Biomedical subjects

G A Gaesser

Publications and source records attributed to G A Gaesser.

32 records · Page 2Linked to original sources

PubMed1991

Exercise training below and above the lactate threshold in the elderly.

In this study we report the effects of training at intensities below and above the lactate threshold on parameters of aerobic function in elderly subjects (age range 65-75 yr). The subjects were randomized into high-intensity (HI, N = 8; 75% of heart rate reserve = approximately 82% VO2max = approximately 121% of lactate threshold) and low-intensity (LI, N = 9; 35% of heart rate reserve = approximately 53% VO2max = approximately 72% of lactate threshold) training groups which trained 4 d.wk-1 for 30 min.session-1 for 8 wk. Before and after the training, subjects performed an incremental exercise test for determination of maximal aerobic power (VO2max) and lactate threshold (LT). In addition, the subjects performed a 6-min single-stage exercise test at greater than 75% of pre-training VO2max (SST-High) during which cardiorespiratory responses were evaluated each minute of the test. After training, the improvements in VO2max (7%) for LI and HI were not different from one another (delta VO2max for LI = 1.8 +/- 0.7 ml.kg-1.min-1; delta VO2max for HI = 1.8 +/- 1.0 ml.kg-1.min-1) but were significantly greater (P = 0.02) than the post-testing change observed in the control group (N = 8). Training improved the LT significantly (10-12%; P less than 0.01) and equally for both LI and HI (delta LT for for LI = 2.3 +/- 0.6 ml O2.kg-1.min-1; delta LT for HI = 1.8 +/- 0.8 ml O2.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Blood lactate during exercise: time course of training adaptation in humans.

We determined the time course of adaptation in blood lactate concentration ([La]) during constant-load exercise in response to training. Thirteen healthy subjects (11 males, 2 females) exercised on a cycle ergometer for 30 min/day at a work rate calculated to elicit 70% of pre-training VO2max, 6 days/week for 3 weeks. VO2max and blood [La] during constant-load exercise (training work rate) were determined at the end of each week of training. Training increased VO2max 8.5% (from 48.2 +/- 1.5 ml.kg-1.min-1 pre-training to 52.3 +/- 1.4 ml.kg-1.min-1 post-training, P less than 0.01) and decreased constant-load blood [La] 53% (from 7.8 +/- 0.6 mM pre-training to 3.7 +/- 0.3 mM post-training, P less than 0.01). The training-induced reduction in exercise blood [La] was well fit to an exponential (5.5e (-t/2.2) + 2.3, r = 0.99) with a half-time of 10.7 days. However, this was not the case for the time course of VO2max adaptation. The absolute decrease in blood [La] was correlated with the initial blood [La] (r = 0.88, P less than 0.01), but changes in VO2max were not significantly correlated with initial blood [La] (r = -0.14) nor with changes in blood [La] (r = -0.02). We conclude that (1) blood [La] response to constant-load exercise decreases rapidly and exponentially with training, with a t1/2 of 10.7 days, (2) the magnitude of training adaptation is positively related to the initial blood [La], and (3) the time course and extent of the training-induced adaptations of blood [La] and VO2max appear to be independent of one another.

Adaptation, Physiological↗

PubMed1988

Effects of continuous and interval training on the parameters of the power-endurance time relationship for high-intensity exercise.

The purpose of this study was to evaluate the effects of 6 weeks of low-intensity continuous exercise training (CE; 40 min at 50% VO2peak, 3 days/week) and high-intensity interval exercise training (IE: 10 x 2 min at VO2peak, 3 days/week) on the parameters of the power-endurance time relationship for cycle ergometry. The hyperbolic relationship between power and endurance time was linearized by expressing the power against the inverse of time, as described by Whipp et al. (22). This model consists of two parameters: theta f, a fatigue threshold reflecting the capability for sustained aerobic power, and W', a constant postulated to reflect a finite energy store (i.e., those factors comprising the O2 deficit: Phosphagen stores, anaerobic glycogenolysis, myoglobin O2 stores). Prior to training, test-retest reliability coefficients (r2) for theta f and W' were 0.92 and 0.62, respectively (P less than 0.01). Training resulted in significant (P less than 0.01) increases in theta f for both CE [27 +/- 3 W (13.4%) increase] and IE [33 +/- 5 W (15.0%) increase], with no difference between groups. Increases in theta f were not dependent upon improvements in VO2peak. W' was not changed significantly in either group after training. However, a significant negative correlation between the training-induced changes in theta f and W' (R = 0.76; P less than 0.01) was obtained. The minimum intensity threshold for exercise training necessary to elicit increases in theta f has yet to be identified, but is at least as low as 50% of VO2peak.

Adult↗

PubMed1988

Ventilatory muscle training in the elderly.

To test the hypothesis that declining ventilatory function in the elderly impairs exercise capacity, we tested maximal exercise capacity and ventilatory function before and after a program of ventilatory muscle training in 25 elderly subjects (ages 65-75 yr). Ventilatory muscle training was performed by means of isocapnic hyperpnea for 30 min/day, 4 days/wk for 8 wk. Before and after the training, we measured maximal exercise capacity by means of an incremental exercise test (IET) and ventilatory muscle endurance by means of the maximum sustained ventilatory capacity (MSVC). Ratings of perceived exercise (RPE) for breathlessness and leg effort were evaluated each minute by means of a modified Borg scale during both the IET and a 12-min single-stage exercise test (SST) performed at approximately 70% of the maximal exercise capacity. The trained group showed a significant increase in the MSVC, from 71.9 +/- 26.4 to 86.9 +/- 20.9 l/min (P less than 0.01), whereas the control group showed no change (66.3 +/- 22.5 to 65.1 +/- 22.1 l/min). In addition, the maximal voluntary ventilation increased in the trained group, from 115 +/- 41 to 135 +/- 36 l/min (P less than 0.01). Neither the trained nor the control group showed an increase in maximum O2 uptake, maximum CO2 consumption, or maximum minute ventilation during the IET. Evaluation of the RPE during both the IET and SST showed that although there was a small decrease in RPE for breathing and leg discomfort, changes between the control and treated groups were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Postexercise muscle and liver glycogen metabolism in male and female rats.

Male and female Wistar rats were run for 5 min at 1.7 mph at a 17% grade to determine whether a sex difference exists in the rate of glycogen resynthesis during recovery in fast-twitch red muscle, fast-twitch white muscle, and liver. Rats were killed at one of three time points: immediately after the exercise bout, and at 1 or 4 h later. Males had significantly higher resting muscle glycogen levels (P less than 0.05). Exercise resulted in significant glycogen depletion in both sexes (P less than 0.01). Males utilized approximately 50% more glycogen during the exercise bout than females (P less than 0.05). During the food-restricted 4-h recovery period, muscle glycogen was repleted significantly during the 1st h (P less than 0.05). Liver glycogen was not depleted as a result of the exercise bout, but fell during the first h of recovery (P less than 0.05) and remained low during the subsequent 3 h. The greater glycogen utilization in red and white fast-twitch muscle during exercise by males could represent a true sex difference but could also be attributable in part to the males having performed more work as a result of 20% greater body mass. We conclude that no sex difference was observed in the rates of muscle glycogen repletion after exercise or in liver glycogen metabolism during and after exercise, and rapid postexercise muscle glycogen repletion occurred at a time of accelerated liver glycogen depletion.

Animals↗

PubMed1986

Lactate and ventilatory thresholds: disparity in time course of adaptations to training.

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1985

Influence of caffeine on blood lactate response during incremental exercise.

To test the hypothesis that caffeine ingestion prior to exercise would delay the onset of blood lactate accumulation, eight male subjects were studied during incremental exercise to maximal work rates on a cycle ergometer under two conditions: 1 h after ingestion of 200 ml of either decaffeinated, calorie-free cola (control trial) or the same cola drink with 5 mg caffeine/kg body weight added (caffeine trial). Maximal exercise values for oxygen consumption (VO2 max), ventilation, heart rate, respiratory exchange ratio (R), work rate, and blood lactate were not affected by caffeine. Submaximal exercise VO2, ventilation, and R also were unaffected by caffeine. During the caffeine trial, submaximal exercise blood lactate was significantly higher and heart rate significantly lower than during the control trial (P less than 0.05). The lower exercise heart rate at the same VO2 resulted in a significantly greater O2 pulse during all submaximal exercise intensities for the caffeine trial (P less than 0.05). Data on R indicated that caffeine had no effect on substrate utilization during exercise. Data on exercise blood lactate response suggested that caffeine does not delay and may accelerate the onset of blood lactate accumulation during incremental exercise. When defined as either a "breakpoint," delta l mM (above resting lactate), or fixed level of 4 mM, the lactate threshold (LT) did not differ between caffeine and control trials. However, in using a 2 mM lactate level as a criterion, the LT during the caffeine trial (2.13 +/- 0.22 l X min-1) was significantly (P less than 0.05) lower than during the control trial (2.71 +/- 0.17 l X min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Response of ventilatory and lactate thresholds to continuous and interval training.

The purpose of this study was to evaluate the effects of continuous and interval training on changes in lactate and ventilatory thresholds during incremental exercise. Seventeen males were assigned to one of three training groups: group 1:55 min continuous exercise at approximately 50% maximum O2 consumption (VO2max); group 2: 35 min continuous exercise at approximately 70% VO2max; and group 3: 10 X 2-min intervals at approximately 105% VO2max interspersed with rest intervals of 2 min. All of the subjects were tested and trained on a cycle ergometer 3 day/wk for 8 wk. Lactate threshold (LT) and ventilatory threshold (VT) (in addition to maximal exercise measures) were determined using a standard incremental exercise test before and after 4 and 8 wk of training. VO2max increased significantly in all groups with no statistically significant differences between the groups. Increases (+/- SE) in LT (ml O2 X min-1) for group 1 (569 +/- 158), group 2 (584 +/- 125), and group 3 (533 +/- 88) were significant (P less than 0.05) and of the same magnitude. VT also increased significantly (P less than 0.05) in each group. However, the increase in VT (ml O2 X min-1) for group 3 (699 +/- 85) was significantly greater (P less than 0.05) than the increases in VT for group 1 (224 +/- 52) and group 2 (404 +/- 85). For group 1, the posttraining increase in LT was significantly greater than the increase in VT (P less than 0.05). We conclude that both continuous and interval training were equally effective in augmenting LT, but interval training was more effective in elevating VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1984

Dissociation between VO2max and ventilatory threshold responses to endurance training.

The purpose of this investigation was to determine whether the ventilatory gas exchange threshold (Tvent) changes significantly during the first 1-3 weeks of endurance training. Six men were studied during 3 weeks of training, which consisted of pedaling on a cycle ergometer 6 d X wk 30 min per session at 70% of pretraining VO2max. At the end of each week, VO2max, Tvent, and maximal and submaximal heart rates were determined during an incremental exercise test on the cycle ergometer. Constant-load submaximal exercise blood lactate concentrations were determined during training sessions on Monday, Wednesday, and Friday of each week of training. Tvent did not change significantly during the 3 weeks of training (+ 0.091 X min-1; P greater than 0.05). In contrast, significant changes occurred in all other training indexes measured. VO2max increased by 0.36 1 X min-1 (P less than 0.05) after just 2 weeks of training and did not change further after 3 weeks. Significant reductions (40-45%; P less than 0.05) in blood lactate levels during training sessions occurred by the middle of the 2nd week of training. Decreases in maximal (approximately 11 bt X min-1) and submaximal (approximately 14 bt X min-1) exercise heart rates after 1 week of training were significant (P less than 0.05). The results demonstrate that changes in Tvent lag behind alterations in several other cardiovascular and metabolic parameters in response to endurance training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Metabolic bases of excess post-exercise oxygen consumption: a review.

The classical "oxygen debt" hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2 consumption in excess of resting that occurs after exercise. The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a "reservoir of carbon," which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial O2 consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

Amphibians↗

PubMed1984

Effects of high- and low-intensity exercise training on aerobic capacity and blood lipids.

Sixteen non-obese, non-smoking males, ages 20-30 yr, were assigned to one of two training groups, exercising on a cycle ergometer 3 d/wk for 18 wk: high-intensity (H; N = 7; 80-85% Vo2max, 25 min/session) or low-intensity (L; N = 9; 45% VO2max, 50/min/session). Data were obtained at 3-wk intervals for Vo2max, body weight, percent body fat, and 12-h fasting blood levels of cholesterol (CHOL), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). The average post-training increase in VO2max for group H (0.56 l X min-1, 8.5 ml X min-1 X kg-1) was not significantly (P greater than 0.05) greater than for group L (0.45 l X min-1, 6.5 ml X min-1 X kg-1). Significant reductions in percent body fat occurred in both groups, amounting to an average fat loss of approximately 1.35 kg. No statistically significant changes in CHOL, TG, HDL-C, LDL-C, CHOL/HDL-C, or HDL-C/LDL-C occurred in either group. However, changes in HDL-C after 18 wk of training were inversely correlated (r = -0.57, P less than 0.05) with pre-training levels. We conclude that 1) the minimum exercise training-intensity threshold for improving aerobic capacity is at least 45% Vo2max; 2) 18 wk of high- or low-intensity exercise training is ineffective in significantly altering CHOL, TG, HDL-C, LDL-C, CHOL/HDL-C, and HDL-C/LDL-C in young male subjects with low blood lipid levels, and 3) exercise training-induced changes in HDL-C are dependent upon initial pre-training levels.

Adult↗

PubMed1980

Glycogen repletion following continuous and intermittent exercise to exhaustion.

Patterns of postexercise glycogen repletion in heart, skeletal muscle, and liver in the absence of exogenously supplied substrates during the first 4 h of recovery were assessed. Female Wistar rats were run to exhaustion using continuous (1.0 mph, 15% grade) and intermittent (alternate 1-min intervals at 0.5 and 1.5 mph, 15% grade) exercise protocols. Rats at exhaustion were characterized by marked depletion of glycogen in heart (55%), skeletal muscle (94%), and liver (97%). Blood glucose levels at exhaustion (1.33 mumol/g) were only 37% of preexercise levels. There were no significant differences between continuous and intermittent exercise groups for any of the tissue glycogen or blood glucose values. Cardiac muscle was the only tissue capable of complete restoration of glycogen levels while relying exclusively upon endogenous substrates. Concentrations of endogenous substrates present at the end of exercise were insufficient to support restoration of blood glucose levels to preexercise values nor support glycogen repletion in skeletal muscle and liver during the initial 4-h food-restricted postexercise period. With subsequent feeding, skeletal muscle demonstrated a glycogen supercompensation effect at 24 h (181.1 and 191.8% of preexercise levels for continuous and intermittent exercise, respectively). Lactate concentration in all tissues at the point exhaustion (1.5--2.5 times resting levels) were only moderately elevated and returned to preexercise levels within 15 min. It was concluded that lactate removal after exercise contributed only minimally to the repletion of muscle glycogen.

Animals↗

PubMed1980

End points of lactate and glucose metabolism after exhausting exercise.

To determine the extent of metabolite oxidation, rats were injected with [U-14C]lactate, -glucose, or -bicarbonate (n = 5, each) during rest or after continuous (CE) and intermittent (IE) exercises to exhaustion. Tissue analyses of resting rats, or rats killed following CE and IE and pulse injection with [14C]lactate or -glucose (n = 72, each), were used to determine the metabolic pathways of these two substrates. Oxygen consumption (VO2) declined rapidly for the first 15 min after exercise; thereafter, VO2 declined slowly and remained elevated above resting levels for 120 min. The slow phase of decline in VO2 during recovery did not coincide with lactate removal, which occurred within 15 min. Two-dimensional radiochromatograms produced from blood, kidney, liver, skeletal muscle, and heart indicated a rapid incorporation of 14C into several amino acid pools, including alanine, glutamine, glutamate, and aspartate. Four-hour postexercise recoveries (means of CE and IE) of injected [14C]lactate were lactate (0.75%), glucose (0.52%), protein (8.57%), glycogen (18.30%), CO2 (45.18%), and HCO3- (17.72%). Greater (P < 0.05) incorporation of 14C into protein and glycogen constituents after exercise, compared with rest, was demonstrated. Incorporation of [14C]lactate into glycogen represented a significant but only minor fraction of the metabolism of lactate after exhausting exercise. It is suggested that classical explanations of excess postexercise O2 consumption (i.e., "O2 debt") are too simplistic.

Amino Acids↗

PubMed1975

Muscular efficiency during steady-rate exercise: effects of speed and work rate.

In a comparison of traditional and theoretical exercise efficiency calculations male subjects were studied during steady-rate cycle ergometer exercises of "0," 200, 400, 600, and 800 kgm/min while pedaling at 40, 60, 80, and 100 rpm. Gross (no base-line correction), net (resting metabolism as base-line correction), work (unloading cycling as base-line correction), and delta (measurable work rate as base-line correction) efficiencies were computed. The result that gross (range 7.5-20.4%) and net (9.8-24.1%) efficiencies increased with increments in work rate was considered to be an artifact of calculation. A LINEAR OR SLIGHTLY EXPONENTIAL RELATIONSHIP BETWEEN CALORIC OUTPUT AND WORK RATE DICTATES EITHER CONSTANT OR DECREASING EFFICIENCY WITH INCREMENTS IN WORK. The delta efficiency (24.4-34.0%) definition produced this result. Due to the difficulty in obtaining 0 work equivalents, the work efficiency definition proved difficult to apply. All definitions yielded the result of decreasing efficiency with increments in speed. Since the theoretical-thermodynamic computation (assuming mitochondrial P/O = 3.0 and delta G = -11.0 kcal/mol for ATP) holds only for CHO, the traditional mode of computation (based upon VO2 and R) was judged to be superior since R less than 1.0. Assuming a constant phosphorylative-coupling efficiency of 60%, the mechanical contraction-coupling efficiency appears to vary between 41 and 57%.

Adult↗