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Biomedical subjects

J M Stager

Publications and source records attributed to J M Stager.

At least 19 recordsLinked to original sources

Clothing fabric does not affect thermoregulation during exercise in moderate heat.

PURPOSE: We investigated whether temperature regulation is improved during exercise in moderate heat by the use of clothing constructed from fabric that was purported to promote sweat evaporation compared with traditional fabrics. METHODS: Eight well-trained, euhydrated males performed three exercise bouts wearing garments made from an evaporative polyester fabric (SYN), wearing garments made from traditional cotton fabric (COT), or dressed seminude (S-N) in random order. Bouts consisted of 15 min seated rest, 30 min running at 70% .VO(2max), 15 min walking at 40% .VO(2max), and 15 min seated rest, all at 30 +/- 1 degrees C and 35 +/- 5% relative humidity. COT and SYN clothing ensembles consisted of crew neck, short sleeve T-shirts, cycling shorts, and anklet socks made from their respective materials, and running shoes. The S-N condition consisted of a Lycra swim suit, polyester socks, and running shoes. RESULTS: Mean skin temperature was lower for S-N during preexercise rest when compared with SYN and COT. No differences in mean body temperature, rectal temperature, or mean skin temperature were observed during or after exercise. No differences in VO2 or heart rate were observed. No differences in comfort sensations were observed. CONCLUSION: In summary, before, during, or after exercise in a moderately warm environmental condition, neither the addition of a modest amount of clothing nor the fabric characteristics of this clothing alters physiological, thermoregulatory, or comfort sensation responses.

Adult↗

Expiratory flow limitation confounds ventilatory response during exercise in athletes.

INTRODUCTION: A significant number of highly trained endurance runners have been observed to display an inadequate hyperventilatory response to intense exercise. Two potential mechanisms include low ventilatory responsiveness to hypoxia and ventilatory limitation as a result of maximum expiratory flow rates being achieved. PURPOSE: To test the hypothesis that expiratory flow limitation can complicate determination of ventilatory responsiveness during exercise the following study was performed. METHODS/MATERIALS: Sixteen elite male runners were categorized based on expiratory flow limitation observed in flow volume loops collected during the final minute of progressive exercise to exhaustion. Eight flow limited (FL) (VO2max, 75.9+/-2.4 mL x kg(-1) x min(-1); expiratory flow limitation, 47.3+/-20.4%) and eight non-flow limited subjects (NFL) (VO2max, 75.6+/-4.8 mL x kg(-1) x min(-1); expiratory flow limitation, 0.3+/-0.8%) were tested for hypoxic ventilatory responsiveness (HVR). RESULTS: Independent groups ANOVA revealed no significant differences between FL and NFL for VO2max, VE max (136.2+/-16.0 vs 137.5+/-21.6 L x min(-1)), VE/VO2, (28.4+/-3.2 vs 27.6+/-2.9 L x lO2(-1)), VE/VCO2 (24.8+/-3.1 vs 24.4+/-2.0 L x lCO2(-1)), HVR (0.2+/-0.2 vs 0.3+/-0.1 L x %SaO2(-1)), or SaO2 at max (89.1+/-2.4 vs 86.6+/-4.1%). A significant relationship was observed between HVR and SaO2 (r = 0.92, P < or = 0.001) in NFL that was not present in FL. Conversely, a significant relationship between VE/VO2 and SaO2 (r = 0.79, P < or = 0.019) was observed in FL but not NFL. Regression analysis indicated that the HVR-SaO2 and SaO2-VE/VO2 relationships differed between groups. DISCUSSION: When flow limitation is controlled for, HVR plays a more significant role in determining SaO2 in highly trained athletes than has been previously suggested.

Adult↗

The effect of exercise modality on exercise-induced hypoxemia.

To investigate the effect of exercise mode on arterial oxyhemoglobin saturation (SaO2), 13 healthy, actively training men who displayed exercise-induced hypoxemia (EIH) performed two incremental maximal exercise tests: uphill treadmill running and cycle ergometry. At maximum, treadmill running resulted in a lower SaO2 (88.6+/-2% versus 92.6+/-2.0%) a lower ventilatory equivalent for carbon dioxide (VE/VCO2; 28.8+/-0.6 versus 31.2+/-0.9), and a higher maximal oxygen consumption (VO2, MAX; 4.83+/-0.11 l x min(-1) versus 4.61+/-0.14 l x min(-1) when compared to cycle ergometry. When data were combined from maximal running and cycling. SaO2 was correlated to VE/VCO2 (r = 0.54). However, there was no relationship between the differences in SaO2 and ventilation between exercise modes. This suggests that ventilation is important in the maintenance of SaO2, but that the difference observed in SaO2 between treadmill running and cycle ergometry cannot be explained by differences in ventilation and must be due to differences in diffusion limitation or ventilation-perfusion inequality.

Adult↗

Degree of arterial desaturation in normoxia influences VO2max decline in mild hypoxia.

PURPOSE: Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at VO2max--a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and VO2max in EIH athletes while non-EIH athletes would be unaffected. METHODS: Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at VO2max (EIH <90%, Non-EIH >92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed--one in normoxia, one in mild hypoxia (FIO2 = 0.187; approximately 1,000 m). RESULTS: EIH subjects demonstrated a significant decline in VO2max from normoxia to mild hypoxia (71.1+/-5.3 vs. 68.1+/-5.0 mL x kg(-1) min(-1), P<0.01), whereas the non-EIH group did not show a significant deltaVO2max (67.2+/-7.6 vs. 66.2+/-8.4 mL x kg(-1) x min(-1)). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in VO2max from normoxia to mild hypoxia (r = -0.54, P<0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (deltaSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect VO2max in mild hypoxia. CONCLUSIONS: We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in VO2max in mild hypoxia compared with normoxemic athletes.

Adult↗

Extent of expiratory flow limitation influences the increase in maximal exercise ventilation in hypoxia.

Increasing ventilation (VE) during hypoxic exercise may help to defend arterial O2 saturation (SaO2) and VO2max however, many athletes experience limitations to ventilatory flow and are not able to increase VE at high workrates. Five of 19 highly trained endurance athletes screened had < 5% of their tidal flow volume loop during maximal exercise meet the boundary set by their maximal resting flow volume loop. These five athletes were grouped as non-flow limited and compared to the five athletes who demonstrated the greatest percent of tidal volume flow limitation (56 +/- 11%) during maximal exercise (flow limited). Each athlete completed two incremental treadmill tests to exhaustion: normoxia and hypoxia (FI(O2) = 0.187). Non-flow limited athletes increased VE at VO2max from normoxia to hypoxia (140.9 +/- 13.4 vs. 154.7 +/- 11.9 L/min, P < 0.05), while flow limited athletes did not (159.5 +/- 9.4 vs. 162.3 +/- 6.0 L/min). The decline in SaO2 at VO2max from normoxia to hypoxia was not significantly different between groups. We conclude that athletes with little or no expiratory flow limitation are able to increase VE during maximal exercise in mild hypoxia, compared to athletes with significantly higher degrees of mechanical limitation. However this 'mechanical ventilatory reserve' does not appear to influence the ability to defend SaO2 or VO2max during maximal exercise in mild hypoxia.

Adult↗

Ventilation's role in the decline in VO2max and SaO2 in acute hypoxic exercise.

The role of ventilation in the response in aerobic capacity and arterial oxygen saturation (SaO2) to acute hypoxic exercise was studied in 13 healthy active men divided into two groups based on their normoxic maximal exercise VE/VO2 (LOW < or =27.7; HIGH > or = 30.2) and PAO2 estimates (LOW < or = 107 mm Hg; HIGH > or = 110 mm Hg). Groups performed two incremental progressive maximal cycle exercise (VO2max) tests: normoxia (FIO2 = 20.9%) and acute hypoxia (FIO2 = 13.3%). To evaluate the influence of hypoxic ventilatory drive on ventilation, resting hypoxic ventilatory response (rHVR) was measured. LOW demonstrated lower ventilatory responses (VE, VE/VO2, and VE/VCO2) during both normoxic and hypoxic exercise (P < or = 0.05). During maximal hypoxic exercise, LOW had a greater decline in both VO2max (21.6 mL x kg(-1) x min(-1) vs 16.6 mL x kg(-1) x min[-1]) and SaO2 (31.9% vs 22.1%). Modest but significant correlations were identified between normoxic VE/VO2 and the decline in both VO2max (r = -0.62) and SaO2 (r = -0.60). No correlations were identified between rHVR and any ventilatory response or SaO2. In summary, the results from this study suggest that a low exercise-induced hyperventilatory response is a significant mechanism in the arterial desaturation observed during hypoxic exercise and the decline in aerobic capacity associated with this desaturation. However, the ventilatory response to hypoxic exercise is not dependent upon hypoxic ventilatory drive.

Adult↗

Partitioned weight loss and body composition changes during a mountaineering expedition: a field study.

Weight loss and changes in body composition are recognized phenomena associated with high-altitude mountaineering expeditions. Attempts to partition the weight loss between fat mass (FM) and fat-free mass (FFM) have been inconclusive. Therefore, five male subjects, average age 40.0 +/- 5.5 years, were studied prior to, during, and following a 21-day expedition between 2200 m and 4300 m on Mt. McKinley, Alaska. Pre- to postexpedition body composition changes were determined by densitometry, skinfold thickness (12 sites), body girth measurements (14 sites), and cross-sectional area from magnetic resonance imaging (MRI) (three sites). Data analysis by Student's t-test (p < 0.05(1) tail) indicated decreases in body weight (4.2 +/- 2.8 kg, 220 g/day, 5.4% of initial weight), total skinfold thickness (10.8%), total body girth (2.8%), and percentage of fat by densitometry (15%). Total cross-sectional area of the three MRI slices (upper arm + thigh + calf) decreased 4.7%, muscle area decreased 9.1%, and fat area decreased 3.9%. The three methods used to partition the weight loss between FM and FFM did not agree: 77% FM vs 23% FFM by densitometry, 25% FM vs 75% FFM by skinfolds, and 38% FM vs 62% FFM by MRI. Energy intake (3640 +/- 1250 kcal/day) was negatively correlated (Pearson r > 0.88(2) tail) with losses in weight (r = -0.89), skinfolds (r = -0.93), and girths (r = -0.88), ie the greater the intake the less the decline. Therefore, insufficient energy intake appeared primarily responsible for the weight loss and changes in body composition during the expedition.

Absorptiometry, Photon↗

Acetazolamide reduces peripheral afferent transmission in humans.

Carbonic anhydrase has been localized in skeletal muscle and nerve, thus, inhibition with acetazolamide (ACZ) may alter nerve and/or muscle function in healthy humans. ACZ (3 oral doses 14, 8, and 2 h prior to testing) reduced isometric force (37%) and peak to peak electromyographic (EMG) amplitude (1.38 mV to 0.83 mV), while increasing EMG latency associated with a unilateral Achilles tendon-tap. Reflex recovery profiles, following a contralateral conditioning tap, were similar in both placebo and ACZ experiments. ACZ led to significant changes in Hmax/Mmax ratio (52.19/14.42 to 45.73/15.65) and H-reflex latency (34.18 +/- 2.54 ms to 35.24 +/- 2.74 ms). Motor nerve conduction velocity and maximal voluntary isometric torque (knee extensors) were unaltered by ACZ. These data suggest that inhibition of the tendon-tap reflex and associated isometric force, following ACZ, is related to impairment of synaptic integrity between la fibers of the muscle spindle and the alpha motor neuron and not impairment of the muscle spindle or force-generating capacity.

Acetazolamide↗

Mood, neuromuscular function, and performance during training in female swimmers.

The effect of seasonal changes in training load on mood, neuromuscular function, and measures of physical power were examined in 12 collegiate women swimmers. These subjects were studied at three training stages during a competitive swim season: baseline (5,000 m.d-1), peak training (8,300 m.d-1), and taper (2,300 m.d-1). Mood was evaluated with the Profile of Mood States. Neuromuscular function was measured via the soleus Hoffmann-reflex (H-reflex). Anaerobic swimming power was assessed with a 30-s tethered swim test, and maximal aerobic power was determined following a maximal 378-m swim. Repeated measures ANOVA revealed that at peak training H-reflex and peak anaerobic swimming power were reduced (P < 0.05) below baseline values by 8.6% and 9.4%, respectively, and total mood disturbance was elevated above baseline (P < 0.01). These variables returned to baseline values at the taper assessment. H-reflex values were correlated with peak (r = 0.52, P < 0.01) and mean (r = 0.39, P < 0.05) anaerobic swimming power. Total mood disturbance was correlated (r = -0.34, P < 0.05) with mean swimming power. The results suggest that neurological mechanisms play a role in the adaptations that result from periodized training.

Adult↗

Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia.

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Energy balance in highly trained female endurance runners.

Anecdotal and scientific reports have suggested that some female endurance athletes may have an inexplicable imbalance between energy intake and energy expenditure. We compared energy intake (EI) from food diaries (FD) with assessment of free-living energy expenditure (EE) using doubly labeled water (DLW) and a food attitude survey for 7 d in nine female distance runners. Daily EE via DLW (2990 +/- 415 kcal) was greater (P < 0.01) than daily EI via FD (2037 +/- 298 kcal): a 32% imbalance. Body weight did not change during the 7 d (day 1, 55.3 +/- 6.2 kg; day 7, 55.1 +/- 5.6 kg). A positive relationship was observed between EE and body weight (r = 0.82) while a negative correlation existed between EE vs EI (r = -0.83) and between EI vs body weight (r = -0.74). A negative correlation was observed between body weight and food attitude/body image (r = -78), i.e., the heavier women self-reported lower EI and also reported lower body image scores. These female athletes had a significant imbalance between EI and EE by our measures. Since body image and EI were related to body weight, the estimates of EI may be low due to underreporting particularly by the heavier athletes.

Adult↗

Lung volumes and maximal respiratory pressures in collegiate swimmers and runners.

To determine whether respiratory muscle strength is related to pulmonary volume differences in athletes and nonathletes, 11 intercollegiate female swimmers, 11 female cross-country runners, and two nonathletic control groups, matched to the athletes in height and age, were evaluated for pulmonary parameters including maximal inspiratory pressure (PImax) and maximal expiratory pressure (PEmax). Swimmers exhibited larger (p less than .05) vital capacities (VC), residual lung volumes (RV), inspiratory capacities (IC), and functional residual capacities (FRC) than both the runners or the controls but no difference (p greater than .05) in either PImax or inspiratory flow (FIV 25%-75%). Timed expiratory volumes (FEV 0.5 and FEV 1.0) were significantly (p less than .05) lower in the swimmers than in the controls. These data suggest that an adaptational growth may be responsible, in part, for the augmented static lung volumes demonstrated in swimmers.

Adolescent↗

Body water and electrolyte responses to acetazolamide in humans.

Acetazolamide (ACZ), a potent carbonic anhydrase inhibitor, is a known diuretic and causal agent in metabolic acidosis. Its diuretic qualities are well established with respect to urine flow and electrolyte excretion. However, the impact of ACZ on body hydration status has not been adequately quantified. Thus, to establish the influence of ACZ treatment on body water, nine healthy males were evaluated for hydration status after clinically prescribed doses of ACZ. The drug was administered in three 250-mg oral doses 14, 8, and 2 h before determination of body water compartments. ACZ led to a significant 1.7-liter reduction in total body water (3.4%). A significant reduction in extracellular water of 3.3 liters is partitioned as the loss of total body water and a significant increase in intracellular water (1.6 liters). Venous blood pH and plasma HCO3- were significantly reduced 0.09 units and 5.9 mM, respectively, with ACZ. Plasma protein concentration was increased, but plasma osmolality did not change. Plasma Na+, K+, and Cl- concentrations were not different with ACZ, but total electrolyte content was significantly decreased 45.2, 1.17, and 44.1 meq, respectively, for all three. Urine K+, HCO3-, flow, and pH were elevated after ACZ treatment, whereas Na+ and Cl- were the same as placebo levels. In conclusion, acute clinical doses of ACZ reduce body fluid compartments, leading to a moderate isosmotic hypovolemia with an intracellular volume expansion as well as metabolic acidosis.

Acetazolamide↗

Acetazolamide alters temperature regulation during submaximal exercise.

Acetazolamide (ACZ), a potent carbonic anhydrase inhibitor, is known to decrease submaximal exercise tolerance under normoxic and hypoxic conditions. These decrements in performance occur despite the maintenance of O2 consumption and CO2 removal. Because ACZ is a diuretic, it induces a moderate hypohydration that may have a role in reducing the ability to sustain exercise through cardiovascular and thermoregulatory impairment. To investigate this potential impairment, seven healthy males between 21 and 35 yr of age were studied in a double-blind crossover design (placebo vs. ACZ). ACZ was administered in three 250-mg oral doses 14, 8, and 2 h before exercise. Subjects exercised at 70% peak O2 uptake for 30 min on a cycle ergometer in a normoxic thermoneutral environment (25 degrees C, 40% relative humidity). Results indicate that exercise minute ventilation was greater but O2 uptake, CO2 output, and respiratory exchange ratio did not differ with ACZ. ACZ led to lower mean skin (0.7 degrees C), higher rectal (0.6 degrees C), and higher mean body temperatures (0.4 degrees C) after 30 min of exercise. Whole-body sweat loss was reduced 23%, and heat storage during the exercise bout was increased 55%. Stroke volume decreased 25%, and arteriovenous O2 difference increased 15%. A significant inverse relationship (r = -0.63) between heart rate and stroke volume was observed. It is concluded that previously reported decreases in the ability to sustain submaximal exercise with ACZ may be related to hypohydration-induced impairment of the cardiovascular and thermoregulatory systems.

Acetazolamide↗

Interpreting the relationship between age of menarche and prepubertal training.

It has been concluded from studies using retrospective data and thus quasi-experimental designs that menarche may be delayed by prepubertal athletic training. Furthermore, a causal relationship between the age of initiation of training (AIT) and the age of menarche (AOM) has been proposed. To investigate the possibility that these conclusions were erroneous and based upon analytical artifact, a computer program was used to generate random and independent AOM and AIT for a population of 30,000 "athletes". The generated mean AOM (means = 13.4 yr) and mean AIT (means = 10.0 yr) were similar to those reported in recent literature. The sampling procedure was designed such that no relationship existed between AOM and AIT in these hypothetical athletes (r = 0.002). When two subgroups (pre- or post-menarcheal training) were compared, the pre-training group was found to have a significantly later AOM than the post-trained group (means = 13.9 yr vs means = 11.7 yr; P less than 0.05). Significant correlations were found for each subgroup between AOM and AIT (r = 0.46 and 0.40 pre- and post-menarcheal training, respectively), similar to values previously reported. In conclusion, the sampling procedures performed in the present study and in similar data sets result in biased estimates of the statistical parameters. This bias accounts for the reported relationship between AOM and AIT derived using this type of quasi-experimental design, and therefore it would appear appropriate to state that the age of menarche in athletes is "later" rather than "delayed".

Adolescent↗

Normoxic and acute hypoxic exercise tolerance in man following acetazolamide.

The influence of acetazolamide (ACZ) upon the ability to perform and sustain maximal and submaximal exercise bouts under normoxic and hypoxic conditions was examined in four groups of healthy male subjects (N = 27). ACZ (500 mg) or inert placebo (Pla) was administered prior to exercise in a quasi-randomized, double-blind, crossover fashion. ACZ was shown to lower venous pH (ACZ, 7.31 +/- 0.01, vs Pla, 7.35 +/- 0.08) and bicarbonate (ACZ, 22.4 +/- 0.27 mM, vs Pla, 25.4 +/- 0.6 mM) and to elevate urine pH (ACZ, 7.36 +/- 0.06, vs Pla, 5.84 +/- 0.19) and tended to elevate VE (P = 0.07) at rest. Peak VO2 measured using a continuous incremental protocol was unaltered in normoxia, while peak VCO2 and RER were lowered by ACZ. No significant effect of ACZ upon VO2, VCO2, RER, or heart rate (HR) was observed during submaximal exercise (75% of peak VO2) although VE was increased by 14% and time to exhaustion (EXHt) was reduced by 29%. During acute hypoxia at a simulated altitude of 4,270 m (Pbar = 446 mm Hg), no significant differences were noted in VE, VO2, VCO2, RER, HR, or arterial saturation (SaO2) at rest. Prior to exercise, venous pH (ACZ, 7.39 +/- 0.04, vs Pla, 7.44 +/- 0.007) and bicarbonate were lower with ACZ (ACZ, 21.6 +/- 0.46 mM, vs Pla, 24.2 +/- 0.25 mM), while urine pH was higher (ACZ, 7.6 +/- 0.07, vs Pla, 5.9 +/- 0.25). Other than a higher PCO2 and lower venous lactate with ACZ, no significant differences were identified at peak VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗

Oxygen delivery and cardiac output during exercise following oral phosphate-glucose.

Phosphate has been proposed as an ergogenic aid since it may enhance O2 delivery and cardiac work efficiency by increasing plasma phosphate (P Pi), red blood cell phosphate (RBC Pi), 2,3-diphosphoglycerate (DPG), RBC adenosine triphosphate (ATP), and P50. In 10 normal, fasting males we measured cardiac output (Q) by CO2 rebreathing, heart rate (HR), O2 deficit (O2DEF), and O2 consumption (VO2) during cycle ergometer exercise (60% of peak VO2). Stroke volume (SV) and arteriovenous O2 difference (A-VO2) were calculated. Following a baseline blood sample (BASE) for P Pi, RBC Pi, DPG, RBC ATP, and P50 (3 h before exercise), a single oral dose of dicalcium phosphate (129 mmol) and glucose (500 ml/10% sol, PHOS), or placebo (PLA), was administered in a random, crossover, double-blind fashion. Blood sampling was repeated immediately before and after exercise (PRE-EX and POST-EX). PHOS induced increases in P Pi (3.87 to 4.35 mg.dl-1, P less than 0.05), RBC Pi (3.86 to 4.63 mg.dl-1, P = 0.08), DPG (11.8 to 13.1 mumol.g-1 Hb, P less than 0.05), RBC ATP (4.2 to 4.4 mumol.g-1 Hb, P less than 0.05), and P50 (26.8 to 27.9 mm Hg, P less than 0.05) from BASE to PRE-EX. All variables remained elevated through the exercise period, as evidenced by higher levels than BASE at POST-EX (P less than 0.05). However, P50 was not different across conditions at PRE-EX (PHOS P50 = 27.9, PLA P50 = 28.3 mm Hg) or POST-EX (PHOS P50 = 28.0, PLA P50 = 28.1 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗