Biomedical subjects

W J Fink

Publications and source records attributed to W J Fink.

At least 73 records · Page 4Linked to original sources

PubMed1986

Effects of exercise and carbohydrate composition on gastric emptying.

To examine the gastric emptying characteristics of selected test drinks varying in carbohydrate composition and concentration, twenty-five runners ingested 400 ml of a solution in one or more of a series of trials followed by either 15 min seated rest or 15 min running (50 to 70% VO2 max). The solutions tested at rest included water, 5.0% maltodextrin, 3.0% maltodextrin + 2% glucose (MG5.0), and 4.5% maltodextrin + 2.6% fructose (MF7.1). Solutions tested during running included water, MG5.0, MF7.1, 5.5% maltodextrin + 2% glucose, and 5.5% maltodextrin + 2% fructose. At rest and during running, water emptied significantly (P less than 0.5) faster than all other drinks. In the running trials, the volume of gastric residue of 5.5% maltodextrin + 2% fructose (221.7 +/- 11.0 ml) was significantly greater than water (103.4 +/- 19.0 ml), MG5.0 (153.3 +/- 16.8 ml), and MF7.1 (167.3 +/- 14.8), suggesting an inhibitory role of glucose on gastric emptying. Running resulted in a significantly lower volume of gastric residue of water, MG5.0, and MF7.1 (103.4 +/- 19.0, 153.3 +/- 16.8, and 167.3 +/- 14.8 ml, respectively) as compared to the corresponding drinks at rest (209.3 +/- 12.6, 287.7 +/- 16.0, and 271.0 +/- 17.8 ml, respectively). These results suggest a possible advantage for including maltodextrin and fructose as carbohydrate sources in athletic drinks. Furthermore, the rate of gastric emptying is enhanced while running, possibly due to increased mechanical movement of fluid within the stomach.

Beverages↗

PubMed1985

Effects of dietary sodium on body and muscle potassium content during heat acclimation.

It has been suggested that renal conversion of sodium (Na+) during training in hot environments results in potassium (K+) deficiencies. This investigation examined the influence of two levels of dietary Na+ intake (399 vs 98 mmol X d-1) on intramuscular, urinary, sweat, and whole body K+ homeostasis. Nine unacclimated, untrained males underwent heat acclimation during two 8 day dietary-exercise regimens (40.1 +/- 0.1 degrees C, 23.5 +/- 0.4% RH). Both diets resulted in depressed urinary K+ excretion. Sweat K+ and muscle K+ concentrations were not altered by diets or acclimation. The whole body stores of Na+ increased 31.1% (+916.8 mmol) during the high Na+ diet and decreased 7.8% (-230.4 mmol) during the low Na+ diet; whole body stores of K+ increased 4.1% (+137.6 mmol) during the high Na+ diet and increased 3.4% (+113.6 mmol) during the low Na+ diet. This dietary-acclimation protocol did not result in whole-body or intramuscular K+ deficits and offers no evidence to support previous claims that dietary sodium levels affect K+ balance.

Acclimatization↗

PubMed1985

Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans.

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.

Acclimatization↗

PubMed1985

Influence of diuretic-induced dehydration on competitive running performance.

A diuretic drug (40 mg of furosemide) was utilized to study the effects of dehydration (D) on competitive running performance, without prior thermal or exercise stress. Eight men competed in randomized races of 1,500, 5,000, and 10,000 m, while normally hydrated (H) and with mean plasma volume reductions of 9.9, 12.3, and 9.9%, respectively. As a result of the reduced body water (change in body weight = -1.9, -1.6, and -2.1%), mean outdoor performance times on a running track increased 0.16 min, 1.31 min (P less than 0.05), and 2.62 min (P less than 0.05) in the 1,500-m, 5,000-m, and 10,000-m trials. Running performance decrements due to dehydration were more strongly correlated with changes in body weight (r = -0.79, -0.65, and -0.40) than with urine volume or plasma volume differences. In addition, subjects were studied during submaximal and maximal treadmill exercise while H and D (mean change in plasma volume = -7.1%). Neither submaximal nor maximal oxygen uptake was significantly altered (P greater than 0.05) as a consequence of D. Mean treadmill run time to volitional exhaustion was reduced by 41.4 s (P less than 0.05) during the D treadmill trial. Therefore, it appears that competitive performance in trials of long duration (5,000 and 10,000 m) was affected to a greater extent by D than the shorter 1,500-m event, even though submaximal and maximal oxygen uptake was not altered.

Adult↗

PubMed1985

Effect of carbohydrate feeding frequencies and dosage on muscle glycogen use during exercise.

Nine men were studied during three 4-h cycling bouts to determine the effect of frequency and dosage of solid carbohydrate (CHO) feedings (86 g) on muscle glycogen utilization and exercise performance. In the frequency trial (F), the subjects ingested 10.75 g of CHO along with 200 ml of water at 30-min intervals; in the dosage trial (D), the subjects ingested 21.5 g of CHO with 400 ml of water at 60-min intervals. During the control trial (C), the subjects ingested 400 ml of an artificially sweetened placebo at 60-min intervals. Respiratory exchange ratios were significantly elevated in both trials D and F (P less than 0.05). Blood glucose was significantly elevated in trial D 20 min post-feeding but had returned to control levels by 50 min. In trial F, blood glucose was maintained at a constant level throughout the entire 4 h. In trial C, blood glucose declined steadily during the entire 4 h. Despite the differences in blood glucose levels between the three trials, there were no significant differences in the rate of muscle glycogen utilization in any of the trials (D = 82.9 +/- 6.6 [SE] mmol X kg-1 vs C = 80.9 +/- 6.9 mmol X kg-1 vs F = 74.4 +/- 12.2 mmol X kg-1). In a sprint ride (100% VO2max) to exhaustion at the end of each trial, the subjects performed significantly longer in trial F compared to C (120.97 +/- 9.6 vs 81.0 +/- 7.1 s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Metabolic characteristics of skeletal muscle during detraining from competitive swimming.

After 5 months of intense training, eight male swimmers were studied during 4 wk of inactivity. Biopsy specimens from the deltoid muscle revealed that its respiratory capacity (QO2) decreased by 50% (5174 to 2559 microliter X h-1 X g-1) after 1 wk of inactivity. Subsequent weeks of detraining did not change the QO2. Although the trained swimmers' muscle phosphofructokinase and phosphorylase activities were significantly higher (P less than 0.05) than those from a group (N = 8) of untrained men, 4 wk of detraining had no effect on these enzyme activities. Mean (+/-SE) resting muscle glycogen concentrations were significantly higher (P less than 0.05) for the trained swimmers (153 +/- 3 mmol X kg-1) than for the untrained men (85 +/- 7.5 mmol X kg-1). Over the 4 wk of inactivity, the swimmers' muscle glycogen progressively decreased from 153 (+/- 3) to 93 (+/-7) mmol X kg-1. After a standard 183-m swim at 90% of the swimmer's best time for that distance, blood lactate rose from a mean of 4.2 (+/-0.8) at week 0 to 9.7 (+/-0.8) mmol X 1(-1) at week 4. These observations demonstrate dramatic changes in the metabolic characteristics of the swimmer's muscle with a 1-4-wk interruption in training.

Adult↗

PubMed1985

Effect of fructose ingestion on muscle glycogen usage during exercise.

Eight healthy males were studied to compare the effects of preexercise fructose and glucose ingestion on muscle glycogen usage during exercise. Subjects performed three randomly assigned trials, each involving 30 min of cycling exercise at 75% VO2max. Forty-five min prior to commencing each trial, subjects ingested either 50 g of glucose (G), 50 g of fructose (F), or sweet placebo (C). No differences in VO2 or respiratory exchange ratio were observed between the trials. Blood glucose was elevated (P less than 0.05) as a result of the glucose feeding. With the onset of exercise, blood glucose declined rapidly during G, reaching a nadir of 3.18 +/- 0.15 (SE) mmol X 1(-1) at 20 min of exercise. This value was lower (P less than 0.05) than the corresponding values in F (3.79 +/- 0.20) and C (3.99 +/- 0.18). No differences in exercise blood glucose levels were observed between F and C. Muscle glycogen utilization was greater (P less than 0.05) during G (55.4 +/- 3.3 mmol X kg-1 w.w.) than C (42.8 +/- 4.2). No difference was observed between F (45.6 +/- 4.3) and C. There was a trend (P = 0.07) for muscle glycogen usage to be lower during F than G. These results suggest that the adverse effects of preexercise glucose ingestion are, in general, not observed with either fructose or sweet placebo.

Adult↗

PubMed1984

Effect of high intensity interval training on 2,3-diphosphoglycerate at rest and after maximal exercise.

The purpose of this study was to examine the effect of intense interval training on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels at rest and after maximal exercise. Eight normal men, mean +/- SE = 24.2 +/- 4.3 years, trained 4 days X week-1 for a period of 8 weeks. Each training session consisted of eight maximal 30-s rides on a cycle ergometer, with 4 min active rest between rides . Prior to and after training the subjects performed a maximal 45-s ride on an isokinetic cycle ergometer at 90 rev X min-1 and a graded leg exercise test ( GLET ) to exhaustion on a cycle ergometer. Blood samples were obtained from an antecubital vein before, during and after the GLET only. Training elicited significant increases in the amount of work done during the 45-s ride (P less than 0.05), and also in maximal oxygen uptake (VO2 max: Pre = 4.01 +/- 0.13; Post = 4.29 +/- 0.07 1 X min-1; P less than 0.05) during exercise and total recovery VO2 (Pre = 19.14 +/- 0.09; Post = 21.45 +/- 0.10 1 X 30 min-1; P less than 0.05) after the GLET . After training blood lactate was higher, base excess lower and pH lower during and following the GLET (P less than 0.05 for all variables).(ABSTRACT TRUNCATED AT 250 WORDS)

2,3-Diphosphoglycerate↗

PubMed1984

Maximal exercise tolerance after induced alkalosis.

Eight healthy males performed two rides to exhaustion at a work load corresponding to 125 VO2 max, 1 h after ingesting either 0.2 g NaHCO3/kg body weight (E) or NaCl (C). Mean +/- SE pre-exercise blood pH, HCO-3, and base excess (BE) values were respectively 7.42 +/- 0.01, 28.2 +/- 1.5 mmol/l, and 2.02 +/- 0.10 mmol/l for the E condition, and 7.39 +/- 0.01, 24.4 +/- 0.07 mmol/l, and -0.40 +/- 0.07 mmol/l for the C condition (P less than 0.05 for all variables). Cycling time to exhaustion (E = 100.6 +/- 6.1; C = 98.6 +/- 5.7 s) and total VO2 during recovery (E = 17.7 +/- 0.9; C = 17.3 +/- 0.8 1/30 min) did not differ significantly between treatments. Blood pH, HCO-3, and BE were significantly higher while the hydrogen ion to lactate ratio (nmol/mmol) was significantly lower in E than in C during recovery. Blood LA levels were also greater in E than in C during the latter part of recovery although peak individual values were not significantly different between trials (E = 14.4 +/- 0.4; C = 13.3 +/- 0.0 mmol/l). In view of the insignificant differences in cycling time, peak individual LA, and total recovery VO2, it is not likely that LA production was greater in E than in C. Rather it appears that LA efflux was enhanced by the NaHCO3 feeding. Additionally, the return of the acid-base status in blood to resting conditions was more rapid during alkalosis. Given this protocol, alkalosis does not help to sustain an intense exercise bout. These data suggest, however, that NaHCO3 may be of benefit following repeated work bouts.

Bicarbonates↗

PubMed1984

Effect of carbohydrate feedings on muscle glycogen utilization and exercise performance.

Ten men were studied during 4 h of cycling to determine the effect of solid carbohydrate (CHO) feedings on muscle glycogen utilization and exercise performance. In the experimental trial (E) the subjects ingested 43 g of sucrose in solid form along with 400 ml of water at 0, 1, 2 and 3 h of exercise. During the control trial (C) they received 400 ml of an artificially sweetened drink without solid CHO. No differences in VO2, heart rate, or total energy expenditure were observed between trials; however, respiratory exchange ratios were significantly (P less than 0.05) higher during E. Blood glucose was significantly (P less than 0.05) elevated 20 min post-feeding in E; however, by 50 min no differences were observed between trials until 230 min (E = 4.5 +/- 0.2 mmol X l-1 vs C = 3.9 +/- 0.2, means +/- SE; P less than 0.05). Muscle glycogen utilization was significantly (P less than 0.05) lower during E (100.7 +/- 10.2 mmol X kg-1 w.w.) than C (126.2 +/- 5.5). During a sprint (100% VO2max) ride to exhaustion at the end of each trial, subjects performed 45% longer when fed CHO (E = 126.8 +/- 24.7 s vs C = 87.2 +/- 17.5; P less than 0.05). It was concluded that repeated solid CHO feedings maintain blood glucose levels, reduce muscle glycogen depletion during prolonged exercise, and enhance sprint performance at the end of such activity.

Adult↗

PubMed1983

Effect of a 42.2-km footrace and subsequent rest or exercise on muscle glycogen and enzymes.

The purpose of this study was to determine the effect of running a marathon and subsequent rest or exercise during a 7-day recovery period on muscle glycogen, glycogen synthase, hexokinase, and the activity of hexose monophosphate pathway enzymes. Ten well-trained runners were randomly assigned to either a postmarathon rest or exercise group. The rest group (n = 5) performed no physical activity, whereas the exercise group ran at their highest tolerable volitional intensity for 20-45 min during the recovery period. Muscle biopsies were obtained from the gastrocnemius before and after the marathon and 1, 3, 5, and 7 days after the marathon. Muscle glycogen was supercompensated before the marathon (196 mmol glucosyl units kg wet tissue wt-1, mmol X kg-1) and was reduced to 25 mmol X kg-1 after the marathon. Seven days later it was 141 and 109 mmol X kg-1 in the rest and exercise groups, respectively. Measurement of glycogen synthase activity ratio indicated an active enzyme only immediately postmarathon, whereas measurement of glycogen synthase fractional velocity and relative velocity indicated an active enzyme immediately postmarathon and 1 day postmarathon. Hexokinase activity was significantly elevated immediately after the marathon and remained elevated through 5 days postmarathon. The activities of the hexose monophosphate pathway enzymes declined steadily during the experimental period and were significantly reduced 5 and 7 days postmarathon. Low-intensity exercise during the recovery week did not significantly differentiate the exercise group from the rest group.

Adult↗

PubMed1983

Leg muscle pH following sprint running.

In an effort to compare the disturbances in leg muscle pH during sprint running, muscle biopsies were obtained from the gastrocnemius and vastus lateralis muscles of six healthy men (three endurance-trained and three nonendurance-trained) before and after a treadmill sprint run (TSR) to fatigue (54-105 s) at roughly 125% of their aerobic capacities. Following the TSR, repeated blood samples were taken from a hand vein and later analyzed for pH, PCO2, and lactic acid (HLa). The muscle specimens were analyzed in duplicate for pH and HLa. Resting-muscle pH was 7.03 +/- 0.02 (means +/- SE) and 7.04 +/- 0.01 for the gastrocnemius and vastus lateralis muscles, respectively. At the termination of the TSR, the pH in these muscles was 6.88 +/- 0.05 and 6.86 +/- 0.03, respectively. After a 400-m timed run on the track, the pH in the gastrocnemius of four of the subjects averaged 6.63 +/- 0.03, while blood pH and HLa were 7.10 +/- 0.03 and 12.3 mM, respectively. Although no differences in pH and HLa were observed between the vastus lateralis and gastrocnemius muscles at the end of the treadmill trial, it is speculated that the lesser disturbance in acid-base balance seen in endurance performers may have been due to a lesser production of metabolites in their running musculature when compared to nonendurance performers.

Adult↗

PubMed1983

Effect of glycerol feeding on endurance and metabolism during prolonged exercise in man.

This study evaluated the effectiveness of pre-exercise glycerol feeding in protecting against development of hypoglycemia and sparing muscle glycogen during prolonged, intense exercise. Thirty minutes after ingesting either glycerol (1 gm X kg-1 body weight) or a placebo, 10 cyclists performed as much exercise on a cycle ergometer as they were able in 150 min. The average exercise intensity was 72% of VO2max during both trials. Glycerol ingestion increased blood glycerol concentration 100-fold, but did not alter the respiratory exchange ratio (R), plasma levels of insulin and free-fatty acids, or blood lactate and beta-hydroxybutyrate. The only significant effect of glycerol feeding was to postpone the decline in blood glucose by about 30 min. This suggests that glycerol served, to a limited extent, as a gluconeogenic substrate; however, glycerol ingestion did not spare muscle glycogen during 90 min of treadmill exercise at 71% VO2max. It appears that man cannot utilize glycerol as gluconeogenic substrate rapidly enough to serve as a major energy source during strenuous exercise.

Administration, Oral↗

PubMed1982

Muscle glycogen storage and its relationship with water.

This study examined the relationship between muscle glycogen and muscle water content. Exercise dietary manipulations were used to vary skeletal muscle glycogen levels in four groups of rodents: (1) eight animals were sedentary controls (SC); (2) ten animals were treadmill familiarized and allowed to recover 24 h before sacrifice (F); (3) ten animals were treadmill familiarized and exercised to exhaustion (E); (4) ten animals were treadmill familiarized, exercised to exhaustion, and allowed to recover with food and water ad libitum for 72 h (ER). All animals were sacrificed in a resting state to normalize intracellular, extracellular, and interstitial water compartments; thus, the E group was sacrificed 45 m in following their run. The treatments altered skeletal muscle glycogen to values ranging from 10.0 to 30.2 mumol glucosyl units/g wet tissue weight. Neither muscle triglyceride nor protein levels were affected by the treatments. Muscle water content expressed as mumol H2O lost/g wet tissue weight or made relative to protein content showed no consistent relationship to the glycogen content. These data, therefore, do not support the commonly accepted muscle glycogen-to-water ratio of 1.0:2.7 (g:g). Further work is necessary to quantify the exact amount of water that is actually associated with the glycogen complex.

Animals↗

PubMed1982

Dietary potassium and heavy exercise: effects on muscle water and electrolytes.

Eight men were studied during two 4-day exercise-dietary regimens, once under a control diet (80 mEq K+/day) and again with a diet low in K+ (25 mEq/day). Muscle K+ increased 5 to 6% as a result of the two exercise-dietary regimens, while no change was observed for muscle Na+ or Mg++. Plasma volume increased throughout the 4 days of each exercise-diet sequence, with the low K+ regimen resulting in the largest plasma volume gain (+15%) and a marked reduction in urinary K+ excretion. Despite the losses of K+ in sweat and the low K+ intake, there was a relatively small decrease in total body K+ content (less than 2% of body content). Based on these measurements of extracellular (plasma) and tissue (muscle) water and electrolytes, we have concluded that in combination with 4 days of heavy exercise and sweating, a low K+ diet will not significantly diminish the total body K+ content.

Adult↗

PubMed1982

Determination of human muscle pH in needle-biopsy specimens.

The homogenate technique for the determination of muscle pH (pHm) has been studied to assess the influence of delayed freezing and the composition and volume of the homogenizing medium on human muscle pH at rest and after exhaustive exercise. It was concluded that resting muscle samples must be frozen within 2 s to prevent falsely high pHm values. Muscle specimens used for lactate determinations (HLam), on the other hand, can be delayed in freezing for up to 30 s without altering the HLam content. A 30- to 40-s delay in biopsying the muscle after the cessation of exhaustive exercise does not appear to alter pHm or HLam values. Although the homogenate method does not provide information relative to the status of selected muscle fibers, it does offer a reliable sensitive measure of mean changes in the acidification of muscle with intense exercise.

Biopsy, Needle↗

PubMed1981

Effect of exercise-diet manipulation on muscle glycogen and its subsequent utilization during performance.

This study examined the effect of three exercise-diet regimens on muscle glycogen supercompensation and subsequent performance during a 20.9-km run. A diet containing 15% carbohydrate (CHO,L), 50% CHO (M), or 70% (CHO (H) was arranged in three trials as follows: trial A = 3 days L, 3 days H; trial B = 3 days M, 3 days H; trial C = 6 days M. For each trial a 5-day depletion-taper exercise sequence was conducted on the treadmill at 73% VO2 max. The runs were 90, 40, 40, 20, and 20 min, respectively. A day of rest preceded the 20.9-km performance run. Muscle biopsies were obtained from the gastrocnemius on days 4 and 7 (both prior to and after the performance run). Trials A, B, and C elevated muscle glycogen to 207, 203, and 159 mmol glucosyl units/kg wet tissue (mmG), respectively. The performance run in both trials A and B utilized significantly more glycogen than in trial C: 5.0 and 5.1 mmG/km vs. 3.1 mmG/km. There were, however, no differences in either performance run times or post-performance run glycogen levels between the trials. These data demonstrate that (1) muscle glycogen can be elevated to high levels with a moderate exercise-diet regimen; (2) initial muscle glycogen levels influence the amount subsequently utilized during exercise; (3) carbohydrate loading is of no benefit to performance for trained runners during a 20.9-km run.

Adult↗

PubMed1981

Muscle water and electrolyte distribution during prolonged exercise.

In an effort to describe the changes in water and electrolyte contents of active and inactive muscles during prolonged effort, seven healthy men were studied during 120 min of cycling. Needle biopsy samples were taken from the deltoid (inactive) and vastus lateralis (active) muscles before, at 10 and 120 min of exercise, and 30 min after exercise. Water and electrolyte contents of blood and active muscle tissue showed a significant change with the onset of exercise, while the inactive muscle was unaffected. As a consequence of the exercise, the subjects lost an average of 2.40 liters of body water, 93 mEq Na+, 22 mEq K+, 95 mEq Cl-, and 5 mEq Mg++. These water and electrolyte losses were not detectable in the muscle tissue sampled at the end of exercise or after 30 min recovery. Based on the loss of Cl-, body weight and plasma volume, extracellular, intracellular, and total body water volumes were calculated to decrease approximately 9%, 3% and 7.5%, respectively, at the end of the exercise. These observations confirm earlier findings that exercise and electrolyte losses in sweat and urine do not alter the calculated membrane potential of active and inactive muscle.

Adult↗