Nitric oxide and neurally mediated regulation of skin blood flow during local heating.

The mechanisms underlying the skin blood flow (SkBF) response to local heating are complex and poorly understood. Our goal was to examine the role of axon reflexes and nitric oxide (NO) in the SkBF response to a local heating protocol. We performed 40 experiments following a standardized heating protocol with different interventions, including blockade of the axon reflex (EMLA cream), antebrachial nerve blockade (0.5% bupivacaine injection), and NO synthase (NOS) inhibition (> or =10 mM N(G)-nitro-L-arginine methyl ester; microdialysis). Appropriate controls were performed to verify the efficacy of the various blocks. Values are expressed as a percentage of maximal SkBF (SkBF(max); 50 mM sodium nitroprusside). At the initiation of local heating, SkBF rose to an initial peak, followed by a brief nadir, and a secondary, progressive rise to a plateau. Axon reflex block decreased the initial peak from 75+3 to 32 +/- 2% SkBF(max) (P < 0.01 vs. control) but did not affect the plateau. NOS inhibition before and throughout local heating reduced the initial peak from 75 +/- 3 to 56 +/- 3% SkBF(max) (P < 0.01) and the plateau from 87 +/- 4 to 40 +/- 5%. NOS inhibition during axon reflex block did not further reduce the initial SkBF peak compared with axon reflex block alone. Antebrachial nerve block did not affect the local heating SkBF response. The primary finding of these studies is that there are at least two independent mechanisms contributing to the rise in SkBF during nonpainful local heating: a fast-responding vasodilator system mediated by the axon reflexes and a more slowly responding vasodilator system that relies on local production of NO.     

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function.

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca(2+) cycling and whether alterations in SR Ca(2+) cycling are related to the blunted peak mechanical power output (PO(peak)) and peak oxygen consumption (Vo(2 peak)) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 +/- 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of Vo(2 peak) (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca(2+)-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) PO(peak) and Vo(2 peak), respectively. During progressive exercise in N, Ca(2+)-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca(2+) concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca(2+) uptake (before exercise = 357 +/- 29 micromol x min(-1) x g protein(-1); at fatigue = 306 +/- 26 micromol x min(-1) x g protein(-1); P < 0.05) when measured at free Ca(2+) concentration of 2 microM and in phase 2 Ca(2+) release (before exercise = 716 +/- 33 micromol x min(-1) x g protein(-1); at fatigue = 500 +/- 53 micromol x min(-1) x g protein(-1); P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca(2+)-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO(peak) and Vo(2 peak) observed during H.     

Acute hypothyroidism slows the rate of left ventricular diastolic relaxation

The effect of acute thyroid hormone deficiency on left ventricular diastolic filling was studied by radionuclide ventriculography with simultaneous right heart catheterization in nine athyreotic patients without cardiovascular disease. The patients were studied when they were hypothyroid and when they were euthyroid on replacement therapy. Peak filling rate and the time to peak filling were used to characterize diastolic function. The time to peak filling was defined as the interval from end-systole on the radionuclide time-volume curve to the time of occurrence of peak filling. The peak filling rate was determined in absolute terms from the normalized radionuclide peak filling rate and from the end-diastolic volume, which was derived from the radionuclide ejection fraction and from the thermodilution stroke volume. In all patients, the values for peak filling rate were lower in the hypothyroid than in the euthyroid state (287 +/- 91 mL/s vs. 400 +/- 118 mL/s, delta = 41 +/- 13%, p less than 0.01). Peak filling always occurred during the first half of the diastolic interval. The time to peak filling was not significantly affected by the thyroid state (170 +/- 10 ms vs. 159 +/- 21 ms, delta = 7 +/- 10%). Left ventricular filling pressure as reflected by the pulmonary capillary wedge pressure and end-systolic volume were similar in both thyroid states (6 +/- 2 mmHg vs. 8 +/- 2 mmHg (1 mmHg = 133.32 Pa) and 32 +/- 11 mL vs. 32 +/- 7 mL, respectively). The data suggest that the rate of active diastolic relaxation is decreased in short-duration hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Isotopic evidence for breastfeeding and possible adult dietary differences from Late/Sub-Roman Britain

Historical documents indicate that breastfeeding and weaning practices have fluctuated in England through history. In order to obtain evidence for general breastfeeding patterns in Late/Sub-Roman Britain, stable carbon and nitrogen isotope values were measured in juvenile and adult skeletons (n = 87) from the cemetery of Queenford Farm, Dorchester-on-Thames, Oxfordshire. As the site contained few individuals between 0-1.5 years of age, it was not possible to determine the initial timing for the introduction of weaning foods. Between ages 2-4 years, the mean +/- SD delta(13)C results (-20.2 +/- 0.3 per thousand) are significantly more negative (t = -4.03, P < 0.001) compared to adult females (-19.7 +/- 0.3 per thousand). This is interpreted as evidence of a different diet being fed to children during weaning. After age 2, the delta(15)N values gradually decline, indicating complete cessation of breastfeeding by 3-4 years. Among adults, stature (males = 1.68 +/- 0.06 m; females = 1.58 +/- 0.07 m) and sexual dimorphism (106) were low, suggesting that the population was possibly under environmental stress. The delta(13)C results for adults are similar, but females show a small but statistically significantly (t = -2.86, P < 0.01) lower mean delta(15)N value (9.9 +/- 0.9 per thousand) compared to males (10.6 +/- 0.5 per thousand). These lower female delta(15)N values possibly reflect the different physiology of the sexes (pregnancy and/or lactation) or the reduced consumption of animal/fish protein by women, and this may have been influenced by individual preference, family needs, or societal values of the era.     

Effects of elastase-induced emphysema on airway responsiveness to methacholine in rats

We examined the effects of elastase-induced emphysema on lung volumes, pulmonary mechanics, and airway responses to inhaled methacholine (MCh) of nine male Brown Norway rats. Measurements were made before and weekly for 4 wk after elastase in five rats. In four rats measurements were made before and at 3 wk after elastase; in these same animals the effects of changes in end-expiratory lung volume on the airway responses to MCh were evaluated before and after elastase. Airway responses were determined from peak pulmonary resistance (RL) calculated after 30-s aerosolizations of saline and doubling concentrations of MCh from 1 to 64 mg/ml. Porcine pancreatic elastase (1 IU/g) was administered intratracheally. Before elastase RL rose from 0.20 +/- 0.02 cmH2O.ml-1.s (mean +/- SE; n = 9) to 0.57 +/- 0.06 after MCh (64 mg/ml). A plateau was observed in the concentration-response curve. Static compliance and the maximum increase in RL (delta RL64) were significantly correlated (r = 0.799, P less than 0.01). Three weeks after elastase the maximal airway response to MCh was enhanced and no plateau was observed; delta RL64 was 0.78 +/- 0.07 cmH2O.ml-1.s, significantly higher than control delta RL64 (0.36 +/- 0.7, P less than 0.05). Before elastase, increase of end-expiratory lung volume to functional residual capacity + 1.56 ml (+/- 0.08 ml) significantly reduced RL at 64 mg MCh/ml from 0.62 +/- 0.05 cmH2O.ml-1.s to 0.50 +/- 0.03, P less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adrenal androgens in children with short stature

Recent data suggest that adolescent individuals with growth hormone (GH) deficiency have subnormal levels of adrenal androgens (AA). In order to determine the developmental pattern of AA in GH deficiency and to assess whether AA levels can help identify children with GH deficiency, we measured plasma concentrations of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), delta 4-androstenedione (delta 4A), and cortisol in the basal state and during prolonged adrenocorticotropin (ACTH) infusion (8 h) in a group of 34 individuals, 26 males and 8 females, with short stature. Their chronological ages (CA) ranged from 1.75 to 17.5 years (median 10.35 years). The subjects were grouped into two categories according to the results of pituitary testing: group 1 = short, non-GH-deficient (n = 16), and group 2 = GH-deficient, ACTH-sufficient (n = 18). Patients in groups 1 and 2 had similar bone ages (BA: 7.2 +/- 0.7 vs. 7.5 +/- 1.0 years) and Z scores for height (-3.0 +/- 0.2 vs. -3.2 +/- 0.3 units) and height velocity (-2.5 +/- 0.4 vs. -2.6 +/- 0.2 units). For both groups there were significant increases from basal to peak levels for DHEA, DHEA-S, delta 4A and cortisol following prolonged ACTH infusion. Although both basal and peak levels of DHEA-S overlapped in groups 1 and 2 for all CA and BA, levels in group 2 tended to be lower, especially for BA greater than 10 years.(ABSTRACT TRUNCATED AT 250 WORDS)     

The amplitude and time course of the myoplasmic free [Ca2+] transient in fast-twitch fibers of mouse muscle

Bundles of 10-100 fibers were dissected from the extensor digitorum longus muscle of mouse, mounted in an apparatus for optical recording, and stretched to long sarcomere length (> or = 3.6 microns). One fiber within the bundle was microinjected with furaptra, a fluorescent indicator that responds rapidly to changes in myoplasmic free [Ca2+] (delta [Ca2+]). Twitches and brief tetani were initiated by external stimulation. At myoplasmic furaptra concentrations of approximately 0.1 mM, the indicator's fluorescence signal during fiber activity (delta F/F) was well resolved. delta F/F was converted to delta [Ca2+] under the assumption that furaptra's myoplasmic dissociation constant for Ca2+ is 98 microM at 16 degrees C and 109 microM at 28 degrees C. At 16 degrees C, the peak amplitude of delta [Ca2+] during a twitch was 17.8 +/- 0.4 microM (+/-SEM; n = 8) and the half-width of delta [Ca2+] was 4.6 +/- 0.3 ms. At 28 degrees C, the peak and half-width values were 22.1 +/- 1.8 microM and 2.0 +/- 0.1 ms, respectively (n = 4). During a brief high-frequency tetanus, individual peaks of delta [Ca2+] were also well resolved and reached approximately the same amplitude that resulted from a single shock; the initial decays of delta [Ca2+] from peak slowed substantially during the tetanus. For a single twitch at 16 degrees C, the amplitude of delta [Ca2+] in fast-twitch fibers of mouse is not significantly different from that recently measured in fast- twitch fibers of frog (16.5 +/- 0.9 microM; Zhao, M., S. Hollingworth, and S.M. Baylor. 1996. Biophys. J. 70:896-916); in contrast, the half- width of delta [Ca2+] is surprisingly brief in mouse fibers, only about half that measured in frog (9.6 +/- 0.6 ms). The estimated peak rate at which Ca2+ is released from the sarcoplasmic reticulum in response to an action potential is also similar in mouse and frog, 140-150 microM/ms (16 degrees C).     

Human temperature regulation during narcosis induced by inhalation of 30% nitrous oxide.

The study investigated the effect of inhalation of 30% nitrous oxide (N2O) on temperature regulation in humans. Seven male subjects were immersed to the neck in 28 degrees C water on two separate occasions. They exercised at a rate equivalent to 50% of their maximum work rate on an underwater cycle ergometer for 20 min and remained immersed for an additional 100 min after the exercise. In one trial (AIR) the subjects inspired compressed air, and in the other trial (N2O) they inspired a gas mixture containing N2O (20.93% O2-30% N2O-49.07% N2). Sweating, measured at the forehead, and shivering thermogenesis, as reflected by O2 uptake, were monitored throughout the 100-min recovery period. The threshold core temperatures at which sweating was extinguished and shivering was initiated were established relative to resting preexercise levels. Neither the magnitude of the sweating response nor the core threshold at which it was extinguished was significantly affected by the inhalation of N2O. In contrast, shivering thermogenesis was both significantly reduced during the N2O condition and initiated at significantly lower core temperatures [change in esophageal temperature (delta T(es)) = -0.98 +/- 0.33 degrees C and change in rectal temperature (delta T(re)) = -1.26 degrees C] during the N2O than during the AIR condition (delta T(es) = -0.36 +/- 0.31 degrees C and delta T(re) = -0.44 +/- 0.22 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)     

Decreased nitric oxide- and axon reflex-mediated cutaneous vasodilation with age during local heating.

Cutaneous vasodilation is reduced in healthy older vs. young subjects; however, the mechanisms that underlie these age-related changes are unclear. Our goal in the present study was to determine the role of nitric oxide (NO) and the axon reflexes in the skin blood flow (SkBF) response to local heating with advanced age. We placed two microdialysis fibers in the forearm skin of 10 young (Y; 22 +/- 2 yr) and 10 older (O; 77 +/- 5 yr) men and women. SkBF over each site was measured by laser-Doppler flowmetry (LDF; Moor DRT4). Both sites were heated to 42 degrees C for ~60 min while 10 mM N(G)-nitro-L-arginine methyl ester (L-NAME) was infused throughout the protocol to inhibit NO synthase (NOS) in one site and 10 mM L-NAME was infused after 40 min of local heating in the second site. Data were expressed as a percentage of maximal vasodilation (%CVC(max); 28 mM nitroprusside infusion). Local heating before L-NAME infusion resulted in a significantly reduced initial peak (Y: 61 +/- 2%CVC(max) vs. O: 46 +/- 4%CVC(max)) and plateau (Y: 93 +/- 2%CVC(max) vs. O: 82 +/- 5%CVC(max)) CVC values in older subjects (P < 0.05). When NOS was inhibited after 40 min of heating, CVC declined to the same value in the young and older groups. Thus the overall contribution of NO to the plateau phase of the SkBF response to local heating was less in the older subjects. The initial peak response was significantly lower in the older subjects in both microdialysis sites (Y: 52 +/- 4%CVC(max) vs. O: 38 +/- 5%CVCmax; P < 0.05). These data suggest that age-related changes in both axon reflex-mediated and NO-mediated vasodilation contribute to attenuated cutaneous vasodilator responses in the elderly.     

Force-time curve characteristics and hormonal alterations during an eleven-week training period in elite women weightlifters

The purpose of this investigation was to study the effects of an 11-week training period performed by female weightlifters. Two weeks before this investigation, baseline measures for total testosterone, cortisol, and testosterone:cortisol ratio were collected. The 11-week training program consisted of the core exercises (i.e., clean, clean and jerk, and snatch) and other supplemental exercises (i.e., clean pull, snatch pull, squat, and front squat). Hormonal, isometric, and dynamic middle thigh pull force-time curve characteristics were assessed biweekly throughout the duration of the investigation, whereas volume load and training intensity were assessed weekly throughout the investigation. The testosterone:cortisol ratio of the baseline (1.19 +/- 0.64) was significantly different from the ratio of weeks 1 (0.67 +/- 0.36) and 9 (0.94 +/- 0.66). When the week-to-week values were compared, week 1 (0.67 +/- 0.36) was significantly different (P < 0.05; eta = 0.84) from week 3 (1.06 +/- 0.54). A very strong correlation (r = -0.83; r = 0.69) was found between the percentage change of the testosterone:cortisol ratio and volume load from weeks 1 to 11. Moderate to very strong correlations were noted between the percentage change in volume load and isometric peak force, peak force during the 30% isometric peak force trial, and peak force during the 100-kg trial during the 11 weeks of training. The primary finding of this study was that alterations in training volume load can result in concomitant changes in the anabolic-to-catabolic balance, as indicated by the testosterone:cortisol ratio, and the ability to generate maximal forces.     

Neuronal application of capsaicin modulates somatic pressor reflexes

Static contraction of skeletal muscle elicits a reflex increase in cardiovascular function. Likewise, noxious stimuli activate somatic nociceptors eliciting a reflex increase in cardiovascular function. On the basis of recent work involving spinothalamic cells in the dorsal horn, we hypothesized that the dorsal horn cells involved in the aforementioned reflexes would be sensitized by applying capsaicin (Cap) to a peripheral nerve. If correct, then Cap would enhance the cardiovascular increases that occur when these reflexes are evoked. Cats were anesthetized, and the popliteal fossa was exposed. Static contraction was induced by electrical stimulation of the tibial nerve at an intensity that did not directly activate small-diameter muscle afferent fibers, whereas nociceptors were stimulated by high-intensity stimulation (after muscle paralysis) of either the saphenous nerve (cutaneous nociceptors) or a muscular branch of the tibial nerve (muscle nociceptors). The reflex cardiovascular responses to these perturbations (contraction or nociceptor stimulation) were determined before and after direct application of Cap (3%) onto the common peroneal nerve, using a separate group of cats for each reflex. Compared with control, application of Cap attenuated the peak change in mean arterial pressure (MAP) evoked by static contraction (DeltaMAP in mmHg: 38 +/- 10 before and 24 +/- 8 after ipsilateral Cap; 47 +/- 10 before and 33 +/- 10 after contralateral Cap). On the other hand, Cap increased the peak change in MAP evoked by stimulation of the saphenous nerve from 57 +/- 8 to 77 +/- 9 mmHg, as well as the peak change in MAP elicited by activation of muscle nociceptors (36 +/- 9 vs. 56 +/- 14 mmHg). These results show that the reflex cardiovascular increases evoked by static muscle contraction and noxious input are differentially affected by Cap application to the common peroneal nerve. We hypothesize that a Cap-induced alteration in dorsal horn processing is the locus for this divergent effect on these reflexes.     

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

The cardiovascular adaptation at the onset of voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one is central command descending from higher brain centers, and the other is a muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in producing the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous administration of gadolinium (55 micromol/kg), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of voluntary static exercise (pressing a bar with a forelimb) in conscious cats. HR increased by 31 +/- 5 beats/min and MAP increased by 15 +/- 1 mmHg at the onset of voluntary static exercise. Gadolinium affected neither the baseline values nor the initial increases of HR and MAP at the onset of exercise, although the peak force applied to the bar tended to decrease to 65% of the control value before gadolinium. Furthermore, we examined the effect of gadolinium on the reflex responses in HR and MAP (18 +/- 7 beats/min and 30 +/- 6 mmHg, respectively) during passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted the passive stretch-induced increases in HR and MAP, suggesting that gadolinium blocks the stretch-activated ion channels and thereby attenuates the reflex cardiovascular responses to passive mechanical stretch of a limb. We conclude that the initial cardiovascular adaptation at the onset of voluntary static exercise is predominantly induced by feedforward control of central command descending from higher brain centers but not by a muscle mechanoreflex.     

Serum leptin and adiponectin concentrations in patients infected with human immunodeficiency virus type 1 (HIV-1) on antiretroviral therapy

The lipodystrophy syndrome with dyslipidaemia and insulin resistance is side-effect of combined antiretroviral therapy (CART). Aim of the study: to describe the influence of CART on leptin and adiponectin concentration in connection with lipids levels in HIV-infected patients on antiretroviral therapy. BMI, serum leptin, adiponectin, triglycerides, total cholesterol, HDL- and LDL-cholesterol concentrations were measured in 56 HIV(+) patients before and on CART; average of treatment duration 38.4 +/-13.2 months. Significant increase of BMI (p=0.0268) of (22.6 +/- 3.3 before and 23.5 +/- 3.4 kg/m2 on therapy, respectively) and all analyzed lipids were found. Mean adiponectin concentration in treated patients was significantly (7.256 +/- 3.551 microg/ml) lower than mean value before treatment (8.395 +/- 3.568 microg/ml; p=0.0011). Mean values of leptin concentrations did not differ significantly (before therapy 3.721 +/- 0.347 log10; on therapy 3.1737 +/- 0.353 log10). Significant positive correlation between BMI and leptin concentrations was found before, as well as during CART (r=0.5333; p<0.0001), but negative correlation between adiponectin and leptin concentrations (r=-0.2677; p=0.042). Leptin and adiponectin concentrations did not revealed significant correlation with lipids levels before therapy. The decrease of adiponectin concentration on CART correlated negatively with total (r=-0.2912; p=0.0310) and LDL-cholesterol (r=-0.310; p=0.0225). CART lasting longer than 2 years resulted in the decrease of adiponectin concentration, with lack of influence on leptin concentration in analyzed group. The increase of total cholesterol and LDL-cholesterol in correlation with the decrease of adiponectin concentration confirms that CART induces metabolic disturbances related to higher risk of atherosclerosis and its sequel.     

Local ascorbate administration augments NO- and non-NO-dependent reflex cutaneous vasodilation in hypertensive humans

Full expression of reflex cutaneous vasodilation (VD) is dependent on nitric oxide (NO) and is attenuated with essential hypertension. Decreased NO-dependent VD may be due to 1) increased oxidant stress and/or 2) decreased L-arginine availability through upregulated arginase activity, potentially leading to increased superoxide production through uncoupled NO synthase (NOS). The purpose of this study was to determine the effect of antioxidant supplementation (alone and combined with arginase inhibition) on attenuated NO-dependent reflex cutaneous VD in hypertensive subjects. Nine unmedicated hypertensive [HT; mean arterial pressure (MAP) = 112 +/- 1 mmHg] and nine age-matched normotensive (NT; MAP = 81 +/- 10 mmHg) men and women were instrumented with four intradermal microdialysis (MD) fibers: control (Ringer), NOS inhibited (NOS-I; 10 mM N(G)-nitro-L-arginine), L-ascorbate supplemented (Asc; 10 mM L-ascorbate), and Asc + arginase inhibited [Asc+A-I; 10 mM L-ascorbate + 5 mM (S)-(2-boronoethyl)-L-cysteine-HCl + 5 mM N(omega)-hydroxy-nor-L-arginine]. Oral temperature was increased by 0.8 degrees C via a water-perfused suit. N(G)-nitro-L-arginine was then ultimately perfused through all MD sites to quantify the change in VD due to NO. Red blood cell flux was measured by laser-Doppler flowmetry over each skin MD site, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/MAP) and normalized to maximal CVC (%CVC(max); 28 mM sodium nitroprusside + local heating to 43 degrees C). During the plateau in skin blood flow (Delta T(or) = 0.8 degrees C), cutaneous VD was attenuated in HT skin (NT: 42 +/- 4, HT: 35 +/- 3 %CVC(max); P < 0.05). Asc and Asc+A-I augmented cutaneous VD in HT (Asc: 57 +/- 5, Asc+A-I: 53 +/- 6 %CVC(max); P < 0.05 vs. control) but not in NT. %CVC(max) after NOS-I in the Asc- and Asc+A-I-treated sites was increased in HT (Asc: 41 +/- 4, Asc+A-I: 40 +/- 4, control: 29 +/- 4; P < 0.05). Compared with the control site, the change in %CVC(max) within each site after NOS-I was greater in HT (Asc: -19 +/- 4, Asc+A-I: -17 +/- 4, control: -9 +/- 2; P < 0.05) than in NT. Antioxidant supplementation alone or combined with arginase inhibition augments attenuated reflex cutaneous VD in hypertensive skin through NO- and non-NO-dependent mechanisms.     

Ionic current of an identifiable giant neurone, d-RPLN, of an African giant snail (Achatina fulica Férussac), measured under voltage clamping--II. Outward currents

1. The outward currents of d-RPLN (dorsal-right parietal large neurone), one of the largest identifiable neurones of an African giant snail, were studied. 2. At the holding potential (-90 mV) and at the command voltage (Vc20 mV), the current values were 3.05 +/- 0.13 microA (M +/- SE) for the peak (n = 38), and 1.96 +/- 0.10 microA for the plateau (n = 37). 3. The peak time constant (Vc = 0 mV) was 2.05 +/- 0.08 msec. 4. Tetraethylammonium at 50 mM reduced the plateau value up to 50-55% of the normal, but had little effect on the peak. 5. 5-Aminopyridine at 5.0 mM diminished the peak value to about 50-55%, and delayed the peak time. 6. Quinine at 0.25 mM decreased both the peak and the plateau approximately to 55-65% of their controls, but shortened the peak time when Vc was beyond 0 mV, in contrast to the case of 4-AP. 7. The calcium-free state (replaced with cobalt) reduced these currents to about 75% of the normal, and evidently delayed the peak time.     

Energy storage in the primary photochemical events of rhodopsin and isorhodopsin

The energetics associated with the photoequilibrium (Formula: see text) are measured at 77 K by using pulsed-laser photocalorimetry and a range of excitation wavelengths and relative starting concentrations. Enthalpies for the photochemical transformations R hv----B and I hv----B are measured to be delta HRB = 32.2 +/- 0.9 kcal mol-1 and delta HIB = 27.1 +/- 3.2 kcal mol-1, respectively. Although the value of delta HRB is slightly lower than that reported previously by Cooper of 34.7 +/- 2.2 kcal mol-1 [Cooper, A. (1979) Nature (London) 282, 531-533], the two values are in agreement within experimental error. The energy difference delta HRB - delta HIB = 5.1 +/- 3.3 kcal mol-1 is identical within experimental error with the difference in enthalpies of isorhodopsin and rhodopsin [5.2 +/- 2.3; Cooper, A. (1979) FEBS Lett. 100, 382-384]. We suggest that this result is consistent with the theory that bathorhodopsin is a single, common photochemical intermediate connecting rhodopsin and isorhodopsin.     

The thyroid reserve in children with chronic lymphocytic thyroiditis revealed by the thyrotropin-releasing hormone and thyroid-stimulating hormone tests

Serum thyroid hormone and TSH concentrations were measured before and after the administration of TRH (10 micrograms/kg body weight) and bovine TSH (10 IU) in 14 children with chronic lymphocytic thyroiditis. The TRH test showed that the responsiveness of TSH was positively correlated with the basal TSH (P less than 0.001) and inversely with the increase in serum thyroid hormones, for delta T3 (P less than 0.05) and for delta T4 (P less than 0.001). Overall, the patients had significantly lower mean values for basal T4, but not for T3. The TSH test revealed that the delta T3 was positively correlated with delta T4 (P less than 0.05). delta T3 after TSH administration was positively correlated with it after TRH (P less than 0.05). The patients were divided into three groups on the basis of their peak TSH values after TRH administration. In Group 1 (peak value below 40 microU/ml; N = 5); T3 increased significantly after TRH and TSH administrations (P less than 0.05 and P less than 0.025, respectively). In addition, delta T4 was significant after TSH administration. In Group 2 (peak TSH above 40 and less than 100 microU/ml; N = 6); only delta T3 after TRH was significant (P less than 0.05). In Group 3 (peak TSH above 100 microU/ml; N = 3); the response of thyroid hormones was blunted. Thus, the thyroid hormone responses to endogenous TSH coincided with that to exogenous TSH, and the exaggerated TSH response to TRH indicates decreased thyroid reserve.     

Electromyographic amplitude ratio of serratus anterior and upper trapezius muscles during modified push-ups and bench press exercises

Imbalance and weakness of the serratus anterior and upper trapezius force couple have been described in patients with shoulder dysfunction. There is interest in identifying exercises that selectively activate these muscles and including it in rehabilitation protocols. This study aims to verify the UT/SA electromyographic (EMG) amplitude ratio, performed in different upper limb exercises and on two bases of support. Twelve healthy men were tested (average age = 22.8 +/- 3.1 years), and surface EMG was recorded from the upper trapezius and serratus anterior using single differential surface electrodes. Volunteers performed isometric contractions over a stable base of support and on a Swiss ball during the wall push-up (WP), bench press (BP), and push-up (PU) exercises. All SEMG data are reported as a percentage of root mean square or integral of linear envelope from the maximal value obtained in one of three maximal voluntary contractions for each muscle studied. A linear mixed-effect model was performed to compare UT/SA ratio values. The WP, BP, and PU exercises showed UT/SA ratio mean +/- SD values of 0.69 +/- 0.72, 0.14 +/- 0.12, and 0.39 +/- 0.37 for stable surfaces, respectively, whereas for unstable surfaces, the values were 0.73 +/- 0.67, 0.43 +/- 0.39, and 0.32 +/- 0.30. The results demonstrate that UT/SA ratio was influenced by the exercises and by the upper limb base of support. The practical application is to show that BP on a stable surface is the exercise preferred over WP and PU on either surfaces for serratus anterior muscle training in patients with imbalance between the UT/SA force couple or serratus anterior weakness.     

Effect of Roman chair exercise training on the development of lumbar extension strength

The purpose of this study was to determine the effect of 45 degrees Roman chair exercise training on the development of lumbar extension strength. Fifteen healthy volunteers (9 women, 6 men) were recruited from a university setting and were randomly assigned to 1 of 2 groups. One group (n = 9) performed progressive resistance back extension exercise on a 45 degrees Roman chair once weekly for 12 weeks. Training consisted of one set of 8-20 dynamic repetitions to volitional exhaustion using hand-held metal plates for additional resistance. The other group did not train (control, n = 6). Peak isometric lumbar extension torque was measured on a lumbar extension dynamometer before and after the 12-week program. Following training, peak isometric lumbar extension torque did not increase for the Roman chair group (before: 224.0 +/- 134.1 N x m; after: 240.3 +/- 137.4 N x m; p > 0.05) compared with the control group (before: 175.6 +/- 68.9 N x m; after: 178.2 +/- 69.9 N x m; p > 0.05), despite an increase in dynamic exercise load.     

Plasma catecholamines and heart rate at the beginning of muscular exercise in man

The relationship between the time course of heart rate and venous blood norepinephrine (NE) and epinephrine (E) concentrations was studied in 7 sedentary young men before and during 3 bicycle exercises of 5 min each (respectively 23 +/- 2.8%, 45 +/- 2.6% and 65 +/- 2.4% VO2max, mean +/- SE). During the low level exercise the change in heart rate is monoexponential (tau = 5.7 +/- 1.2 s) and no increment above the resting level of NE (delta NE) or of E (delta E) occurs. At the medium and highest intensity of exercise: a) the change in heart rate is biexponential, tau for the fast and the slow component averaging about 3 and 80 s respectively; b) delta NE (but not delta E) increases continuously with time of exercise; c) at the 5th min of exercise heart rate increments are related to delta NE; d) between 20 s and 5 min, at corresponding sampling times, the heart rate of the slow component is linearly related to delta NE. At exercise levels higher than 33% VO2max the increase in heart rate described by the slow component of the biexponential kinetic could be due to an augmented sympathetic activity revealed by increased NE blood levels.