Active and passive recovery and acid-base kinetics following multiple bouts of intense exercise to exhaustion.

The purpose of this study was to profile the effect of active versus passive recovery on acid-base kinetics during multiple bouts of intense exercise. Ten males completed two exercise trials. The trials consisted of three exercise bouts to exhaustion with either a 12 min active (20% workload max) or passive recovery between bouts. Blood pH was lower in the passive (p) recovery compared to active (a) throughout the second and third recovery periods [second recovery: 7.18 +/- 0.08 to 7.24 +/- 0.09 (p), 7.23 +/- 0.07 to 7.32 +/- 0.07 (a), P < 0.05; third recovery: 7.17 +/- 0.08 to 7.22 +/- 0.09 (p), 7.23 +/- 0.08 to 7.32 +/- 0.08 (a), P < 0.05]. Exercise performance times did not differ between recovery conditions (P = 0.28). No difference was found between conditions for recovery kinetics (slope and half-time to recovery). Subsequent performance during multiple bouts of intense exercise to exhaustion may not be influenced by blood acidosis or mode of recovery.

Accumulation of acetyl groups following cycling: a 1H-MR spectroscopy study.

Using in vivo proton magnetic resonance spectroscopy (1H-MRS), a new peak resonating at 2.13 ppm post-exercise has been attributed in the literature to the acetyl groups of acetylcarnitine. Since this peak is inconsistently generated by various submaximal exercise regimens, this study aimed at (a) verification of the previous chemical assignment, (b) determination of exercise conditions necessary for its induction, and (c) documentation of the recovery kinetics through 60 minutes following exercise. Ten healthy males (31 +/- 4 yr) cycled continuously for 45 minutes with intensity alternating between 50% (3 min) and 110% (2 min) of ventilatory threshold (VT). 1H-MR spectra were acquired from the vastus lateralis before and for 60 minutes following exercise. The peak at 2.13 ppm was not quantifiable at rest in any subject. However, it was present in all subjects following intense exercise (p < 0.0001), and expressed the chemical characteristics of an acetyl-containing compound. The estimated concentration, accumulation with high-intensity exercise, the presence as a single peak at 2.13 ppm, and the chemical shift were all consistent with the chemical and biophysical characteristics of acetyl groups associated with acetylcarnitine. This study provides further evidence that acetyl groups are robustly generated by intense exercise, and that the accumulation of acetyl groups in healthy subjects is dependent on the degree of exercise intensity. 1H-MRS may be used for the noninvasive study of muscle metabolism during exercise and recovery and may have special applications for studying the generation and transport of acetyl compounds, including acetylcarnitine.

A review of the stroke volume response to upright exercise in healthy subjects.

Traditionally, it has been accepted that, during incremental exercise, stroke volume plateaus at 40% of Vo(2)max. However, recent research has documented that stroke volume progressively increases to Vo(2)max in both trained and untrained subjects. The stroke volume response to incremental exercise to Vo(2)max may be influenced by training status, age, and sex. For endurance trained subjects, the proposed mechanisms for the progressive increase in stroke volume to Vo(2)max are enhanced diastolic filling, enhanced contractility, larger blood volume, and decreased cardiac afterload. For untrained subjects, it has been proposed that continued increases in stroke volume may result from a naturally occurring high blood volume. However, additional research is needed to evaluate the importance of blood volume, or other mechanisms, that influence the stroke volume response to exercise in untrained subjects.

Non-linear relationships between central cardiovascular variables and VO2 during incremental cycling exercise in endurance-trained individuals.

AIM: The purpose of this study was to examine the relationships between the central cardiovascular variables (cardiac output, stroke volume and heart rate) and oxygen uptake (VO2) during continuous, incremental cycle exercise to maximal aerobic capacity (VO2max). METHODS: Twenty-one moderately to highly trained males (n=19) and females (n=2) participated in the study. A baseline maximal exercise test was performed to measure VO2max. Following the initial VO2max test, cardiac output was measured (CO2 rebreathing technique) at rest and 3 times during each of 4 exercise trials (2 submaximal tests to 90% VO2max and 2 maximal tests). Stroke volume and arteriovenous O2 difference were calculated using standard equations. RESULTS: Significant non-linear relationships were found between all central cardiovascular variables and VO2 (P<0.01). A plateau in cardiac output at VO2max was identified in 3 subjects. Stroke volume plateaued at an average of 37+/-12.5% of VO2max in 18 subjects and increased continuously to VO2max in 3 subjects. The arteriovenous O2 difference progressively increased to VO2max in 17 subjects and revealed a plateau response in 4 subjects. CONCLUSIONS: Our data suggest that there is a significant non-linear relationship between the central cardiovascular variables and VO2 during incremental exercise to VO2max. Furthermore, depending on the person, VO2max may be limited by cardiac output (evidence of cardiac output[Q] plateau) or peripheral factors (continued increase in Q).

Breathing patterns and cardiovascular autonomic modulation during hypoxia induced by simulated altitude.

OBJECTIVE: To assess the influence of different breathing patterns on autonomic cardiovascular modulation during acute exposure to altitude-induced hypoxia. DESIGN: We measured relative changes in minute ventilation (VE), oxygen saturation (%SaO2), spectral analysis of RR interval and blood pressure, and response to stimulation of carotid baroreceptors (neck suction) at baseline and after acute (1 h) hypobaric hypoxia (equivalent to 5,000 m, in a hypobaric chamber). METHODS: We studied 19 human subjects: nine controls and 10 Western yoga trainees of similar age, while breathing spontaneously, at 15 breaths/min (controlled breathing) and during 'complete yogic breathing' (slow diaphragmatic + thoracic breathing, approximately 5 breaths/min) in yoga trainees, or simple slow breathing in controls. RESULTS: At baseline %SaO2, VE and autonomic pattern were similar in both groups; simulated altitude increased VE in controls but not in yoga trainees; %SaO2 decreased in all subjects (P< 0.0001), but more in controls than in yoga trainees (17 versus 12%, 14 versus 9%, 14 versus 8%, all P< 0.05 or better, during spontaneous breathing, controlled breathing and yogic or slow breathing, respectively). Simulated altitude decreased RR interval (from 879 +/- 45 to 770 +/- 39, P < 0.01) and increased indices deducted from spectral analysis of heart rate variability (low frequency/high frequency (LF/HF) ratio from 1.6 +/- 0.5 to 3.2 +/- 1.1, P < 0.05) and systolic blood pressure (low-frequency fluctuations from 2.30 +/- 0.31 to 3.07 +/- 0.24 In-mmHg2, P< 0.05) in controls, indicating sympathetic activation; these changes were blunted in yoga trainees, and in both groups during slow or yogic breathing. No effect of altitude was seen on stimulation of carotid baroreceptors in both groups. CONCLUSIONS: Well-performed slow yogic breathing maintains better blood oxygenation without increasing VE (i.e. seems to be a more efficient breathing) and reduces sympathetic activation during altitude-induced hypoxia.

Exercise exacerbates acute mountain sickness at simulated high altitude.

We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, approximately 4,800 m (J. B. West, J. Appl. Physiol. 81: 1850-1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (VE), pulmonary function, arterial oxygen saturation (Sa(O(2))), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 +/- 1.0 and 1.3 +/- 0.4 in Ex and Sed, respectively (P < 0.01); but resting VE and Sa(O(2)) were not different between trials. However, Sa(O(2)) during the exercise bouts in Ex was at 76.3 +/- 1.7%, lower than during either Sed or at rest in Ex (81.4 +/- 1.8 and 82.2 +/- 2.6%, respectively, P < 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3-6 h (P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

Detraining from total body exercise ergometry in individuals with spinal cord injury.

This study was designed to investigate the effects of detraining that occurred during an 8 week period of muscular inactivity following a 12 week training program of artificial computerized functional electrical stimulation cycle ergometry (CFES LE) and arm ergometry. Six spinal cord injured male individuals were followed through an 8 week detraining period that was preceded by a 12 week exercise program including CFES LE and arm ergometry. Maximal graded exercise tests were completed and measurements of peak oxygen consumption (VO2), heart rate (HR), ventilation (VE) workload, and creatine kinase were taken. Testing occurred at initial training (0T), after 12 weeks of training (12T), and after 8 weeks of detraining (DT). After the training program, peak VO2 increased significantly from 0.562 +/- 0.126 (0T) to 1.021 +/- 0.247 l/min (12T, P < 0.05). After DT, peak VO2 decreased to 0.791 +/- 0.216 l/min, which was lower than 12T (P < 0.05), yet higher than 0T (P < 0.05). After DT, peak workoad had decreased from 0.675 +/- 0.203 (12T) to 0.32 +/- 0.203 kp (P < 0.05), which was not different than 0T. Creatine kinase levels were significantly lower both at 12T and DT compared to 0T (P < 0.05). In addition, this training program induced linear increases in both VO2 and HR with workload, which were retained after DT. These increases did not reach statistical significance. however. No apparent relationship existed between these values at baseline. There were no significant differences in submaximal or peak HR of VE between the three testing periods. The results indicate that both peripheral muscular adaptations and central distribution adaptations in SCI individuals are partially maintained following 8 weeks of DT from CFES LE and arm ergometry.

Glycerol. Biochemistry, pharmacokinetics and clinical and practical applications.

Glycerol is a naturally occurring 3-carbon alcohol in the human body. It is the structural backbone of triacylglycerol molecules, and can also be converted to a glycolytic substrate for subsequent metabolism. Serum glycerol concentrations approximate 0.05 mmol/L at rest, and can increase to 0.30 mmol/L during increased lipolysis associated with prolonged exercise or caloric restriction. When glycerol is ingested or infused at doses greater than 1.0 g/kg bodyweight, serum concentrations can increase to approximately 20 mmol/L, resulting in more than a 10 mOsmol/kg increase in serum osmolality. Glycerol infusion and ingestion have been used in research settings for almost 60 years, with widespread clinical use between 1961 and 1980 in the treatment of cerebral oedema resulting from acute ischaemic stroke, intraocular hypertension (glaucoma), intracranial hypertension, postural syncope and improved rehydration during acute gastrointestinal disease. Since 1987, glycerol ingestion with added fluid has been used to increase total body water (glycerol hyperhydration) by up to 700 ml, thereby providing benefits of improved thermoregulation and endurance during exercise or exposure to hot environments. Despite the small number of studies on glycerol hyperhydration and exercise, it appears to be an effective method of improving tolerance to exercise and other heat-related stressors.

Video-assisted cycling alters perception of effort and increases self-selected exercise intensity.

Two studies were conducted to assess whether indoor video-assisted cycling influenced a person's quality of exercise (subjectively and quantitatively), compared to indoor cycling alone. In the first study 12 recreationally active subjects completed an initial test of VO2max, and three randomized trials of cycling at 70% VO2max (35 min.) watching a commercial cycling tape (cycle video), a test pattern displayed on the ergometer screen (blank video), or no video. Subjects' ratings of perceived exertion (RPE) and Affect were recorded, and heart rate and oxygen consumption (VO2) were measured during testing. The second study required 12 different subjects first to complete an assessment of VO2max and then two randomized trials (cycle video and no video) on a cycle ergometer where they freely set the intensity of their own exercise. Measurements of VO2, heart rate, blood lactate, power output, RPE, and Affect were recorded during testing. Results of Exp. 1 indicated that subjects' perceived effort equally between the two conditions, yet reported significantly (p < .05) higher affect at 25 and 35 min. of cycling during the cycle video condition than no video condition. Results of Exp. 2 indicated that despite similar levels of blood lactate, subjects exercised at a significantly higher intensity during the cycle video condition compared to no video condition, with a higher VO2 and heart rate. The data support the use of indoor exercise videos to improve the exercise experience and also to increase the physiological demands of indoor exercise.

Multiple variables explain the variability in the decrement in VO2max during acute hypobaric hypoxia.

PURPOSE: We used multiple regression analyses to determine the relationships between the decrement in sea level (SL, 760 Torr) VO2max during hypobaric hypoxia (HH) and variables that could alter or be related to the decrement in VO2max. METHODS: HH conditions consisted of 682 Torr, 632 Torr, and 566 Torr, and the measured independent variables were SL-VO2max, SL lactate threshold (SL-LT), the change in hemoglobin saturation at VO2max between 760 and 566 Torr (delta SaO2max), lean body mass (LBM), and gender. Male (N = 14) and female (N = 14) subjects of varied fitness, training status, and residential altitude (1,640-2,460 m) completed cycle ergometry tests of VO2max at each HH condition under randomized and single-blinded conditions. RESULTS: VO2max decreased significantly from 760 Torr after 682 Torr (approximately 915 m) (3.5 +/- 0.9 to 3.4 +/- 0.8 L.min-1, P = 0.0003). Across all HH conditions, the slope of the relative decrement in VO2max (%VO2max) during HH was -9.2%/100 mm Hg (-8.1%/1000 m) with an initial decrease from 100% estimated to occur below 705 Torr (610 m). Step-wise multiple regression revealed that SL-VO2max, SL-LT, delta SaO2max, LBM, and gender each significantly combined to account for 89.03% of the variance in the decrement in VO2max (760-566 Torr) (P < 0.001). CONCLUSIONS: Individuals who have a combination of a large SL-VO2max, a small SL-LT (VO2, L.min-1), greater reductions in delta SaO2max, a large LBM, and are male have the greatest decrement in VO2max during HH. The unique variance explanation afforded by SL-LT, LBM, and gender suggests that issues pertaining to oxygen diffusion within skeletal muscle may add to the explanation of between subjects variability in the decrement in VO2max during HH.

Blood glucose and glucoregulatory hormone responses to solid and liquid carbohydrate ingestion during exercise.

This study was conducted to compare blood glucose and glucoregulatory hormone responses to the ingestion of solid and liquid carbohydrate (CHO) during prolonged cycling, followed by 30 min of isokinetic cycling. Eight male cyclists randomly completed three cycling trials (LC = liquid CHO, SCE = solid CHO with water equal to LC, SCA = solid CHO + ad libitum water). Each subject cycled for 120 min at 65% of VO2max with CHO ingestion (0.6 g CHO/ kg/hr) at 0, 30, 60, 90, and 120 min. Subjects then completed a 30-min maximal isokinetic ride at 90 rpm. There was no significant (p < .05) difference between the trials for plasma glucose, insulin, glucagon, glycerol, lactate, RER, HR, VO2, RPE, and total work performed during the isokinetic ride. However, serum glucose was significantly lower in the SCE and SCA trials compared to LC at 80 min. The ingestion of a solid food containing CHO, protein, and fat with added water produced similar blood glucose, metabolic, glucoregulatory hormone, and exercise performance responses to those seen with the ingestion of liquid CHO.

Effects of estradiol on substrate turnover during exercise in amenorrheic females.

The purpose of this investigation was to determine the effects of transdermal estradiol (E2) replacement on substrate utilization during exercise. Amenorrheic females (N = 6) performed three exercise trials following 72 h of placebo (C 72) and 72 and 144 h of medicated transdermal estradiol (E2) treatment (E2 72 and E2 144). Exercise involved 90 min of treadmill running at 65% VO2max followed by timed exercise to exhaustion at 85% VO2max. Resting blood samples were obtained for glucose, insulin, free fatty acids (FFA), and E2. Exercise blood samples were obtained for E2, lactate, epinephrine, and norepinephrine. Rates of appearance and disposal were calculated for glucose and glycerol using a primed, continuous infusion of [6,6-2H] glucose and [2H5] glycerol. Medicated transdermal placement increased E2 significantly at rest, before exercise (35.03 +/- 12.3, 69.5 +/- 20.1, and 73.1 +/- 31.6 pg.mL-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Resting FFA increased significantly following E2 treatment (0.28 +/- 0.16, 0.41 +/- 0.27, and 0.40 +/- 0.21 mmol.L-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Glucose Ra was significantly decreased during exercise as a result of E2 replacement (21.9 +/- 7.7, 18.9 +/- 6.2, and 18.9 +/- 5.6 mumol.kg-1.min-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Average glucose Rd also decreased during exercise as a result of E2 replacement (21.3 +/- 7.8, 18.5 +/- 6.4, and 18.6 +/- 5.8 mumol.kg-1.min-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). However, the estimated relative contribution of plasma glucose and muscle glycogen to total carbohydrate oxidation was similar among the trials. Epinephrine values were significantly lower late in exercise during the E2 72 and E2 144 trials, compared with the C 72 trial (P < 0.05). These results indicate that elevated E2 levels can alter glucose metabolism at rest and during moderate intensity exercise as a result of decreased gluconeogenesis, epinephrine secretion, and/or glucose transport.

Energy expenditure and physiological responses during indoor rock climbing.

OBJECTIVES: To report the physiological responses of indoor rock climbing. METHODS: Fourteen experienced climbers (nine men, five women) performed three climbing trials on an indoor climbing wall. Subjects performed three trials of increasing difficulty: (a) an easy 90 degrees vertical wall, (b) a moderately difficult negatively angled wall (106 degrees), and (c) a difficult horizontal overhang (151 degrees). At least 15 minutes separated each trial. Expired air was collected in a Douglas bag after four minutes of climbing and heart rate (HR) was recorded continuously using a telemetry unit. Arterialised blood samples were obtained from a hyperaemised ear lobe at rest and one or two minutes after each trial for measurement of blood lactate. RESULTS: Significant differences were found between trials for HR, lactate, oxygen consumption (VO2), and energy expenditure, but not for respiratory exchange ratio. Analysis of the HR and VO2 responses indicated that rock climbing does not elicit the traditional linear HR-VO2 relationship characteristic of treadmill and cycle ergometry exercise. During the three trials, HR increased to 74-85% of predicted maximal values and energy expenditure was similar to that reported for running at a moderate pace (8-11 minutes per mile). CONCLUSIONS: These data indicate that indoor rock climbing is a good activity to increase cardiorespiratory fitness and muscular endurance. In addition, the traditional HR-VO2 relationship should not be used in the analysis of this sport, or for prescribing exercise intensity for climbing.

Exercise training by individuals with predialysis renal failure: cardiorespiratory endurance, hypertension, and renal function.

The purpose of this study was to determine the effects of 4 months of exercise training (ET) on cardiorespiratory function and endurance, blood pressure, muscle strength, hematology, blood lipids, and renal function in individuals with chronic renal failure (CRF) who were not yet on dialysis. Sixteen subjects were recruited to volunteer for participation in this study, but only eight completed all study phases. Subjects were first evaluated before and after a 2-month baseline (BL1 and BL2), after 4 months of ET, and again after 2 months of detraining (DT). ET did not change hematology, blood lipids, or echocardiographic measurements of left ventricular function and mass. Resting systolic and diastolic blood pressures decreased significantly from BL after the ET (146 +/- 15.7/87 +/- 9 mm Hg to 124 +/- 17.5/78 +/- 9.5 mm Hg; P < 0.02), and then increased significantly after DT (139 +/- 14.7 mm Hg and 87 +/- 9.9 mm Hg; P < 0.01). Peak oxygen consumption (pVO2) changed significantly during the study (1.3 +/- 0.3 L/min, 1.5 +/- 0.3 L/min, and 1.4 +/- 0.3 L/min for BL2, ET, and DT, respectively; P < 0.02), as did the VO2 at the ventilatory threshold (0.65 +/- 0.18 L/min, 0.92 +/- 0.19 L/min, and 0.68 +/- 0.23 L/min for BL2, ET, and DT, respectively; P < 0.01). Knee flexion peak torque increased after ET (43.4 +/- 25.6 Nm to 51.0 +/- 30.5 Nm; P < 0.02). GFR, as measured by creatinine clearance, continued to deteriorate during the course of the study (25.3 +/- 12.0 mL/min, 21.8 +/- 13.2 mL/min, and 21.8 +/- 13.2 mL/min for BL2, ET, and DT, respectively; P < 0.001). Individuals with predialysis CRF who undergo ET improve in functional aerobic capacity, muscular strength, and blood pressure.

Temporal inhomogeneity in brachial artery blood flow during forearm exercise.

The purpose of this study was to measure the influences of muscle contraction and exercise intensity on brachial artery blood flow during incremental forearm wrist flexion exercise to fatigue. Twelve subjects performed incremental forearm exercise (increments of 0.1 W every 5 min) with their nondominant arms. Doppler waveforms and two-dimensional images of the brachial artery were recorded during the last 2 min of each stage. Exercise intensities were expressed as a percent of the maximal workload achieved (%WLmax). Blood flow was calculated during each of the concentric (CP), eccentric (EP), and recovery phases (RP) of the contraction cycle. Blood flow during the CP of the contraction did not increase above resting values (25.0 +/- 10.5 mL.min-1) at any intensity (100%WLmax = 21.6 +/- 6.5 mL.min-1). Conversely, blood flow during the EP and RP increased from 25.6 +/- 3.0 to 169.1 +/- 12.8 (P < 0.05), and from 24.7 +/- 3.1 to 137.9 +/- 19.5 mL.min-1 (P < 0.05), respectively from rest to maximal exercise. Time averaged blood flow increased linearly from rest to maximal exercise (75.3 +/- 26.3 to 334.6 +/- 141.6 mL.min-1, P < 0.05). Thus, a significant impairment in blood flow occurs with concentric contractions during forearm dynamic exercise. The implications of a temporal disparity in blood flow to oxygen delivery and skeletal metabolism during exercise are discussed.

Exercise mode and gender comparisons of energy expenditure at self-selected intensities.

The purpose of this study was to compare oxygen consumption (VO2) and energy expenditure after 20 min of self-selected submaximal exercise for four modes of exercise. Eighteen subjects (9 male and 9 female) first completed a test of VO2max during treadmill running. On separate days, subjects then completed 20 min submaximal treadmill running (TR), simulated cross-country skiing (XC), cycle ergometry (CE), and aerobic riding (AR) exercise. Total VO2 and energy expenditure were significantly higher for TR than all other modes for both males and females (43.6 +/- 10.4, 39.1 +/- 9.7, 36.1 +/- 7.6, 28.4 +/- 6.1 LO2, for TR, XC, CE, and AR, respectively, P < 0.0001). For males and females, heart rate was similar during TR and XC and lower during CE and AR (154.8 +/- 14.2, 152 +/- 13.1, 143.4 +/- 14.9, and 126.2 +/- 12.0 beats.min-1 for TR, XC, CE, and AR, respectively, P < 0.0001). Compared with females, males had significantly greater VO2 (P < 0.005) and energy expenditure (P < 0.004), while females had higher heart rates (P < 0.003). Ratings of perceived exertion (RPE) were not different between TR, XC, and CE, but were significantly lower during AR (13.4 +/- 1.3, 13.6 +/- 0.8, 13.2 +/- 0.9, and 12.6 +/- 1.0 for TR, XC, CE, and AR, respectively, P < 0.003). TR elicited the greatest VO2 and energy expenditure during self-selected exercise despite and RPE similar to XC and CE. Therefore, treadmill exercise may be the modality of choice for individuals seeking to improve cardiorespiratory endurance and expend a larger number of kjoules.

Blood pressure measurement during exercise: a review.

This review summarizes research dealing with the validity of commonly used methods for measuring systemic blood pressure during exercise. Arterial blood pressures measured from within peripheral arteries exaggerate systolic blood pressures because of wave form reflection but provide representative mean and diastolic pressures of the central arterial circulation. Manual and automated sphygmomanometry are the best noninvasive indirect methods of blood pressure measurement to estimate ascending aorta systolic pressures; however, both methods significantly underestimate diastolic pressures at rest and during exercise. The error in diastolic pressure measurement increases with increasing exercise intensity. The accuracy of many indirect noninvasive devices for blood pressure measurement at rest and during exercise can be questioned because of the use of unsuitable criterion methods. Ascending aorta pressures should ideally be used as a gold standard or criterion method for blood pressure measurement during exercise and instrument/method validation. However, given the constraints of varied criterion standards and current recommendations for blood pressure measurement, the following units were found to be acceptable devices for measuring systolic blood pressure during exercise: Accutracker II, A&D TM 2421, Colin 630 (auscultation), Critikon 1165, and possibly the Paramed 9350.

Oxygen consumption and energy expenditure of level versus downhill running.

OBJECTIVE: The purpose of this study was to assess and compare submaximal oxygen consumption (VO2) and energy expenditure (kJ) while running at 0, -1.8, -3.6, and -5.4% grades for three individually selected running speeds (9.4 + 0.79, 10.3 + 0.74, 11.3 + 0.73 km.h-1). EXPERIMENTAL DESIGN: Subjects completed the four grade conditions in random order via a modified Latin squares design at three self-selected submaximal running speeds for each condition. PARTICIPANTS: Thirteen (5 females and 8 males) recreational (< 35 km.wk-1) runners (age: 27.7 +/- 4.3 yrs) volunteered for the study. MEASURES: Two-way repeated measures ANOVA (Grade x Speed) was used to analyze steady-state VO2 and kJ expenditure. Stepwise linear multiple regression was used to develop an equation for predicting VO2 for running at recreational speeds on moderately negative grades. RESULTS: VO2 and kJ mean values were significantly different between all speed and % grade comparisons. Compared to level grade, the average reductions in VO2 and kJ expenditure ranged from approximately 9% at a grade of -1.8% to 22% at a grade of -5.4%. The relationship between VO2 and % grade for each running speed was linear. CONCLUSIONS: For a given speed, running at a modest negative grade can significantly decrease VO2 and kJ expenditure compared to level running. The following regression equation can be used to estimate VO2 (ml.kg-1.min-1) for running at recreational speeds on slight downhills: VO2 = 6.8192 + 0.1313 (speed in m.min-1) + 1.2367 (% grade).

Changes in muscle proton transverse relaxation times and acidosis during exercise and recovery.

We studied changes in muscle proton (1H) transverse relaxation times (T2) by magnetic resonance imaging during exercise and compared these changes with alterations in muscle metabolism measured by phosphorus-31 magnetic resonance spectroscopy (31P-MRS). Eleven subjects completed two trials of intermittent incremental forearm wrist flexion exercise requiring 30 contractions/min for 5 min, 7 min of recovery between stages, and 5-N load increments/stage. Between stages of the first trial, T2 images of muscle 1H were obtained. Muscle T2 increased from 27.3 +/- 1.1 (SD) ms at rest to 35.8 +/- 3.6 ms after volitional fatigue (P < 0.05), whereas less active wrist extensor muscle T2 remained unchanged (26.8 +/- 0.9 to 28.8 +/- 1.6 ms; P > 0.05). After localizing the predominant muscle recruited from the T2 images, subjects completed an identical trial at least 1 wk later but involving surface coil 31P-MRS of the T2-enhanced muscle to measure the H+ concentration ([H+]). Intramuscular [H+] of T2-enhancing muscle increased from 1.1 +/- 0.1 x 10(-7) M at rest to 4.1 +/- 2.0 x 10(-7) M after volitional fatigue. Both muscle T2 and intramuscular [H+] increased in a bimodal manner, with T2 increasing before muscle [H+] (P < 0.05). The correlation coefficient between the percent change in T2 and muscle [H+] during exercise was +0.74 (range 0.48-0.98; P < 0.05) and +0.47 during recovery. After 12 min of recovery, muscle [H+] decreased to 1.4 +/- 0.3 x 10(-7) M (P < 0.05), and T2 remained close to postexercise values (32.2 +/- 3.1 ms, P > 0.05). The data indicate that 1) the T2 increases during increases in exercise intensity are nonlinear, 2) the T2 increases during exercise are significantly correlated with increases in [H+], and 3) the slow recovery of T2 compared with [H+] indicates that [H+] has a minor contribution to the recovery in T2.