarthey P: Exercise options for person with diabetic complications. Diabetes Educ 16:212-20, 1990.
52U. S. Department of Health and Human Services: Physical Activity and Health: A Report of the Surgeon General. Atlanta, Ga., U. S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996.
53Marrero DG, Sizemore JM: Motivating patients with diabetes to exercise. In Practical Psychology for Diabetes Physicians: How to Deal with Key Behavioral Issues Faced by Health Care Teams. Anderson BJ, Ruben RR, Eds. Alexandria, Va., American Diabetes Association, 1996.
54Albright AL, Franz M, Hornsby G, Kriska A, Marrero D, Ullrich I, Verity L: ACSM position stand: physical activity and type 2 diabetes mellitus. Med Sci Sports Exercise. In preparation.
Ann L. Albright, PhD, RD, is director of the California Department of Health Services Diabetes Control Program in Sacramento.
Copyright © 1998 American Diabetes Association
Last updated: 11/98