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Women who are estrogen deficient have an increased risk of osteoporosis and future fractures. In recent years, improving technology and a consensus on the definition of osteoporosis have made it easier to measure bone density and assess the risk of osteoporosis. Density should be measured at two sites, the lumbar spine and the femoral neck. If only one measurement is possible, the site should be the lumbar spine in women younger than 65 and the femoral neck in women 65 and older. Treatment is recommended if a woman's bone density is more than one standard deviation below the young adult reference value.

Plasma free fatty acid (FFA) levels tend to be lower and the plasma lipolytic hormone response to prolonged exercise of the same intensity is blunted after endurance exercise training. To determine whether training elicits a corresponding decrease in plasma FFA turnover and metabolism during prolonged exercise, we measured plasma [1-13C]palmitate kinetics and oxidation and respiratory gas exchange in 13 subjects during the latter portion of a 90- to 120-min bout of cycle ergometer work performed before and after 12 wk of alternate-day cycling and running. Training increased total fat oxidation during prolonged exercise by 41% (P < 0.005). However, for the final 30-60 min of the cycle ergometer protocol, the rate of 13CO2 production from [1-13C]palmitate oxidation was 27% lower (P < 0.05), the rate of palmitate turnover was 33% less (P < 0.05), and plasma FFA and glycerol concentrations were 32 and 20% lower (P < 0.05), respectively, than in the untrained state. Thus endurance exercise training results in decreased plasma FFA turnover and oxidation during a 90- to 120-min bout of submaximal exercise because of a slower rate of FFA release from adipose tissue.

The purpose of this study was to examine the relationship of bone mineral density (BMD) to muscular strength in highly trained young male athletes in order to gain insights concerning the influence of heavy resistance training on BMD. Twenty-five elite junior weightlifters (age, 17.4 +/- 1.4 yr) and 11 age-matched controls (16.9 +/- 1.1 yr) volunteered for this investigation. Measurements of BMD (g.cm-2) utilizing dual energy x-ray absorptiometry were obtained for the lumbar spine (L2-4) and the proximal femur (neck; trochanter, Ward's triangle). The BMD values for the junior lifters were found to be significantly greater at all sites for the junior weightlifters compared with their age-matched control group. The BMD values of the spine and femoral neck of the junior weightlifters when compared with adult reference data (i.e., 20-39 yr old men) were found to be significantly greater. Both simple and multiple regression analyses demonstrated significant relationships of BMD with strength accounting for 30-65% of the variance. These data suggest that in elite junior weightlifters, muscle strength, highly specific to the sport of weightlifting, has a major influence on BMD due to the influence of the chronic overloads experienced in training.

This study examined the effects of age and physical activity on body composition and fat distribution by comparing differences between young and older endurance trained men and women with differences between young and older sedentary people. Although indices of total body adiposity (fat mass, percent body fat) were higher in the older than in the young people in both the trained and the sedentary groups, the magnitude of the difference was markedly less in the trained group (P less than 0.01). The average differences in fat mass between young and old sedentary men and women were 10.1 kg and 12.2 kg, respectively, but only 4.3 kg and 5.5 kg in trained men and women. Skinfold thicknesses were approximately 24% and approximately 47% larger at all sites (triceps, thigh, subscapula, pectoralis, umbilicus, suprailiac) in the older than in the young trained men and women, respectively. Similar differences were found between young and older sedentary people except at central, upper body sites, where the relative differences in skinfold thicknesses between young and older sedentary people were 2- to 6-fold greater than in trained people. Thus, people who exercise regularly appear to accumulate less adipose tissue in upper, central body regions as they get older, potentially reducing the risk for the metabolic disorders associated with upper body obesity.

Insulin secretion in response to glucose stimulation is reduced in endurance-trained humans. In this study, a modified hyperglycemic clamp, with a superimposed arginine infusion and fat meal, was performed on eight endurance-trained and nine untrained men to determine whether insulin secretory capacity is reduced by exercise training. Raising the plasma glucose concentration to approximately 450 mg/dl resulted in a plasma insulin response in the trained men that was approximately 64% lower than that of the untrained (peak values: 54 +/- 8 vs. 149 +/- 35 microU/ml; P less than 0.001). When a primed continuous infusion of arginine was superimposed on the hyperglycemia, the plasma insulin response was also markedly lower (66%) in the trained subjects, reaching peak values of 333 +/- 68 and 974 +/- 188 microU/ml for trained and untrained subjects, respectively (P less than 0.005). When insulin secretion was further stimulated during the arginine-infused hyperglycemia by the ingestion of a high-fat meal, peak insulin concentrations averaged 989 +/- 205 microU/ml in the trained compared with 2,232 +/- 455 microU/ml in the untrained subjects (P less than 0.01). The response of gastric inhibitory polypeptide (GIP) to the fat meal was delayed and blunted, suggesting that some enteric factor(s) other than GIP mediated the insulinotropic effect of the fat meal. The reduced plasma insulin response in trained people to the stimuli investigated suggests that regular exercise produces either several adaptations within the beta-cell or a single alteration of the beta-cell that results in an attenuation of the insulin secretory response to glucose, arginine, and fat ingestion.

Estrogen deficiency in postmenopausal women is associated with low lumbar bone mineral density and an increased incidence of fractures of the vertebrae and proximal femur. Estrogen deficiency in premenopausal women with secondary amenorrhea related to athletic training or anorexia nervosa is also associated with decreased lumbar bone mineral density. The purpose of this review is to present four concepts related to the adaptations of bone to physical exercise, as a basis to explain the loss of bone mass in women with athletic amenorrhea. These concepts are based on Lanyon's theory of a Minimum Effective Strain-Related Stimulus. The bone remodeling response to estrogen deficiency is an increase in the rate of bone remodeling activity and in the rate of bone resorption relative to formation, resulting in a net loss of bone mass. In the presence of estrogen deficiency, the stimulus of physical activity is thought first to decrease the rate of turnover and secondly to increase bone formation. Endurance exercise training appears to be an insufficient stimulus to accomplish both tasks, which may explain why these athletes often have low lumbar bone mineral density.

Thirteen healthy, untrained males (age 44 +/- 1 yr, range 40-55 yr) were studied to determine the effects of 16 wk of high-intensity, variable-resistance, Nautilus strength training on cardiovascular function. A control group consisting of 10 untrained males (age 52 +/- 2 yr, range 40-64 yr) underwent the same evaluation procedures as the training group. Maximal oxygen uptake (VO2max), cardiac output during submaximal exercise, and body composition were determined before and after training. In addition, the physiological responses to an acute training session were evaluated. Muscular strength increased markedly, as evidenced by a 44% average increase in the "one-repetition maximum" in the various exercises. Body weight and percent body fat did not change with training, though fat-free weight did increase (66.9 +/- 2.6 vs 68.8 +/- 2.7 kg, P less than 0.05) significantly. Maximal oxygen uptake did not change significantly in either the training or the control group, and there were no changes in the hemodynamic responses to submaximal exercise after training. These findings indicate, therefore, that high-intensity, variable-resistance strength training produces no adaptative improvement in cardiovascular function. The physiological responses measured during a training session provide evidence that this lack of cardiovascular adaptation may be due to the low percentage of VO2max elicited by this form of exercise.

We employed the hyperglycemic clamp technique to investigate the effects of short-term inactivity on insulin secretion in nine (8 men, 1 woman) well-trained subjects. A 3-h hyperglycemic clamp (plasma glucose approximately 180 mg/100 ml) was performed approximately 16 h after a usual training bout and again 14 days after stopping exercise training. There was no significant change in body composition during this short period of inactivity. The mean plasma insulin response to an identical glycemic stimulus was 67% higher after 14 days without exercise (45 +/- 7 after vs. 27 +/- 4 microU/ml before stopping exercise training). Marked increases in the early (0-10 min, 150 +/- 28 vs. 101 +/- 15 microU.ml-1.min) and late (10-180 min, 6,051 +/- 1,257 vs. 3,521 +/- 749 microU.ml-1.min) incremental insulin areas were observed as a result of the physical inactivity. Incremental areas for C-peptide were also elevated significantly in the inactive state for early (12 +/- 2.0 vs. 7 +/- 1 ng.ml-1.min) and late (567 +/- 90 vs. 467 +/- 85 ng.ml-1.min) phases. Urinary excretion of C-peptide increased from 12.1 +/- 1.5 ng/240 min in the exercising state to 21.8 +/- 3.6 ng/240 min in the inactive state. Rates of whole body glucose disposal were not different between exercising and inactive states, indicating a large increase in resistance to the action of insulin. These findings indicate that the decreased insulin secretory response to a glucose stimulus in people who exercise regularly is a relatively short-term effect of exercise.

The respiratory exchange ratio (RER) is lower during exercise of the same intensity in the trained compared with the untrained state, even though plasma free fatty acids (FFA) and glycerol levels are lower, suggesting reduced availability of plasma FFA. In this context, we evaluated the possibility that lipolysis of muscle triglycerides might be higher in the trained state. Nine adult male subjects performed a prolonged bout of exercise of the same absolute intensity before and after adapting to a strenuous 12-wk program of endurance exercise. The exercise test required 64% of maximum O2 uptake before training. Plasma FFA and glycerol concentrations and RER during the exercise test were lower in the trained than in the untrained state. The proportion of the caloric expenditure derived from fat, calculated from the RER, during the exercise test increased from 35% before training to 57% after training. Muscle glycogen utilization was 41% lower, whereas the decrease in quadriceps muscle triglyceride concentration was roughly twice as great (12.7 +/- 5.5 vs. 26.1 +/- 9.3 mmol/kg dry wt, P less than 0.001) in the trained state. These results suggest that the greater utilization of FFA in the trained state is fueled by increased lipolysis of muscle triglyceride.

Groups of endurance-trained masters athletes (60 +/- 2 yr), older untrained men (62 +/- 1 yr), lean older untrained men (61 +/- 2 yr), endurance-trained young athletes (26 +/- 1 yr), and young untrained men (28 +/- 1 yr) were studied to obtain information on the separate effects of age, physical activity, and body fatness on glucose tolerance and insulin sensitivity. Each subject underwent an oral 100-g glucose tolerance test. Skinfold thickness was determined at six sites. The trained groups had a higher maximum O2 uptake capacity and lower sum of skinfolds than their sedentary peers. The lean older untrained group had a sum of skinfolds similar to that of the young untrained group. The masters athletes, young athletes, and young untrained men exhibited similar glucose tolerance whereas the two older untrained groups had an almost twofold greater total area under the glucose curve (P less than 0.05). The masters and young athletes had significantly blunted plasma insulin responses compared with the other three groups (P less than 0.05). The young and the lean older untrained groups had similar plasma insulin responses with significantly lower insulin levels than the older untrained group (P less than 0.05). These results provide evidence that regularly performed vigorous exercise can, in some individuals, prevent the deterioration of glucose tolerance and insulin sensitivity with age.

To evaluate insulin sensitivity and responsiveness, a two-stage hyperinsulinemic euglycemic clamp procedure (insulin infusions of 40 and 400 mU.m-2.min-1) was performed on 11 endurance-trained and 11 untrained volunteers. A 3-h hyperglycemic clamp procedure (plasma glucose approximately 180 mg/dl) was used to study the insulin response to a fixed glycemic stimulus in 15 trained and 12 untrained subjects. During the 40-mU.m-2.min-1 insulin infusion, the glucose disposal rate was 10.2 +/- 0.5 mg.kg fat-free mass (FFM)-1.min-1 in the trained group compared with 8.0 +/- 0.6 mg.kg FFM-1.min-1 in the untrained group (P less than 0.01). In contrast, there was no significant difference in maximally stimulated glucose disposal: 17.7 +/- 0.6 in the trained vs. 16.7 +/- 0.7 mg.kg FFM-1.min-1 in the untrained group. During the hyperglycemic clamp procedure, the incremental area for plasma insulin was lower in the trained subjects for both early (0–10 min: 140 +/- 18 vs. 223 +/- 23 microU.ml–1.min; P less than 0.005) and late (10–180 min: 4,582 +/- 689 vs. 8,895 +/- 1,316 microU.ml–1.min; P less than 0.005) insulin secretory phases. These data demonstrate that 1) the improved insulin action in healthy trained subjects is due to increased sensitivity to insulin, with no change in responsiveness to insulin, and 2) trained subjects have a smaller plasma insulin response to an identical glucose stimulus than untrained individuals.

The sympathochromaffin system, probably sympathetic neural norepinephrine, plays a primary role in the prevention of hypoglycemia during exercise in humans. Our previous data indicated that changes in pancreatic islet hormones are not normally critical but decrements in insulin, increments in glucagon, or both become critical when catecholamine actions are blocked pharmacologically. To distinguish between the role of insulin and that of glucagon in this secondary line of defense against hypoglycemia during exercise in humans, glucoregulation during moderate exercise (approximately 55% of maximum O2 consumption over 60 min) was studied in people who could not decrease insulin but could increase glucagon, i.e., patients with insulin-dependent diabetes mellitus (IDDM). While receiving constant intravenous infusions of regular insulin, in individualized doses shown to result in stable plasma glucose concentrations of approximately 95 mg/dl before exercise, patients with IDDM were studied under two conditions: 1) a control study (n = 13) and 2) an adrenergic blockade study (propranolol infusion, n = 8). In the control study, mean plasma glucose concentrations did not change (from 95 +/- 2 to 100 +/- 11 mg/dl) during exercise despite constant plasma free insulin levels. In the adrenergic blockade study plasma glucose declined (from 96 +/- 2 to 74 +/- 7 mg/dl, P less than 0.01) but stabilized; hypoglycemia did not occur. Exercise-associated increments in plasma glucagon were comparable in the two studies. These data confirm that decrements in insulin are not critical to the prevention of hypoglycemia during moderate exercise in humans and indicate that compensation for deficient catecholamine action does not require decrements in insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

We documented stability of plasma glucose concentrations and glucose production and utilization rates, and levels of other metabolic substrates and regulatory factors, during the islet clamp (somatostatin infusion with glucagon and insulin replacement) in the absence of an intervention in five normal humans and further applied this technique to the study of glucoregulation during moderate exercise. Based on previous evidence that sympathochromaffin activation plays a primary role in the prevention of hypoglycemia during exercise, the role of adrenomedullary catecholamines was assessed by exercise (60% of maximum oxygen consumption for 60 min) studies in four bilaterally adrenalectomized, epinephrine-deficient humans under two conditions: control (saline infusion) and islet clamp. Increased glucose utilization and production rates were matched and plasma glucose was unchanged during exercise under both conditions. Thus adrenomedullary catecholamines including epinephrine are not critical to glucoregulation during moderate exercise in humans even when changes in insulin and glucagon are prevented. These findings provide further support for the suggestion that sympathetic neural norepinephrine is the operative catecholamine in the prevention of hypoglycemia during exercise in humans.

In an effort to assess the effects of caffeine ingestion on metabolism and performance during prolonged exercise, nine competitive cyclists (two females and seven males) exercised until exhaustion on a bicycle ergometer at 80% of Vo2 max. One trial was performed an hour after ingesting decaffeinated coffee (Trial D), while a second trial (C) required that each subject consume coffee containing 330 mg of caffeine 60 min before the exercise. Following the ingestion of caffeine (Trial C), the subjects were able to perform an average of 90.2 (SE +/- 7.2) min of cycling as compared to an average of 75.5 (SE +/- 5.1) min in the D Trial. Measurements of plasma free fatty acids, glycerol and respiratory exchange ratios evidenced a greater rate of lipid metabolism during the caffeine trial as compared to the decaffeinated exercise treatment. Calculations of carbohydrate (CHO) metabolism from respiratory exchange data revealed that the subjects oxidized roughly 240 g of CHO in both trials. Fat oxidation, however, was significantly higher (P less than 0.05) during the C Trial (118 g or 1.31 g/min) than in the D Trial (57 g or 0.75 g/min). On the average the participants rated (Perceived Exertion Scale) their effort during the C Trial to be significantly (P less than 0.05) easier than the demands of the D treatment. Thus, the enhanced endurance performance observed in the C Trial was likely the combined effects of caffeine on lipolysis and its positive influence on nerve impulse transmission.

Insulin action is enhanced in people who exercise regularly and vigorously. In the present study, the hyperinsulinemic, euglycemic clamp procedure was used to determine whether this enhanced insulin action is due to an increased sensitivity and/or an increased responsiveness to insulin. To avoid the variability that exists between individuals and complicates cross-sectional studies, the same subjects were studied in the trained exercising state and again after 10 days of physical inactivity. When the plasma insulin concentration was maintained at approximately 78 microU.ml-1 (a submaximal level), glucose disposal rate averaged 8.7 +/- 0.5 mg.kg-1.min-1 before and 6.7 +/- 0.6 mg.kg-1.min-1 after 10 days of activity (P less than 0.001). When the plasma insulin concentration was maintained at approximately 2,000 microU.ml-1 (a maximally effective concentration), the rate of glucose disposal was not significantly different before (15.3 +/- 0.5 mg.kg-1.min-1) compared with after (14.5 +/- 0.4 mg.kg-1.min-1) 10 days without exercise. These results provide evidence that the reversal of enhanced insulin action that occurs within a few days when exercise-trained individuals stop exercising is due to a decrease in sensitivity to insulin, not to a decrease in insulin responsiveness.

The response of an individual's bone mass to exercise training will depend, in part, on their present level of functional activity and on the hormonal and nutritional milieus of bone tissue. For normally active, but not trained persons, an exercise training program may lead to a new bone mass as much as 5% to 10% above baseline. In an individual with a bone mass which is markedly reduced because of inactivity, poor nutrition, or hormonal deficiency (or excess, depending on the hormone), it is possible that exercise will result in even larger gains in bone mass. Training with weight-bearing exercises may serve as an osteogenic stimulus to both young and older individuals. If the training program is limited or restricted, however, older people may not show the same magnitude of change as do younger subjects. In women, low estrogen levels may reduce the apparent benefit from exercise training, as seen from the studies of amenorrheic athletes. Low bone mass may be related to an estrogen withdrawal effect as well as to the basic estrogen deficiency. Exercise training is likely to provide an osteogenic stimulus for the maintenance of bone mass when it is done in an environment of optimal hormonal levels and nutrition. Physical activity, however, may not be an effective substitute for estrogen therapy. Under optimal conditions, exercise training does provide an osteogenic stimulus to bone, resulting in an increase or maintenance of bone mass, when a loss might otherwise be expected. It is not realistic, however, to expect that exercise training will bring about a large increase in bone mass.(ABSTRACT TRUNCATED AT 250 WORDS)

To ascertain whether older (masters) athletes exhibit a more favorable plasma lipoprotein/lipid profile than sedentary men of similar age, 14 endurance-trained masters athletes (mean age 60 +/- 2 years [+/- standard error of the mean]), 12 older, untrained-not lean men (mean age 62 +/- 1 years), 9 older untrained-lean men (mean age 61 +/- 2 years), 15 young endurance-trained athletes (mean age 26 +/- 1 years) and 15 young untrained men (mean age 28 +/- 1 years) were studied. The athletes had higher values for maximal oxygen uptake and lower levels of body fatness compared with the untrained men, regardless of age (p less than 0.05). High-density lipoprotein (HDL) cholesterol was markedly higher in the masters athletes than in the other groups (66 vs 42 to 55 mg/dl, p less than 0.05). The total cholesterol (TC) and low-density lipoprotein cholesterol concentrations of the masters athletes generally were higher than those of the younger groups, similar to those of the older lean men, and lower than those of the older-not lean men (p less than 0.05). The TC/HDL cholesterol ratios were similarly low (2.8 to 3.4) for the athletes and the young untrained men compared with the older untrained men (4.0 to 5.6) (p less than 0.05). Thus, some older endurance athletes exhibit markedly higher HDL cholesterol levels and lower TC/HDL cholesterol ratios compared with their sedentary peers. This favorable plasma lipoprotein profile may indicate a reduced risk of developing coronary artery disease for older men who exercise regularly.

During mild or moderate nonexhausting exercise, glucose utilization increases sharply but is normally matched by increased glucose production such that hypoglycemia does not occur. To test the hypothesis that redundant glucoregulatory systems including sympathochromaffin activation and changes in pancreatic islet hormone secretion underlie this precise matching, eight young adults exercised at 55-60% of maximal oxygen consumption for 60 min on separate occasions under four conditions: (a) control study (saline infusion); (b) islet clamp study (insulin and glucagon held constant by somatostatin infusion with glucagon and insulin replacement at fixed rates before, during and after exercise with insulin doses determined individually and shown to produce normal and stable plasma glucose concentrations prior to each study); (c) adrenergic blockage study (infusions of the alpha- and beta-adrenergic antagonists phentolamine and propranolol); (d) adrenergic blockade plus islet clamp study. Glucose production matched increased glucose utilization during exercise in the control study and plasma glucose did not fall (92 +/- 1 mg/dl at base line, 90 +/- 2 mg/dl at the end of exercise). Plasma glucose also did not fall during exercise when changes in insulin and glucagon were prevented in the islet clamp study. In the adrenergic blockade study, plasma glucose declined initially during exercise because of a greater initial increase in glucose utilization, then plateaued with an end-exercise value of 74 +/- 3 mg/dl (P less than 0.01 vs. control). In contrast, in the adrenergic blockade plus islet clamp study, exercise was associated with glucose production substantially lower than control and plasma glucose fell progressively to 58 +/- 7 mg/dl (P less than 0.001); end-exercise plasma glucose concentrations ranged from 34 to 72 mg/dl. Thus, we conclude that: (a) redundant glucoregulatory systems are involved in the precise matching of increased glucose utilization and glucose production that normally prevents hypoglycemia during moderate exercise in humans. (b) Sympathochromaffin activation, perhaps sympathetic neural norepinephrine release, plays a primary glucoregulatory role by limiting glucose utilization as well as stimulating glucose production. (c) Changes in pancreatic islet hormone secretion (decrements in insulin, increments in glucagon, or both) are not normally critical but become critical when catecholamine action is deficient. (d) Glucoregulation fails, and hypoglycemia can develop, both when catecholamine action is deficient and when changes in islet hormones do not occur during exercise in humans.

To assess the effect of weight-bearing exercise training and subsequent detraining on lumbar bone mineral content in postmenopausal women.Non-randomized, controlled, short-term (9 months) trial and long-term (22 months) exercise training and detraining (13 months).Section of applied physiology at a university school of medicine.Thirty-five healthy, sedentary postmenopausal women, 55 to 70 years old. All women completed the study. There was 90% compliance with exercise training.All women were given calcium, 1500 mg daily. The exercise group did weight-bearing exercise (walking, jogging, stair climbing) at 70% to 90% of maximal oxygen uptake capacity for 50 to 60 min, 3 times weekly.Bone mineral content increased 5.2% (95% confidence interval [CI], 2.0% to 8.4%; P = 0.0037) above baseline after short-term training whereas there was no change (-1.4%) in the control group. After 22 months of exercise, bone mineral content was 6.1% (95% CI, 3.9% to 8.3% above baseline; P = 0.0001) in the long-term training group. After 13 months of decreased activity, bone mass was 1.1% above baseline in the detraining group.Weight-bearing exercise led to significant increases above baseline in bone mineral content which were maintained with continued training in older, postmenopausal women. With reduced weight-bearing exercise, bone mass reverted to baseline levels. Further studies are needed to determine the threshold exercise prescription that will produce significant increases in bone mass.