American College of Sports Medicine position stand. Exercise and type 2 diabetes.

Physical activity, including appropriate endurance and resistance training, is a major therapeutic modality for type 2 diabetes. Unfortunately, too often physical activity is an underutilized therapy. Favorable changes in glucose tolerance and insulin sensitivity usually deteriorate within 72 h of the last exercise session: consequently, regular physical activity is imperative to sustain glucose-lowering effects and improved insulin sensitivity. Individuals with type 2 diabetes should strive to achieve a minimum cumulative total of 1,000 kcal x wk(-1) from physical activities. Those with type 2 diabetes generally have a lower level of fitness (VO2max) than nondiabetic individuals. and therefore exercise intensity should be at a comfortable level (RPE 10-12) in the initial periods of training and should progress cautiously as tolerance for activity improves. Resistance training has the potential to improve muscle strength and endurance, enhance flexibility and body composition, decrease risk factors for cardiovascular disease, and result in improved glucose tolerance and insulin sensitivity. Modifications to exercise type and/or intensity may be necessary for those who have complications of diabetes. Individuals with type 2 diabetes may develop autonomic neuropathy, which affects the heart rate response to exercise, and as a result, ratings of perceived exertion rather than heart rate may need to be used for moderating intensity of physical activity. Although walking may be the most convenient low-impact mode, some persons, because of peripheral neuropathy and/or foot problems, may need to do non-weight-bearing activities. Outcome expectations may contribute significantly to motivation to begin and maintain an exercise program. Interventions designed to encourage adoption of an exercise regimen must be responsive to the individual's current stage of readiness and focus efforts on moving the individual through the various "stages of change."

Ageing of the cardiovascular system during 33 years of aerobic exercise.

BACKGROUND: increasing age affects aerobic capacity, with an average loss of 10% or more per decade. AIM: to determine the effect of ageing on the circulatory system in middle-aged men during 33 years of physical training. METHODS: 15 men initially aged 45 years took part in an exercise training programme for 25-33 years. Nine serial measurements were made at rest and during maximal effort. Aerobic training consisted of swimming, jogging, walking and cycling 3-4 times per week. Sessions were for 61-70 min at 77-84% of heart rate reserve. RESULTS: there was no change in resting heart rate, blood pressure, percentage fat or body composition. Minimal cardiovascular losses at maximal work included 5.8-6.8% in maximal oxygen uptake per decade, 25 beats in maximum heart rate and 26 beats in heart rate reserve. CONCLUSION: exercise training has a favourable effect on ageing of the cardiovascular system in older men, resulting in minimal loss of oxygen uptake, no rise in resting blood pressure and no change in body composition.

Cardiovascular changes with age and exercise. A 28-year longitudinal study.

Various studies report a 0-22% per decade decline in circulatory function (VO2max) with advancing age. Twelve exercising men (E) were followed for 28 years, mean age 43 and 71 years, initial to final measurement, while 12 dropouts (C) detrained for 21 years, with a mean age from first to last measurement of 48 and 69 years, respectively. VO2 max in E changed from 45.9 to 39.4 ml.min-1.kg-1, 5% per decade, whereas C declined from 36.0 to 21.4 ml.min-1.kg-1, 19% per decade. Resting blood pressure was unchanged in E, 119/75 mmHg, whereas C rose from 128/85 to 149/90 mmHg. The data suggest that regular aerobic exercise forestalls the usual loss of circulatory function with increasing age.

Effect of exercise on cardiovascular ageing.

Ageing of the cardiovascular system presents several costly public health problems, loss of quality of life, dependency, and other various health hazards. Large declines of 0-24% per decade in cardiovascular function have been cited in the literature but no long-term longitudinal studies have been reported. Serially measured cardiovascular function was performed on 12 normal men, aged 44-79 years, at 0, 10, 15, 20 and 25 years. Over the same time period, daily exercise training data were reported monthly including mode, frequency, intensity, and duration. Although seven men developed some form of pathological disease, the total group's cardiovascular function remained 60% greater than the average of ten investigations. The overall decline in cardiovascular function (Vo2 max) was 13%, or 5% per decade, 45.4 ml.min-1.kg-1 to 39.5 ml.min-1.kg-1. In summary, cardiovascular function was one-half, or 0.24 ml.min-1.kg-1.year-1 of the 0.45 ml.min-1.kg-1.year-1 reported to be the average decline for ageing cited in the literature.

The Effect of Physical Activity and Inactivity on Aerobic Power in Older Men (A Longitudinal Study).

In brief To assess the decline in maximal aerobic power (V O2max) with age, two groups of men were studied: Fifteen exercisers were followed from age 45 to 68, and 15 controls were measured while training at age 52 and again at age 70 after being detrained for 18 years. Resting blood pressure of 120/78 was unchanged in the exercisers but rose from 135/85 to 150/90 in the nonexercisers. V O2max measured by open circuitry declined 13% in the exercisers from 44.4 to 38.6 ml-min(-1)-kg(-1); in the nonexercisers it declined 41% from 34.2 to 20.3 ml-min(-1)· kg(-1). The V Omax loss was primarily due to a combined loss of maximal heart rate and stroke volume. The data suggest that regular aerobic exercise retards the usual loss in aerobic power with age and present important implications for the aging population in relation to social, economic, and health benefits.

Effects of exercise on cardiovascular disease risk in women with NIDDM.

The effect of a 4-month exercise program on measures of cardiovascular disease (CHD) risk was observed in women (mean age = 59.2 +/- 3.9 years) of postmenopausal years with NIDDM, who demonstrated fair to normal control of blood glucose control. The women were randomly assigned to either an exercise (n = 5) or control (n = 5) group. Initially, both groups had a similar body mass index, resting heart rate and blood pressures, blood glucose and hemoglobin A1. After 4 months, the exercise group demonstrated a 32% increase (P less than 0.03) in both absolute and relative maximum oxygen uptake (VO2) while the control group remained unchanged. Significant differences were found between the exercisers and non-exercisers for absolute (F(1,8) 4.94, P = 0.057) and relative (F(1,8) 7.67, P = 0.024) maximum VO2 from pretest to posttest. Body weight (kg) and body fat (%) remained unchanged for both groups. Although total cholesterol was found to be reduced by 13% for the exercise group (P less than 0.03) and 11% for the controls (P less than 0.01), a 15% decrease (P less than 0.03) in high-density lipoprotein (HDL) was observed for the control group, only. Hence, a marked difference (P less than 0.03) in the risk ratio was observed between the exercise and control groups. These data suggest that physical exercise may play an important role in the maintenance of HDL mass and in the reduction of CHD risk factors in women of postmenopausal years with NIDDM.

Effects of insulin infusion on human skeletal muscle pyruvate dehydrogenase, phosphofructokinase, and glycogen synthase. Evidence for their role in oxidative and nonoxidative glucose metabolism.

To determine whether activation by insulin of glycogen synthase (GS), phosphofructokinase (PFK), or pyruvate dehydrogenase (PDH) in skeletal muscle regulates intracellular glucose metabolism, subjects were studied basally and during euglycemic insulin infusions of 12, 30, and 240 mU/m2 X min. Glucose disposal, oxidative and nonoxidative glucose metabolism were determined. GS, PFK, and PDH were assayed in skeletal muscle under each condition. Glucose disposal rates were 2.37 +/- 0.11, 3.15 +/- 0.19, 6.71 +/- 0.44, and 11.7 +/- 1.73 mg/kg X min; glucose oxidation rates were 1.96 +/- 0.18, 2.81 +/- 0.28, 4.43 +/- 0.32, and 5.22 +/- 0.52. Nonoxidative glucose metabolism was 0.39 +/- 0.13, 0.34 +/- 0.26, 2.28 +/- 0.40, and 6.52 +/- 1.21 mg/kg X min. Both the proportion of active GS and the proportion of active PDH were increased by hyperinsulinemia. PFK activity was unaffected. Activation of GS was correlated with nonoxidative glucose metabolism, while activation of PDH was correlated with glucose oxidation. Sensitivity to insulin of GS was similar to that of nonoxidative glucose metabolism, while the sensitivity to insulin of PDH was similar to that of glucose oxidation. Therefore, the activation of these enzymes in muscle may regulate nonoxidative and oxidative glucose metabolism.