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Biomedical subjects

W M Kohrt

Publications and source records attributed to W M Kohrt.

At least 55 records · Page 3Linked to original sources

Hormone replacement therapy does not augment gains in muscle strength or fat-free mass in response to weight-bearing exercise.

Lower extremity strength and fat-free mass were examined in 58 postmenopausal women aged 60-72 yr. Subjects were studied before and after an 11-mo control period (n = 16) or before and after an 11-mo weight-bearing exercise training program designed to generate relatively high ground reaction forces (n = 42). Twenty-two of the exercisers initiated hormone replacement therapy (HRT) at the outset of exercise and continued HRT for 11 mo. Hip extension and abduction strength were assessed using a hand-held dynamometer. Force production during knee extension and flexion was evaluated on an isokinetic dynamometer at 60, 90, and 180 degrees/s. Simultaneous knee and hip extension strength was also assessed on a leg press machine. Total body and lower extremity fat-free mass were determined using dual-energy x-ray absorptiometry. There were no significant changes in muscle strength or body composition in control subjects. Both exercise groups had significant increases in fat-free mass and in all strength measures. Fat-free mass increased from 38.8 +/- 4.3 to 39.7 +/- 4.3 kg in the exercise group and from 37.7 +/- 3.9 to 38.9 +/- 4.6 kg in the exercise-plus-HRT group. The average relative increase in strength was 16.2 +/- 11.0% in the exercise group and 17.0 +/- 13.0% in the exercise-plus-HRT group. Women receiving HRT did not have a gain in fat-free mass or in strength over and above that demonstrated by the women not on HRT. Our results provide evidence that HRT does not augment the increases in muscle mass or strength that occur in response to weight-bearing exercise in older women.

Absorptiometry, Photon↗

Regional differences in interstitial glycerol concentration in subcutaneous adipose tissue of women.

The aims of this study were to 1) compare two methods of determining interstitial glycerol concentration in subcutaneous adipose tissue (AT) and 2) determine whether there are regional differences in interstitial glycerol concentration in subcutaneous AT of nonobese, premenopausal women. Microdialysis probes were inserted under local anesthesia into the abdominal (2 probes) and femoral (1 probe) subcutaneous AT in each subject (n = 5) and perfused with a Ringer solution containing 2.5 mM glucose and glycerol in concentrations ranging from 0 to 900 microM. Microdialysis probe relative recoveries and interstitial glycerol concentrations were determined by the no-net-flux method (NNF) and the internal reference method (IR) with the use of [13C]glycerol. Microdialysis probe relative recoveries were 57.4 +/- 3.6% by NNF and 61.2 +/- 10.1% by IR in femoral AT [P = not significant (NS)] and were 55.2 +/- 6.0% by NNF and 66.6 +/- 4.2% by IR in abdominal AT (P = NS). The calculated interstitial glycerol concentrations determined by NNF and IR were 236.4 +/- 42.7 and 241.1 +/- 39.6 microM (P = NS) in femoral AT and 151.4 +/- 29.7 and 129.4 +/- 18.7 microM in abdominal AT (NNF vs. IR, P = NS; femoral vs. abdominal, P < 0.05). It can be concluded that the interstitial glycerol concentration in the femoral AT of nonobese, premenopausal females is approximately 240 microM and is higher than in abdominal AT (140 microM). Furthermore, the use of a stable isotope of glycerol as an internal reference is suitable for determining interstitial glycerol concentrations in subcutaneous adipose tissue in humans at rest.

Abdomen↗

Whole body leptin kinetics and renal metabolism in vivo.

Leptin metabolism was investigated in male Sprague-Dawley rats by use of 125I-labeled leptin plasma kinetic and arteriovenous balance studies. When conscious rats received bolus venous injections of 125I-leptin, intact (precipitable) leptin quickly disappeared from circulation in a biexponential manner during the 2-h experimental period. After substantial delay, most of the injected radioactivity appeared in the urine. The data were described by a two-compartment model, which postulated that plasma leptin exchanged with a nonplasma pool and that all of the tracer cleared from plasma appeared in urine or in a degraded form in plasma. The half-life of leptin was 9.4 +/- 3.0 min, and the leptin production rate was 3.6 +/- 1.2 ng 100 g fat-1.min-1. The left kidney extracted 21 +/- 1.5% of intact arterial 125I-leptin 5 min after femoral venous injection. Endogenous arterial leptin was reduced 21 +/- 8 and 18 +/- 12%, respectively, in simultaneously sampled left and right renal veins. Renal elimination appears to be the major elimination mechanism for leptin in normal rats, and the kinetic studies suggest that uptake of leptin by renal tissue rather than glomerular filtration is the predominant elimination mechanism.

Adipose Tissue↗

Role of nitric oxide in skeletal muscle blood flow at rest and during dynamic exercise in humans.

The role of nitric oxide at rest and in the active hyperemic response within skeletal muscle was investigated in eight physically active men. Three microdialysis probes were inserted into the vastus lateralis of the quadriceps femoris muscle group in each subject. Microdialysis probes were perfused with a Ringer solution containing 5.0 mM ethanol, 2.5 mM glucose, and either 10 mg/ml of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) monoacetate salt, 30 mg/ml of the nitric oxide precursor L-arginine, or no additional substance (control probe). Subjects performed one-legged cycling exercise at work rates ranging from 25 to 100 W. Dialysate and perfusate ethanol concentrations were presented as the ratio of [ethanol]dialysate to [ethanol]perfusate (ethanol outflow-to-inflow ratio), an indicator that is inversely related to blood flow. The ethanol outflow-to-inflow ratios at rest were 0.614 +/- 0.032, 0.523 +/- 0.023, and 0.578 +/- 0.039 in the L-NMMA, L-arginine, and control probes, respectively. Calculated resting blood flows were therefore 8.7 +/- 4.1, 20.5 +/- 4.6, and 14.0 +/- 4.7 ml.min-1.100 g-1 around the L-NMMA, L-arginine, and control probes, respectively. The ethanol outflow-to-inflow ratios were significantly higher at all exercise intensities in the L-NMMA probe than in the control and L-arginine probes, resulting in calculated blood flows of 195 +/- 55, 407 +/- 47, and 352 +/- 60 ml.min-1.100 g-1 at 25 W and 268 +/- 65, 602 +/- 129, and 519 +/- 113 ml.min-1.100 g-1 at 100 W around the L-NMMA, L-arginine, and control probes, respectively. Skeletal muscle blood flow was therefore reduced both at rest and during continuous, dynamic exercise by the action of L-NMMA, whereas blood flow was increased only at rest by L-arginine.

Adult↗

Effects of exercise involving predominantly either joint-reaction or ground-reaction forces on bone mineral density in older women.

This study compared the effects of two exercise training programs, 11 months in duration, on bone mineral density (BMD) in older, sedentary women. Thirty-nine women, aged 60-74 years, were assigned to the following groups: (a) a group that performed exercises that introduced stress to the skeleton through ground-reaction forces (GRF) (i.e., walking, jogging, stairs); (b) a group that performed exercises that introduced stress to the skeleton through joint-reaction forces (JRF) (i.e., weight lifting, rowing); or (c) a no-exercise control group. BMD of the whole body, lumbar spine, proximal femur, and distal forearm was assessed five times at approximately 3-month intervals. The GRF and JRF exercise programs resulted in significant and similar increases in BMD of the whole body (2.0 +/- 0.8% and 1.6 +/- 0.4%, respectively), lumbar spine (1.8 +/- 0.7% and 1.5 +/- 0.5%, respectively), and Ward's triangle region of the proximal femur (6.1 +/- 1.5% and 5.1 +/- 2.1%, respectively). There was a significant in BMD of the femoral neck only in response to the GRF exercise program (GRF, 3.5 +/- 0.8%; JRF, -0.2 +/- 0.7%). There were no significant changes in BMD in control subjects. Among all exercisers, there was a significant inverse (r = -0.52, p < 0.01) relationship between increases in whole body BMD and reductions in fat mass, suggesting a dose response effect of exercise on bone mass. Although femoral neck BMD was responsive only to the GRF exercise program, some adaptations (i.e., increase in lean body mass and strength) that were specific to the JRF exercise program may be important in preventing osteoporotic fractures by reducing the risk for falls. It remains to be determined whether all of these benefits can be gained through a training program that combines the different types of exercises employed in this study.

Aged↗

Effects of endurance exercise and hormone replacement therapy on serum lipids in older women.

OBJECTIVE: To determine the effects of 11 months of exercise training and hormone replacement therapy (HRT), alone or in combination, on serum lipids and lipoproteins, in postmenopausal women. DESIGN: Controlled, prospective, 11-month clinical trial. Healthy postmenopausal women (n = 71, age range 60-72 yrs) were assigned to four groups in a 2 X 2 design (control, exercise, HRT, exercise + HRT). SETTING: Large, midwestern urban community; subjects were recruited from the community-at-large. The exercise program was conducted at a university exercise facility. INTERVENTIONS: HRT consisted of conjugated estrogens at 0.625 mg/day and trimonthly medroxyprogesterone acetate 5 mg/day for 13 days. Exercise consisted of 2 months of low intensity exercise followed by 9 months of vigorous exercise for 45 min/day, 3 or more days/week, at 65-85% of maximal heart rate. MEASUREMENTS: Maximal aerobic power (VO2max), resting blood pressure, body composition, serum lipids and lipoproteins, and dietary intake at baseline and after 11 months. MAIN RESULTS: At the end of 11 months, subjects in the exercise group had decrease total cholesterol (TC; P < .01) and LDL-cholesterol (LDL-C; P < .05), but there was no change in HDL-cholesterol (HDL-C) or triglycerides. Women in the HRT group had decreased LDL-C (P < .001) and increased HDL-C (P < .01) and triglycerides (P < .01), but there was no change in TC. Exercise + HRT subjects had decreased TC (P < .05) and LDL-C (P < .001), and increased HDL-C (P < .001); exercise prevented the HRT-related increase in triglycerides. CONCLUSIONS: Endurance exercise training and HRT have independent and complimentary effects on serum lipids profiles in healthy postmenopausal women. Such effects are likely to reduce the risk of cardiovascular morbidity in this population.

Aged↗

Regulation of carbohydrate and fat metabolism during and after exercise.

During vigorous exercise, carbohydrate, in the form of muscle glycogen and blood glucose, is the primary energy source, whereas fatty acids play a secondary, carbohydrate-sparing role. In the postabsorptive state, nearly all of the carbohydrate used during exercise comes from muscle and liver glycogen. The size of these glycogen stores plays a major role in determining how long vigorous endurance exercise can be performed if other causes of fatigue, such as dehydration or heat exhaustion, are avoided. In a "fight or flight" situation, individuals whose muscles are glycogen depleted are helpless, as they are unable to either run or fight. The same is true of someone who has become markedly hypoglycemic as a result of liver glycogen depletion.

Blood Glucose↗

Changes in insulin action and GLUT-4 with 6 days of inactivity in endurance runners.

The purpose of this investigation was to determine whether decreased insulin action after 6 days of inactivity in endurance-trained runners was associated with a decrease in skeletal muscle glucose transporter protein levels (GLUT-4) in the gastrocnemius muscle. Seven endurance runners (5 men and 2 women) volunteered to participate in this investigation. All subjects had normal glucose tolerance as determined by the National Diabetes Data Group guidelines. Each individual completed two hyperinsulinemic euglycemic clamps at insulin infusion rates of 15 (LO) and 40 (HI) mU.m-2.min-1, one approximately 18 h after a training bout and the second after 6 days of inactivity (IA). Muscle biopsies for the measurement of GLUT-4 were obtained from the gastrocnemius before each clamp. Glucose disposal rates during the last 30 min of each insulin infusion were significantly reduced after 6 days of IA, averaging 6.45 +/- 1.04 mg.kg fat-free mass (FFM)-1.min-1 before and 4.55 +/- 0.56 mg.kg FFM-1.min-1 after detraining for the LO insulin infusion rate and 13.77 +/- 0.88 mg.kg FFM-1.min-1 before and 11.81 +/- 0.60 mg.kg FFM-1.min-1 after detraining for the HI insulin infusion rate (both P < 0.05), despite the fact that plasma insulin was higher in the inactive state (LO, 19.2 +/- 0.9 microU/ml before and 23.4 +/- 1.5 microU/ml after detraining; HI, 56.0 +/- 2.0 microU/ml before and 61.6 +/- 1.6 microU/ml after detraining; P < 0.05)). Calculated insulin clearance was greater in the trained than in the inactive state (P < 0.03). Muscle GLUT-4 transporter protein after 6 days of IA was reduced by 17.5 +/- 5.4% (P < 0.02). These results demonstrate that 6 days of IA reduces insulin action in endurance-trained runners and suggest that a reduction in muscle GLUT-4 transporter level plays a role in the decrease in glucose disposal rates.

Adult↗

Endurance exercise training decreases capillary basement membrane width in older nondiabetic and diabetic adults.

The objectives of these studies were to 1) evaluate the relationships among age, glucose intolerance, and skeletal muscle capillary basement membrane (CBM) width (CBMW) and 2) determine the effects of exercise training on CBMW by comparing values of young (28 +/- 4 yr) and older (63 +/- 7 yr) athletes with those of age-matched sedentary control subjects and by measuring CBMW in older men and women before and after a 9-mo endurance-exercise training program. CBMW was measured in tissue samples obtained from the gastrocnemius muscle. CBMW in sedentary 64 +/- 3-yr-old subjects was 25% thicker than in sedentary 24 +/- 3-yr-old subjects. CBMW was similar in young and older athletes and was thinner than the CBMW of age-matched sedentary control subjects. There were no differences in CBMW among older sedentary individuals with normal or impaired glucose tolerance or mild non-insulin-dependent diabetes mellitus. Nine months of endurance exercise training reduced CBMW in older men and women by 30-40%, to widths that were not different from those of the young subjects; this response was independent of glucose tolerance status. These findings suggest that habitual exercise prevents the thickening of the skeletal muscle CBM that is characteristic of advancing age. Moreover, the thickening of the CBM appears to be readily reversed as a result of exercise training, even in older individuals.

Adult↗

Serum leptin levels are reduced in response to exercise training, but not hormone replacement therapy, in older women.

The aim of this study was to evaluate the effects of exercise training and hormone replacement therapy (HRT) on serum leptin levels in older women. Previously sedentary, healthy women, aged 60-72 yr, were assigned to control (n = 16), exercise (n = 17), HRT (n = 15), or exercise + HRT (n = 13) groups. Exercise training consisted of a 2-month flexibility-exercise program followed by a 9-month exercise program that included walking, jogging, and stair climbing. HRT consisted of 11 months of continuous conjugated estrogens (0.625 mg/day) and medroxyprogesterone acetate (5 mg/day) for 13 days every third month. Body composition was assessed by dual-energy x-ray absorptiometry, and serum insulin levels were measured in the fasted state and in response to a glucose challenge. Leptin levels were reduced by 23 +/- 25% and 22 +/- 27% (both P < 0.01) in response to exercise and exercise + HRT, respectively. There was no effect of HRT on leptin. Fat mass was the strongest predictor of serum leptin concentration, both before (r = 0.81; P < 0.001) and after (r = 0.85; P < 0.001) the study period, and the change in fat mass in the exercisers was significantly correlated with the change in leptin (r = 0.55; P < 0.01). There did not seem to be an effect of exercise, independent of the reduction in fat mass, on leptin. Insulin levels were significantly correlated with leptin levels, but this was not independent of the association with adiposity. The curvilinear relationship between leptin level and fat mass and the finding that the ratio of leptin mass to fat mass decreased after weight loss suggest that fat cell size is an important determinant of circulating leptin levels.

Adipose Tissue↗

Additive effects of weight-bearing exercise and estrogen on bone mineral density in older women.

The separate and combined effects of weight-bearing exercise and hormone replacement therapy (HRT) on bone mineral density (BMD) were studied in 32 women, 60 to 72 years of age. HRT consisted of continuous conjugated estrogens 0.625 mg/day and trimonthly medroxyprogesterone acetate 5 mg/day for 13 days. Exercise consisted of 2 months of low-intensity exercise followed by 9 months of more vigorous weight-bearing exercise approximately 45 minutes/day, > or = 3 days/week, at 65-85% of maximal heart rate. Lumbar spine and proximal femur BMD were significantly increased in response to exercise and to HRT, and total body BMD was significantly increased in response to HRT; neither exercise nor HRT had an effect on wrist BMD. The combination of exercise + HRT resulted in increased BMD at all sites except the wrist, with effects being additive for the lumbar spine and Ward's triangle and synergistic for the total body. Based on reductions in serum osteocalcin levels, it appears that increases in BMD in response to HRT and exercise + HRT were due to decreased bone turnover. The lack of change in serum osteocalcin and IGF-I in response to exercise alone suggests that increases in BMD were due to decreased bone resorption and not increased formation. Results indicate that weight-bearing exercise + HRT may be effective in preventing and/or treating osteoporosis. It is likely that the additive effects of weight-bearing exercise and HRT on bone mineral accretion, coupled with other adaptations to the exercise (i.e., increased strength and functional capacity), could effectively reduce the incidence of falls and osteoporotic fractures.

Aged↗

Differential effects of estrogen treatment on bone mineral density of the spine, hip, wrist and total body in late postmenopausal women.

It is commonly believed that estrogen is effective only in preventing menopause-related loss of bone mineral. However, recent studies found significant increases in bone mineral density (BMD) of the spine in response to estrogen, particularly in older women. The degree to which estrogen can restore BMD of the hip is uncertain. In the present study, changes in BMD of the lumber spine (L2-4), hip (neck, trochanter and Ward's triangle), wrist (ultradistal) and total body in response to 1 year of hormone replacement therapy (HRT) were evaluated by dual-energy X-ray absorptiometry (DXA) in women 10 or more years past menopause. Twelve women, aged 61-74 years, received conjugated estrogens 0.625 mg and cyclic medroxyprogesterone acetate 5 mg; 12 women who did not receive HRT were controls. Calcium intake was adjusted to approximately 1500 mg/day in all subjects. There were no differences between the groups in BMD prior to treatment. Increases in BMD of the lumbar spine (mean +/- SD, 0.041 +/- 0.030 g/cm2), hip (neck, 0.019 +/- 0.018 g/cm2; trochanter, 0.017 +/- 0.012 g/cm2; Ward's triangle, 0.026 +/- 0.029 g/cm2) and total body (0.013 +/- 0.016 g/cm2) occurred in response to HRT, and these changes were significantly different from those in controls (spine, 0.005 +/- 0.020 g/cm2; neck, -0.007 +/- 0.026 g/cm2; trochanter, 0.002 +/- 0.014 g/cm2; Ward's triangle, 0.003 +/- 0.019 g/cm2; total body, -0.001 +/- 0.017 g/cm2). HRT appears to be most effective at weight-bearing sites that have a high cancellous bone content.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Loss of skeletal muscle mass with aging: effect on glucose tolerance.

It is generally believed that aging results in glucose intolerance. Since skeletal muscle is the major site of glucose uptake following an oral glucose tolerance test (OGTT), it is reasonable to hypothesize that loss of muscle mass with aging causes glucose intolerance. Evidence against this concept comes from extensive data demonstrating the usefulness of the recommended procedures for performing an OGTT. This involves giving 75 g of glucose to all subjects regardless of body weight, and the criteria for categorizing glucose intolerance are the same for all individuals. That this works well, with no evidence that larger people have better glucose tolerance than smaller people, suggests that muscle mass does not usually play a role. Recent studies on humans and rats indicate that aging per se does not result in glucose intolerance. In most of those older people with decreased glucose tolerance, this problem appears to be due to accumulation of abdominal fat with development of insulin resistance. We conclude that the loss of muscle mass with aging does not usually result in glucose intolerance.

Adipose Tissue↗

Body composition by DXA: tried and true?

Dual-energy x-ray absorptiometry (DXA) is unquestionably the method of choice for the assessment of bone mass. Recent generations of DXA instruments also have the capability of assessing soft tissue mass, thereby providing a three-compartment model of body composition, i.e., bone mineral, fat, and bone-free lean masses. Although hydrodensitometry has long been considered the reference method of assessing body composition, assumptions regarding the constancy of the constituents of fat-free mass may compromise its validity in some populations. Because DXA appears to be less dependent on assumptions regarding biological consistency, it is possible that it has the potential to provide a more accurate assessment of body composition across populations than does hydrodensitometry, and that it should be considered the reference method. DXA has been shown to provide precise measures of body composition, but it remains questionable as to whether those measures are accurate. Contributing to the uncertainty regarding validity is the variability among manufacturers of DXA instruments in the methods of calibration, data acquisition, and data analysis. Although DXA holds great promise in becoming the criterion method of assessing body composition, and has been promoted as such by some investigators, available data indicate that this endorsement is premature.

Absorptiometry, Photon↗

Effect of exercise training on left ventricular performance in older women free of cardiopulmonary disease.

Endurance exercise training increases aerobic exercise capacity (maximal oxygen consumption rate [VO2max]) and attenuates the age-related decline in left ventricular (LV) function during exercise in older men. To determine whether similar adaptations occur in older women, 10 subjects (aged 63 +/- 4 years mean +/- SE) were studied before and after 9 to 12 months of endurance exercise training. They exercised 3.85 +/- 0.06 days/week at 81 +/- 0.3% of maximal heart rate. LV function at rest and during supine exercise was assessed by radionuclide ventriculography. VO2max was increased by 21% (from 1.40 +/- 0.1 to 1.7 +/- 0.1 liter/min; p < 0.001) in response to training. Maximal heart rate and systolic blood pressure during treadmill exercise were unchanged (161 +/- 5 beats/min before vs 164 +/- 3 beats/min after; p = NS, and 208 +/- 7 mm Hg before vs 214 +/- 8 mm Hg after; p = NS, respectively) after training. LV ejection fraction at rest (70.4 +/- 2% before vs 70 +/- 1% after) and during peak exercise (78.6 +/- 2% before vs 79.3 +/- 2% after) did not change in response to training. Furthermore, the increases in ejection fraction from rest to exercise were similar before and after training (change: 8.8 +/- 1 vs 9.1 +/- 1%). Stroke volume and cardiac output at peak exercise also did not change in response to training.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Endurance exercise training reduces glucose-stimulated insulin levels in 60- to 70-year-old men and women.

BACKGROUND: Aging is frequently associated with development of insulin resistance and deterioration of glucose tolerance. Plasma glucose and insulin concentrations tend to be higher than in young people, even in those older individuals whose glucose tolerance is within the normal range. A sedentary life style could play a role in the development of insulin resistance and hyperinsulinemia with advancing age. METHODS: We evaluated the effect of 9 mo of vigorous endurance exercise training (approximately 80% of maximal heart rate) on the glucose-stimulated insulin response and glucose disposal rate, using the hyperglycemic clamp procedure, in 12 people aged 65 +/- 1 yr (mean +/- SE) with normal glucose tolerance. The post-training hyperglycemic clamps were performed approximately 16 h after a usual exercise session. RESULTS: VO2max increased approximately 23% in response to the exercise program. The plasma insulin concentration (I) during hyperglycemia (180 mg.dL-1) was significantly lower (mean 36 +/- 6 microU.mL-1 before vs 26 +/- 5 microU.mL-1 after; p < .05) after the exercise program. Insulin action was improved by the exercise, as the glucose disposal rate (M) during hyperglycemia was unchanged despite the blunted insulin response, resulting in an increase in the M/I ratio from 24 +/- 5 to 30 +/- 5 (p < .05), a value similar to the M/I ratio of 33 +/- 4 found in normally active young subjects. CONCLUSION: These results provide evidence that regular exercise is effective in reducing hyperinsulinemia and improving insulin action in 65-yr-olds to levels typical of young people.

Age Factors↗

Relationship between glucose tolerance and glucose-stimulated insulin response in 65-year-olds.

BACKGROUND: Decreased insulin secretion may contribute to the deterioration of glucose tolerance associated with aging. METHODS: We studied the insulin response to a 3-hour hyperglycemic clamp (10 mM) of 19 young (24 +/- 1 y) subjects with normal glucose tolerance and 60 older (65 +/- 1 y) subjects with various levels of glucose tolerance. RESULTS: The noninsulin dependent diabetic (NIDDM) group had a diminished first phase immunoreactive (IR)-insulin response compared to young and nondiabetic older groups (p < .05). The older groups had a lower rate of change in IR insulin concentration during the third hour of hyperglycemia compared to the young group (p < .05). This was not, however, a universal finding, because a decreased third hour response was not seen in a subgroup of older subjects whose glucose tolerance was similar to that of the young group. Another subgroup of older subjects with a decrease in glucose tolerance mild enough to be considered normal by the National Diabetes Group Criteria tended to have both an increase in the early insulin response and a decrease in the third hour response. More severe decreases in glucose tolerance were associated with blunting of the early response. CONCLUSION: Aberrations in early and late phase glucose-stimulated insulin responses appear to be present in older subjects with even mildly decreased glucose tolerance. Some individuals, however, show no evidence of deterioration of glucose tolerance or insulin response to glucose with aging, at least up to age 70 years.

Adult↗

Effect of prolonged exercise on muscle citrate concentration before and after endurance training in men.

It has been hypothesized that endurance training reduces carbohydrate utilization during exercise via citrate-mediated inhibition of phosphofructokinase (PFK). To test this hypothesis, vastus lateralis muscle biopsy samples were obtained from eight men before and immediately (approximately 10 s) after 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake, both before and after 12 wk of endurance exercise training (3 days/wk running, 3 days/wk interval cycling). Training increased muscle citrate synthase (CS) activity from 3.69 +/- 0.48 (SE) to 5.30 +/- 0.42 mol.h-1.kg protein-1 and decreased the mean respiratory exchange ratio during exercise from 0.92 +/- 0.01 to 0.88 +/- 0.01 (both P < 0.001). Muscle citrate concentration at the end of exercise correlated significantly with CS activity (r = 0.70; P < 0.005) and was slightly but not significantly higher after training (0.80 +/- 0.19 vs. 0.54 +/- 0.19 mmol/kg dry wt; P = 0.16). Muscle glucose 6-phosphate (G-6-P) concentration at the end of exercise, however, was 31% lower in the trained state (1.17 +/- 0.10 vs. 1.66 +/- 0.27 mmol/kg dry wt; P < 0.05), in keeping with a 36% decrease in the amount of muscle glycogen utilized (133 +/- 22 vs. 209 +/- 19 mmol.kg dry wt-1.2 h-1; P < 0.01). The lower G-6-P concentration after training suggests that the training-induced reduction in carbohydrate utilization results from attenuation of flux before the PFK step in glycolysis and is not due to citrate-mediated inhibition of PFK.

Adult↗