Biomedical subjects

A Bonen

Publications and source records attributed to A Bonen.

At least 109 records · Page 6Linked to original sources

PubMed1990

Determination of luteal phase length by quantitative basal temperature methods: validation against the midcycle LH peak.

Basal temperature data are known to provide unreliable assessments of luteal phase length when they are evaluated by qualitative, visual-pattern methods. This study of 24 cycles in 24 women compared the serum LH peak day with the luteal phase onset day determined by three quantitative basal temperature methods: a) a new computerized least mean square method developed by the authors; b) the mean temperature method reported by Vollman; and c) a computerized version of the World Health Organization cumulative sum method of Royston. The luteal phase onset day determined by the three quantitative basal temperature methods, (a, b, and c) correlated well with the midcycle LH peak (r = 0.879, 0.891, and 0.791, respectively, all p less than 0.001). The cumulative sum method, however, was only able to analyze 19/24 cycles. The mean delay between the LH peak day and the luteal phase onset day determined by thermal shift was 2.4 +/- 1.5, 2.7 +/- 1.4, and 4.1 +/- 2.0 d (mean +/- SD), respectively. The mean temperature method, but not the other two methods, showed an increasing delay between the LH peak day and the thermal shift day with longer follicular phase lengths. Rectal and oral temperature data from the same cycle give identical luteal onset days when analyzed by the least mean square and mean temperature methods, but discrepant days by the cumulative sum analysis. The least mean square technique is a reliable and precise method for population documentation of luteal phase lengths.

Adult↗

PubMed1989

Dissociation between insulin binding and glucose utilization after intense exercise in mouse skeletal muscles.

Since there are data to indicate that heavy exercise decreases insulin binding to skeletal muscle at a point when glucose uptake is known to be augmented, we tested the hypothesis that insulin-stimulated glucose uptake and metabolism are dissociated from insulin binding after exercise. Therefore, insulin binding, 2-deoxy-d-glucose (2-DOG) uptake and glucose incorporation into glycogen and glycolysis were compared in soleus and EDL muscles of intensively exercised (2-3 h) mice and non-exercised mice. Basal 2-DOG uptake was increased in the exercised EDL (P less than 0.05) but not in the exercised soleus (P greater than 0.05). However, in both muscles intense exercise increased insulin-stimulated (0.1-16 nM) 2-DOG uptake (P less than 0.05). The rates of glycogenesis were increased in both the exercised muscles (P less than 0.05) as was the rate of glycolysis in the exercise soleus (P less than 0.05). Glycolysis was not altered in the EDL (P greater than 0.05). In the face of the increased 2-DOG uptake and glucose metabolism in the exercised muscles, insulin binding was not altered in the exercised soleus muscle (P greater than 0.05) and was decreased in the exercised EDL (P less than 0.05). These results indicate that after intense exercise there is a dissociation of insulin binding from insulin action on glucose uptake and metabolism in skeletal muscles.

Animals↗

PubMed1989

Carbohydrate metabolism in skeletal muscle: an update of current concepts.

We have reviewed carbohydrate metabolism in skeletal muscle with an emphasis on recent information. In this review a significant number of points have been made. These are summarized below. 1. CP and glycogen are concomitantly metabolized during short-term (less than or equal to 10 s) intense exercise. 2. Both epinephrine and contractile activity regulate glycogen use in muscle. 3. Glycogen sparing during exercise is promoted by fatty acids and probably glucose. 4. Glycogenesis increases during exercise in exercising muscle. 5. Ingested glucose is easily metabolized during exercise. 6. The heterogeneity in glucose uptake among muscles at rest and during exercise is likely not caused by blood flow differences per se. 7. Insulin binding, glucose transporters, glucose uptake, and glycogenesis are greater in ST than in FT muscles. 8. Acute changes in glucose metabolism are not always attributable to concomitant changes in insulin binding to its receptor. 9. Contractile activity alone will increase glucose uptake in muscle, and insulin is not required. 10. Insulin and contractile effects on glucose uptake are additive, suggesting that these stimuli mobilize different pools of glucose transporters. 11. Glycogen loss occurs in exercising and non-exercising muscle; therefore this substrate is not an appropriate index of muscle contractile activity. 12. Carbohydrate mobilization does not appear to be strictly determined by need for this substrate nor by the rate of muscle metabolism. 13. Glyconeogenesis from lactate occurs in ST and FT muscles and is regulated by pH.

Animals↗

PubMed1989

The use of a cell-free perfusate in the perfused rat hindquarter: methodological concerns.

The viability of using a cell-free perfusate in a rat hindlimb preparation to assess skeletal muscle glycogenesis was investigated. A perfusate containing 10 mM glucose and 10 microCi (1 Ci = 37 GBq) of D-[5-3H]glucose was recycled for a 60-min period. In agreement with other studies using more complex media, oxygen uptake of the preparation indicated adequate tissue oxygenation (8 mumol.min-1.g-1). Skeletal muscle fiber type heterogeneity in basal glycogen synthesis from glucose was shown (slow oxidative greater than fast oxidative glycolytic greater than fast glycolytic fibres). Insulin (4.2 mU/mL) markedly stimulated glycogenesis from D-[5-3H]glucose in the soleus (slow oxidative fiber), red gastrocnemius (fast oxidative glycolytic fiber), and white gastrocnemius muscles (p less than 0.05). A recent report indicates that tissue edema in this preparation did not affect insulin responsiveness of the tissue. In contrast, our observations indicate that glucos uptake was enhanced by insulin when edema was absent (p less than 0.05), but not when edema was present (p less than 0.05). In addition, the presence of tissue edema negated insulin-mediated glycogenesis in slow oxidative and fast oxidative glycolytic muscle (p less than 0.05 compared with control) but not in fast glycolytic muscle (p less than 0.05). These data warrant caution when using a cell-free media in the perfused rat hindquarter; however, in the absence of edema, normal responses of glucose metabolism are observed.

Animals↗

PubMed1989

Glycogenesis in muscle and liver during exercise.

We hypothesized that glycogenesis increases in muscle during exercise before significant glycogen depletion occurs. Therefore, rats ran for 15 or 90 min at speeds of 8-22 m/min. D-[5-3H]glucose (10 microCi/100 g body wt) was administered 10 min before the end of exercise. Hindlimb muscles [soleus (SOL), plantaris (PL), extensor digitorum longus (EDL), and red (RG) and white gastrocnemius (WG)] and a portion of liver were analyzed for glycogen concentrations and rates of glycogen synthesis (i.e., D-[3H]glucose incorporated into glycogen). At rest, marked differences were observed among muscles in their rates of glucose incorporation into glycogen: i.e., SOL = 24.3 +/- 3.1, RG = 5.4 +/- 1.9, PL = 2.8 +/- 1.1, EDL = 0.54 +/- 0.10, WG = 0.12 +/- 0.02 (SE) dpm.micrograms glycogen-1.10 min-1 (P less than 0.05 between respective muscles). Compared with the glucose incorporation into glycogen at rest, increments in the PL (272%), RG (189%), WG (400%), EDL (274%), and liver (175%) were observed after 90 min of exercise (P less than 0.05, all data). In contrast, a decrease in glucose incorporation into glycogen (-62%) occurred in the SOL at min 15 (P less than 0.05), but this returned to the rates observed at rest after 90 min of exercise. This measure for rates of net glycogen synthesis (dpm.microgram glycogen-1.10 min-1) was weakly related to the ambient glycogen levels in most muscles; the exception was the SOL (r = -0.79; P less than 0.05). There was up to a 50-fold difference in glycogen synthesis among muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Thermal and metabolic responses to cold by men and by eumenorrheic and amenorrheic women.

Previous work has suggested that men (M) are more sensitive to cold stress than women. There have also been observations that suggest that amenorrheic women (AW) are less thermally responsive than eumenorrheic women (EW). We investigated the hypothesis that M, EW, and AW would have different responses to cold stress. The subjects (6/group) were tested four times: twice at rest for 60 min (5 and 22 degrees C) and twice in a progressive exercise test (5 and 22 degrees C). At rest at 22 degrees C AW had a lower O2 uptake (VO2) than M and lower rectal (Tre) and finger temperatures than EW. At rest at 5 degrees C both AW and EW had lower skin temperature (Tsk) than M, but there were no group differences in peripheral Tsk sites. M increased VO2 after 10 min and EW after 20 min of cold stress; however, AW did not increase metabolism until 60 min. In the two exercise tests Tre increased in proportion to relative work load; in the 5 degrees C test there was little evidence that exercise increased Tsk sites above rest levels. Few of the metabolic or thermal differences could be accounted for by body fatness, body surface area (BSA), or BSA/kg. The data support the hypothesis that M, EW, and AW have different responses to cold stress.

Adult↗

PubMed1988

Hindlimb suspension increases insulin binding and glucose metabolism.

After 28 days of hindlimb-suspension, insulin binding, 2-deoxy-D-glucose (2-DG) uptake, and glucose metabolism (glycolysis and glycogenesis) were determined at various insulin concentrations (0.2-30 nM) in soleus muscle of young (18-day-old) and adult (150-day-old) rats. Compared with age-matched controls the young (YS) and adult suspended (AS) rats had lower soleus and body weights and insulin levels (P less than 0.05). Per milligram of protein, insulin binding, 2-DG uptake, and the rate of glycolysis were increased by approximately 200%, and the rate of glycogenesis was increased approximately 100% in the YS group (P less than 0.05). Except for a reduction in glycogenesis (P less than 0.05) all other parameters also increased in the AS rats (P less than 0.05). On the basis of the whole muscle the rate of glucose metabolism (glycogenesis + glycolysis) was reduced in the YS rats (P less than 0.05), but in the AS rats glucose metabolism was similar to the controls. Thus the increased glucose metabolism (i.e., per milligram of protein) in the YS and AS groups may represent a compensatory response by atrophied muscle to attempt to sustain glucose removal from the circulation. Because greater insulin binding occurred in YS muscle [35% slow-twitch (ST)] than in the control group (70% ST), and greater insulin binding occurred in the AS (81% ST) than in the control group (90% ST), higher insulin binding capacities are not always related to a high proportion of ST muscle fibers. In conclusion, after hindlimb suspension, marked increments in insulin binding and glucose metabolism occur in the soleus muscle.

Aging↗

PubMed1987

Pituitary, ovarian, and adrenal hormone responses to marathon running.

We have described the responses of selected hormones [luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), progesterone (P), androstenedione (delta 4-A), testosterone (T)] and substrates (glucose, lactate) before, during, and after a marathon run in five women of varying gynecological status. Blood samples (15 ml) were obtained 60 and 30 min before the race, during the race at 10, 20, and 30 km, and after the race at min 5, 60, and 120. The relative intensity of running varied between 60% and 85% VO2 max, and weight loss ranged from 2.6 to 3.0 kg. The new observations from our data include the fact that FSH was increased during exercise, whereas this was not observed for LH. This latter hormone appears to be linked more closely to the exercise intensity as defined by blood lactate increments. Increments occurred in all steroid hormones and paralleled those observed in controlled laboratory studies, although the magnitude of these changes was larger at the end of the marathon run. Except for dehydroepiandrosterone sulfate (DHEA-S), most of the hormones returned to basal levels in the 2 h after the marathon. DHEA-S exhibited no change until the 30-km point, when a sharp increase was observed, and then remained elevated for 2 h after exercise, suggesting that a) adrenocortical production of steroids continues for a long time after exercise, b) there is a marked reduction in hepatic clearance of this hormone. In summary, the present study shows that prolonged exercise has a marked effect on both steroid and pituitary hormones.

Adrenal Cortex Hormones↗

PubMed1987

Effect of exercise training on insulin binding and glucose metabolism in mouse soleus muscle.

Training stimulates glucose uptake and metabolism by muscles independent of a rise in serum glucose. Whether this increased insulin action is associated with enhanced insulin binding in muscles is unknown. We studied the effect of 6 weeks of treadmill running on insulin binding, uptake of 2-deoxy-D-glucose, glycolysis, and glycogenesis by the soleus muscle of Swiss Webster mice. Training was progressively increased. The in vitro studies using intact soleus preparations were done 48 h after the last exercise bout. Training increased insulin binding, insulin-stimulated uptake of 2-deoxy-D-glucose, and glycogenesis but not glycolysis in the soleus. Our data suggest that the enhanced glucose uptake and metabolism in muscles induced by exercise training are associated with an increase in insulin binding.

Animals↗

PubMed1987

Exercise- and cold-induced changes in plasma beta-endorphin and beta-lipotropin in men and women.

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response of men, eumenorrheic women, and amenorrheic women (n = 6) to 1 h of rest or to a bicycle ergometer test [20 min at 30% maximum O2 uptake (VO2max), 20 min at 60% VO2max, and at 90% VO2max to exhaustion] was studied in both normal (22 degrees C) and cold (5 degrees C) environments. beta-EP and beta-LPH was measured by radioimmunoassay in venous samples collected every 20 min during rest or after each exercise bout. Exhaustive exercise at ambient temperature (Ta) 22 degrees C induced significant increases in plasma beta-EP and beta-LPH in all subjects as did work at 60% VO2max in amenorrheic and eumenorrheic women. During work at Ta 5 degrees C, the relative increase in beta-EP and beta-LPH was suppressed in eumenorrheic women and completely prevented in amenorrheic women. Although significant lowering of beta-EP and beta-LPH was observed in men and eumenorrheic women during rest at 5 degrees C, amenorrheic women maintained precold exposure levels. These findings suggest that plasma beta-EP and beta-LPH may reflect a thermoregulatory response to heat load. There appears to be a sexual dimorphism in exercise- and cold-induced release of beta-EP and beta-LPH and amenorrhea may be accompanied by alterations in these responses.

Adult↗

PubMed1987

Adrenal hormones enhance glycogenolysis in nonexercising muscle during exercise.

The purpose of this study was to investigate whether epinephrine exerts an effect on glycogen metabolism in nonexercising (Non-Ex) as well as in exercising (Ex) skeletal muscle. Rats ran (15 m/min; 8% grade) on their forelimbs while their hindlimbs (Non-Ex) were suspended above the treadmill. Electromyographic records confirmed the lack of significant contractile activity in muscles during suspension. Plasma epinephrine levels were manipulated in three experimental groups (n = 20 for each group): adrenalectomized (ADX), intact adrenals (IA), and IA + epinephrine injection (+Ep). Another group of rats performed normal exercise on all four limbs (15 m/min; 8% grade). Muscle glycogen levels were measured in selected hindlimb muscles at t = 0 and after 90 min exercise (15 m/min; 8% grade) or suspended rest. In the absence of epinephrine (ADX), no glycogen loss was found (P greater than 0.05) in Non-Ex muscles during the exercise period. In the IA group (epinephrine levels elevated sixfold above basal at t = 90 min), glycogen levels in the nonexercising soleus, plantaris, and red and white gastrocnemius were significantly (P less than 0.05) depleted to 62 +/- 6, 67 +/- 6, 58 +/- 5, and 67 +/- 9% of control values, respectively. Similar decrements occurred in these muscles when exercise was performed on all four limbs (P greater than 0.05). We conclude that glycogenolysis occurs in nonexercising skeletal muscle independent of contractile activity, probably due to the effect of epinephrine. Furthermore, the present data strongly suggest that glycogen depletion patterns in muscles during exercise cannot be used as an index of motor unit recruitment.

Adrenalectomy↗

PubMed1987

Endurance exercise potentiates the stimulatory influence of oestrogen-progesterone on LH and FSH release in the rat.

Ovariectomized rats were treated with oestradiol benzoate and progesterone or GnRH. Prolonged exercise (running 4 days per week for 6 weeks) markedly potentiated the oestrogen/progesterone-induced release of LH and FSH, but the pituitary response to an injection of GnRH was unaffected. In contrast, at 24 h after a single exercise bout there was no apparent effect on steroid and GnRH stimulated LH and FSH responses although an acute exercise session given on the day of the LH surge inhibited steroid-induced LH release in some rats. We conclude that strenuous, prolonged exercise-training in the ovariectomized rat seems to modify the ability of the hypothalamus to release GnRH. The results were not attributable to a single bout of exercise since the gonadotrophin responses immediately or 24 h after such exercise did not parallel the results observed in the trained rats.

Animals↗

PubMed1986

Chronic exercise increases insulin binding in muscles but not liver.

It has been postulated that the improved glucose tolerance provoked by chronic exercise is primarily attributable to increased insulin binding in skeletal muscle. Therefore, we investigated the effects of progressively increased training (6 wk) on insulin binding by five hindlimb skeletal muscles and in liver. In the trained animals serum insulin levels at rest were lower either in a fed (P less than 0.05) or fasted (P less than 0.05) state and after an oral glucose tolerance test (n = 8) (P less than 0.05). Twenty-four hours after the last exercise bout sections of the liver, soleus (S), plantaris (P), extensor digitorum longus (EDL), and red (RG) and white gastrocnemius (WG) muscles were pooled from four to six rats. From control animals, killed at the same time of day, muscles and liver were also obtained. Insulin binding to plasma membranes increased in S, P, and EDL (P less than 0.05) but not in WG (P = 0.07), RG (P greater than 0.1), or in liver (P greater than 0.1). There were insulin binding differences among muscles (P less than 0.05). Comparison of rank orders of insulin binding data with published glucose transport data for the same muscles revealed that these parameters do not correspond well. In conclusion, insulin binding to muscle is shown to be heterogeneous and training can increase insulin binding to selected muscles but not liver.

Animals↗

PubMed1985

The in vitro effect of corticosterone on insulin binding and glucose metabolism in mouse skeletal muscles.

We studied the in vitro effect of corticosterone on insulin binding, uptake of 2-deoxy-D-glucose, glycolysis, and glycogenesis in the soleus and extensor digitorum longus (EDL) of Swiss-Webster mice. In each experiment, one muscle (soleus/EDL) was incubated with corticosterone (0.1, 1, 50, and 100 micrograms/mL) and the respective contralateral muscle was incubated without corticosterone, but at the same insulin and pH levels. Corticosterone did not affect insulin binding in both muscles. However, corticosterone decreased the uptake of 2-deoxy-D-glucose and the rate of glycolysis and glycogenesis in both muscles when the dose was pharmacologic (50 and 100 micrograms/mL), but not when it was physiologic (0.1 and 1 microgram/mL). For glycolysis and glycogenesis, the suppression was greater in the EDL when compared with the soleus. This suppression was seen in both basal and insulin-stimulated conditions. In this in vitro system, where the experimental muscle is not exposed to prior hyperinsulinemia as in the in vivo model, corticosterone, at pharmacologic doses, affects postreceptor events without altering the insulin binding in the skeletal muscle.

Animals↗

PubMed1985

Effects of exercise on insulin binding to human muscle.

A procedure was developed to measure insulin binding to human skeletal muscle obtained via the percutaneous muscle biopsy technique. With this method the effects of exercise on insulin binding were investigated. Subjects (n = 9) exercised for 60 min on a bicycle ergometer at intensities ranging from 20-86% maximum O2 consumption (VO2max). Blood samples were obtained before, during, and after exercise and analyzed for glucose and insulin. Muscle samples (250 mg) for the vastus lateralis were obtained 30 min before exercise, at the end of exercise, and 60 min after exercise. Two subjects rested during the experimental period. There was no linear relationship between exercise intensities and the changes in insulin binding to human muscle. At rest (n = 2) and at exercise intensities below 60% VO2max (n = 5) no change in insulin binding occurred (P greater than 0.05). However, when exercise occurred at greater than or equal to 69% VO2max (n = 4), a pronounced decrement in insulin binding (30-50%) was observed (P less than 0.05). This persisted for 60 min after exercise. These results indicate that insulin binding in human muscle is not altered by 60 min of exercise at less than or equal to 60% VO2max but that a marked decrement occurs when exercise is greater than or equal to 69% VO2max.

Adult↗

PubMed1985

Mild exercise impedes glycogen repletion in muscle.

Bicycle ergometric exercise was used to deplete glycogen by either 80 or 35% in the vastus lateralis of both legs. Thereafter, subjects from each group rested or maintained single-leg exercise [20% of maximal O2 consumption (Vo2max) for 4 h. All subjects ingested glucose (1.5 g/kg wt; 20% solution) at min 10-12 and min 130-132 of the 4-h period. With bed rest, significant glycogen increases occurred after exhaustive (+36%; P less than 0.05) and nonexhaustive exercise (+13%; P less than 0.05). With single-leg exercise, 1) a diminished glycogen repletion occurred in exercising (+11%; P less than 0.05) and nonexercising (+15%; P less than 0.05) muscle after exhaustive exercise, or 2) further glycogen loss occurred in exercising (-26%; P less than 0.05) and nonexercising muscle (-19%; P less than 0.05) after nonexhaustive exercise. Within both groups, glycogen concentrations did not differ between exercising and nonexercising muscles (P greater than 0.05). Single-leg exercise, not preceded by exercise, provoked differences in glycogen loss in exercising (-47%) and nonexercising (-24%) muscle (P less than 0.05). These experiments demonstrate that mild exercise 1) impedes glycogen resynthesis or 2) provokes glycogen loss in both exercising and nonexercising muscle. These findings cannot be ascribed to circulating glucose and insulin concentrations in these studies.

Adult↗

PubMed1985

Insulin receptors: their roles in the pathogenesis and management of type II diabetes mellitus.

In Type II Diabetes Mellitus associated with insulin resistance, the defect is in insulin action. This may take the form of decreased insulin sensitivity, responsiveness, or both. The decrease in insulin binding is due to a decrease in the number of insulin receptors per cell. When the obese Type II diabetic loses weight after being on a weight reducing diet, the insulin sensitivity abnormality is restored towards normal. In so doing the number of insulin receptors per adipocyte or monocyte is restored towards normal. The effect of exercise on insulin binding in skeletal muscles of Type II diabetics has not been studied. Recent experiments in rodents and humans indicate that insulin binding is not affected by acute exercise but the post-receptor events are increased. Finally oral hypoglycemic medications can increase the insulin sensitivity and/or the insulin responsiveness of various tissues.

Administration, Oral↗

PubMed1984

Insulin binding in human skeletal muscle.

Insulin binding to crude plasma membranes derived from human skeletal muscle was characterized. Incubations were performed for 22 h at 4 degrees C. Typical insulin binding characteristics were found, i.e., (a) specificity for insulin, (b) pH sensitivity, (c) dissociation of insulin by the addition of excess insulin and (d) concave Scatchard curves. Half-maximal inhibition of 125I-labeled-insulin binding occurred at 1 X 10(-8) M. Affinity constants were 0.76 X 10(9) and 0.02 X 10(9) M-1 for the high- and low-affinity receptor (2-site model), respectively, and the corresponding receptor numbers were 89 and 1450 fmol/mg protein, respectively. The procedures employed permit the determination of insulin binding to small quantities of human muscle (approx. 250 mg).

Adult↗