Comparative effects of caffeine and albuterol on the bronchoconstrictor response to exercise in asthmatic athletes.

The main aim of this study was to evaluate the comparative and additive effects of caffeine and albuterol (short-acting beta (2)-agonist) on the severity of EIB. Ten asthmatic subjects with EIB (exercise-induced bronchoconstriction) participated in a randomized, double-blind, double-dummy crossover study. One hour before an exercise challenge, each subject was given 0, 3, 6, or 9 mg/kg of caffeine or placebo mixed in a flavored sugar drink. Fifteen minutes before the exercise bout, an inhaler containing either albuterol (180 microg) or placebo was administered to each subject. Pulmonary function tests were conducted pre- and post-exercise. Caffeine at a dose of 6 and 9 mg/kg significantly reduced (p<0.05) the mean maximum % fall in post-exercise FEV (1) to -9.0+/-9.2% and -6.8+/-6.5% respectively compared to the double-placebo (-14.3+/-11.1%) and baseline (-18.4+/-7.2%). There was no significant difference (p>0.05) in the post-exercise % fall in FEV (1) between albuterol ( PLUS CAFFEINE PLACEBO) (-4.0+/-5.2%) and the 9 mg/kg dose of caffeine (-6.8+/-6.5%). Interestingly, there was no significant difference (p>0.05) in the post-exercise % fall in FEV (1) between albuterol ( PLUS CAFFEINE PLACEBO) (-4.0+/-5.2%) and albuterol with 3, 6 or 9 mg/kg of caffeine (-4.4+/-3.8, -6.8+/-5.6, -4.4+/-6.0% respectively). Similar changes were observed for the post-exercise % fall in FVC, FEF (25-75%) and PEF. These data indicate that moderate (6 mg/kg) to high doses (9 mg/kg) of caffeine provide a significant protective effect against EIB. It is feasible that the negative effects of daily use of short-acting beta (2)-agonists by asthmatic athletes could be reduced simply by increasing caffeine consumption prior to exercise.

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)

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.

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.

Phosphate supplementation, cardiovascular function, and exercise performance in humans.

The use of oral phosphate (Pi) supplements to improve muscular work performance has long been proposed without substantiating data. In a double-blind, crossover experiment 11 male runners ingested calcium Pi (176 mmol/day) or placebo for 4 days. On the 3rd treatment day, subjects ran an incremental maximal aerobic capacity test (VO2 max) on a treadmill, and on the 4th day a treadmill run to exhaustion at approximately 70% VO2max. By the 4th day of Pi loading, plasma Pi was significantly higher than control (P less than 0.05); however, erythrocyte Pi, 2,3-diphosphoglycerate, and O2 half-saturation pressure of hemoglobin (P50) were not elevated. VO2 max was not changed by the treatments (mean 62.9, 64.2, 64.9 ml.kg-1.min-1 for control, Pi, and placebo bouts, respectively) nor was submaximal run time to exhaustion (61.6 min for Pi, 65.5 min for placebo). Stroke volume at steady-state VO2 was decreased with Pi (P less than 0.05), whereas cardiac output tended (P = 0.07) to be lower. Greater arteriovenous O2 difference (P less than 0.05) with Pi suggested a peripheral effect that increased O2 extraction. We concluded that in healthy individuals Pi loading produced no improvement in work tolerance or aerobic capacity but did alter some aspects of cardiovascular function.

Ventilatory endurance in athletes and non-athletes.

Do the ventilatory muscles (VM) of normal persons become fatigued while high ventilation is maintained during strenuous exercise? If so, then one effect of the intense training performed by endurance athletes should be an increase in VM endurance. To investigate this possibility, eight female endurance-athletes and eight female non-athletes were compared in studies of both short-term and long-term maximal ventilation. The two groups were matched for age, body size, and vital capacity. While athletes and non-athletes had similar short-term maximal ventilation (12-s MVV), the athletes displayed greater ventilatory endurance on two-long-term breathing tests. In the first, ventilation was increased 30 1/min every 4 min. Before exhaustion, athletes reached a ventilation that was a significantly greater fraction of their 12-s MVV (75% vs 67%, P less than 0.01), than did non-athletes. Although the energy cost (VO2) of submaximal levels of ventilation was identical in the two groups, athletes reached a significantly greater peak VO2 during this progressive test (P less than 0.05). In the second test of ventilatory endurance, 80% of the 12-s MVV was sustained until exhaustion. Endurance times averaged 11 min for athletes and 3 min for non-athletes (P less than 0.01). While these results do not rule out the possibility of genetic predisposition to high VM endurance in athletes, they are consistent with the possibility that VM training may occur in normal persons during forms of endurance exercise training.

Menarche in athletes: the influence of genetics and prepubertal training.

It is unclear whether the later menarche observed in competitive athletes is due to genetic factors or environmental factors related to intense prepubertal training. In order to investigate the importance of these factors upon the age of menarche (AOM), 263 competitive swimmers and 71 women with no athletic experience were asked to complete questionnaires concerning general health and reproductive development. Based upon their responses, similar questionnaires were sent to the sisters of both groups. Complete data were obtained from 140 athlete/sister pairs and 43 control/sister pairs. Results indicate that the athletes were older at menarche than their sisters, the non-athletes, and the sisters of the non-athletes (14.3 yr, 13.7 yr, 12.9 yr, and 13.0 yr, respectively). The sisters of the athletes were significantly older at menarche than the controls and their sisters, while the AOM of the non-athletic controls and their sisters did not differ. The interpretation of the data is complicated by the fact that the sisters of the athletes were likely to be athletes (75%), while those of the control group tended to be non-athletic (74%). The athletes differed from their sisters who trained prior to menarche (13.9 years) and from those who did not engage in prepubertal training (13.1 years). Controls did not differ from any of their sister groups, nor did they differ from the untrained sisters of athletes. In terms of the similarity of the AOM within the sister pairs, the athletes/sisters and controls/sisters were equally similar. Significant correlations were observed between athletes and their sisters who trained prior to menarche and controls and their sisters who did not.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Delayed menarche in swimmers in relation to age at onset of training and athletic performance.

Competitive swimmers have been considered to be different from other female athletes in that their mean age at menarche is similar to that of nonathletes. However, it was hypothesized that if the delayed menarche observed in athletes of other sports is caused by prepubertal training, then swimmers should also exhibit delayed menarche as the majority of swimmers begin training prior to puberty. Furthermore, if early prepubertal training is the important factor in delaying menarche, then it was hypothesized that a relationship between performance and age at menarche in swimming is unlikely to exist. Thus, 345 competitive female swimmers and 549 control subjects completed questionnaires concerning general health, athletic training history, and age at menarche. Results indicated that, as a population, the mean age at menarche of the swimmers (13.4 yr) was significantly later than the controls (13.0 yr). When swimmers and controls were compared on an age-group basis, it was found that the difference in age at menarche was due to the data obtained from the older and more highly competitive swimmers. Assigning swimmers to different competitive levels or by performance in specific swimming events (50- or 100-yd freestyle; 45.7- or 91.4-m, respectively) indicated a significantly later age at menarche for the more competitive swimmers. Thus, there is evidence that the age at menarche and subsequent athletic performance in swimming are related; the later menarche observed in swimmers appears to be associated with factors that select for superior performance.

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)

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.

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".

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.

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.

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)

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.

Bone mineral content and menstrual regularity in female runners.

The relationship between bone mineral content and menstrual regularity in 10 amenorrheic runners (0-3 menses during the past year), 12 runners with regular menstrual cycles (10-12 menses during the past year), and 15 non-athletic women with regular menstrual cycles was investigated. Comparisons of the two groups of runners indicated no significant differences in body fatness, average weekly running distance, or average daily intake of calcium (Ca), phosphorus (P), and Ca/P ratios. Mean bone mineral content for the three groups, measured by photon absorptiometry, was 0.508, 0.529, and 0.544 g X cm-2, respectively, at 3 cm distal radius, and 0.707, 0.700, and 0.707 g X cm-2, respectively, at one-third distal radius, indicating no significant differences among the groups (P less than 0.05). However, a significant relationship (r = 0.77) was noted between bone mineral content and body fatness only in the amenorrheic runners. Within the amenorrheic population, the five thinnest runners had significantly lower mean bone mineral content values at 3 cm distal radius (0.457 g X cm-2) than the five runners with higher relative body fatness (0.559 g X cm-2). We conclude, therefore, that amenorrhea, independent of body composition, was not related to reduced bone mineral content in female runners. However, the combination of excessive thinness and amenorrhea may, in fact, predispose female athletes to reduced bone mass.

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.

The thyroid and hypoxic moderation of systemic hypertension in the spontaneously hypertensive rat.

Surgically thyroidectomized (TX), sham-operated euthyroid (EU), or thyroidectomized with dietary hormone replacement (RPL), 8-week-old male spontaneously hypertensive rats were subjected to 4 weeks of either of two altitude treatments: normoxia (N; lab altitude = 1520 m) or hypobaric hypoxia (H; simulated altitude = 3658 m). Systolic blood pressure (SBP) was attenuated in all hypoxic and in TX-N rats (p less than 0.05). Thyroidectomy reduced oxygen consumption, rectal temperature, and hormonal indices of thyroid function, as well as attenuating hypoxia-induced polycythemia and right ventricular hypertrophy. Thyroidectomy decreased the sensitivity of aortic rings to KCl and isoproterenol with no differences between EU-N and EU-H or between TX-N and TX-H apparent. Vessel responsiveness in RPL-H was consistent with the hypothyroid status indicated by hormonal measurement, while RPL-N vessel responsiveness was characteristic of euthyroid vessels. Since EU-H rats were euthyroid, with similar vascular responses to EU-N, hypoxia-induced attenuation of SBP does not require hypothyroid-like vascular alterations. Thus, hypoxia and thyroidectomy appear to mitigate systemic hypertension by different mechanisms.