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.

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.

The effect of training and epinephrine infusion on ratings of perceived exertion (RPE).

Seven untrained males (mean age [+/-SD] = 25.6+/-3.9 yr, mean ht = 177.0+/-5.9 cm, mean wt = 65.8+/-7.4 kg) completed a 6-week exercise program (cycle ergometer). Prior to training, and at the end of each week of training, each subject performed a 20 min constant-power exercise test (absolute power was the same each week). At the end of the six week training program (within a few days), an additional 20 min constant-power test was performed, during which epinephrine was infused at a rate of 100 ng x kg(-1) x min(-1) over the final 10 min of exercise. Training significantly (P<0.05) reduced end-exercise ratings of perceived exertion (RPE), plasma epinephrine concentration [Epi], plasma norepinephrine concentration [NE], blood lactate concentration [La-], minute ventilation (V(E)), heart rate (HR), and blood glucose concentration [Glc]. Epinephrine infusion failed to increase RPE despite significant (p < 0.05) increases in [Epi], [La-], V(E) and [Glc]. Therefore, the present data indicate that RPE during exercise is not causally related to changes in plasma [Epi]. It also appears that modest changes in plasma [NE], blood [La-], V(E) and blood [Glc] during constant-power cycle ergometry (as observed during Epi infusion) do not impact RPE.

Exercise training decreases the growth hormone (GH) response to acute constant-load exercise.

To assess the influence of exercise training on the growth hormone (GH) response to acute exercise, six untrained males completed a 20-min, high-intensity, constant-load exercise test prior to and after 3 and 6 wk of training (the absolute power output (PO) during each test remained constant x PO = 182.5 +/- 29.5 W). Training increased (pre- vs post-training) oxygen uptake (VO2) at lactate threshold (1.57 +/- 0.33 L.min-1 vs 1.97 +/- 0.24 L.min-1 P < or = 0.05). VO2 at 2.5 mM blood lactate concentration ([HLa]) (1.83 +/- 0.38 L.min-1 vs 2.33 +/- 0.38 L.min-1, P < or = 0.05), and VO2peak (3.15 +/- 0.54 L.min-1 vs 3.41 +/- 0.47 L.min-1, P < or = 0.05). Power output at the lactate threshold (PO-LT) increased with training from 103 +/- 28 to 132 +/- 23W (P < or = 0.05). Integrated GH concentration (20 min exercise + 45 min recovery) (microgram.L-1 x min) after 3 wk (138 +/- 106) and 6 wk (130 +/- 145) were significantly lower (P < or = 0.05) than pre-training (238 +/- 145). Plasma epinephrine and norepinephrine responses to training were similar to the GH response (EPI-pre-training = 2447 +/- 1110; week 3 = 1046 +/- 144; week 6 = 955 +/- 322 pmol.L-1; P < or = 0.05; NE pre-training = 23.0 +/- 5.2; week 3 = 13.4 +/- 4.8; week 6 = 12.1 +/- 6.8 nmol.L-1; P < or = 0.05). These data indicate that the GH and catecholamine response to a constant-load exercise stimulus are reduced within the first 3 wk of exercise training and support the hypothesis that a critical threshold of exercise intensity must be reached to stimulate GH release.

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.

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.

Effects of carbohydrate supplementation on performance during 1 hour of high-intensity exercise.

The effects of carbohydrate supplementation on high-intensity exercise performance were examined in 5 moderately-trained subjects (age = 28.4 +/- 1.5 yr; ht = 171.0 +/- 4.3 cm; wt = 66.25 +/- 6.32 kg). High-intensity exercise tests (initiated at the power output (PO) associated with 90% VO2 peak [mean = 201 +/- 21 watts] x 60 min, with drop-off in PO allowed over time) were completed under the following randomized double blind conditions: 1) pre-exercise glucose polymer (G)/placebo during exercise (G/P), 2) G pre-exercise and during exercise (G/G), and 3) placebo pre-exercise and during exercise (P/P). Subjects ingested 300 ml of a sweetened placebo or a similarly flavored 10% G solution, immediately prior to and every 15 min during exercise. No differences were observed in PO among the 3 treatments until min 40-60 where PO was greater with G. This resulted in significantly greater total work (and less drop-off in PO) with G (G/P = 619 +/- 234kJ [14.5% lower than the value associated with 201 watts maintained for 60 min (724kJ)], G/G = 599 +/- 235 kJ [17.3% lower than the value associated with 201 watts maintained for 60 min]) compared with placebo (P/P = 560 +/- 198 kJ [22.7% drop-off in average PO]) (p < 0.05). VO2 followed a similar pattern with no difference in VO2 over min 0-40 and significantly higher VO2 in G/P and a trend for higher VO2 in G/G during min 40-60 compared to placebo. Results of the present study indicate that, compared to placebo, pre-exercise ingestion of G (30 g in 10% solution) results in less drop-off in PO during 1 hour of high-intensity exercise performance, and that no further benefit is observed when the same amount of G is also ingested every 15 min during exercise.

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)

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.

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.

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.

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.

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)

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.

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.