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)

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)

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.

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)

Effects of infused epinephrine on slow phase of O2 uptake kinetics during heavy exercise in humans.

We tested the hypothesis that infused epinephrine (Epi) would augment the slow phase of oxygen uptake (VO2) during heavy exercise. Six normal healthy males initially performed a ramp test on a cycle ergometer to estimate the lactate threshold (LT) and determine peak VO2. Each subject then performed two 20-min constant-load tests at a power output calculated to elicit a VO2 equal to estimated LT + 0.2(peak VO2--estimated LT) under control conditions throughout and with an intravenous infusion of Epi from minutes 10 to 20 at a rate of 100 ng.kg-1.min-1. Pulmonary gas exchange variables were determined breath by breath. Arterialized venous blood was repeatedly sampled from the dorsum of the heated hand. Epi infusion elevated (P < 0.05) plasma Epi concentration (i.e., from 420 +/- 130 pg/ml at minute 10 to 2,190 +/- 410 pg/ml at minute 20) but had no effect on plasma norepinephrine or K+ concentrations. Concentrations of blood lactate and pyruvate were increased, pH was decreased, and base excess became more negative by infusion of Epi (P < 0.05). Epi infusion increased (P < 0.05) CO2 production and the respiratory exchange ratio but had no effect on ventilation or VO2. VO2 increased (P < 0.05) to the same extent in both control (3.14 +/- 0.12 l/min at minute 10, 3.28 +/- 0.12 l/min at minute 20) and Epi infusion (3.10 +/- 0.11 l/min at minute 10, 3.25 +/- 0.11 l/min at minute 20) trials. We therefore concluded that neither Epi nor its associated humoral consequences contribute significantly to the slow phase of VO2 kinetics during heavy exercise.

Pulmonary and leg VO2 during submaximal exercise: implications for muscular efficiency.

Insights into muscle energetics during exercise (e.g., muscular efficiency) are often inferred from measurements of pulmonary gas exchange. This procedure presupposes that changes of pulmonary O2 (VO2) associated with increases of external work reflect accurately the increased muscle VO2. The present investigation addressed this issue directly by making simultaneous determinations of pulmonary and leg VO2 over a range of work rates calculated to elicit 20-90% of maximum VO2 on the basis of prior incremental (25 or 30 W/min) cycle ergometry. VO2 for both legs was calculated as the product of twice one-leg blood flow (constant-infusion thermodilution) and arteriovenous O2 content difference across the leg. Measurements were made 3-5 min after each work rate imposition to avoid incorporation of the VO2 slow component above the lactate threshold. For all 17 subjects, the slope of pulmonary VO2 (9.9 +/- 0.2 ml O2.W-1.min-1) was not different (P greater than 0.05) from that for leg VO2 (9.2 +/- 0.6 ml O2.W-1.min-1). Estimation of "delta" efficiency (i.e., delta work accomplished divided by delta energy expended, calculated from slope of VO2 vs. work rate and a caloric equivalent for O2 of 4.985 cal/ml) using pulmonary VO2 measurements (29.1 +/- 0.6%) was likewise not significantly different (P greater than 0.05) from that made using leg VO2 measurements (33.7 +/- 2.4%). These data suggest that the net VO2 cost of metabolic "support" processes outside the exercising legs changes little over a relatively broad range of exercise intensities. Thus, under the conditions of this investigation, changes of VO2 measured from expired gas reflected closely those occurring within the exercising legs.

Catecholamine and blood lactate responses to incremental rowing and running exercise.

Ten collegiate rowers performed discontinuous incremental exercise to their tolerable limit on two occasions: once on a rowing ergometer and once on a treadmill. Ventilation and pulmonary gas exchange were monitored continuously, and blood was sampled from a venous catheter located in the back of the hand or forearm for determination of blood lactate ([La]) and plasma epinephrine ([Epi]) and norepinephrine ([NE]) concentrations. Thresholds for lactate (LT), epinephrine (Epi-T), and norepinephrine (NE-T) were determined for each subject under each condition and defined as breakpoints when plotted as a function of O2 uptake (VO2). For running, LT (3.76 +/- 0.18 l/min) was lower (P < 0.05) than Epi-T (4.35 +/- 0.14 l/min) and NE-T (4.04 +/- 0.19 l/min). For rowing, LT (3.35 +/- 0.16 l/min) was lower (P < 0.05) than Epi-T (3.72 +/- 0.22 l/min) and NE-T (3.70 +/- 0.18 l/min) and was lower (P < 0.05) than LT for running. Within each mode of exercise, Epi-T and NE-T did not differ. Because LT occurred at a significantly lower VO2 than either Epi-T or NE-T, we conclude that catecholamine thresholds, per se, were not the cause of LT. However, for both modes of exercise LT occurred at a plasma [Epi] of approximately 200-250 pg/ml (rowing, 221 +/- 48 pg/ml; running, 245 +/- 45 pg/ml); these concentrations are consistent with the plasma [Epi] reported necessary for eliciting increments in blood [La] during Epi infusion at rest. Plasma [NE] at LT differed significantly between modes (rowing, 820 +/- 127 pg/ml; running, 1,712 +/- 217 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men.

We examined the relationship between energy expenditure (in kcal) and epinephrine (Epi), norepinephrine (NE), and growth hormone (GH) release. Ten men [age, 26 yr; height, 178 cm; weight, 81 kg; O(2) uptake at lactate threshold (LT), 36.3 ml. kg(-1). min(-1); peak O(2) uptake, 49.5 ml. kg(-1). min(-1)] were tested on six randomly ordered occasions [control, 5 exercise: at 25 and 75% of the difference between LT and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT) (0900-0930)]. From 0700 to 1300, blood was sampled and assayed for GH, Epi, and NE. Carbohydrate (CHO) expenditure during exercise and fat expenditure during recovery rose proportionately to increasing exercise intensity (P = 0.002). Fat expenditure during exercise and CHO expenditure during recovery were not affected by exercise intensity. The relationship between exercise intensity and CHO expenditure during exercise could not be explained by either Epi (P = 1.00) or NE (P = 0.922), whereas fat expenditure during recovery increased with Epi and GH independently of exercise intensity (P = 0. 028). When Epi and GH were regressed against fat expenditure during recovery, only GH remained statistically significant (P < 0.05). We conclude that a positive relationship exists between exercise intensity and both CHO expenditure during exercise and fat expenditure during recovery and that the increase in fat expenditure during recovery with higher exercise intensities is related to GH release.

Slow component of O2 uptake during heavy exercise: adaptation to endurance training.

Seven untrained male subjects [age 25.6 +/- 1.5 (SE) yr, peak O2 uptake (VO2) 3.20 +/- 0.19 l/min] trained on a cycle ergometer 4 days/wk for 6 wk, with the absolute training workload held constant for the duration of training. Before and at the end of each week of training, the subjects performed 20 min of constant-power exercise at a power designed to elicit a pronounced slow component of VO2 (end-exercise VO2-VO2 at minute 3 of exercise) in the pretraining session. An additional 20-min exercise bout was performed after training at this same absolute power output during which epinephrine (Epi) was infused at a rate of 100 ng.kg-1.min-1 between minutes 10 and 20. After 2 wk of training, significant decreases in VO2 slow component, end-exercise VO2, blood lactate ([La-] and glucose concentrations, plasma Epi ([Epi]) and norepinephrine concentrations, ventilation (VE), and heart rate (HR) were observed (P < 0.05). Although the rapid attenuation of the VO2 slow component coincided temporally with reductions in plasma [Epi], blood [La-], and VE, the infusion of Epi after training significantly increased plasma [Epi] (delta 2.22 ng/ml), blood [La-] (delta 2.4 mmol/l) and VE (delta 10.0 l/min) without any change in exercise VO2. We therefore conclude that diminution of the VO2 slow component with training is attributable to factors other than the reduction in plasma [Epi], blood [La-] and VE.

Influence of endurance training and catecholamines on exercise VO2 response.

For constant-load, heavy exercise (i.e., above the lactate threshold (TLac)), a slow component of oxygen uptake (VO2) is observed. Endurance training reduces the magnitude of the slow component and, hence, end-exercise VO2. Reductions in exercise VO2 have been reported after 7-8 wk of training; unpublished observations suggest that the VO2 slow component may be attenuated after just 2 wk of training. A minimum training intensity for eliciting reductions in constant-load exercise VO2 has not been established; however, in the elderly, training at an intensity below TLac resulted in similar reductions in exercise VO2 as did training above TLac. Mechanisms responsible for the reduced slow component of VO2 after training remain to be firmly established. Evidence both for and against blood lactate concentration ([L-]) as a mediator of the slow component has been published; high correlations between [L-] and the slow component, and between the training-induced reductions in these variables, appear to be more coincidental than causal. Decreased pulmonary ventilation after training may account for between 14% and 30% of the reduction in the slow component of VO2. Epinephrine infusion does not augment exercise VO2, nor does beta-adrenergic blockade diminish the magnitude of the slow component of VO2.

Thinness and weight loss: beneficial or detrimental to longevity?

This review examined the hypotheses that 1) low body mass index (BMI) is optimal for longevity and 2) weight loss reduces mortality rates. The preponderance of epidemiological evidence fails to support either of these hypotheses. Indeed, a number of studies show that thinness and weight loss (regardless of initial BMI) are associated with increased mortality rates. These findings cannot be attributed to smoking status or to weight loss resulting from subclinical disease. The effect of intentional weight loss on mortality rates depends upon health status. For overweight individuals in good health, there is no compelling evidence to show that mortality rates are reduced with weight loss. Even among overweight persons with one or more obesity-related health conditions, specific weight loss recommendations may be unnecessary: 1) the reduction in mortality rate associated with intentional weight loss is independent of the amount of weight loss, 2) the reductions in all-cause mortality rate associated with increased physical activity and fitness (23-44%), independent of changes in body weight, are greater than that reported for intentional weight loss (approximately 20%), and 3) many obesity-related health conditions (e.g., hypertension, dyslipidemias, insulin resistance, glucose intolerance) can be ameliorated independently of weight loss. In view of the potential risks associated with weight loss and weight cycling, it is suggested that public health may be better served by placing greater emphasis on lifestyle changes and less attention to weight loss per se.

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)

Effects of pedaling speed on the power-duration relationship for high-intensity exercise.

Seven males (age = 20.4 +/- 0.3 yr) each performed a total of eight exhaustive exercise bouts (four at 60 rpm and four at 100 rpm) in order to determine the influence of pedaling frequency on the parameters of the power-duration relationship for high-intensity cycle ergometry. The power-endurance time data for each subject at each rpm were fit by nonlinear regression to extract parameters of the hyperbolic: (P - theta PA). t = W', where P = power output, t = time to exhaustion, and theta PA and W' are constants. theta PA (the power asymptote, in watts (W] reflects an inherent characteristic of aerobic energy production during exercise, above which only a finite amount of work (W', in joules) can be performed, regardless of the rate at which the work is performed. theta PA at 60 rpm (235 +/- 8 W) was significantly (15.9 +/- 4.5%, P less than 0.05) greater than theta PA at 100 rpm (204 +/- 11 W), thus confirming our hypothesis that endurance would be compromised while cycling at the higher pedaling frequency. In contrast, W' was not significantly (P greater than 0.05) affected by cadence (16.8 +/- 1.7 kJ at 60 rpm vs 18.9 +/- 2.2 kJ at 100 rpm). Our data are consistent with the implications of previous investigations which demonstrated a greater cardiorespiratory and blood/muscle lactate response during constant-power exercise while cycling at high vs low rpm and indicate that the theoretical maximum sustainable power (i.e., theta PA) during cycle ergometry in untrained males is greater at 60 rpm than at 100 rpm.

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.

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.

Rating of perceived exertion and blood lactate concentration during submaximal running.

We examined whether the relation between of ratings of perceived exertion (RPE) and exercise intensities associated with the lactate threshold (LT) and blood lactate concentrations (BLC) of 2.5 and 4.0 mM, established with an incremental protocol, held during 30-min treadmill run at constant velocity (V). RPE (11.6, 14.9, 16.8, 18.9), oxygen uptake (VO2) (3.2, 3.7, 3.9, 4.2 l.min-1), and V (168, 196, 215, 227 m.min-1) at LT, BLC of 2.5, and 4.0 mM and peak were determined for nine males during incremental exercise. Subjects then completed three 30-min runs at the V associated with LT and BLC of 2.5 and 4.0 mM, with RPE, VO2, and blood [HLa] determined every 5 min. After min 10 during the 30-min runs, RPE, VO2, and BLC were not significantly different from corresponding values observed during the incremental protocol. Regression equations predicting BLC from RPE were generated from results obtained during the incremental protocol. RPE values from the 30-min runs were used to predict BLC, and the measured BLC was used to validate the use of RPE as a predictor of BLC. Correlations ranged from r = 0.79 to r = 0.98 [total error (TE) ranged from 0.6-1.3 mM]. We conclude that RPE is a physiologically valid tool for prescribing exercise intensity when the intent is to use LT and/or BLC as the intensity criterion.

VO2 slow component: physiological and functional significance.

This paper offers a brief synopsis of the five preceding papers which constitute the proceedings of the symposium "Mechanistic basis of the slow component of VO2 kinetics during heavy exercise." The key features have been taken from each paper and a coherent position regarding the site and potential underlying mechanisms for the "excess" VO2 is presented. The hypothesis is developed that some aspect of fiber type recruitment patterns might be responsible for this phenomenon. Elucidation of the precise determinants of VO2 during heavy exercise is fundamental to our understanding of muscle energetics. Furthermore, certain patient populations, whose exercise tolerance is limited by impaired cardiovascular and/or respiratory capacity, may benefit from interventions designed to constrain the magnitude of the VO2 slow component.

The validity of regulating blood lactate concentration during running by ratings of perceived exertion.

We examined whether ratings of perceived exertion (RPE) observed during an incremental (response) protocol could be used to produce target blood [HLa] of 2.5 mM and 4.0 mM during a 30-min treadmill run at a constant RPE. RPE (15.3, 17.6, 19.1), oxygen uptake (VO2) (3.31, 3.96, 4.00 l.min-1), velocity (V) (198, 218, 223 m.min-1), and heart rate (HR) (179, 185, 190 bpm) at blood [HLa] of 2.5 mM and 4.0 mM, and peak were determined for nine subjects (5 males, 4 females) during incremental exercise. Subjects then completed two 30-min runs at the RPE corresponding to blood [HLa] of 2.5 mM (RPE 2.5 mM) and 4.0 mM (RPE 4.0 mM) measured during the incremental protocol. For both 30-min runs, VO2 was not different from VO2 corresponding to either 2.5 or 4.0 mM blood [HLa] during the incremental test. During the 30-min run at RPE 2.5 mM: (a) only during minutes 25-30 was the blood [HLa] significantly different than 2.5 mM (3.2 +/- 0.6 mM, P < 0.05), (b) for the first 20 min HR was significantly lower than the HR at 2.5 mM during the incremental protocol, and (c) V did not differ from V at 2.5 mM during the incremental protocol. During the 30-min run at RPE 4.0 mM: (a) blood [HLa] was not significantly different from 4.0 mM, (b) HR at every time point was significantly lower than HR 4.0 mM during the incremental protocol, and (c) V was decreased over time by an average of 24.6 m.min-1 (P < 0.05). Because RPE from the response protocol was able to produce a blood [HLa] close to the criterion value during each 30-min run, we conclude that RPE is a valid tool for prescribing exercise intensities corresponding to blood [HLa] of 2.5 mM and 4.0 mM.

Assessment of the aerosport TEEM 100 portable metabolic measurement system.

The present study evaluated the utility of a portable metabolic measurement system, the Aerosport TEEM 100. A total of 505 data points [242 from incremental (INC) and 263 from constant load (CL) exercise] were collected on 12 subjects (age = 25 +/- 4 yr), by placing the Aerosport TEEM 100 medium flow pneumotach and mouthpiece in-line with a validated system, the Rayfield system. When VO2 values were separated into categories (< 1.5, 1.5-2.0, 2.0-2.5, 2.5-3.0, > 3.0 l.min-1), there was a small but statistically significant difference between the two metabolic measurement systems for VO2, VCO2, VE, RER, %ECO2, and %EO2 during both INC and CL exercise and measurement error for VO2 ranged between 2% and 11%. Correlations for VO2 values during INC and CL exercise between the two systems were r = 0.95 (SEest +/- 0.18 l.min-1) and r = 0.96 (SEest +/- 0.29 l.min-1), respectively. Correlations for RER were r = 0.82 (SEest +/- 0.08) and r = 0.47 (SEest +/- 0.11), for INC and CL, respectively. Results from the present investigation indicate that the Aerosport TEEM 100 has utility for the assessment of VO2, but the estimation of carbohydrate and fat utilization from RER should be used with caution.

Estimation of critical power with nonlinear and linear models.

Sixteen young, healthy males each performed five to seven randomly assigned, exhaustive exercise bouts on a cycle ergometer, with each bout on a separate day and at a different power, to compare estimates of critical power (PC) and anaerobic work capacity (W') among five different models: t = W'/(Pmax-PC) (two-parameter nonlinear); t = (W'/P-PC))-(W'/(Pmax-PC)) (three-parameter nonlinear); P.t = W' + (PC.t) (linear (P.t)); P = (W'/t) + PC (linear (P)); P = PC + (Pmax-PC)exp(-t/tau) (exponential). The data fit each of the models well (mean R2 = 0.96 through 1.00 for each model). However, significant differences among models were observed for both PC (mean +/- standard deviation (SD) for each model was 195 +/- 29 W through 242 +/- 21 W) and W' (18 +/- 5 kJ through 58 +/- 19 kJ). PC estimates among models were significantly correlated (r = 0.78 through 0.99). For W', between-model correlations ranged from 0.25 to 0.95. For a group of six subjects, the ventilatory threshold for long-term exercise (LTE Tvent; 189 +/- 34 W) was significantly lower than PC for all models except the three-parameter nonlinear (PC = 197 +/- 30 W); PC for each model was, however, positively correlated with LTE Tvent (r = 0.69 through 0.91).(ABSTRACT TRUNCATED AT 250 WORDS)