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Biomedical subjects

I A Macdonald

Publications and source records attributed to I A Macdonald.

At least 19 recordsLinked to original sources

In vivo measurement of colonic butyrate metabolism in patients with quiescent ulcerative colitis.

BACKGROUND: Butyrate, a short chain fatty acid produced by bacterial fermentation, is a major fuel source for the colonocyte. In vitro work has shown that ulcerative colitis may be characterised by a metabolic defect in colonocyte butyrate oxidation. AIMS: To investigate the rate of metabolism of rectally administered butyrate in patients with quiescent colitis. METHODS: [1-(13)C]-butyrate enemas were administered to 11 patients with long standing quiescent ulcerative colitis and to 10 control patients. The rate of production of (13)CO(2) in exhaled breath over four hours was measured by isotope ratio mass spectrometry combined with indirect calorimetry in order to measure CO(2) production. This allowed calculation of the patients' resting energy expenditure and respiratory quotient. RESULTS: Over a four hour period, 325 (SEM 21) micromol (13)CO(2) was recovered in breath samples from the colitis group compared with 322 (17) micromol from the control group (NS). The respiratory quotient of the colitic group was significantly lower than that of the control group. CONCLUSION: There was no difference in the rate of metabolism of butyrate between the two groups. It is unlikely that there is a primary metabolic defect of butyrate metabolism in patients with quiescent ulcerative colitis.

Adult

Repeatability and methodology of resting energy expenditure in patients with cystic fibrosis.

In this study, intra-individual variation of resting energy expenditure (REE) in adults with cystic fibrosis (CF) and the effect of measurement duration were determined. Twelve adults with CF and chronic Pseudomonas aeruginosa (Ps. aeruginosa) infection and 12 healthy volunteers, matched for age and sex were studied whilst clinically stable on days 1.2, and 15. Respiratory gas exchange was monitored by continuous measurement of oxygen uptake (VO2) and carbon dioxide production (VCO2) using a ventilated hood indirect calorimeter. Coefficients of variation (CVs) were 4.3% in patients and 2.4% in controls comparing days 1 and 2. The CV for patients was 5.0% and for controls 2.9% comparing days 1 and 15. The effect of measurement duration on REE was assessed in eight of the CF patients. REE remained stable for 40 min but tended to rise by 80 min. Plasma catecholamine concentrations were stable between study days in patients but fell with time in controls suggesting some adaptation to experimental procedure. The greater variability of REE in patients was related to change in serum CRP over 2 weeks. REE is a repeatable measurement in clinically stable patients with CF, though variability was greater in patients than healthy subjects. This has implications for the design and interpretation of longitudinal studies of REE in patients with chronic lung disease.

Adrenal Cortex Hormones

The assay of the catecholamine content of small volumes of human plasma.

Plasma catecholamines are routinely measured using high-performance liquid chromatography (HPLC) with electrochemical detection. Most of the present assays require sample volumes of at least 500 microL and are complex and labour-intensive procedures, or require large capital investment to reduce the sample size. This paper describes a liquid/liquid plasma catecholamine extraction procedure, HPLC separation and electrochemical detection method which is simple, sensitive and reproducible. The resting catecholamine concentration of 50 microL adult human plasma can be assayed using standard electrochemical detection. The limits of detection were 0.1 fmol injected onto the column for each catecholamine. This method allows the routine assay of plasma catecholamine concentrations within the normal adult ranges in both 500 and 50 microL samples. The within assay coefficient of variation (CV) for noradrenaline (NA) was 1.2% in 500 microL plasma and 1.9% for 50 microL plasma, corresponding values for adrenaline (A) were 8.5 and 6.6%. The between assay CVs were 3.9 and 7.8% for NA, and 9.9 and 5.7% for A.

Acids

Euglycaemic hyperinsulinaemia does not affect gastric emptying in type I and type II diabetes mellitus.

Hyperglycaemia slows gastric emptying in both normal subjects and patients with diabetes mellitus. The mechanisms mediating this effect, particularly the potential role of insulin, are uncertain. Hyperinsulinaemia has been reported to slow gastric emptying in normal subjects during euglycaemia. The purpose of this study was to evaluate the effect of euglycaemic hyperinsulinaemia on gastric emptying in Type I (insulin-dependent) and Type II (noninsulin-dependent) diabetes mellitus. In six patients with uncomplicated Type I and eight patients with uncomplicated Type II diabetes mellitus, measurements of gastric emptying were done on 2 separate days. No patients had gastrointestinal symptoms or cardiovascular autonomic neuropathy. The insulin infusion rate was 40 mU x m(-2) x min(-1) on one day and 80 mU x m(-2) x min(-1) on the other. Gastric emptying and intragastric meal distribution were measured using a scintigraphic technique for 3 h after ingestion of a mixed solid/liquid meal and results compared with a range established in normal volunteers. In both Type I and Type II patients the serum insulin concentration had no effect on gastric emptying or intragastric meal distribution of solids or liquids. When gastric emptying during insulin infusion rates of 40 mU x m(-2) x min(-1) and 80 mU x m(-2) x min(-1) were compared the solid T50 was 137.8+/-24.6 min vs. 128.7+/-24.3 min and liquid T50 was 36.7+/-19.4 min vs. 40.4+/-15.7 min in the Type I patients; the solid T50 was 94.9+/-19.1 vs. 86.1+/-10.7 min and liquid T50 was 21.8+/-6.9 min vs. 21.8+/-5.9 min in the Type II patients. We conclude that hyperinsulinaemia during euglycaemia has no notable effect on gastric emptying in patients with uncomplicated Type I and Type II diabetes; any effect of insulin on gastric emptying in patients with diabetes is likely to be minimal.

Adult

The reduction in postprandial lipemia after exercise is independent of the relative contributions of fat and carbohydrate to energy metabolism during exercise.

A single session of exercise several hours before a high-fat meal reduces postprandial lipemia. The purpose of the present study was to test the hypothesis that this effect is independent of substrate metabolism during exercise. Twelve men aged 21 to 36 years underwent three oral fat tolerance tests with intervals of at least 1 week. On one occasion, only activities of daily living were allowed the preceding day (control). On the other two occasions, subjects ran on a treadmill for 90 minutes on the afternoon preceding the fat tolerance test; 90 minutes before running, they ingested either acipimox, an inhibitor of lipolysis in adipose tissue, or placebo. Acipimox abolished the increase in the nonesterified fatty acid (NEFA) concentration observed during the run after placebo and reduced lipid oxidation (placebo, 37 +/- 7 g; acipimox, 21 +/- 3 g; P < .05, mean +/- SEM), but had no effect on gross energy expenditure (placebo, 4.86 +/- 0.20 MJ; acipimox, 4.83 +/- 0.18 MJ). Before each of the three fat tolerance tests, subjects reported to the laboratory after an overnight fast. Blood samples were obtained in the fasted state and for 6 hours after consumption of a high-fat meal (per kilogram of body mass: 1.2 g fat, 1.2 g carbohydrate, and 61 kJ energy). Plasma concentrations of NEFA were higher postprandially with acipimox, compared with control and placebo (P < .05), as were glucose concentrations measured over the first 4 hours. The insulin response to the meal was lower in placebo compared with control and acipimox (P < .05). Despite these counterregulatory responses, postprandial lipemia was reduced to the same degree (compared with control, P < .05) by exercise preceded by acipimox and by exercise preceded by placebo (area under the plasma triacylglycerol concentration v time curve: control, 8.77 +/- 1.17 mmol/L x 6 h; placebo, 6.95 +/- 0.97 mmol/L x 6 h; acipimox, 6.81 +/- 0.81 mmol/L x 6 h). These findings suggest that some factor other than the nature of the metabolic substrate used during exercise determines the attenuating effect of prior exercise on postprandial lipemia.

Adult

Carbohydrate as a nutrient in adults: range of acceptable intakes.

This review considers the acute and chronic effects of different levels of carbohydrate (CHO) intakes. The type of CHO consumed, especially glucose vs fructose, affects the glycaemic, insulinaemic and thermogenic responses. In addition, other aspects of food (type of starch, method of processing or cooking, presence of other nutrients) affects the glycaemic response (glycaemic index). In general, the greatest benefit to health is derived from consuming foods with a low glycaemic index and a high non-starch polysaccharide (fibre) content. Healthy, moderately active adults require at least 200g CHO per day to sustain normal brain metabolism and muscle function. Moreover, the CHO content should represent at least 50% of energy intake. Higher intakes of CHO can have deleterious effects on blood lipids (especially plasma triacylglycerol) in middle-aged and elderly subjects, and are really only appropriate for subjects with a high level of physical activity who need to maintain muscle glycogen content. Meals with a high carbohydrate content can lead to problems of postprandial hypotension in the elderly, and impaired exercise capacity in patients with angina.

Adult

The effect of sibutramine on energy expenditure and appetite during chronic treatment without dietary restriction.

OBJECTIVE: To assess the contribution of a thermogenic effect to weight loss induced by eight weeks treatment with sibutramine (15mg/d) vs placebo in obese subjects. DESIGN: Randomised, placebo controlled, double blind study. SUBJECTS: Thirty-two (7 male, 25 female) healthy obese body mass index (BMI) 33.9+/-0.5 kg/m2 subjects completed the trial. MEASUREMENTS: Energy expenditure (EE) was measured by indirect calorimetry during a 32 h stay in a respiration chamber before and after 8 weeks treatment. Visual analogue scales were completed for assessment of appetite sensation. No dietary restriction was given. RESULTS: Sibutramine caused a significant weight loss compared with placebo (-2.4 kg vs+0.3 kg, P<0.001). Despite the larger weight loss after 8 weeks, 24-h EE did not decrease more in the sibutramine than in the placebo group (-2. 6% vs -2.5%, P=ns). When the changes in 24-h EE were adjusted for changes in body weight, 24-h EE decreased significantly less in the sibutramine group than in the placebo group (0.8% vs 3.8%, P<0.02). Sibutramine significantly decreased both hunger and anticipated food consumption, and increased satiety scores. CONCLUSIONS: The weight reducing effect of sibutramine in humans is caused by a dual mechanism: reduction of energy intake by increasing satiety and decreasing hunger and prevention of the decline in EE that follows weight loss.

Adult

Effect of different times of administration of a single ethanol dose on insulin action, insulin secretion and redox state.

AIMS: Ethanol (EtOH) can affect glucose metabolism by altering the redox state, insulin-mediated glucose uptake and insulin secretion. We sought to determine the effects of an acute oral EtOH load on insulin secretion and glucose tolerance and the importance of a different timing of administration relative to a glucose load. METHODS: Eleven subjects underwent a frequently sampled intravenous glucose tolerance test (FSIGT) on three occasions in random order. In one, EtOH was given 50 min 'before' the FSIGT; on the second, the same amount was administered 6 min after the glucose pulse ('during' study); on the third no EtOH was given. RESULTS: Blood EtOH peaked at 4.43+/-0.24 mmol/l (mean +/- SD) in the 'during' and 4.16+/-0.31 mmol/l in the 'before' study. No differences were noticed in S(I), the index of insulin sensitivity, or in S(G), the glucose effectiveness, between the 'before', 'during' and control studies. There were no differences in the first-phase insulin secretion between the three studies but a significant increase in the sensitivity to glucose of second-phase dynamic insulin response, phi2, in the 'before' (0.062+/-0.036 pmol x min(-2) x (mg(-1) x dl(-1))(-1)) and 'during' (0.063+/-0.059) studies, compared to the control study (0.017+/-0.010, P<0.05) was observed. No differences were observed in the hepatic extraction of insulin. In the 'before' study, there was a significant decline in NEFA (non-esterified fatty acid) concentration from the baseline (mean 602+/-51 micromol/l) to the O min value (mean 353+/-37, P<0.01). During the FSIGT, the mean plasma NEFA concentration was significantly lower in the 'before' and in the 'during' than in the control study. CONCLUSION: An acute oral EtOH load does not impair glucose metabolism, at least in part because of an increased second-phase insulin secretion. Since this effect is observed irrespective of whether EtOH is consumed either before or during the glucose load, the existence of a priming effect is questioned.

Adult

Counterregulation during spontaneous nocturnal hypoglycemia in prepubertal children with type 1 diabetes.

OBJECTIVE: To examine counterregulatory responses during spontaneous nocturnal hypoglycemia in prepubertal children with type 1 diabetes. RESEARCH DESIGN AND METHODS: A total of 29 prepubertal patients with type 1 diabetes underwent two overnight profiles. Data were analyzed from 16 children (median [range] 8.7 [5.9-12.9] years of age) with a night of hypoglycemia and a nonhypoglycemic night. Children hypoglycemic (< 3.5 mmol/l) on night 1 were given 25% extra carbohydrate as uncooked cornstarch with their usual evening snack on night 2 to avoid hypoglycemia. Glucose, growth hormone, and cortisol were measured every 15 min, catecholamines every 30 min, and glucagon, pancreatic polypeptide, insulin, and ketones every 60 min. A group of 15 healthy control subjects, aged 9.5 (5.6-12.1) years, underwent one overnight profile. RESULTS: Median duration of hypoglycemia was 225 (30-630) min, and glucose nadir was 2.0 (1.2-3.3) mmol/l. Insulin levels were not different on the two nights (P = 0.9, analysis of variance), but children with diabetes had higher insulin levels than normal control subjects between 2300 and 0300, maximal at 0200 (mean +/- SEM 57.4 +/- 5.7 vs. 31.6 +/- 5.0 pmol/l, P = 0.002). Peak epinephrine was higher on the night of hypoglycemia (0.98 [0.52-2.09] nmol/l) versus nonhypoglycemia (0.32 [0.21-0.62] nmol/l), P = 0.001, but norepinephrine (1.29 [1.07-2.64] vs. 1.26 [1.04-1.88] nmol/l, P = 0.5), glucagon (93 [64.2-125.6] vs. 100.5 [54.6-158] ng/l, P = 0.6), pancreatic polypeptide (410.2 [191-643.2] vs. 270.8 [158.2-777.8] ng/l, P = 0.5), and cortisol (513 [300-679] vs. 475 [235-739] nmol/l, P = 0.6) were not different. Glucose threshold for epinephrine release was very low, 1.9 +/- 0.2 mmol/l. There was a short-lived rise in growth hormone from 75-105 min after onset of hypoglycemia, maximal at 90 min (7.8 +/- 1.2 vs. 3.5 +/- 0.9 ng/ml, P = 0.02). CONCLUSIONS: The prolonged nature of nocturnal hypoglycemic episodes may be explained in part by defective counterregulation. The risk of nocturnal hypoglycemia needs to be reduced before intensification of insulin therapy can be contemplated in this age-group.

Blood Glucose

Occult hypoglycemia caused by hemodialysis.

BACKGROUND: Previous studies have ignored hypoglycemia in patients undergoing hemodialysis. The fall in plasma glucose may not have been considered to be clinically relevant because the patients were asymptomatic. The present study was designed to assess the effect of hemodialysis on plasma glucose, insulin, glucagon, cortisol and catecholamines in non diabetic patients. METHODS: 21 non diabetic patients with chronic renal failure were hemodialyzed using a glucose-free dialysis fluid. They did not take any medication prior to dialysis and were asked not to eat during the first hour on hemodialysis. Blood and dialysate fluid was sampled at regular intervals during the first hour of dialysis for analysis. RESULTS: Plasma glucose fell below 4.0 mmol/l (72 mg/dl) in 9 of the 21 patients, below 3.5 mmol/l (63 mg/dl) in 6 and below 3.0 mmol/l (54 mg/dl) in 3. The lowest recorded value was 2.1 mmol/l (38 mg/dl). The mode glucose loss in the waste dialysate fluid was 6 g/h. In the group of 9 patients whose plasma glucose fell below 4.0 mmol/l (72 mg/dl), no symptoms of hypoglycemia were shown but 4 of the 7 patients who felt very hungry and ate were in this group. When 7 patients from this group were subsequently dialysed with a dialysis fluid containing 5.5 mmol/l (100 mg/dl) glucose, their plasma glucose became stabilized within the fasting reference range. There were no significant hormonal changes during the dialysis or between euglycemic and hypoglycemic patients. CONCLUSIONS: Patients undergoing hemodialysis may become hypoglycemic and not be aware of it. There is no hormonal imbalance causing the hypoglycemia and the hormonal response to the hypoglycemia is blunted. Patients with an initial plasma glucose of 4.5 mmol/l (81 mg/dl) or less who are hemodialyzed and who do not eat during dialysis may be particularly at risk. They should be dialysed with a dialysis fluid containing at least 5.5 mmol/l (100 mg/dl) glucose.

Blood Glucose

Effects of carbohydrate and lipid on resting energy expenditure, heart rate, sleepiness, and mood.

The effects of gastric infusions of fat and carbohydrate on physiological and psychological measures were compared using a within subject design in 9 healthy subjects (6 males). Each subject received isovolaemic rapid gastric infusions of sucrose solution (100% energy carbohydrate), lipid emulsion (100% energy fat, 20% Intralipid), and a non-nutrient control (0.9% saline) in a randomised order. Nutrient infusions were isoenergetic, containing one-third of an individual subject's estimated daily energy requirements (mean, 3227 kJ; range, 2479-3971 kJ). Measures of heart rate (HR), energy expenditure (EE), mood, and sleepiness were collected before the infusions and every 0.5 h for 3.5 h. Mean postingestive HR, EE, and satiation were significantly greater after the nutrient infusions than after the control. Sucrose induced a rapid increase in HR and EE, whereas lipid had a lesser and more delayed effect. Thirty minutes after the gastric infusions, HR and EE were significantly higher after the sucrose than after the lipid and saline. Hedonic tone was greater and tension lower after the saline and sucrose infusions than after the lipid infusion. From 3 to 3.5 h after ingestion, subjects felt significantly more sleepy after the lipid infusion than they did at these times after the saline infusion, and significantly more dreamy after the lipid infusion than they did after the sucrose infusion. In conclusion, the presence of lipid and sucrose in the intestine induces significant and differing physiological and psychological effects, which are independent of cognitive and orosensory influences.

Adult

Substrate availability limits human skeletal muscle oxidative ATP regeneration at the onset of ischemic exercise.

We have demonstrated previously that dichloroacetate can attenuate skeletal muscle fatigue by up to 35% in a canine model of peripheral ischemia (Timmons, J.A., S.M. Poucher, D. Constantin-Teodosiu, V. Worrall, I.A. Macdonald, and P.L. Greenhaff. 1996. J. Clin. Invest. 97:879-883). This was thought to be a consequence of dichloroacetate increasing acetyl group availability early during contraction. In this study we characterized the metabolic effects of dichloroacetate in a human model of peripheral muscle ischemia. On two separate occasions (control-saline or dichloroacetate infusion), nine subjects performed 8 min of single-leg knee extension exercise at an intensity aimed at achieving volitional exhaustion in approximately 8 min. During exercise each subject's lower limbs were exposed to 50 mmHg of positive pressure, which reduces blood flow by approximately 20%. Dichloroacetate increased resting muscle pyruvate dehydrogenase complex activation status by threefold and elevated acetylcarnitine concentration by fivefold. After 3 min of exercise, phosphocreatine degradation and lactate accumulation were both reduced by approximately 50% after dichloroacetate pretreatment, when compared with control conditions. However, after 8 min of exercise no differences existed between treatments. Therefore, it would appear that dichloroacetate can delay the accumulation of metabolites which lead to the development of skeletal muscle fatigue during ischemia but does not alter the metabolic profile when a maximal effort is approached.

Acetylcarnitine

Effect of euglycaemic hyperinsulinaemia on gastric emptying and gastrointestinal hormone responses in normal subjects.

Several studies have shown that hyperglycaemia slows gastric emptying in normal subjects and patients with diabetes mellitus but whether hyperinsulinaemia per se has an effect remains debatable. In the present study we have assessed the effect of hyperinsulinaemia on gastric emptying of a solid and liquid meal in normal subjects. Ten men were studied three times in random order. After an overnight fast, subjects were infused with 0.9% NaCl on two occasions and on the third with insulin, at 40 mU x m(-2) x min(-1) with 20% glucose simultaneously to maintain euglycaemia. Steady-state glucose infusion rate was ensured before the subjects ate a standard meal of a pancake labelled with 99mTc and milkshake labelled with (111)In-DTPA. Gamma-scintigraphic images were then obtained every 20 min for the next 3 h. There were no significant differences between the mean half-emptying times (T50) of the solid and liquid during the two saline infusions (129.6 +/- 28.5 vs 128.4 +/- 23.8 min for the solid and 25.4 +/- 7.0 vs 34.7 +/- 18.0 min for the liquid, mean +/- SD). Hyperinsulinaemia delayed both solid (mean T50 149.6 +/- 30.7, p = 0.031) and liquid emptying (mean T50 39.8 +/- 13.9, p = 0.042). There were no significant differences in the cholecystokinin and glucagon-like peptide 1 responses to the meal during either saline or insulin infusions. There was a tendency towards a greater insulin response to the meal during the hyperinsulinaemic study. Thus, hyperinsulinaemia delayed emptying of both the solid and liquid components of the meal.

Adult

The effect of single doses of pramlintide on gastric emptying of two meals in men with IDDM.

In a previous study we have shown that an intravenous infusion of pramlintide (an analogue of human amylin) delayed gastric emptying, but the dose of pramlintide was supraphysiological in relation to the amylin response to food in non-diabetic subjects. The purpose of this study was to examine the dose response relationship of subcutaneous injections of pramlintide on gastric emptying and to determine whether administration of the drug before one meal has an impact on the subsequent meal. Eleven men with insulin-dependent diabetes mellitus were studied in a double-blind, randomised, four-way crossover design. None had autonomic neuropathy. Euglycaemia was maintained overnight before the study day. At -30 min the patients self-injected their usual morning insulin and at -15 min they injected the study drug (either placebo or 30, 60 or 90 microg pramlintide) subcutaneously. At 0 min they ate a standard meal consisting of a pancake, labelled with 99mTc, and a milkshake containing 3-ortho-methylglucose (3-OMG). Gastric emptying images were obtained for the next 8 h. At 240 min the subjects ate a similar meal, but on this occasion the pancake was labelled with (111)In. All three doses of pramlintide delayed emptying of the solid component of the first meal (p < 0.004) with no significant difference between the drug doses. There were no differences between placebo and pramlintide after the second meal. All three doses of pramlintide resulted in a prolongation in the time to peak plasma 3-OMG level (p < 0.0001) after the first meal but there was no difference after the second meal.

3-O-Methylglucose

The influence of cold stress and a 36- h fast on the physiological responses to prolonged intermittent walking in man.

In a previous study, rectal temperature (Tre) was found to be lower, and oxygen consumption (VO2) and the respiratory exchange ratio (R) were higher in a cold (+5 degrees C), wet and windy environment (COLD), compared with a thermoneutral environment during intermittent walking at approximately 30% of peak VO2 (Weller AS, Millard CE, Stroud MA et al. Am J Physiol 272:R226-R233, 1997). The aim of the present study was to establish whether these cold-induced responses are influenced by prior fasting, as impaired thermoregulation has been demonstrated in cold-exposed, resting men following a 48-h fast. To address this question, eight men attempted a 360-min intermittent (15 min rest, 45 min exercise) walking protocol under COLD conditions on two occasions. In one condition, the subjects started the exercise protocol approximately 120 min after a standard meal (FED/ COLD), whereas in the other the subjects had fasted for 36 h (FASTED/COLD). The first two exercise periods were conducted at a higher intensity (HIGHER, 6 km x h[-1] and 10% incline), than the four subsequent exercise periods (LOW, 5 km x h[-1] and 0% incline). There was no difference in the time endured in FED/ COLD and FASTED/COLD. In FASTED/COLD compared with FED/COLD, R was lower during HIGHER and LOW, and Tre was lower during LOW, whereas there was no difference in VO2, mean skin temperature and heart rate. Therefore, although the 36-h fast impaired temperature regulation during intermittent low-intensity exercise in the cold, wet and windy environment, it was unlikely to have been the principal factor limiting exercise performance under these experimental conditions.

Adult

Cardiorespiratory responses to underwater treadmill walking in healthy females.

This study compared the cardiorespiratory responses of eight healthy women (mean age 30.25 years) to submaximal exercise on land (LTm) and water treadmills (WTm) in chest-deep water (Aquaciser). In addition, the effects of two different water temperatures were examined (28 and 36 degrees C). Each exercise test consisted of three consecutive 5-min bouts at 3.5, 4.5 and 5.5 km x h(-1). Oxygen consumption (VO2) and heart rate (HR), measured using open-circuit spirometry and telemetry, respectively, increased linearly with increasing speed both in water and on land. At 3.5 km x h(-1) VO2 was similar across procedures [chi = 0.6 (0.05) l x min(-1)]. At 4.5 and 5.5 km x h(-1) VO2 was significantly higher in water than on land, but there was no temperature effect (WTm: 0.9 and 1.4, respectively; LTm: 0.8 and 0.9 l x min(-1), respectively). HR was significantly higher in WTm at 36 degrees C compared to WTm at 28 degrees C at all speeds, and compared to LTm at 4.5 and 5.5 km x h(-1) (P < or = 0.003). The HR-VO2 relationship showed that at a VO2 of 0.9 l x min(-1) x HR was higher in water at 36 degrees C (115 beats x min[-1]) than either on land (100 beats min[-1]) or in water at 28 degrees C (99 beats x min[-1]). The Borg scale of perceived exertion showed that walking in water at 4.5 and 5.5 km x h(-1) was significantly harder than on land (WTm: 11.4 and 14, respectively; LTm: 9.9 and 11, respectively; P < or = 0.001). These cardiorespiratory changes occurred despite a slower cadence in water (the mean difference at all speeds was 27 steps/min). Thus, walking in chest-deep water yields higher energy costs than walking at similar speeds on land. This data has implications for therapists working in hydrotherapy pools.

Adult

Depressor action of insulin on skeletal muscle vasculature: a novel mechanism for postprandial hypotension in the elderly.

OBJECTIVES: We sought to assess the role of insulin in postprandial blood pressure regulation in the elderly. BACKGROUND: Insulin is both a positive inotropic and chronotropic hormone that also vasodilates skeletal muscle vasculature. Insulin may thus mediate aspects of postprandial cardiovascular homeostasis. METHODS: Ten healthy elderly subjects were studied in the fasting state on three separate days. After baseline supine hemodynamic and neurohumoral measurements were taken (cardiac output and superior mesenteric artery blood flow were measured using Doppler ultrasound, and calf blood flow was measured using venous occlusion plethysmography), subjects ate on one occasion a 2.5-MJ high carbohydrate meal and on the other two occasions, an isoenergetic high fat meal. One high fat meal was accompanied by an insulin infusion reproducing the plasma insulin profile seen after a high carbohydrate meal while maintaining the glycemic profile seen after a high fat meal alone. After meal ingestion, measurements were repeated every 20 min for 2 h. RESULTS: After the three meals, there were similar increments in cardiac output and heart rate. After the high carbohydrate meal and high fat meal with insulin, mean arterial blood pressure fell by between 8 to 10 mm Hg, but did not change after the high fat meal. After the high carbohydrate meal and the high fat meal with insulin, calf vascular resistance did not change, whereas after the high fat meal, it increased by 15.5 +/- 4.4 U (mean +/- SEM). CONCLUSIONS: Insulin contributes to the failure of calf vasoconstriction seen after a high carbohydrate meal. By this vasodepressor action, insulin is at least in part responsible for the fall in blood pressure after a high carbohydrate meal.

Aged