Canadian journal of applied physiology = Revue canadienne de physiologie appliquée

The purpose of this study was to evaluate the potential ergogenic benefit of caffeine in the performance of a 1,500-meter swim. Caffeine (6 mg.kg-1) or placebo was administered 2-1/2 hrs prior to the swim trial in a double-blind crossover design. Caffeine resulted in a significantly lower perceived exertion for 100-m warm-up swims. Subjects swam significantly (p < 0.05) faster with caffeine (20:58.8 +/- 0:36.4, mean +/- SEM) than without (21:21.8 +/- 0:38). Plasma potassium was significantly lower prior to the swim with caffeine, and blood glucose was higher after that swim. Caffeine provides an ergogenic benefit for a 1,500-meter swim, an event that is completed in less than 25 min. Lower plasma potassium concentration prior to exercise and higher blood glucose following the trial suggest that electrolyte balance and glucose availability may be important aspects of the ergogenic effects of caffeine.

This study examined the effects of a 14-week running program on VO2max, as well as cardiac output (Q) and arterial-venous O2 difference (a-vO2 dif) at submaximal intensities corresponding to 50 and 75% of VO2max. Thirteen boys (mean age 10.6 +/- 1.2 yrs) served as experimental subjects while 13 other boys of similar age (mean age 10.2 +/- 1.2 yrs) served as controls. Mean VO2max in the runners increased 13%, from 44.2 +/- 7.0 to 49.9 +/- 6.3 ml.kg-1.min-1. Posttraining VO2 during submaximal and maximal exercise was significantly (p < 0.05) greater in the runners than in the controls. Q and SV exhibited an increase of 10% at each intensity, but posttraining differences between groups were not significant (p > 0.05). A-vO2 dif increased by 8% at 50% of VO2max and by 6% at 75% of VO2max, and was significantly greater in the runners following training. These results indicate that increases in submaximal relative VO2 in children are mediated by increases in a-vO2 dif and Q.

The purpose of this study was to determine the effects of a 1,500-m swim on energy expenditure during a subsequent cycle task. Eight well-trained male triathletes (age 26.0 +/- 5.0 yrs; height 179.6 +/- 4.5 cm; mass 71.3 +/- 5.8 kg; VO(2)max 71.9 +/- 7.8 ml.kg(-1).min(-1)) underwent two testing sessions in counterbalanced order. The sessions consisted of a 30-min ride on the cycle ergometer at 75% of maximal aerobic power (MAP), and at a pedaling frequency of 95 rev.min(-1), preceded either by a 1,500-m swim at 1.20 m.s(-1) (SC trial) or by a cycling warm-up at 30% of MAP (C trial). Respiratory and metabolic data were collected between the 3rd and the 5th min, and between the 28th and 30th min of cycling. The main results indicated a significantly lower gross efficiency (13.0%) and significantly higher blood lactate concentration (56.4%), VO(2) (5.0%), HR (9.3%), VE (15.7%), and RF (19.9%) in the SC compared to the C trial after 5 min, p < 0.05. After 30 min, only VE (7.9%) and blood lactate concentration (43.9%) were significantly higher in the SC compared to the C trial, p < 0.05. These results confirm the increase in energy cost previously observed during sprint-distance triathlons and point to the importance of the relative intensity of swimming on energy demand during subsequent cycling.

Age, sex, geographic and temporal trends in leisure-time physical activity levels were examined using data from five national surveys conducted between 1981 and 1998. Physical activity energy expenditure (AEE) was higher among men compared to women, and in younger versus older adults. AEE increased from Eastern to Western Canada, with a significant temporal trend of increasing AEE. The prevalence of physical inactivity (expending <12.6 kJ x kg(-1) x day(-1) has decreased; however, it remains high (women: 77%; men: 74%). The high prevalence of physical inactivity emphasizes the importance of population-level physical activity surveillance and interventions.

The aim of this study was to determine the anthropometric and physiological profile of 200-m sprint kayakers and to examine relationships with 200-m race performance. Twenty-six male kayakers who were categorised in two ability groups, international (Int) and national (Nat) level, underwent a battery of anthropometric and physiological tests and a 200-m race. Race time was significantly lower in Int than Nat (39.9 +/- 0.8 s and 42.6 +/- 0.9 s, respectively). Int demonstrated significantly greater measures of mesomorphy, biepycondylar humeral breadth, circumferences of the upper arm, forearm and chest, peak power and total work in a modified Wingate test, total work in a 2-min ergometry test, peak isokinetic power, and peak isometric force. Significant relationships were found between 200-m time and a number of anthropometric variables and anaerobic and dynamometric parameters. Stepwise multiple regression revealed that total work in the modified Wingate alone predicted 200-m race time (R2 = 0.53, SEE = 1.11 s) for all 26 subjects, while biepycondylar humeral breadth alone predicted race time (R2 = 0.54, SEE = 0.52 s) in Int. These results demonstrate that superior upper body dimensions and anaerobic capacities distinguish international-level kayakers from national-level athletes and may be used to predict 200-m performance.

The purpose of this study was to determine the race profile for a 2000-m simulated rowing race as well as the effect of training and gender on the race profile. Nineteen men and 19 women undertook a 2000-m simulated rowing race before and after 10 weeks of a typical off-season training program for rowing. Velocity was calculated every 200 m and the deviation in velocities from the mean race velocity (MRV) was plotted every 200 m to produce race profiles for each gender before and after training. The three fastest male rowers varied approximately 0.02 m.s from the MRV after training and displayed a constant-pace model. The fastest female rowers displayed an all-out strategy after training, producing large deviations from MRV. Average squared deviations from the mean (SDM) determined that all groups except the fastest females had a reduction in MRV deviation after training. These results suggest that the optimal race profile for a simulated 2000-m rowing race may be different between genders. Training reduces SDM and influences both male and female pacing patterns such that both exhibit a pacing strategy that is more similar to that of elite athletes in other events of similar and shorter duration.

It is commonly held that the structural capacity of the normal lung is "overbuilt" and exceeds the demand for pulmonary O2 and CO2 transport in the healthy, exercising human. On the other hand, the adaptability of pulmonary system structures to habitual physical training is substantially less than are other links in the O2 transport system. Accordingly, in some highly fit, and even in some not so fit habitually active individuals, the lung's diffusion surface, airways, and/or chest-wall musculature are underbuilt relative to the demand for maximal O2 transport. Two specific pulmonary limitations to exercise performance are proposed: (1) exercise-induced arterial hypoxemia secondary to excessive widening of the alveolar to arterial O2 difference, inadequate hyperventilation, and metabolic acidosis; and (2) highly fatiguing levels of respiratory muscle work which effectively steals blood flow from locomotor muscles via sympathetically mediated reflexes and heightens the perception of limb discomfort and dyspnea. In this brief review, we describe the characteristics and causes of each of these proposed pulmonary limitations and their consequences to maximal O2 uptake and exercise performance.

We investigated the effect of a 21-day climbing expedition to 6,194 m on the oxygen uptake (V022) and leg blood flow (LBF) responses to submaximal exercise in five healthy, fit men during two-leg kicking exercise a 0-W and 50-W. Tests were completed 1 week before and 3 days after altitued acclimatization. The adaptation of VO2 at exercise onset was described by the time to 63% of the new steady state. Steady state VO2 during 50-W exercise was less post-climb (1290+/- 29 mL/min, mean +/- SE) than pre-climb (1413+/- 63 mL/min, P <.05). VO2 adapted more slowly at the onset of 50-W exercise post climb. There were no differences in the steady state LBF during the 50-W exercise, the increase above baseline, or the adaptation post-climb. Respiratory exchange ratio was greater at 50-W post-climb compared to pre-climb. Reduced steady state V02 during exercise after exposure to high altitude is consistent with an increase in metabolic efficiency.

The goals of pre-exercise nutritional strategies are to optimise the availability of carbohydrate (CHO) and fluid. Ingestion of CHO 3-4 hr prior to exercise can increase liver and muscle glycogen stores and has been associated with enhanced endurance exercise performance. The metabolic effects of CHO ingestion persist for at least 6 hr. Although an increase in plasma insulin following CHO ingestion in the hour prior to exercise inhibits lipolysis and liver glucose output, and can lead to transient hypoglycemia during subsequent exercise, there is no convincing evidence that this is always associated with impaired exercise performance. Having said that, individual experience should inform individual practice. Interventions to increase plasma FFA availability prior to exercise have been shown to reduce CHO utilisation during exercise, but do not appear to have major ergogenic benefits. It is more difficult to hyperhydrate prior to exercise and although there has been interest in glycerol ingestion, to date research results have been equivocal. At the very least, athletes should ensure euhydration prior to exercise.

The purpose of the present study was to examine, in highly trained cyclists, the reproducibility of cycling time to exhaustion (T(max)) at the power output equal to that attained at peak oxygen uptake (.VO2peak) during a progressive exercise test. Forty-three highly trained male cyclists (M +/- SD; age = 25 +/- 6 yrs; weight = 75 +/- 7 kg; .VO2peak = 64.8 +/- 5.2 ml.kg-1.min-1) performed two T(max) tests one week apart. While the two measures of T(max) were strongly related (r = 0.884; p < 0.001), T(max) from the second test (245 +/- 57 s) was significantly higher than that of the first (237 +/- 57 s; p = 0.047; two-tailed). Within-subject variability in the present study was calculated to be 6 +/- 6%, which was lower than that previously reported for T(max) in sub-elite runners (25%). The mean T(max) was significantly (p < 0.05) related to both the second ventilatory turnpoint (VT(2); r = 0.38) and to .VO2peak (r = 0.34). Despite a relatively low within-subject coefficient of variation, these data demonstrate that the second score in a series of two T(max) tests may be significantly greater than the first. Moreover, the present data show that T(max) in highly trained cyclists is moderately related to VT(2) and .VO2peak.

This study examined the effect of diet and exercise on tumour growth, and the effect of dietary fatty acids on glucose uptake. Male Fischer 344 rats were divided into 4 dietary groups and fed for 2 weeks. The diets were 5% (wt/wt) safflower oil, 10% safflower oil, 5% docosahexaenoic acid(DHA)-rich, and 10% DHA-rich. On Day 14 the animals were injected with rat fibrosarcoma tumour cells. After 3 days of tumour growth the animals in each diet group were divided into exercise and nonexercise groups. Exercise was achieved by voluntary wheel running. Dietary intake, body weight, tumour growth, and distance run were determined daily. Two weeks later the animals were euthanized and the following tissues were dissected out: tumour, liver, heart, epididymal fat pads, gastrocnemius, epitrochlearis, and soleus muscles. Glucose transport experiments were performed on the epitrochlearis and soleus muscles whereas phospholipid analysis was completed on the gastrocnemius muscle. We observed no effect of either diet or exercise on tumour growth. The glucose transport data demonstrates that short-term voluntary running can cause increased insulin-sensitive transport and that DHA may inhibit transport. DHA-containing diets were associated with increased oxidation products TBARM. In conclusion, exercise benefits on glucose disposal are maintained in tumour-bearing animals but are influenced by fat content and composition. High DHA diets may also increase oxidative damage in muscle through enhanced TBARM production.

The aim of this study was to analyse the variations of the metabolic and technical parameters during a maximal 400-m freestyle event. Seven trained male swimmers swam a maximal 400-m freestyle as if in competition (255.8 +/- 6.9 s). Intermediate time and stroke rate (SR) were recorded at each length (25 m). To estimate the changes in metabolic parameters during the 400-m event, they swam a 300-, 200-, and 100-m test set from each length of the 400-m event results, resting 90 min between each test. The exact speed at each length was given with a visual light pacer. Oxygen uptake (VO(2)) and blood lactate concentration ( [Lac]) were measured before and immediately after each test. VO(2) and [Lac] were stable during the 100-, 200-, and 300-m test but significantly higher (p < 0.05) during 400-m test. The estimated contribution of anaerobic metabolism (EsCANA ) during the first 100-m and the 400-m represented 45 % and 20 % of total energy output, respectively. Speed decreased significantly (p < 0.05) after the first 100-m and remained stable until the end. SR decreased significantly after the first 100-m, then increased until the end, while stroke length (SL) decreased linearly throughout the 400-m. During the first or the last 100-m, EsCANA was not correlated with the changes in V, SR, or SL between the second and the first 100-m, and between the fourth and the third 100-m, respectively. To conclude, this study showed that the swimmers were not able to maintain stable SL during the 400-m event. Thus, to sustain stable velocity and to compensate for the decrease in SL, swimmers increased SR throughout the last 300-m.

Changes in physiological variables during a 60-min continuous test at maximal lactate steady state (MLSS) were studied using highly conditioned cyclists (1 female and 9 males, aged 28.3 +/- 8.1 years). To determine power at MLSS, we tested at 8-min increments and interpolated the power corresponding to a blood lactate value of 4 mmol/L. During the subsequent 60-min exercise at MLSS, we observed a sequential increase of physiological parameters, in contrast to stable blood lactate. Heart rate drifted upward from beginning to end of exercise. This became statistically significant after 30 min. From 10-60 min of exercise, a change of +12.6 +/- 3.2 bpm was noted. Significant drift was seen after 30 min for the respiratory exchange ratio, after 40 min for the rate of perceived exertion using the Borg scale, and after 50 min for % VO(2)max/kg and minute ventilation. This slow component of VO(2)max may be the result of higher recruitment of type II fibers.

Eleven women (TRW; 64 +/- 4 yrs) and ten men (TRM; 65 +/- 5 yrs) participated in the strength/power training twice a week for 24 weeks. Basal concentrations of serum total and free testosterone, growth hormone (GH), dehydroepiandrosterone sulfate (DHEAS), cortisol and sex hormone binding globulin (SHBG) as well as acute responses of serum total and free testosterone, growth hormone (GH) were measured. Maximal 1RM strength in the squat, chair rise time and muscle fibre distribution and areas of type I and IIa and IIb of the vastus lateralis were also examined. 1RM squat increased in TRW by 26 (SD10)% (p < .001), and in TRM by 35 (7)% (p < .001) and chair rise time improved in both groups (p < .001). Fibre areas increased in type I, (p < .01), IIa (p < .01) and IIb (p < .01) in TRM and type I (p < .05) and IIa (p < .05) in TRW. The proportion of type IIa increased from 31% to 43% (p < .05) in TRW and that of type IIb decreased from 27% to 17% (p < .05) in TRW and from 25% to 17% (p < .05) in TRM. Individual concentrations of testosterone/cortisol ratios correlated (r = 0.63; p < .05) with the individual increases in 1RM strength in TRW. The exercise sessions resulted in acute increases in serum GH in both groups (p < .05) with a further increase (p < .01) up to 10 minutes post-loading in TRM at post-training.

The purpose of this investigation was to determine whether the Rockport one-mile walk test equation to predict maximal oxygen uptake was valid for application to treadmill walking. When the Rockport model was found to be inappropriate, a new regression model was developed for predicting peak oxygen uptake (VO2peak) from a one-mile treadmill walk. 304 healthy volunteers ages 40 to 79 years (mean age = 57.6 years, 154 men and 150 women) completed a VO2peak test and a one-mile treadmill walk. Stepwise regression was used to build a model for the relationship between VO2peak and a variety of predictor variables in a sub-sample development group (n = 154). This new model was then applied to a sub-sample validation group (n = 150). The new equation produced a correlation of 0.87, SEE = 4.7 ml x kg (-1) x min (-1) with a mean residual of 0.96 ml x kg (-1) x min (-1). The equation for predicting VO2peak developed in this investigation provides a means of assessing VO2peak that is easy to administer, allows for careful supervision of subjects, and can be completed at a low financial and temporal cost.

The aim of this study was to determine whether peak oxygen uptake (PVO2) attained in a 90-s maximal intensity cycle sprint is comparable to that from a conventional ramp test. Sixteen participants (13 boys and 3 girls, 14.6 +/- 0.4 yr) volunteered for the study. On Day 1 they completed a PVO2 test to exhaustion using a 25 W x min(-1) ramp protocol beginning at 50 W. Peak VO2 was defined as the highest VO2 value achieved, and aerobic power (Wmax) as the power output of the final 30 s. On Day 2 the participants completed two 90-s maximal sprints (S1 and S2). A 45-min recovery period separated each sprint. Mean oxygen uptake over the last 10 s of each sprint was determined as PVO2, and minimum power (MinP-30 s) as the mechanical power attained in the final 30 s. A one-way ANOVA was used to analyse differences between S1, S2, and the ramp test for PVO2 and MinP-30 s. Peak VO2 was not significantly different between the ramp, S1, or S2 (2.64 +/- 0.5, 2.49 +/- 0.5, and 2.53 +/- 0.5 L x min(-1), respectively, p > 0.68). The S1 and S2 PVO2 scores represented 91 +/- 10% and 92 +/- 10% of the ramp aerobic test. The MinP-30 s for S1 and S2 were significantly lower than the Wmax of the ramp test, p < 0.05. Hence, for researchers solely interested in PVO2 values, a shorter but more intensive protocol provides an alternative method to the traditional ramp aerobic test.

The purpose of this study was to determine the influence of simple, progressive lower body exercise training, focusing on strength and power, on functional abilities in frail older adults. Twenty-five residents of a long-term care facility (75-94 yrs) participated in this randomized controlled trial of 10-wks duration. The exercise group (Ex, n = 18) underwent simple, progressive lower body resistance exercises, specifically aimed at improving muscle power, 3 times/wk; the control subjects (Con, n = 7) maintained their usual daily activities. Knee extensor strength and power were measured on an isokinetic dynamometer (180 degrees/s), and functional performance was assessed from a 6-m walk timed test, a 30-s chair stand, and an 8-ft up-and-go timed test, before and after the 10-wk intervention period. Significant increases were found in the Ex group for eccentric (44%) and concentric (60%) average power (p < 0.05), and improvements were seen on each functional test: the 8-foot up-and-go, chair stand, and walk time improved by 31%, 66%, and 33%, respectively (p < 0.05). No significant change occurred in the Con group. In conclusion, simple progressive exercise training, even in the 10th decade, increases muscle power and is associated with an improved performance of functional activities using the trained muscles.

The purpose of the present study was to compare the heat strain while wearing nuclear, biological, and chemical (NBC) protective clothing following a hot-wet (HW) or hot-dry (HD) heat acclimation protocol. Twenty-two males were assigned to groups HW (n = 7), HD (n = 8), or control (C, n = 7). Subjects were evaluated during continuous treadmill walking while wearing lightweight combat clothing and during intermittent exercise while wearing the NBC protective clothing. While wearing Combat clothing, greater decreases in rectal temperature (Tre), mean skin temperature (Tsk), and heart rate were observed for both acclimation groups. For the NBC clothing trials, lower Tre, Tsk, and heart rates were observed only for group HW. The time required for Tre to increase 1.0 degrees C and 1.5 degrees C was significantly delayed for groups HW and HD. Sweat evaporation increased for HW, whereas no change was found for HD. The most significant changes in Tre, Tsk, and heart rate while wearing the NBC protective clothing occur following heat acclimation that involves wearing the clothing during exercise.

In order to study the acclimatization process over 14 days of exposure to tropical climate, 9 triathletes performed 4 outdoor indirect continuous multistage tests in both thermoneutral and tropical conditions. The thermoneutral test (TN, 14 degree C, 45% rh) was performed before traveling to the tropical area (Martinique, FWI). The tropical tests were performed 2, 8, and 14 days after arrival (32.9 degree C, 78% rh). During each trial, we measured tympanic temperature, sweat rate, body mass loss, heart rate (HR), and performance. The results showed that 1). the mean tympanic temperature was greater in T2 (P <.001), T8 (P <.01) and T14 (P <.01) than in TN and significantly lower in T14 than in T2 (P <.05); 2). the mean sweat rate was significantly greater (P <.001) in T2, T8 and T14 than in TN and significantly greater (P <.05) in T8 and T14 than in T2; 3). the body mass loss after trials was significantly greater (P <.001) in T2, T8 and T14 than in TN and significantly greater (P <.05) in T8 and T14 than in T2; 4). the mean HR and HR at rest were significantly higher (P <.005) in T2 than in TN, T8, T14 and the mean HR was significantly lower (P <.05) in T14 than in the other trials; and 5). the performance time was significantly lower in T2 (P < 0.02), T8 (P < 0.03) and T14 (P < 0.05) than in TN. We concluded that 14 days of exposure to tropical climate led to changes in physiological parameters but were still insufficient to ensure complete acclimatization in well-trained athletes. The hot/wet climate induced impairment of physiological responses and performance that were still evident on the 14th day.

The purpose of this study was to compare values for maximal accumulated O2 deficit measured in running and cycling. Nine university students performed five fatiguing constant-velocity treadmill tests and five fatiguing constant-power cycle ergometer tests at intensities within the severe domain. O2 deficit was determined making the traditional assumptions that (1) the O2 demand increases linearly with the exercise intensity and (2) the O2 demand is constant from the onset of exercise if the intensity is kept constant (Medbø, 1996). VO2max was 11% higher in running than in cycling. In contrast, O2 deficit was approximately 50% higher in cycling than treadmill running. Inspection of the data suggested that the O2 demand may have been underestimated, especially in the treadmill tests. It was concluded that assumptions associated with measuring maximal accumulated O2 deficit in running must be revisited.

The purpose of this study was to test the hypothesis that ingestion of creatine monohydrate increases anaerobic exercise capacity, as reflected by the maximal accumulated oxygen deficit (MAOD). Subjects were assigned, double-blind, to placebo (PL, n = 12) or creatine (CR, n = 14) groups and ingested 5-g doses 4 times daily of artificial sweetener or artificially sweetened creatine monohydrate, respectively, for 5 days. On a separate day subjects exercised to exhaustion at 125% VO2max. After two familiarization trials, MAOD was again determined before treatment, after 5 days of PL or CR treatment, and 7 days later. MAOD increased after CR treatment from 4.04 +/- 0.31 to 4.41 +/- 0.34 L (p < .001) and remained elevated for another 7 days (4.31 +/- 0.33, p < .001). Time to exhaustion also increased in CR from 130 +/- 7 to 141 +/- 7 s (p < .01) and remained increased for another 7 days (139 +/- 8 s, p < .01). These data demonstrate that ingesting creatine monohydrate for 5 days increases the MAOD, and is likely to have an ergogenic effect on supramaximal exercise performance that persists for at least a week after treatment.

The primary purpose of the study was to compare maximal accumulated oxygen deficit (MAOD) in resistance-trained (RT), endurance-trained (ET), and untrained men (UT). A secondary purpose was to determine the influence of leg muscle mass (MM) on MAOD by examining the relationship between MM and MAOD and by comparing MAOD expressed relative to MM between the groups. MAOD was determined during 2-4 min of constant-load fatiguing cycling. MM, estimated via anthropometric measurements, was higher (p < .05) for RT (mean +/- SE; 25.5 +/- 3.4 kg) compared to ET (20.3 +/- 3.5) and UT (21.6 +/- 3.4). MAOD in liters O2eq was larger in RT (4.75 +/- 0.3) compared to UT (3.07 +/- 0.3) and ET (3.75 +/- 0.3). A significant positive correlation was observed between MAOD (LO2eq) and MM (kg) for RT only (RT, r = .85; ET, r = .55; UT, r = .20). Based on the correlational and mean MM data, the higher MAOD (LO2eq) in RT relative to ET and UT is predominantly the result of their larger leg muscle mass.

Usually, an initial step in determining accumulated O2 deficit is the estimation of the O2 demand of high intensity exercise by extrapolation from VO2 measured during steadystate submaximal exercise. It was hypothesized that O2 deficit could be determined without the need to estimate O2 demand by extrapolation. Ten women performed all-out cycle ergometer exercise tests at each of four power outputs selected so that exhaustion would occur after 90 to 600 s. Power output (W), accumulated VO2 (ml), and time to exhaustion (s) were measured in each test and then fit to the following equation: O2 deficit (ml) = O2 demand (ml.min-1.W-1).time (min).power (W) - accumulated VO2 (ml). This procedure generated values for two parameters (O2 demand and O2 deficit) for each subject. The O2 deficit was also calculated for each individual using conventional methods. The values for O2 deficit obtained using the two methods were correlated (r = .96, p < .01), and the value obtained using the experimental method tended to be larger, t(9) = 2.15, p = .06. It is concluded that O2 demand and O2 deficit can be determined from the results of several high-intensity tests without the need to extrapolate from submaximal exercise to estimate the O2 demands of supramaximal exercise.

The present investigation evaluates a maximal anaerobic running test (MART) against the maximal accumulated oxygen deficit (MAOD) for the determination of anaerobic capacity. Essentially, this involved comparing 18 male students performing two randomly assigned supramaximal runs to exhaustion on separate days. Post warm-up and 1, 3, and 6 min postexercise capillary blood samples were taken during both tests for plasma blood lactate (BLa) determination. In the MART only, blood ammonia (BNH3) concentration was measured, while capillary blood samples were additionally taken after every second sprint for BLa determination. Anaerobic capacity, measured as oxygen equivalents in the MART protocol, averaged 112.2 +/- 5.2 ml.kg-1.min-1. Oxygen deficit, representing the anaerobic capacity in the MAOD test, was an average of 74.6 +/- 7.3 ml.kg-1. There was a significant correlation between the MART and MAOD (r = .83, p < .001). BLa values obtained over time in the two tests showed no significant difference, nor was there any difference in the peak BLa recorded. Peak BNH3 concentration recorded was significantly increased from resting levels at exhaustion during the MART.

This study aimed to determine the skeletal muscle fiber sample size required for a reliable, valid representation of an individual's average fiber area and capillary contacts (CC) per fiber. Biopsies were obtained from the biceps brachii of 11 college-age, recreational resistance-trained men in conjunction with a study investigating how muscle morphology changed after 12 weeks of resistance training. The effect of additional measurements on the rolling cumulative means for fiber area and CC per fiber was evaluated using sequential estimation analysis. Results showed that group cumulative mean and standard deviation had stabilized by 50 fiber measurements per individual for type I and II fibers and CC per fiber. Significant correlations (.96-.99; p < .05) existed between the 50th and 95th/100th cumulative individual means. These results indicate that a typical skeletal muscle needle biopsy would be sufficient to characterize type I and II fiber areas and CC per fiber of an individual in most subject populations, although the required sample size for characterizing fiber subtypes might be different.

The aim of this study was to assess the food habits and nutritional status of high level adolescent soccer players (N = 33; ages 14-16 yrs) living in their home environment. Body composition (height, mass, skinfolds), biochemical and hematological parameters, performance in soccer-specific tests (sprinting, jumping, intermittent endurance), and dietary intake (weighed food intake method) and related behaviors (nutrient supplement use, daily activity profile) were assessed. Daily energy expenditure and energy intake were 12.5 MJ and 12.6 MJ, respectively. Protein (16% of energy intake; 1.9 g/kg of body mass), lipid (38%), and cholesterol (385 mg) intake were above recommendations, while carbohydrates (45%) were below. The food intake of these adolescents was based on cereals and derivates; meat, fish, and eggs; milk and dairy products; biscuits and confectionery; and oil, butter and margarine, which provided 78% of total energy intake, 85% of proteins, 64% of carbohydrates, 90% of lipids, and 47% of fiber. Although diet provided sufficient iron, 48% of individuals showed iron deficiency without anemia. Based on these results, a well designed nutrition intervention would be advisable for optimizing performance, and especially for promoting healthy eating habits in adolescent soccer players.

I/D polymorphism of the ACE gene may be associated with better endurance performance and a stronger response to exercise training. The aim of this study was to investigate the association between ACE gene polymorphism and athletic performance in a homogeneous cohort. Eighty-eight male non-elite Caucasian Turkish athletes with similar training backgrounds for at least for 6 months were studied for ACE gene polymorphisms by PCR analysis. Performance on the 60-meter sprint and middle-distance running tests were evaluated. The distributions of the ACE I/D genotypes were 20.5%, 40.9%, and 38.6% for II, ID, and DD polymorphisms in the whole group (N = 88), respectively. The ACE DD genotype frequency was significantly higher in the superior group (56.7%) than in the poor (37.9%) and mediocre (20.7%) group in middle-distance running performance (chi2 = 11.778; p = 0.019). The ACE DD genotype may be related to better short-duration aerobic endurance performance. Larger homogeneous cohorts may help clarify the association between ACE I/D polymorphism and physical performance.

The acetate correction factor is used to account for retention of carbon label in exchange reactions of the tricarboxylic acid cycle in studies estimating free fatty acid oxidation with carbon-labeled tracers. Previous evidence indicates that substrate utilisation and metabolic rate vary across the menstrual cycle, which may alter the correction factor. We therefore derived the acetate correction factor for each of three menstrual phases (early follicular [EF], late follicular [LF], and midluteal [ML] phase) from the fractional recovery of 13CO2 from a constant infusion of sodium-[1-13C] acetate during 90 min of submaximal exercise (60% VO2-max) in sedentary eumenorrhoeic women. There was no difference in the correction factor between the EF and LF or the LF and ML phases, but the correction factor derived in the ML phase was significantly lower than in the EF phase (p < 0.05). Neither energy expenditure nor whole body substrate utilisation during exercise varied significantly between menstrual phases and therefore cannot explain the observed difference in the correction factor. The lower correction factor in the ML phase, compared to the EF phase, would result in only a small increase of -6% in the calculated plasma free fatty acid oxidation rate.

The potential of exercise-induced changes in peripheral amino acids to alter blood prolactin levels through a serotonergic system modification was investigated in 8 male athletes. In two trials, subjects (N = 8) exercised on a cycle ergometer for 5 hr. The intensity of exercise corresponded to 55% VO2max (T55) or 75% VO2max (T75), respectively. In each trial, each subject received a 25-g energy bar (111 kcal) every 60 min, as well as 300 ml of a 6% carbohydrate solution (90 kcal) every 30 min of exercise duration. Plasma glucose and insulin declined (p < or = .05) in both trials during exercise. Ammonia was augmented (p < or = .05) above the baseline concentration after 120 min in both trials. During the last 2 hr of exercise, plasma free fatty acids were higher (p < or = .05) in T75 than in T55. During this time, the plasma free TRP/BCAA ratio was also augmented (p < or = .05) in T75, while no change was induced in T55. Plasma prolactin did not change in T55, while an increase (p < or = .05) was found in T75. The findings may further support the hypothesis that during endurance exercise changes in peripheral amino acid concentration may influence prolactin response via serotonergic system modifications.

Five women and 5 men performed maximal isometric and concentric dorsiflexion actions on an isokinetic dynamometer. The concentric actions were done at 10 present velocities ranging from 0.26 to 5.23 rad.s-1. Electromyographic (EMG) recordings were made from one agonist (tibialis anterior (TAI) and two antagonists (soleus [S], lateral gastrocnemius [LG]). The men produced greater absolute torque than the women, but there was no gender difference in the torque/body mass ratio. The shape of the torque-velocity relation was similar in men and women and approximated, but did not match, that obtained in animal preparations or in human studies using electrical stimulation. Agonist TA activation (integrated EMG/movement time) decreased with increasing velocity over the same range of velocities as torque. Antagonist S, but not LG, activation also decreased. The S/TA activation ratio was greater in men than women. In men the S/TA ratio tended to be greater than the LG/TA ratio, whereas the converse was true for women. These data indicate that velocity influences the relative activation of two antagonists in maximal dorsiflexion muscle actions, and that there is an apparent gender difference in the relative activation of two antagonists.

Insulin has well known metabolic effects. However, depending on the magnitude and duration of the insulin stimulus, this hormone can also produce vasodilation and vascular smooth muscle growth. The association of hyperinsulinemia with the metabolic disorders of obesity and non-insulin-dependent diabetes, as well as with the cardiovascular pathologies of hypertension and atherosclerosis, has led to suggestions that perhaps elevated insulin levels are causally related to these diseases. Alternatively, insulin resistance may develop following an increase in skeletal muscle vascular resistance, with or without hypertension, such that a reduction in skeletal muscle blood flow leads to an attenuated glucose delivery and uptake. These hypotheses are explored in this review by examining the effects of insulin on vascular smooth muscle tissue during both acute and prolonged exposure. An interaction among hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with the insulin resistant state is described whereby insulin resistance can be both a cause and a result of elevated vascular resistance. The association between blood flow and insulin stimulated glucose uptake suggests that therapeutic intervention against the development of skeletal muscle vascular resistance should occur early in individuals generally predisposed to cardiovascular pathology in order to attenuate, or avoid, insulin resistance and its sequelae.

Although the proteolytic events accompanying acute and chronic perturbations in striated muscle protein turnover remain to be fully elucidated, the purpose of this paper is to (a) review the chemistry of the nonlysosomal calpain-calpastatin system, and (b) provide evidence for the involvement of a nonlysosomal, calcium-activated neutral protease (calpain) in the response of skeletal muscle protein breakdown to altered nutritional status (diet composition; energy restriction) and increased periods of contractile activity (exercise). In reviewing the literature, it is apparent that calpain is involved in the protein catabolism which accompanies alterations in diet composition and/or energy restriction. The precise mechanism of calpain action remains to be elucidated; however, the role of altered metabolic status contributing to calcium imbalances is discussed relative to increasing protein degradation. Hypotheses for further investigation are provided in regard to identifying the targeting of selected proteins (and organelles) for degradation by calpain.

Movements that are performed with maximal velocity and acceleration can be considered ballistic actions. Ballistic actions are characterized by high firing rates, brief contraction times, and high rates of force development. A characteristic triphasic agonist/antagonist/agonist electromyographic (EMG) burst pattern occurs during ballistic movement, wherein the amount and intensity of antagonist coactivation is variable. In conditions of low-grade tonic muscular activity, a premovement EMG depression (PMD; or silent period, PMS) can occur in agonist muscles prior to ballistic contraction. The agonist PMD period may serve to potentiate the force and velocity of the following contraction. A selective activation of fast twitch motor units may occur in ballistic contractions under certain movement conditions. Finally, high-velocity ballistic training induces specific neuromuscular adaptations that occur as a function of the underlying neurophysiological mechanisms that subserve ballistic movement.

Ten resistance trained (RT) and 6 non-resistance trained (NRT) subjects were used to determine differences in quadriceps activation between isometric single and double knee extensions and squat contractions. Greater inactivation, as measured by the interpolated twitch technique, was recorded with single (RT: 16.5%, NRT: 17.6%) than double leg extensions (RT: 8.4%, NRT: 13.4%) or squats (RT: 4.03%, NRT: 1.7%). There was no significant difference between the maximum voluntary contraction (MVC) force of the dominant leg during single and double leg extensions. However, in NRT subjects, the contralateral or non-dominant leg during double leg extensions exhibited significantly less force than the dominant leg (715.9 vs 566.9 N). This deficit may be due to a lesser reliance on the non-dominant limb. The contractions of multiple lower body muscle groups enhanced the activation of the dominant quadriceps. Greater levels of activation may be necessary to cope with the stabilization necessary for bilateral and multi-articular contractions.

Training with voluntary or electromyostimulation (EMS)-evoked eccentric contractions should produce complete muscle activation, since EMS and eccentric contractions preferentially recruit large motor units. Subjects (22 women ages 18-40) were randomly assigned to a voluntary (VOL; n = 8), EMS (n = 8), or control group. VOL and EMS groups trained the quadriceps at the same, increasing force levels 4 times/week for 6 weeks using voluntary or EMS-evoked eccentric contractions. VOL improved voluntary more than EMS-evoked eccentric strength. EMS improved EMS-evoked strength more than voluntary. EMS training improved EMS-evoked eccentric strength more than VOL training improved voluntary eccentric strength. EMS-evoked to voluntary force ratio increased from 0.57 (+/- 0.11) to 1.20 (+/- 0.35) in EMS and did not change in VOL (all changes p < .05). Six of eight EMS subjects produced greater EMS-evoked force posttraining, suggesting incomplete muscle activation after EMS training.

Since reported changes in muscle activation following fatigue could be affected by alterations in muscle contractile properties, the plantar flexors' activation-force relationship was investigated before and following an isometric, intermittent, submaximal fatigue protocol. Voluntary and evoked force and muscle activation was tested pre- and postfatigue with ischaemic and nonischaemic recovery. The muscle activation-force relationship of ischaemic and nonischaemic groups was best described by a second-order polynomial equation with similar y intercepts, slopes, and curvature of the slopes. A significantly increased muscle activation-force slope during recovery may be attributed to decreased muscle activation and not impaired muscle kinetics. The index of muscle activation immediately postfatigue was not significantly different between ischaemic and nonischaemic groups (88.5% vs. 92.7%). No significant difference in the estimate of muscle activation postfatigue with polynomials and interpolated twitch (IT) ratios (superimposed/potentiated doublets) suggested that IT ratios can be used as a general estimate of muscle inactivation following fatigue.

The purpose of this study was to examine the effect of selective skin cooling over m. vastus lateralis (VL) on the activation patterns of quadriceps femoris muscle during knee extension exercise (KEE) using muscle function magnetic resonance imaging (mfMRI). The isometric force production of the right thigh was tested in 7 healthy young men at maximum voluntary contraction (MVC), and the transverse relaxation time (T2) value was taken from mfMR images at rest and immediately after KEE with 4 sets of 10 repetitions at a load equal to 60% of their 10-rep maximum, with and without skin cooling. The cooling was carried out by ice pack on the surface of the skin of the VL for 3 min before resting mfMRI and MVC tests, and before KEE, during KEE, and during the KEE rest intervals. The percent change in T2 of the m. vastus intermedius was significantly increased by skin cooling in comparison to the change without skin cooling, p < 0.05. This result suggests that skin cooling alters the activation pattern of the different heads of the quadriceps.

The mechanical twitch in response to increasing electrical stimulus intensity, delivered both over the motor point and motor nerve, was recorded in the first dorsal interosseous (FDI) and the adductor pollicis (AP), and only over the motor point in the soleus (Sol), lateral (LG), and medial (MG) gastrocnemius muscles of human subjects. The relationship between intensity of electrical stimulation (ES) and twitch torque showed a positive linear regression in all muscles. In the FDI and AP the relationship was not significantly different when ES was applied at the motor point or over the motor nerve. At small intensities of activation, ES induced larger twitch torques in the MG and LG, which contain a roughly equal proportion of slow and fast motor units (MUs) compared to the Sol, which is composed mainly of slow type fibres. Moreover, the relationship between ES intensity and twitch time-to-peak is best fitted in all muscles by a power curve that shows a greater twitch time-to-peak range in its initial part for muscles containing a larger proportion of fast MUs (LG, MG) than for muscles mainly composed of slow MUs (Sol). In conclusion, these results induced by ES at the motor point and/or over the motor nerve confirm the concept of a reversed sequence of MU activation, as compared to voluntary contractions, and document this viewpoint in muscles of different function and composition. The reversed sequence of MU activation is more clearly evident during motor point ES.

Practitioners and scientists have demonstrated great interest in the physiological and biochemical effects of endurance training on the results of the marathon run. It is well documented that athletes with a large proportion of slow twitch and fast twitch aerobic skeletal muscle fibre, high metabolic enzyme activities and concentrations, large mitochondria concentration and, of course, the ability to increase the power output generated for a given rate of oxygen consumption and energy expenditure, are generally highly successful distance runners. Aerobic and endurance training have been shown to bring about significant adaptations to the skeletal muscle and its inclusions as well as to the delivery system. In particular, enzyme activity levels are readily mutable, mitochondrial concentrations increase, and some evidence suggests that the fibre distribution is changed. This article briefly reports on changes in skeletal muscle brought about by endurance training and those changes that appear most effective in yielding success in endurance events.

The most accurate critical velocity (CV) estimate for the prediction of velocity during a simulated 2,000-m rowing race and the relationship to aerobic power were studied. Sixteen male rowers completed randomized maximal exertion trials (200, 400, 600, 800, 1,000, and 1,200 m), a maximal oxygen consumption (VO(2)max) on a Concept II rowing machine, and an actual 2,000-m simulated rowing race. Three mathematical models were applied to 4 rowing distance combinations producing 12 CV estimates. Seven of the 12 possible CV estimates were not significantly different from actual 2,000-m velocity. Comparison of the 3 CV models using all 6 trial distances revealed that the nonlinear model produced a CV estimate lower than the 2 linear CV models. CV was significantly correlated to VO(2)max (r = 0.91) and the mean velocity achieved during the 2,000-m simulated rowing race (r = 0.97). VO(2)max was significantly correlated to 2,000-m simulated rowing race velocity (r = 0.93).

We examined the effects of androstenedione supplementation on the hormonal profile of 10 males and its interaction with resistance exercise. Baseline testosterone, luteinizing hormone, estradiol, and androstenedione concentrations were established by venous sampling at 3 hr intervals over 24 hr. Subjects ingested 200 mg of androstenedione daily for 2 days, with second and third day blood samples. Two weeks later, they ingested androstenedione or a placebo for 2 days, in a double-blind, cross-over design. On day 2, they performed heavy resistance exercise with blood sampled before, after, and 90 min post. The supplement elevated plasma androstenedione 2--3-fold and luteinizing hormone approximately 70% but did not alter testosterone concentration. Exercise elevated testosterone, with no difference between conditions. Exercise in the supplemented condition significantly elevated plasma estradiol by approximately 83% for 90 min. Androstenedione supplementation, thus, is unlikely to provide male athletes with any anabolic benefit and, with heavy resistance exercise, elevates estrogen.

The purpose of this study was to investigate the acute responses of both stress and fluid regulatory hormones to a single bout of resistance exercise in both trained and untrained men. Seven competitive power lifters (PL) and 12 untrained subjects (UT) performed one set of the leg press exercise to exhaustion at 80% of their respective one-repetition maximum. Blood samples were obtained twice prior to exercise (at P1 and P2), immediately postexercise (IP), and at 5 minutes postexercise (5PE). Compared to P1 and P2, plasma epinephrine, norepinephrine, dopamine, atrial peptide, osmolality, and blood lactic acid increased significantly (p < or = 0.05) at IP. Plasma epinephrine, norepinephrine, atrial peptide, and blood lactic acid concentrations remained elevated at 5PE compared to P1 and P2. Plasma renin activity and angiotensin II were significantly elevated at 5PE compared to P1, P2, and IP, and this increase was significantly greater in PL compared to UT at 5PE. These data indicate that an acute bout of resistance exercise dramatically affects secretion of stress and fluid regulatory hormones.

This study examined the effects of four high-intensity interval-training (HIT) sessions performed over 2 weeks on peak volume of oxygen uptake (VO2peak), the first and second ventilatory thresholds (VT1, VT2) and peak power output (PPO) in highly trained cyclists. Fourteen highly trained male cyclists (VO2peak = 67.5 +/- 3.7 ml.kg-1.min-1) performed a ramped cycle test to determine VO2peak, VT1, VT2, and PPO. Subjects were divided equally into a HIT group and a control group. The HIT group performed four HIT sessions (20 x 60 s at PPO, 120 s recovery); the VO2peak test was repeated < 1 wk after the HIT program. Control subjects maintained their regular training program and were reassessed under the same timeline. There was no change in VO2peak for either group; however, the HIT group showed a significantly greater increase in VT1 (+22% vs. -3%), VT2 (+15% vs. -1%), and PPO (+4.3 vs. -.4%) compared to controls (all P < .05). This study has demonstrated that HIT can improve VT1, VT2, and PPO, following only four HIT sessions in already highly trained cyclists.

Acute and chronic hormonal responses to resistance training were evaluated in 11 college men who completed 12 weeks (33 sessions) of high volume resistance training. No differences in resting concentrations of growth hormone (GH), insulin-like growth factor-I, testosterone, or sex hormone-binding globulin occurred from pre- and posttraining in the trained vs. nontrained control group. However, cortisol (c) decreased 17% for both groups (p < 0.05). There were no differences in exercise-induced responses between Sessions 10 and 20, with all hormone concentrations increasing (p < 0.05) from pre- at mid- and post exercise session. However, after correction for plasma volume decreases, only C and GH showed differences, with C increased from mid- to postsession (48% 10th; 49% 20th), and GH increased from pre- at mid- and postsession for both sessions 10 (0.16 +/- 0.42 pre; 4.77 +/- 6.24 mid; 6.26 +/- 5.19 post; microg x L-1) and 20 (0.33 +/- 0.85 pre; 5.42 +/- 9.08 mid; 8.24 +/- 7.61 post; microg x L-1). Significant correlations (p&lt 0.05) existed only between absolute mean GH increases from presession and the degree of muscle fiber hypertrophy for type I (r = 0.70 mid, 0.74 post) and type II (r = 0.71 post) fibers. In conclusion, resistance training had no effect on resting serum hormone concentrations, whereas similar acute exercise responses occurred between the 10th and 20th training sessions.

In discussion of the physiological mechanisms that regulate fat metabolism, and with consideration of the metabolic stimuli that modulate substrate metabolism, the issue of how an acute state of negative lipid balance can be maximized is addressed. The regulation of lipolysis by catecholamines and insulin is reviewed, and the mechanisms of fatty acid mobilization and uptake by muscle are also briefly discussed. The implications of substrate availability and the hormonal response during physiological states such as fasting, exercise, and after food intake are also addressed, with particular regard to the influences on fatty acid mobilization and/or oxidation from eliciting these stimuli conjointly. Finally, a brief discussion is given of both the nature of exercise and the exercising individual, and how these factors influence fat metabolism during exercise. It is also a primary thrust of this paper to underline gaps in the existing literature with regard to exercise timing concerning food ingestion for maximizing acute lipid utilization.

Fatigue is an inevitable consequence of physical activity; yet its biological cause remains uncertain. During exercise, a polypeptide messenger molecule interleukin-6 (IL-6) is actively produced. Previously, the administration of recombinant IL-6 (rhIL-6) induced a heightened sensation of fatigue in healthy humans at rest. In contrast, anti-IL-6 receptor antibodies reduced the symptoms of chronic fatigue. In the present study, athletic performance during an exercise challenge consisting of a 10-km running time trial was significantly impaired in trained male runners following the administration of a low dose of rhIL-6 compared to the placebo trial.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P<.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P<.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.

The purpose of this study was to determine, in heart failure patients (HF), whether acute or chronic L-arginine supplementation (LAS) might delay the ventilatory threshold (VT) and whether chronic LAS might reduce exercise-induced plasma lactate increase. HF patients undertook 4 cardiopulmonary bicycle exercises tests. The first 3 were maximal without (EX(1)), after acute (EX(2)), or chronic (EX(3)) oral LAS (6 gm twice a day for 6 weeks). The 4th test (EX(4)) performed after chronic LAS, was similar to the first in order to investigate the effect of chronic LAS on circulating lactate levels. Results showed that acute LAS failed to improve both submaximal and maximal exercise capacities. Similarly, maximal exercise capacity remained unmodified after chronic LAS. Nevertheless, chronic LAS delayed significantly the patients' ventilatory threshold. Thus exercise duration prior to VT increased (mean +/- SEM) from 6.04 +/- 0.9 to 7.7 +/- 1.03 min (p = 0.04), resulting in a significant increase in oxygen uptake (1.05 +/- 0.08 to 1.24 +/- 0.12 L.min(-1); p = 0.03), CO(2) release (0.94 +/- 0.10 to 1.2 +/- 0.12 L.min(-1); p = 0.018), minute ventilation (29.31 +/- 2.8 to 34.5 +/- 2.7 L; p = 0.009), and workload (60.7 +/- 9.8 to 78.5 +/- 10.2 watts; p = 0.034). Furthermore, chronic LAS significantly reduced the exercise-induced increase in postexercise plasma lactate concentration (-21 +/- 7%). In conclusion, unlike acute supplementation, chronic LAS significantly delays the ventilatory threshold, and chronic LAS reduces circulating plasma lactate in HF patients. These data suggest that chronic LAS might improve the ability of HF patients to perform their daily-life activities.

This study examined acute systolic (SBP) and diastolic (DBP) blood pressure responses within passive and modified proprioceptive neuromuscular facilitation (PNF) stretching techniques. Nonhypertensives (N = 60) were assigned to one of three treatment groups. Group 1 employed an antagonist passive stretch (APS), 6-sec maximal voluntary isometric contraction (MVIC) of the antagonist, and subsequent APS. Group 2 employed an APS, a 6-sec MVIC of the antagonist, submaximal concentric contraction of the agonist, and APS. Group 3 was similar to Group 2, with the deletion of an MVIC prior to the concentric contraction. Blood pressures were obtained during rest, baseline following passive stretch, and at the end of the three phases of the PNF technique. Range of motion (ROM) data were collected for baseline and treatment in terminal hip flexion for each group. All PNF treatments were effective for increasing ROM. One or two trials of PNF improve ROM and avoid increasing SBP, while a third trial increases SBP.