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Biomedical subjects

D R Lamb

Publications and source records attributed to D R Lamb.

17 recordsLinked to original sources

Arterial-venous difference in atrial natriuretic peptide concentration during exercise in horses.

Six nontrained mares were subjected to steady-state, submaximal treadmill exercise to examine the effect of exercise on the plasma concentration of atrial natriuretic peptide (ANP) in arterial, compared with mixed venous, blood. Horses ran on a treadmill up a 6 degree grade for 20 minutes at a speed calculated to require a power equivalent to 80% of maximal oxygen uptake (VO2MAX). Arterial and mixed venous blood samples were collected simultaneously from the carotid and pulmonary arteries of horses at rest and at 10 and 20 minutes of exercise. Plasma was stored at -80 C and was later thawed; ANP was extracted, and its concentration was determined by radioimmunoassay. Exercise caused significant (P < 0.05) increases in arterial and venous plasma ANP concentrations. Mean +/- SEM arterial ANP concentration increased from 25.2 +/- 4.4 pg/ml at rest to 52.7 +/- 5.2 pg/ml at 10 minutes of exercise and 62.5 +/- 5.2 pg/ml at 20 minutes of exercise. Mean venous ANP concentration increased from 24.8 +/- 4.3 pg/ml at rest to 67.2 +/- 14.5 pg/ml at 10 minutes of exercise and 65.3 +/- 13.5 pg/ml at 20 minutes of exercise. Significant differences were not evident between arterial or mixed venous ANP concentration at rest or during exercise, indicating that ANP either is not metabolized in the lungs or is released from the left atrium at a rate matching that of pulmonary metabolism.

Animals

Plasma renin activity and aldosterone and vasopressin concentrations during incremental treadmill exercise in horses.

Six untrained mares were subjected to incremental treadmill exercise to examine exercise-induced changes in plasma renin activity (PRA) and plasma aldosterone (ALDO) and plasma arginine vasopressin (AVP) concentrations. Plasma renin activity, ALDO and AVP concentrations, and heart rate (HR) were measured at each step of an incremental maximal exercise test. Mares ran up a 6 degree slope on a treadmill set at an initial speed of 4 m/s. Speed was increased 1 m/s each minute until HR reached a plateau. Plasma obtained was stored at -80 C and later was thawed, extracted, and assayed for PRA and ALDO and AVP values by use of radioimmunoassay. Exercise caused significant increase in HR from 40 +/- 2 beats/min (mean +/- SEM) at rest to 206 +/- 4 beats/min (HRmax) at speed of 9 m/s. Plasma renin activity increased from 1.9 +/- 1.0 ng/ml/h at rest to a peak of 5.2 +/- 1.0 ng/ml/h at 9 m/s, paralleling changes in HR. Up to treadmill speed of 9 m/s, strong linear correlations were obtained between exercise intensity (and duration) and HR (r = 0.87, P less than 0.05) and PRA (r = 0.93, P less than 0.05). Heart rate and PRA reached a plateau and did not increase when speed was increased from 9 to 10 m/s. Plasma ALDO concentration increased from 48 +/- 16 pg/ml at rest to 191 +/- 72 pg/ml at speed of 10 m/s. Linear relation was found between exercise intensity (and duration) and ALDO concentration (r = 0.97, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone

Muscle glycogen loading with a liquid carbohydrate supplement.

This study compared two high carbohydrate (CHO) diets in 14 male runners for effects on muscle glycogen deposition, endurance, and sensations of gastrointestinal discomfort. Muscle glycogen was measured in the vastus lateralis at rest and run time to exhaustion at 75% VO2max was measured following 3-1/2 days on a 50% CHO diet. After 14 days the subjects consumed a 20% CHO diet and continued training to reduce glycogen. During the next 3-1/2 days, subjects ran less and consumed a 90% CHO diet emphasizing pasta and rice (Pasta, n = 7) or lesser amounts of pasta and rice supplemented by a maltodextrin beverage (Supplement, n = 7). Glycogen was again measured, followed by a second run to exhaustion. Compared to the 50% CHO diet, Pasta increased muscle glycogen by 27.1 +/- 12.2 mmoles/kg muscle (M +/- SE; P < 0.05) and run time by 15.7 +/- 5.9 min; Supplement increased glycogen by 43.2 +/- 13.5 mmoles/kg (P < 0.05) and run time by 29.0 +/- 7.4 min (P < 0.05). Total glycogen concentrations and run times were not significantly different for Pasta versus Supplement. Subjects reported less gastrointestinal discomfort and greater overall preference for Supplement than for Pasta. Thus, glycogen loading can be accomplished at least as effectively and more comfortably by substituting a maltodextrin drink for some of the pasta and rice in a glycogen loading diet.

Adult

Dietary carbohydrate, muscle glycogen, and power output during rowing training.

The belief that high-carbohydrate diets enhance training capacity (mean power output) has been extrapolated from studies that have varied dietary carbohydrate over a few days and measured muscle glycogen but did not assess power output during training. We hypothesized that a high-carbohydrate (HI) diet (10 g.kg body mass-1.day-1) would promote greater muscle glycogen content and greater mean power output during training than a moderate-carbohydrate (MOD) diet (5 g.kg body mass-1.day-1) over 4 wk of intense twice-daily rowing training. Dietary protein intake was 2 g.kg body mass-1.day-1, and fat intake was adjusted to maintain body mass. Twelve male and 10 female collegiate rowers were randomly assigned to the treatment groups. Training was 40 min at 70% peak O2 consumption (VO2) (A.M.) and either three 2,500-m time trials to assess power output or interval training at 70-90% peak VO2 (P.M.). Mean daily training was 65 min at 70% peak VO2 and 38 min at greater than or equal to 90% peak VO2. Mean muscle glycogen content increased 65% in the HI group (P less than 0.05) but remained constant at 119 mmol/kg in the MOD group over the 4 wk. Mean power output in time trials increased 10.7 and 1.6% after 4 wk in the HI and MOD groups, respectively (P less than 0.05). We conclude that a diet with 10 g carbohydrate.kg body mass-1.day-1 promotes greater muscle glycogen content and greater power output during training than a diet containing 5 g carbohydrate.kg body mass-1.day-1 over 4 wk of intense twice-daily rowing training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Dietary carbohydrate and intensity of interval swim training.

We tested the effects of 9 d of a high-carbohydrate diet (80% of calories as CHO, 80% CHO diet) vs. a moderate-CHO diet (43% of calories as CHO, 43% CHO diet) on the abilities of collegiate swimmers to maintain a high intensity of interval swim training. Interval swim times and other physiological indices were recorded the last 5 d of each diet. Swim-interval distances ranged from 50-m interval sets to continuous 3000-m swims. There were no diet effects on mean swim velocities for any interval distance, and mean (+/- SEM) velocities for all swims were identical for both diets. There were no diet effects on the physiological indices; however, postswim blood lactate concentrations were higher after the 80% CHO diet. When mean +/- SEM daily caloric intake is 19.56 +/- 2.16 MJ (4675 +/- 516 kcal) for swimmers undertaking swim training to develop aerobic capacity, an 80% CHO diet provides no advantage over a 43% CHO diet for maintaining interval-swim-training intensity.

Adult

Indomethacin suppresses the coronary flow response to hypoxia in exercise trained and sedentary rats.

STUDY OBJECTIVE: The aim was to determine if prostaglandin like activity might be involved in changes due to exercise training in the coronary flow responses to hypoxia. DESIGN: The coronary flow response to hypoxia was measured under constant perfusion pressure in isolated perfused hearts from 12 endurance exercise trained rats and 12 control rats. Eight hearts were perfused with a solution containing indomethacin, a cyclo-oxygenase inhibitor, to determine its effect on any training induced changes in the coronary flow response to hypoxic stress. EXPERIMENTAL MATERIAL: 24 male Sprague-Dawley rats, 517 (SD 51) g, were used for this study. The animals were anesthetised and the hearts rapidly excised and perfused with a modified Langendorff perfusion system. MEASUREMENTS AND MAIN RESULTS: Under constant perfusion pressure, the hearts of endurance exercise trained rats had a greater increase in coronary flow during hypoxia relative to normoxia than did hearts of untrained rats, at 13.52(2.15) v 9.56(1.05) ml.min-1.g-1 dry heart weight. Indomethacin treatment abolished this difference and lowered coronary flow: exercise -3.81(3.75) ml.min-1.g-1; control 0.38(2.44) ml.min-1.g-1. CONCLUSIONS: The inhibition by indomethacin of the endurance exercise training induced potentiation of the coronary fluid flow response to hypoxia suggests that prostacyclin or a related compound may be involved in this adaptation to exercise.

Animals

Carbohydrate-electrolyte drinks: effects on endurance cycling in the heat.

On three occasions cyclists completed, as fast as possible, two exercise tasks (T1 and T2) separated by 30 min rest. T1 and T2 were equivalent to the work performed during 2 h cycling at 75% VO2max and 30 min at 75% VO2max, respectively. Every 20 min subjects drank 275 mL of a 6% (MC) or 2.5% (LC) carbohydrate-electrolyte beverage or a water placebo (P). The initial drink during both T1 and the rest period contained 20 g D2O as a marker for entry of ingested fluid into blood. No differences in drink effects were found for heart rate, sweat rate, change in plasma volume, rectal temperature, or D2O accumulation in blood. Blood glucose and respiratory exchange ratios were higher and T2 was performed faster with MC than with P. Ingestion of MC can help maintain blood glucose and enhance performance of prolonged cycling exercise without compromising fluid replenishment.

Adolescent

Opioid modulation of feeding behavior following forced swimming exercise in male rats.

Adult male rats were subjected to an acute bout of swimming exercise for 50 min during the early morning or late afternoon. Compared to nonexercised controls, all exercised groups showed an initial approximately 2-hr period of increased feeding (period I hyperphagia). A 50-min period of sham swimming (wading in water) was followed by period I hyperphagia but not period II hypophagia. Opioid modulation of period I hyperphagia was indicated by the ability of naltrexone to antagonize, in a dose-dependent manner, the postexercise hyperphagia. Furthermore, plasma concentrations of immunoreactive B-endorphin (Ir-B-ep) were increased during period I following exercise. Opioid modulation of the period II hypophagia was equivocal. Plasma Ir-B-ep was not altered in period II, and naltrexone did not modify period II hypophagia. The ability of 2-deoxy-D-glucose to induce feeding was slightly depressed (p less than 0.05) during period II after exercise, and the ability of exogenous insulin to induce feeding was not changed. These differential feeding responses to 2-deoxy-D-glucose (opioid-mediated) and insulin (relatively opioid-independent) suggest that an opioid deficiency may exist during period II and contribute to the hypophagia.

Animals

Opioid modulation of feeding behavior following repeated exposure to forced swimming exercise in male rats.

Patterns of normal and stimulated food intake (FI) as well as its possible endogenous opioid (EO) modulation were investigated in male rats given regular swimming exercise (trained; TR) and compared with nonexercised sedentary (SED) controls. Rats in the TR group had lower body weights as well as reduced 24 hr FI due to lower nocturnal FI. TR rats also ate less food in response to injections of 2-deoxy-D-glucose (2-DG) but not insulin (INS) when injections were given during the first 4-5 weeks of training. However, this difference between TR and SED rats in the 2-DG induced feeding was not demonstrable after 10 or more weeks of training. Plasma concentrations of immunoreactive B-endorphin (IR-B-ep) were elevated, as expected, in TR rats (10-12 weeks) during nocturnal sampling whereas the nocturnal increase of IR-B-ep was absent in SED controls. However, these SED rats did increase daytime IR-B-ep in response to 2-DG and acute exercise, albeit somewhat less in magnitude when compared to TR rats. Injection of naltrexone (NTX) decreased feeding in TR rats (10-12 weeks) but not in contemporary SED controls. In summary, exercise training modified feeding behavior, and at 4 weeks of training, TR rats ate less in response to opioid-related feeding stimulus of 2-DG, but responded similarly to insulin (relatively opioid independent) treatment. At later stages of training this difference between TR and SED rats disappeared. Moreover, SED rats had atypical profiles of IR-B-ep and reduced hypophagic responses to NTX suggesting that TR rats might have greater EO modulation of feeding at this stage.

Animals

Glycogen synthase activation in human skeletal muscle: effects of diet and exercise.

We investigated the role of glycogen synthase in supranormal resynthesis (supercompensation) of skeletal muscle glycogen after exhaustive exercise. Six healthy men exercised 60 min by cycling with one leg at 75% VO2max, recovered 3 days on a low-carbohydrate diet, exercised again, and recovered 4 days on high-carbohydrate diet. Glycogen and glycogen synthase activities at several glucose-6-phosphate (G6P) concentrations were measured in biopsy samples of m. vastus lateralis. Dietary alterations alone did not affect glycogen, whereas exercise depleted glycogen stores. After the second exercise bout, glycogen returned to normal within 24 h and reached supercompensated levels by 48 h of recovery. Glycogen synthase activation state strikingly increased after exercise in exercised muscle and remained somewhat elevated for the first 48 h of recovery in both muscles. We suggest that 1) forms of glycogen synthase intermediate to I (G6P-independent) and D (G6P-dependent) forms are present in vivo, and 2) glycogen supercompensation can in part be explained by the formation of intermediate forms of glycogen synthase that exhibit relatively low activity ratios, but an increased sensitivity to activation by G6P.

Adult

Structure and function of cardiac mitochondria in exhausted guinea pigs.

The ultrastructure and functional capacity of mitochondria from hearts of exhausted guinea pigs were compared to those from rested animals. Electron micrographs of heart ventricles were examined for ultrastructural alterations, and functional capacity was studied by oxygen polarography. General swelling of mitochondria from exhausted animals was indicated by a 41% reduction in mitochondrial surface/volume ratio and a 22% increase in volume density of mitochondria from exercised animals when compared to those from controls. The yield of isolated mitochondria from exhausted guinea pigs was similar to that for control animals. In the presence of all substrates tested the rate of oxygen consumption was lower in the exhausted animals than in the controls. The ADP/O ratios and respiratory control indices for pyruvate, succinate and ascorbate were not systematically affected by exercise. With glutamate as substrate respiratory control was reduced in exercised guinea pigs. These experiments suggest that the structure of myocardial mitochondria from exhausted animals is sufficient to maintain normal ADP/O ratios but is not adequate to maintain normal rates of respiration.

Animals

Skeletal muscle leucine incorporation and testosterone uptake in exercised guinea pigs.

We examined the changes induced by daily treadmill exercise on body weights, plantaris muscle weights, plantaris protein concentrations, and L-leucine-4,5-3H incorporation into plantaris muscles of normal and castrated young male guinea pigs and of castrated animals receiving testosterone replacement therapy, and compared the testosterone-1,2-3H uptake by plantaris muscles of trained normal guinea pigs to that of untrained animals. Trained animals exhibited significantly lower body and muscle weights and greater labeled leucine incorporation into sarcoplasmic and myofibrillar proteins but did not show significant changes in protein concentrations or labeled testosterone uptake. The level of physical activity of the young animals studied appeared to be more important than gonadal endocrine function in altering protein metabolism and muscle and body weights. Because hypertrophy did not occur in the trained plantaris muscles, which had elevated rates of labeled leucine incorporation, it appears that the trained animals had a higher muscle protein turnover rate. It seems unlikely that testosterone plays an important role in these activity-related phenomena.

Animals

Glycogen replenishment following exercise: effects of denervation and tenotomy.

To examine the role of the nervous system in the rapid replenishment of muscle glycogen that occurs after exhaustive exercise, glycogen stores and glycogen synthetase activity of normal gastrocnemius muscles of untrained and trained guinea pigs were compared to glycogen and synthetase activity of trained gastrocnemius muscles that were denervated or tenotomized immediately after exhaustive exercise and then allowed to recover for 48 h. The trained tenotomized muscles, but not the denervated muscles, had significantly (P smaller than 0.05) less glycogen than the trained normal muscles. These results suggest that neither nerve impulse conduction nor tropic substances contained in neural tissue proximal to the site of denervation mediate glycogen replenishment after exercise. The active, glucose 6-phosphate independent (I) form of glycogen synthetase activity was reduced by both denervation and tenotomy at 48 h after exercise with no significant (P greater than 0.05) differences detected for the total of I and D (glucose 6-phosphate dependent) synthetase activity. Synthetase I relative to total synthetase activity was similar in trained and untrained normal muscles, both of which had significantly (P smaller than 0.05) greater relative I activities than denervated or tenotomized muscles. These synthetase data show that elevated glycogen stores following recovery from exercise may be observed in the absence of increased levels of glycogen synthetase activity.

Achilles Tendon

Androgens and exercise.

In this presentation several of the reasons why androgenic hormones might be responsible for some of the effects of physical training and for some of the differences among individuals in athletic ability have been outlined. It seems apparent that minimal amounts of androgen are necessary to produce the normal differences between males and females in aggression, red blood cell production and bone growth, but it seems unlikely that any additional natural androgen, perhaps produced as a result of physical training, can be shown to enhance these characteristics after puberty. It seems more likely that changes in androgen levels or changes in sensitivity to androgens may be shown to be involved in the increases in muscle glycogen, protein synthesis, and lean body mass associated with chronic exercise. However, the data suggesting changes in androgen levels or androgen uptake with exercise are so meager and contradictory that no complete answer to any of these problems can yet be offered. Perhaps the best evidence that androgens are involved in athletic performance is that boys become more athletically proficient than girls at puberty, the time of the greatest changes in blood testosterone. The changes in muscle strength, body weight and lean body mass caused by anabolic steroid treatment are probably greater than many would hope and somwhat less than many think. There is apparently a wide range of individual responses to these drugs.

Adrenal Glands

Postexercise glycogen replenishment in untrained animals: denervation, tenotomy effects.

To test the hypothesis that an intact nerve supply is essential to normal replenishment of muscle glycogen after exhaustive exercise, glycogen concentration in normal gastrocnemius muscles from guinea pigs exhausted 48 hr previously was compared to glycogen in contralateral muscles that had been denervated at the muscle or high in the thigh immediately after exercise. Each animal of another group underwent tenotomy of one Achilles tendon after exercise so that any effect of disuse could be distinguished from effects of denervation. All muscles were able to replenish glycogen to normal control values 48 hr after exercise and surgery; there were no significant (greater than .05) effects of any of the surgical interventions. Therefore, it appears that glycogen concentration in skeletal muscle 48 hr after exhaustive exercise is independent of both neural phenomena and muscle tension.

Animals

Exercise training, indomethacin, and isoproterenol-induced myocardial necrosis in the rat.

It was hypothesized that endurance exercise training would attenuate isoproterenol-induced myocardial necrosis in the rat by increasing the concentration of prostacyclin in the myocardial vasculature. Rats were randomly assigned to exercise and control groups. Exercisers ran on a motorized treadmill 1 h.d-1, 5 d.week-1 for 14 weeks. Immediately following the training program subgroups of rats were injected with 4 mg.kg-1 indomethacin or saline. One day later, all rats were given a subcutaneous injection of isoproterenol (20 mg.kg-1); after another 24 h they were sacrificed. A decrease of myocardial creatine kinase (CK) activity was used as a marker for myocardial necrosis. Endurance exercise training attenuated the isoproterenol-induced decrease in myocardial CK relative to control by approximately 37% (exercise: 16.4 +/- 0.6 U.mg-1 protein; control: 10.5 +/- 0.6 U.mg-1 protein; p less than 0.05). Pretreatment with indomethacin decreased myocardial CK in the exercise-trained rats (indomethacin: 15.4 +/- 0.8 U.mg-1 protein; saline: 17.7 +/- 0.7 U.mg-1 protein; p less than 0.05), but not in the controls (indomethacin: 10.3 +/- 1.0 U.mg-1 protein; saline: 10.8 +/- 0.6 U.mg-1 protein; p greater than 0.05). The concentration of myocardial 6-keto-PGF1 alpha, a marker for prostacyclin, was not altered by exercise but, as expected, was reduced by indomethacin pretreatment (p less than 0.05). Thus, exercise training reduces myocardial damage caused by isoproterenol, but the evidence does not support the hypothesis that prostacyclin mediated this effect of training. Further research is needed to determine the extent to which exercise training-induced alterations in sensitivity to PGI2 or TXA2 affect myocardial damage from isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha

Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats.

The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.

Animals