The relation of adiponectin and tumor necrosis factor alpha levels between endothelial nitric oxide synthase, angiotensin-converting enzyme, transforming growth factor beta, and tumor necrosis factor alpha gene polymorphism in adrenal incidentalomas.

OBJECTIVE: The aim of our study was to demonstrate demographic characteristics, presence of inflammatory markers, distribution of angiotensin-converting enzyme (ACE), tumor necrosis factor (TNF), endothelial nitric oxide synthase (eNOS) genotypes and relations among these parameters in these patients and control subjects. RESEARCH DESIGN AND METHODS: Study samples were collected from 50 patients with adrenal mass and 30 control groups. The eNOS, ACE, TNF-alpha, transforming growth factor (TGF)-beta genes polymorphisms, TNF-alpha, adiponectin levels were analysed in 50 unrelated Turkish patients with a diagnosis of adrenal incidentaloma (AI). RESULTS: There was statistically significant difference between TNF-alpha levels of patient and controls (p=0.048). We have not detected the connection between TGF-beta, TNF-alpha, ACE, eNOS gene polymorphism with serum TNF-alpha and adiponectin levels. In this study, we demonstrated that there were significant differences for ACE genotypes in the patients when compared to the controls (p<0.05). The percentages of the ID, DD, II genotypes for ACE gene polymorphism in the patients group were 30.0, 13.0, 7.0%, respectively. CONCLUSIONS: According to different cases of eNOS, TGF-beta, ACE, and TNF-alpha gene genotypes; no statistical significant difference was found between basal cortisol, ACTH, DHEAS, metanephrine, renin, aldosterone, normetanephrine, 17-hydroxyprogesterone, 1 mg low-dose dexamethasone suppression test-cortisol response and AI size. In this study, I/D genotype was determined to be statistically higher in ACE gene in patients with AI (p=0.014).

Dose-response of inhaled diltiazem on airway reactivity to methacholine and exercise in subjects with mild asthma.

Methacholine challenges were performed by 10 asthmatic subjects, 2 hours before and 15 minutes after placebo (diluent alone) and 5, 10, 15, 30, and 60 mg inhaled diltiazem given in a single-blind crossover manner. There was no significant change from placebo in the dose of methacholine required to produce a 20% decrease in forced expiratory volume in the first second (FEV1) (PD20); the fold increase in PD20 from baseline was 1.1 +/- 0.1 after placebo, 1.4 +/- 0.2 after 5 mg, 1.8 +/- 0.3 after 10 mg, 1.4 +/- 0.2 after 15 mg, 1.6 +/- 0.2 after 30 mg, and 1.2 +/- 0.1 after 60 mg. There was a 1% chance that we missed a twofold difference between placebo and the 10 mg dose because of inadequate sample size. Fifteen minutes before a standardized exercise challenge, 10 subjects received placebo, 10 mg, and the highest dose tolerated during the methacholine study (20 to 45 mg) in a randomized double-blind crossover design. The mean +/- SE maximum postexercise decrease in FEV1 was 28.8% +/- 5.7% after placebo, 23.4% +/- 4.6% after 10 mg, and 20.8% +/- 3.0% after high-dose diltiazem (P greater than 0.05). There was a 12% chance that we missed a 15% difference between placebo and the high-dose regimen because of inadequate sample size. We conclude that diltiazem does not attenuate airway reactivity to methacholine or exercise even when high concentrations are delivered to the lungs.

Natural history and course of acquired lactic acidosis in adults. DCA-Lactic Acidosis Study Group.

STUDY OBJECTIVE: To determine the pathogenesis and clinical course of lactic acidosis in adults receiving standard medical care. DESIGN: Placebo arm of a 5-year prospective, randomized, blinded study comparing placebo and dichloroacetate as specific lactate-lowering therapy. Each patient received intravenous saline placebo in addition to conventional therapy. SETTING: Intensive care units of 10 tertiary care hospitals in North America. PATIENTS: One hundred twenty-six patients with lactic acidosis, defined as arterial blood lactate greater than or equal to 5 mmol/L and either arterial pH of less than or equal to 7.35 or base deficit greater than 6 mmol/L. Patients were followed for up to 6 months. MEASUREMENTS AND MAIN RESULTS: Mean +/- SD demographic entry data for 126 patients included: age 56 +/- 17 years, lactate 10.4 +/- 5.5 mmol/L, pH 7.24 +/- 0.14, calculated base deficit 14.1 +/- 5.4, arterial systolic blood pressure 103 +/- 29 mm Hg, Glasgow Coma score 7.9 +/- 4.9, and APACHE II score 19.2 +/- 8.1. Despite fluids and pressors, 32% of patients had systolic blood pressures of less than or equal to 90 mm Hg in association with sepsis (59%), cardiac failure (18%), or hemorrhage (18%). The most common causes of lactic acidosis in the absence of shock were sepsis (49%), liver disease (15%), and respiratory failure (12%). The median survival was 38.5 hours. Survival at 24 hours was 59%. Arterial pH predicted 24-hour survival better than base deficit or bicarbonate level. Percent survival was 41% at 3 days and 17% at 30 days. Only 21% of patients survived to leave the intensive care unit, and 17% were discharged from the hospital. In patients receiving sodium bicarbonate, neither acid-base nor hemodynamic status improved. CONCLUSIONS: In this first prospective study of the clinical course of acute lactic acidosis in adults, nearly all subjects had both hemodynamic and nonhemodynamic (metabolic) underlying causes, many of which independently predicted survival and most of which were refractory to standard care.

Clinical relevance of the interaction of theophylline with diltiazem or nifedipine.

The results of previously published studies indicate that calcium channel blockers are capable of competitively inhibiting cytochrome P-450 activity in hepatic microsomes, the pathway of theophylline metabolism. In addition, case reports have suggested that theophylline serum concentrations change when a calcium channel blocker has been added to or deleted from a stable theophylline regimen. To determine the clinical relevance of this potential interaction in patients with chronic asthma, we measured a peak steady-state theophylline serum concentration in 21 subjects while receiving theophylline alone (400 to 1,500 mg/day), and again, at least seven days later, after the addition of continuous therapy with maximally tolerated doses of either diltiazem (n = 18) or nifedipine (n = 16). The diltiazem dose was increased in 120 mg/day increments, as tolerated, to a maximum of 240 to 480 mg/day, while the nifedipine dose was increased in increments of 40 mg/day, to a maximum dose of 80 to 160 mg/day. The mean +/- SEM theophylline serum concentrations were 13.6 +/- 1.4 micrograms/ml before and 14.0 +/- 1.2 micrograms/ml during concurrent diltiazem therapy, and 12.6 +/- 1.0 micrograms/ml before and 12.2 +/- 1.1 micrograms/ml during nifedipine (p greater than 0.05). With this sample size there is a 5 percent chance that we missed a 20 percent change in serum concentration (type II error). Thus, maximum tolerated doses of diltiazem or nifedipine do not impair the metabolism of theophylline to a clinically relevant degree and adjustment of theophylline dosage is not required after the addition or discontinuation of diltiazem or nifedipine. In addition, these data suggest that currently available in vitro techniques for evaluating drug interactions in the hepatocyte do not predict the clinical relevance of such an interaction in patients who might require both drugs for different therapeutic indications.

Rapid mucosal absorption of topical lidocaine during bronchoscopy in the presence of oral candidiasis.

Local anesthetic agents are topically applied during diagnostic procedures such as bronchoscopy. These routine procedures are associated with only rare reports of drug toxicity or extensive systemic drug absorption. We report a case of rapid systemic absorption and elevated plasma lidocaine concentrations following a fiberoptic bronchoscopy procedure in a man with oral candidiasis and lung cancer.

Complete remission of pulmonary spindle cell carcinoma after treatment with oral germanium sesquioxide.

Spindle cell carcinoma (SCC) is a rare form of lung cancer representing 0.2 to 0.3% of all primary pulmonary malignancies. Even with combined surgery, chemotherapy, and radiation therapy, these tumors are associated with a poor prognosis and only 10% of patients survive 2 years after diagnosis. We describe a patient with an unresectable SCC who, following no response to conventional treatment with combined modality therapy, chose to medicate herself with daily doses of germanium obtained in a health food store. She noted prompt symptomatic improvement and remains clinically and radiographically free of disease 42 months after starting her alternative therapy.

Inhaled verapamil-induced bronchoconstriction in mild asthma.

Methacholine challenges were performed in ten subjects with mild asthma at 2 h before and 20 min after placebo or 5, 10, 20, 40, 80, and 160 mg of inhaled verapamil given in a single-blind randomized crossover manner on different days. While verapamil did not have a bronchodilator effect, the 10-mg dose modestly increased the concentration of methacholine required to decrease FEV1 by 20 percent (PC20). The mean (+/- SEM) increase in PC20 from baseline was 2.1 +/- 0.2 times baseline after 10 mg of verapamil, compared to 1.1 +/- 0.1 times baseline after placebo (p less than 0.001). Unexpectedly, bronchoconstriction (greater than 10 percent decrease in FEV1) associated with cough or wheezing was observed in seven of ten subjects at doses of 20 mg or more. This adverse effect was not related to the osmolarity of the nebulized solutions. Thirty minutes before a standardized exercise challenge, 13 subjects inhaled placebo, 10 mg, or the highest dose of verapamil tolerated during the methacholine study (20 to 160 mg) in a double-blind randomized crossover manner. The exercise challenge was aborted in three subjects because of bronchospasm that occurred after administration of the higher dose. The mean (+/- SEM) maximum change in FEV1 after exercise in the ten subjects completing all three regimens of treatment was -17.1 +/- 4.0 percent after placebo, -12.7 +/- 4.3 percent after 10 mg (p less than 0.05), and -6.4 +/- 3.6 percent after the highest dose (p less than 0.05). We conclude that increasing the dose of verapamil above 10 mg did not provide greater benefit but, paradoxically, induced bronchoconstriction in most of the subjects. Because of this potential bronchoconstrictor effect, high doses of oral or intravenous verapamil should be used with caution in asthmatic subjects.

Relative amount of albuterol delivered to lung receptors from a metered-dose inhaler and nebulizer solution. Bioassay by histamine bronchoprovocation.

The results of previous studies comparing bronchodilatation from beta agonists administered by metered-dose inhaler (MDI) and nebulizer solution have been conflicting. We therefore evaluated a range of albuterol doses administered by these two methods, using histamine bronchoprovocation as a bioassay for the amount of drug reaching the beta 2 receptors in the lung. Twelve stable asthmatic volunteers received, in a double-blind, randomized, crossover design on different days, placebo or one, two, four, or six puffs from an MDI attached to an InspirEase device (90 micrograms per puff) or 0.625, 1.25, 2.5, or 5.0 mg of solution delivered in 2 ml of buffered saline through a Hudson Updraft II nebulizer. The histamine concentration required to decrease FEV1 by 20 percent (PC20) was measured 1 h before and 30 min after administration of each treatment and expressed as the increase in PC20 from baseline. The dose-response curves for change in PC20 indicated that the higher doses of the nebulizer solution delivered more drug to beta 2 receptors in the lung than the lower doses from the MDI. For example, the geometric mean increase in PC20 was 1.1 +/- 1.6 (SD) after placebo, 7.5 +/- 2.7 after two puffs from the MDI, and 20.0 +/- 2.1 after 2.5 mg of nebulizer solution (p less than 0.05). Using this bioassay method and administration technique, we estimated that ten puffs from the MDI (0.9 mg) would deliver approximately the same amount of albuterol to lung receptors as 2.5 mg of the nebulizer solution. Taking into account previously published reports and the results of the present study, we conclude that differences in dose, administration technique, nebulizer system efficiency, and severity of airway obstruction can alter the amount of drug reaching the beta 2 receptors in the lungs and, thus, the clinical response.

The effect of weight loss on sleep-disordered breathing and oxygen desaturation in morbidly obese men.

Four morbidly obese men who had been found to have significant sleep-disordered breathing and oxygen desaturation were restudied after an average weight loss of 108 kg (range 53-155 kg). In all subjects, weight loss was accompanied by a significant reduction in the number of episodes per hour of sleep-disordered breathing events. In three of the four subjects, there was improvment in the severity of desaturation accompanying abnormal breathing. The two subjects with daytime somnolence and hypercapnia prior to weight loss showed the most dramatic improvement in desaturation. This suggests that obesity is a cause, rather than an effect, of the sleep apnea syndrome.

Sleep-disordered breathing and oxygen desaturation in obese patients.

Fourteen morbidly obese subjects, referred to our institution for bypass surgery for obesity, were studied with regard to pulmonary function and respiratory patterns during sleep. The seven female patients experienced no episodes of desaturation or disordered breathing during sleep. Six of the seven male patients experienced desaturation or disordered breathing. The one who did not had hypogonadism, suggesting that testosterone may have a role in the regulation of breathing during sleep. The two patients with the most frequent episodes of apnea and lowest oxygen saturation had a clinical picture consistent with the pickwickian syndrome. This supports the relationship previously noted between the degree of hypoxia and the presence of hypersomnolence.

Miliary tuberculosis presenting as acute respiratory failure: treatment by membrane oxygenator and ventricle pump.

A 58-year-old woman with high fever, dyspnea, rapidly progressive hypoxemia and opacification of the lung fields presented the clinical picture of catastrophic respiratory failure. Extracorporeal support of oxygenation using a membrane oxygenator and a new ventricle pump was initially successful. At autopsy, miliary tuberculosis was found to be the cause of this "shock lung like" syndrome.

Evaluation of the asthmogenicity of propafenone, a new antiarrhythmic drug. Comparison of spirometry with methacholine challenge.

Propafenone is a new membrane-stabilizing antiarrhythmic agent that structurally resembles the beta-adrenergic receptor antagonist, propranolol. To determine the potential asthmogenicity of this new drug, pulmonary function, airway reactivity to methacholine, blood pressure, the electrocardiogram, and plasma concentrations were measured in 12 patients with mild intermittent asthma after 48 to 72 hours of treatment with placebo and with oral propafenone in low dosage (150 mg every eight hours) and high dosage (300 mg every eight hours) in a double-blind crossover manner. The forced vital capacity (FVC), forced expiratory volume in one second (FEV1), forced expiratory flow over the middle half of the FVC (FEF25-75%), heart rate, and blood pressure during the three regimens of treatment were not significantly different; however, the QRS interval on the ECG was significantly widened with both dosages of active drug, and the mean provocative dose of methacholine (+/- SE) required to reduce FEV1 by 20 percent (PD20) decreased from 3.0 +/- 0.6 mg/ml with placebo to 2.1 +/- 0.7 mg/ml with the high dosage of propafenone (p less than 0.01). The mean PD20 on the low-dose regimen was not significantly different from placebo or high-dose therapy. A potentially relevant increase in airway reactivity, as measured by a ratio of less than 0.5 for PD20 after treatment to PD20 after placebo, occurred in seven subjects with high-dose and in one subject during low-dose treatment (p less than 0.01). These data suggest that propafenone should be used with caution in patients with asthma and that bronchial provocation will provide a more sensitive measure of the asthmogenicity of a drug with beta-adrenergic receptor antagonist activity than pulmonary function tests. Moreover, use of bronchial provocation allows the selection of subjects with mild disease, thus reducing the risk of potentially severe bronchospasm.

FDG SPECT in patients with lung masses.

STUDY OBJECTIVES: To determine whether 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG) single-photon emission CT (SPECT) is useful in characterizing pulmonary masses. DESIGN: Scans were prospectively acquired and interpreted. Interpretations were performed with CT or chest radiograph but interpreters were blinded to eventual diagnosis. SETTING: University hospital practice and affiliated Veterans Administration medical center. PATIENTS OR PARTICIPANTS: Forty patients participated as part of an institutional review board-approved research protocol, and informed consent was obtained in all. Eight additional patient scans were acquired as part of their clinical evaluation for pulmonary mass. MEASUREMENTS AND RESULTS: There were 26 malignant lesions (12 were 1 to 2 cm in size, the rest were larger) and 17 benign lesions (3 were < 1 cm in size, 9 were 1 to 2 cm in size, and 5 were larger). Averaged sensitivity, specificity, positive predictive value, and negative predictive value were, respectively, 50% (12 of 24), 94% (17 of 18), 92% (12 of 13), and 59% (17 of 29) for lesions 1 to 2 cm in size, 100% (28 of 28), 90% (9 of 10), 97% (28 of 29), and 100% (9 of 9) for lesions > 2 cm in size. There was good correlation between readers (p < 0.0001). CONCLUSION: FDG SPECT is useful in characterizing pulmonary masses > 2 cm in size and appears to be equivalent to positron emission tomography for these lesions. Although currently clinically suboptimal for characterizing lesions < or = 2 cm in size, FDG SPECT appears to be better than current anatomic imaging methods. In addition, the positive predictive value of FDG SPECT for small lesions is also high (92%), and this technique appears potentially useful in the subset of patients in whom a positive result would alter clinical diagnostic pathways or care.

Automated data collection and processing for a cycle ergometer.

A system is described for collection and processing of data from a cycle ergometer. Cycle pedals, specially made to withstand the extremely high forces exerted during maximal power cycling, contain transducers to measure pedal angle relative to the crank and foot forces both perpendicular and parallel to the pedal surface. An additional transducer monitors crank position. Output signals are conditioned, amplified, digitized by a 12-bit analog-to-digital converter, fed into a computer at 100 Hz/channel, and mathematically smoothed to attenuate noise. For each sample interval, foot force components perpendicular and parallel to the crank arm are calculated. Power generated on each crank revolution is determined from transducer information. Computer graphics display pedaling parameters vs. crank angle in both rectangular and circular format. Data files containing variables descriptive of pedaling force curves are produced to enable computerized statistical analysis of cycling performance.

Regional body composition changes in women after 6 months of periodized physical training.

Data are lacking regarding regional morphological changes among women after prolonged physical training. This study employed dual-energy X-ray absorptiometry to assess changes in whole body and regional (i.e., trunk, legs, arms) fat mass, lean mass, and bone mineral content body composition adaptations in 31 healthy women pre-, mid-, and post-6 mo of periodized physical training. These results were compared with those of 1) a control group of women who had not undergone the training program and were assessed pre- and post-6 mo and 2) a group of 18 men that was tested only once. Additionally, magnetic resonance imaging was used to assess changes in muscle morphology of the thigh in a subset of 11 members of the training group. Physical training consisted of a combination of aerobic and resistance exercise in which the subjects engaged for 5 days/wk for 24 wk. Overall, the training group experienced a 2.2% decrease, a 10% decrease, and a 2.2% increase for body mass, fat mass, and soft tissue lean mass, respectively. No changes in bone mineral content were detected. The women had less of their soft tissue lean mass distributed in their arms than did the men, both before and after the women were trained. Novel to this study were the striking differences in the responses in the tissue composition of the arms (31% loss in fat mass but no change in lean mass) compared with the legs (5.5% gain in lean mass but no change in fat mass). There was a 12% fat loss in the trunk with no change in soft tissue lean mass. Dual-energy X-ray absorptiometry and magnetic resonance imaging fat mass measurements showed good agreement (r = 0. 72-0.92); their lean mass measurements were similar as well, showing approximately 5.5% increases in leg lean tissue. These findings show the importance of considering regional body composition changes, rather than whole body changes alone when assessing the effects of a periodized physical training program.

Hormonal and growth factor responses to heavy resistance exercise protocols.

To examine endogenous anabolic hormone and growth factor responses to various heavy resistance exercise protocols (HREPs), nine male subjects performed each of six randomly assigned HREPs, which consisted of identically ordered exercises carefully designed to control for load [5 vs. 10 repetitions maximum (RM)], rest period length (1 vs. 3 min), and total work effects. Serum human growth hormone (hGH), testosterone (T), somatomedin-C (SM-C), glucose, and whole blood lactate (HLa) concentrations were determined preexercise, midexercise (i.e., after 4 of 8 exercises), and at 0, 5, 15, 30, 60, 90, and 120 min postexercise. All HREPs produced significant (P less than 0.05) temporal increases in serum T concentrations, although the magnitude and time point of occurrence above resting values varied across HREPs. No differences were observed for T when integrated areas under the curve (AUCs) were compared. Although not all HREPs produced increases in serum hGH, the highest responses were observed consequent to the H10/1 exercise protocol (high total work, 1 min rest, 10-RM load) for both temporal and time integrated (AUC) responses. The pattern of SM-C increases varied among HREPs and did not consistently follow hGH changes. Whereas temporal changes were observed, no integrated time (AUC) differences between exercise protocols occurred. These data indicate that the release patterns (temporal or time integrated) observed are complex functions of the type of HREPs utilized and the physiological mechanisms involved with determining peripheral circulatory concentrations (e.g., clearance rates, transport, receptor binding). All HREPs may not affect muscle and connective tissue growth in the same manner because of possible differences in hormonal and growth factor release.

Quantitation of progressive muscle fatigue during dynamic leg exercise in humans.

There is virtually no published information on muscle fatigue, defined as a gradual decline in force-generating capacity, during conventional dynamic (D) leg exercise. To quantitate progression of fatigue, we developed 1) a model featuring integration of maximal voluntary static contraction (MVC) of knee extension (KE) muscles with ongoing DKE and 2) a device that allows frequent rapid transfer between DKE isolated to the quadriceps femoris muscles and measurement of KE MVC. Eight healthy men performed graded and submaximal constant work rate one-leg DKE to exhaustion while seated. Work rate, a product of a contraction rate (1 Hz), force measured at the ankle, and distance of ankle movement from 90 degrees to 150 degrees of KE, was precisely controlled. Lack of rise in myoelectric activity in biceps femoris of the active leg during DKE and MVC was consistent with restriction of muscle action to quadriceps femoris. The slope of the linear relationship between O2 uptake and work rate was 13.7 ml O2/W (r = 0.93). This slope and the increase of heart rate relative to increasing work intensity agreed with published values for D leg exercise. Test-retest values for O2 uptake were similar (P > 0.05) for matched DKE work rates. To track fatigue, MVC (90 degrees knee angle) was performed every 2 min of DKE. After 4 min of DKE at work rates corresponding to (mean +/- SE) 66 +/- 2, 78 +/- 2, and 100% of peak DKE O2 uptake, MVC fell to 95 +/- 3, 90 +/- 5, and 65 +/- 7%* of MVC of rested muscle, respectively (*P < 0.01 from previous work rates). Virtually identical declines in MVC were observed by the end of graded work rate DKE and submaximal constant work rate DKE tests. Quantitation of progressive muscle fatigue during D leg exercise provides a framework to study the effects of a variety of interventions on the fatigue process and may permit unique insights into the involved mechanisms.

Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia.

Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 +/- 3 W, 79 +/- 2 and 87 +/- 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90-150 degrees at a rate of 1 Hz. MVC (90 degrees knee angle) was performed before dynamic exercise and during < or = 5-s pauses every 2 min of dynamic exercise. MVC force was 578 +/- 29 N in normoxia and 569 +/- 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 +/- 10 and 284 +/- 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher (P < 0.01) than peak force of constant work rate knee extension (98 +/- 10 N, 18 +/- 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 +/- 5 vs. 43 +/- 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = -22.3 vs. -11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to related more closely to impaired shortening velocity than to failure of force-generating capacity.

Hypothalamic-pituitary-adrenal responses to short-duration high-intensity cycle exercise.

beta-Endorphin (beta-EP), adrenocorticotropin (ACTH), and cortisol plasma concentrations were examined before and after maximal exercise at four intensities [36, 55, 73, and 100% of maximal leg power (MLP)] by means of a computerized cycle ergometer. All intensities were greater than those eliciting peak O2 uptake for the individual subjects. Blood samples were collected at rest, immediately after exercise, and at 5 and 15 min postexercise. Significant (P less than 0.05) increases were observed at 36% MLP for beta-EP and ACTH immediately after exercise and at 5 and 15 min postexercise. Plasma cortisol increased at 36% MLP at 15 min postexercise. Blood lactate significantly increased at all postexercise collection points for exercise intensities of 36, 55, and 73% MLP and at 5 min postexercise for 100% MLP. beta-EP concentrations at 36% MLP were significantly correlated (r = 0.75) with capillary density (mm-2), and cortisol concentrations at 36% MLP were significantly correlated (r = 0.89) with percentage of type II muscle fibers. No other significant relationships were observed. These data show that brief, high-intensity exercise up to maximal power production results in a nonlinear response pattern in peripheral blood hormone concentrations. Furthermore, blood lactate levels do not appear to be related to hypothalamic-pituitary-adrenal hormone plasma concentrations at high exercise intensities.

Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations.

Thirty-five healthy men were matched and randomly assigned to one of four training groups that performed high-intensity strength and endurance training (C; n = 9), upper body only high-intensity strength and endurance training (UC; n = 9), high-intensity endurance training (E; n = 8), or high-intensity strength training (ST; n = 9). The C and ST groups significantly increased one-repetition maximum strength for all exercises (P < 0.05). Only the C, UC, and E groups demonstrated significant increases in treadmill maximal oxygen consumption. The ST group showed significant increases in power output. Hormonal responses to treadmill exercise demonstrated a differential response to the different training programs, indicating that the underlying physiological milieu differed with the training program. Significant changes in muscle fiber areas were as follows: types I, IIa, and IIc increased in the ST group; types I and IIc decreased in the E group; type IIa increased in the C group; and there were no changes in the UC group. Significant shifts in percentage from type IIb to type IIa were observed in all training groups, with the greatest shift in the groups in which resistance trained the thigh musculature. This investigation indicates that the combination of strength and endurance training results in an attenuation of the performance improvements and physiological adaptations typical of single-mode training.