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Biomedical subjects

R Bahr

Publications and source records attributed to R Bahr.

At least 73 records · Page 4Linked to original sources
PubMed1995

The clinical presentation of shoulder instability including on field management.

In the athlete, shoulder instability may result from external high-energy trauma or repetitive overuse. Our understanding of how shoulder instability may contribute to and result from shoulder injury has improved considerably during the past decade. In addition, the delicate balance between mobility and stability and the interrelationship between instability and rotator cuff disease make the clinical management of the unstable shoulder and its field treatment a challenge for physicians, therapists, trainers, and others responsible for the care of injured athletes.

Arm Injuries↗
PubMed1994

Atrial natriuretic peptide in plasma after prolonged physical strain, energy deficiency and sleep deprivation.

Plasma concentrations of atrial natriuretic peptide (ANP) were investigated daily in 16 male cadets during a 6-day military training course with continuous heavy physical activities, sleep and energy deficiency (course I). At the end of another similar course (course II) 15 cadets were studied during 30-min cycle exercise at 50% maximal oxygen uptake with and without glucose infusion. A small, but not significant increase was found in the plasma concentrations of ANP during course I from 9.6 (SEM 1.1) pmol.l-1 in the control experiment to 11.1 (SEM 0.5) pmol.l-1 on day 5. During course II a small but significant increase was found from 7.8 (SEM 0.5) pmol.l-1 in the control experiment to 9.1 (SEM 0.5) pmol.l-1 at the end of the course. Plasma osmolality and chloride concentration decreased during the course. During the exercise test a significant increase was seen in ANP concentration from 8.2 (SEM 0.8) to 13.1 (SEM 2.0) pmol.l-1 in the control experiment and from 9.4 (SEM 0.7) to 13.5 (SEM 1.2) pmol.l-1 during the course. This response was attenuated by glucose infusion, an effect which may have been due to an exercise induced increase in plasma chloride concentration being abolished. In contrast, the potassium concentration response to exercise was increased during the course but unaffected by glucose infusion. In conclusion, the large increases in endogenous plasma catecholamine concentration shown to take place during previous courses were not reflected in the plasma concentrations of ANP, indicating only a moderate cardiac stress or no cardiac work overload during such courses.

Adult↗
PubMed1994

Effect of beta-adrenoceptor blockade on post-exercise oxygen consumption.

In the recovery period after strenuous exercise, there is an increase in O2 uptake termed the excess post-exercise O2 consumption (EPOC), consisting of a rapid and a prolonged component. Mechanisms regulating the prolonged component of EPOC are not completely understood, but an effect of catecholamines has been suggested. The purpose of this study was to investigate the effect of beta-adrenoceptor blockade on EPOC. Six healthy young men were randomized to one control experiment and two exercise experiments, one with and one without nonselective beta-adrenoceptor blockade. In the exercise experiments, they exercised for 60 minutes at 78% +/- 3% (mean +/- SD) of maximal O2 uptake (VO2max) on a cycle ergometer followed by 6.5 hours' bedrest. In the beta-adrenoceptor blockade experiment, propranolol (0.1 mg.kg-1 body weight [BW]) was administered intravenously immediately after the exercise bout and again 3.5 hours after exercise. The control experiment was performed without exercise or beta-adrenoceptor blockade. EPOC was calculated as the difference in O2 uptake between the exercise and control experiments. A supplementary study on 15 subjects showed resting O2 uptake to be unaffected by propranolol. O2 uptake was significantly increased during the recovery period after exercise when no beta-adrenoceptor blocker was administered. After 6.5 hours of bedrest, the mean increase (+/- SE) in O2 uptake was 19 +/- 4 mL.min-1. In contrast, when propranolol was administered during recovery from exercise, O2 uptake was significantly increased for only the first 2 hours. Propranolol decreased total EPOC (+/- SE) by about one third, from 14.4 +/- 1.9 to 9.5 +/- 2.5 L.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

[Overtraining among elite athletes--causes, diagnosis and treatment].

Overtraining is an imbalance between training and recovery. We review the pathogenesis of overtraining, with emphasis on the neuroendocrinal changes which occur in response to acute overtraining. At present, no sensitive and specific tests are available to allow early diagnosis of overtraining. The diagnosis is based on medical history, clinical evaluation and exercise testing. The treatment is rest, and may take weeks to months.

Athletic Injuries↗
PubMed1992

Effect of supramaximal exercise on excess postexercise O2 consumption.

This study was undertaken to determine the effect of high intensity exercise on the time course and magnitude of excess postexercise O2 consumption (EPOC). Six healthy male subjects performed three intermittent 2-min exercise bouts on a cycle ergometer at 108% of VO2max with 3-min rest periods (3 x 2 min). O2 uptake, blood lactate, plasma catecholamines, and rectal temperature were measured while the subjects rested in bed for 14 h postexercise, and the results were compared with those of an identical control experiment without exercise. In addition, they were studied on two separate days for 2 h after only two (2 x 2 min) or one (1 x 2 min) exercise bout. O2 uptake was significantly increased for 4 h after 3 x 2 min exercise, for 60 min after 2 x 2 min, and for 30 min after 1 x 2 min exercise. EPOC was 5.6 +/- 0.41 (1 x 2 min), 6.7 +/- 0.41 (2 x 2 min), and 16.3 +/- 3.01 (3 x 2 min), respectively. Over the first hour postexercise, EPOC was linearly related to the change in blood lactate and plasma norepinephrine. However, after exhaustive supramaximal exercise O2 consumption was significantly increased for 4 h, whereas blood lactate and plasma norepinephrine concentrations were significantly increased for only 2 h.

Adult↗
PubMed1991

Effect of intensity of exercise on excess postexercise O2 consumption.

After exercise, there is an increase in O2 consumption termed the excess postexercise O2 consumption (EPOC). In this study, we have examined the effect of exercise intensity on the time course and magnitude of EPOC. Six healthy male subjects exercised on separate days for 80 minutes at 29%, 50%, and 75% of maximal O2 uptake (VO2max) on a cycle ergometer. O2 uptake, R value, and rectal temperature were measured while the subjects rested in bed for 14 hours postexercise, and the results were compared with those of an identical control experiment without exercise. An increase in O2 uptake lasting for 0.3 +/- 0.1 hour (29% exercise), 3.3 +/- 0.7 hour (50%) and 10.5 +/- 1.6 hour (75%) was observed. EPOC was 1.3 +/- 0.46 I(29%), 5.7 +/- 1.7 I (50%), and 30.1 +/- 6.4 I (75%). There was an exponential relationship between exercise intensity and total EPOC, both during the first 2 hours and the next 5 hours of recovery. Hence, prolonged exercise at intensities above 40% to 50% of VO2max is required in order to trigger the metabolic processes that are responsible for the prolonged EPOC component extending beyond 2 hours postexercise.

Adult↗
PubMed1991

Strenuous prolonged exercise elevates resting metabolic rate and causes reduced mechanical efficiency.

Resting O2 consumption, net mechanical efficiency during cycling exercise and excess postexercise O2 consumption (EPOC) was measured in 15 army cadets after 3 or 4 days of continuous simulated combat exercises (estimated energy demand: 40 MJ day-1), no organized sleep and virtually no food intake (stress experiment). They exercised for 30 minutes at a work load corresponding to about 50% of maximal O2 uptake. An identical test using the same absolute work load was repeated when the cadets were completely recovered from the combat course (control experiment). Resting O2 consumption increased by 15% from 279 +/- 7 ml min-1 (control) to 320 +/- 8 ml min-1 (stress, P less than 0.001). Mechanical efficiency decreased from 24.6 +/- 0.4% (control) to 20.9 +/- 0.2% (stress, P less than 0.001). EPOC1h increased from 0.58 +/- 0.41 l (control) to 2.24 +/- 0.2% (stress, P less than 0.05). Glucose infusion during exercise (0.20 g kg-1 body weight) had no effect on mechanical efficiency or EPOC. About 1/5 of the increase in exercise O2 uptake can be explained by a substrate shift from carbohydrates to fat, as evidenced by a reduction in R-value during exercise from 0.90 +/- 0.012 (control) to 0.80 +/- 0.010 (stress). Hence, after severe physical stress combined with sleep deprivation and food restriction, O2 uptake is increased both at rest and during submaximal exercise.

Adult↗
PubMed1991

Effect of exercise on recovery changes in plasma levels of FFA, glycerol, glucose and catecholamines.

The prolonged effects of acute exercise on the plasma concentrations of FFA, glycerol, glucose and catecholamines were examined. Twelve young men performed exhaustive prolonged exercise on a cycle ergometer (80 minutes at 70-75% of VO2 max), and in separate experiments they exercised for shorter durations (20, 40 and 80 minutes) and at lesser intensities (29, 50 and 75% of VO2 max). Carbohydrate-rich meals were given 2, 7 and 12 hours after exercise. Blood samples were taken while the subjects rested in bed during a 12-14-hour recovery period. Control experiments without exercise were also performed. In some subjects the plasma concentration of FFA after exhaustive exercise was increased to levels considered to be potentially hazardous, and the mean plasma level of FFA was increased for 6 hours and that of glycerol was increased for 2.5 hours after exercise. The plasma concentration of glucose was generally reduced for 12 hours after exhaustive exercise. Plasma catecholamines were increased for 2 hours after exhaustive exercise. We observed a preprandial increase in FFA and glycerol concentrations during recovery from exercise which was related to the duration and intensity of exercise. These findings indicate that the rates of FA utilization and TG-FA substrate cycling were increased in the recovery period after exercise, and that the magnitude of both depends on the duration and intensity of exercise.

Adult↗
PubMed1991

Effect of feeding and fasting on excess postexercise oxygen consumption.

This study was undertaken to determine the effect of fasting on the magnitude and time course of the excess postexercise O2 consumption (EPOC). Six lean untrained subjects were studied in the fasted state for 7 h after a previous strenuous exercise bout (80 min at 75% of maximal O2 uptake) and in a control experiment. The results were compared with identical control and exercise experiments where the subjects were fed a 4.5-MJ test meal after 2 h of rest. EPOC was calculated as the difference in O2 uptake between the corresponding control and exercise experiments. The total EPOC (0-7 h postexercise) was 20.9 +/- 4.5 (fasting) and 21.1 +/- 3.6 liters (food, NS). A significant prolonged EPOC component was observed in the fasted and in the fed state. The thermic effect of food (TEF) was calculated from O2 consumption and respiratory exchange ratio as the difference in energy expenditure between the corresponding food and fasting experiments. The total TEF (0-5 h postprandial) was 321 +/- 32.0 (control) and 280 +/- 37.7 kJ/5 h (exercise, NS). It is concluded that the prolonged component of EPOC is present in the fasting state. Furthermore, no major interaction effects between food intake and exercise on the postexercise O2 consumption could be detected.

Adult↗
PubMed1991

Reduced set-point temperature in young men after prolonged strenuous exercise combined with sleep and energy deficiency.

The effects on body temperature of 3-4 days of continuous military exercise combined with energy and sleep deficiency, at rest and in response to an exercise test (45% of VO2max for 30 min) and the following recovery, have been studied in fifteen young male cadets. During the course, at rest before exercise, rectal temperature was reduced by 0.57 +/- 0.15 degrees C, whereas trunk temperature was increased by 1.47 +/- 0.50 degrees C, and thigh temperature by 2.69 +/- 0.64 degrees C. Oxygen uptake increased 14-24% both before and during the exercise test in the stress experiment. During the course slightly lower rectal temperature levels were seen during the exercise test, whereas skin temperatures were significantly increased. Since the cadets' heat production and loss appeared to be increased and core temperature reduced, it is possible that we have observed a lowered set-point for core temperature.

Adult↗
PubMed1990

Triglyceride/fatty acid cycling is increased after exercise.

After exercise, there is a prolonged increase in O2 consumption termed the excess postexercise O2 consumption (EPOC). In this study, we have assessed the relative contribution of the triglyceride/fatty acid (TG/FA) substrate cycle to EPOC. Six healthy, young men exercised for 2 hours at 51% of maximal O2 uptake. The total energy expenditure and the rate of FA oxidation were estimated from measurements of O2 uptake, respiratory exchange ratio, and urinary nitrogen excretion while the subjects rested in bed for 3.5 hours postexercise. During the last part of the recovery period, the rate of FA mobilization was determined by infusion of glycerol. The rate of TG/FA cycling was calculated from the difference between the rate of FA mobilization and oxidation. An identical control study without exercise was also performed. The total EPOC during the recovery period was 7.82 +/- 1.51 L O2 (a 15% +/- 3% increase above the control O2 consumption). The rate of FA oxidation increased from 252 +/- 36 mumol/min (control) to 360 +/- 27 mumol/min (3 hours postexercise). The rate of FA mobilization increased from 666 +/- 108 mumol/min (control) to 1833 +/- 456 mumol/min (3 hours postexercise). TG/FA cycling was found to increase from 414 +/- 90 mumol FA/min (control) to 1473 +/- 435 mumol FA/min (3 hours postexercise). The energy cost of these rates of TG/FA cycling was found to be 0.09 +/- 0.02 kJ/min (control) and 0.31 +/- 0.09 kJ/min (3 hours postexercise). It is concluded that the energy cost of the increased TG/FA cycling rate may account for as much as half of the delayed component of EPOC.

Adult↗
PubMed1990

Thrombolytic therapy in MI: a retrospective study.

Of 123 patients with acute myocardial infarction, 82 percent did not receive thrombolytic therapy; 27 percent of those were because of time delays on patients' part in seeking medical attention. There is a clear need for patient education and public awareness of prodromal symptoms and early intervention.

Adult↗
PubMed1988

Anaerobic capacity determined by maximal accumulated O2 deficit.

We present a method for quantifying the anaerobic capacity based on determination of the maximal accumulated O2 deficit. The accumulated O2 deficit was determined for 11 subjects during 5 exhausting bouts of treadmill running lasting from 15 s to greater than 4 min. The accumulated O2 deficit increased with the duration for exhausting bouts lasting up to 2 min, but a leveling off was found for bouts lasting 2 min or more. Between-subject variation in the maximal accumulated O2 deficit ranged from 52 to 90 ml/kg. During exhausting exercise while subjects inspired air with reduced O2 content (O2 fraction = 13.5%), the maximal O2 uptake was 22% lower, whereas the accumulated O2 deficit remained unchanged. The precision of the method is 3 ml/kg. The method is based on estimation of the O2 demand by extrapolating the linear relationship between treadmill speed and O2 uptake at submaximal intensities. The slopes, which reflect running economy, varied by 16% between subjects, and the relationships had to be determined individually. This can be done either by measuring the O2 uptake at a minimum of 10 different submaximal intensities or by two measurements close to the maximal O2 uptake and by making use of a common Y-intercept of 5 ml.kg-1.min-1. By using these individual relationships the maximal accumulated O2 deficit, which appears to be a direct quantitative expression of the anaerobic capacity, can be calculated after measuring the O2 uptake during one exhausting bout of exercise lasting 2-3 min.

Adenosine Triphosphate↗