bluuebunny/crossref_metadata_2025 huggingface dataset:
Plantar flexor activation capacity and H reflex in older adults: adaptations to strength training
Authors: Scaglioni G. , Ferri A. , Minetti A. E. , Martin A. , Van Hoecke J. , Capodaglio P. , Sartorio A. , Narici M. V.
Published: March 2015

The purpose of this study was to investigate whether the voluntary neural drive and the excitability of the reflex arc could be modulated by training, even in old age. To this aim, the effects of a 16-wk strengthening program on plantar flexor voluntary activation (VA) and on the maximum Hoffman reflex (Hmax)-to-maximum M wave (Mmax) ratio were investigated in 14 elderly men (65–80 yr). After training, isometric maximum voluntary contraction (MVC) increased by 18% ( P < 0.05) and weight-lifting ability by 24% ( P < 0.001). Twitch contraction time decreased by 8% ( P < 0.01), but no changes in half relaxation time and in peak twitch torque were observed. The VA, assessed by twitch interpolation, increased from 95 to 98% ( P < 0.05). Pretraining VA, also evaluated from the expected MVC for total twitch occlusion, was 7% higher ( P < 0.01) than MVC. This discrepancy persisted after training. The interpolated twitch torque-voluntary torque relationship was fitted by a nonlinear model and was found to deviate from linearity for torque levels >65% MVC. Compared with younger men (24–35 yr), the Hmax- to Mmax ratio and nerve conduction velocity (H index) of the older group were significantly lower (42%, P < 0.05; and 29%, P < 0.001, respectively) and were not modulated by training. In conclusion, older men seem to preserve a high VA of plantar flexors. However, the impaired functionality of the reflex pathway with aging and the lack of modulation with exercise suggest that the decrease in the Hmax- to Mmaxratio and H index may be related to degenerative phenomena.
Circulating cytokines and endotoxin are not necessary for the activation of the sickness or corticosterone response produced by peripheralE. colichallenge
Authors: Campisi, J. , Hansen, M. K. , O'Connor, K. A. , Biedenkapp, J. C. , Watkins, L. R. , Maier, S. F. , Fleshner M.
Published: March 2015

Peripheral administration of a variety of inflammatory stimuli, such as endotoxin or cytokines, induces an orchestrated set of brain-mediated events referred to as the sickness response. The mechanism for how immune products signal the brain is not clear, but accumulating evidence supports the existence of neural as well as blood-borne pathways. Although endotoxin or cytokine administration results in sickness responses, few data exist regarding the role of circulating endotoxin or cytokines in the induction of sickness during a real bacterial infection. Thus the present studies examined whether subcutaneously administered Escherichia coli can activate sickness responses and whether circulating endotoxin and/or proinflammatory cytokines are a prerequisite for these responses. Male Sprague-Dawley rats were injected subcutaneously with one of three doses (2.5 × 107, 2.5 × 108, 2.5 × 109colony-forming units) of replicating E. coli, a ubiquitous bacterial strain, or vehicle. Core body temperature (Tc) and activity were measured for 3 days after the injection. A second set of groups of animals were killed 3, 6, 12, 18, 24, and 48 h after the injection, and blood samples and brains were collected. Injections dose dependently and consistently increased Tcand decreased activity, with increases in Tcbeginning 4 h after the injection. In addition, E. coli significantly increased serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and brain IL-1β levels beginning at the 6-h time point. Corticosterone and endotoxin were first elevated in the circulation at 3 and 18 h after the injection, respectively. Because fever onset preceded brain cytokine induction, we also examined cytokine levels in the serum, brain, and inflammation site 2 and 4 h after injection. Cytokines were elevated at the inflammation site but were not detectable in the serum or brain at 2 and 4 h. We conclude that subcutaneous injection of replicating E. coli induces a consistent and naturalistic infection that includes features of the sickness response as well as increases in circulating, brain, and inflammation site tissue cytokines. In addition, injection of replicating E. coli produces a robust fever and corticosterone response at a time when there are no detectable increases in circulating cytokines or endotoxin. These results suggest that elevated levels of circulating cytokines and endotoxin are not necessary for the activation of the sickness or corticosterone response. Therefore, fever, activity reduction, and corticosterone elevation induced by E. coli infection may have been evoked by a neural, rather than a humoral, pathway from the periphery to the brain.
Ozone-induced airway hyperresponsiveness is reduced in immature mice
Authors: Shore S. A. , Johnston R. A. , Schwartzman I. N. , Chism D. , Krishna Murthy G. G.
Published: March 2015

During ozone (O3) exposure, adult mice decrease their minute ventilation (V˙e). To determine whether there are age-related differences in the ventilatory response to O3, A/J mice, aged 2, 4, 8, or 12 wk, were exposed to O3(0.3–3.0 parts/million for 3 h) in nose-only exposure plethysmographs. Baseline V˙e normalized for body weight (V˙e/g) decreased with increasing age, consistent with the higher metabolic rates of younger animals. O3 caused a concentration-related decrease inV˙e in mice of all ages, but the response was significantly less in 2-wk-old than in older mice. The increased baseline V˙e/g and smaller decrements inV˙e induced by O3 in immature mice resulted in an inhaled dose of O3 normalized for body weight that was three to four times higher than in adult mice. O3 exposure caused a dose-related increase in airway responsiveness in 8- and 12-wk-old mice but did not cause airway hyperresponsiveness at any dose in either 2- or 4-wk-old mice, although higher inhaled doses of O3 normalized for body weight were delivered to these younger animals. Interleukin-6 and macrophage inflammatory protein-2 levels in bronchoalveolar lavage fluid were also increased in 8-wk-old compared with 2-wk-old mice exposed to O3. The results suggest that immature mice are less sensitive than adult mice to O3, at least in terms of the ability of O3 to induce airway hyperresponsiveness and promote release of certain cytokines.
Sigmoidal equation for lung and chest wall volume-pressure curves in acute respiratory failure
Authors: Pereira Cécile , Bohé Julien , Rosselli Sylvaine , Combourieu Emmanuel , Pommier Christian , Perdrix Jean-Pierre , Richard Jean-Christophe , Badet Michel , Gaillard Sandrine , Philit François , Guérin Claude
Published: March 2015

To assess incidence and magnitude of the “lower inflection point” of the chest wall, the sigmoidal equation was used in 36 consecutive patients intubated and mechanically ventilated with acute lung injury (ALI). They were 21 primary and 5 secondary ALI, 6 unilateral pneumonia, and 4 cardiogenic pulmonary edema. The lower inflection point was estimated as the point of maximal compliance increase. The low constant flow inflation method and esophageal pressure were used to partition the volume-pressure curves into their chest wall and lung components on zero end-expiratory pressure. The sigmoidal equation had an excellent fit with coefficients of determination >0.90 in all instances. The point of maximal compliance increase of the chest wall ranged from 0 to 8.3 cmH2O (median 1 cmH2O) with no difference between ALI groups. The chest wall significantly contributed to the lower inflection point of the respiratory system in eight patients only. The occurrence of a significant contribution of the chest wall to the lower inflection point of the respiratory system is lower than anticipated. The sigmoidal equation is able to determine precisely the point of the maximal compliance increase of lung and chest wall.
Nonuniform activation of the agonist muscle does not covary with index finger acceleration in old adults
Authors: Laidlaw Douglass H. , Hunter Sandra K. , Enoka Roger M.
Published: March 2015

This study examined the patterns of activation in the superficial and deep parts of the first dorsal interosseus muscle and in the antagonist muscle, second palmar interosseus, during postural tasks (position holding) and slow movements (position tracking) of the index finger performed by young and old adults. The position-tracking task involved the index finger lifting light loads (2.5, 10, and 35% of maximum) with shortening and lengthening contractions as steadily as possible. Steadiness was quantified in both tasks as the standard deviation of index finger acceleration. The fluctuations in acceleration during the two tasks were greater for the old subjects (62–72 yr) compared with young subjects (19–27 yr), especially with the lightest loads. The two groups of subjects activated the superficial and deep parts of first dorsal interosseus at similar intensities during the position-holding task, whereas the deep part was more active during the shortening and lengthening contractions of the position-tracking task. The nonuniform activation of first dorsal interosseus, therefore, was not associated with the difference in the standard deviation of acceleration between the young and old subjects. Furthermore, there was no association between the average level of coactivation by the antagonist muscle and the standard deviation of acceleration for either group of subjects across these tasks. Thus the greater variability in motor output exhibited by the older adults could not be explained by either the nonuniform activation of the agonist muscle or the average level of coactivation by the antagonist muscle.
Thermal regulation and comfort during a mild-cold exposure in young Japanese women complaining of unusual coldness
Authors: Nagashima Kei , Yoda Tamae , Yagishita Tomoko , Taniguchi Aki , Hosono Takayoshi , Kanosue Kazuyuki
Published: March 2015

We examined body core and skin temperatures and thermal comfort in young Japanese women suffering from unusual coldness (C, n = 6). They were selected by interview asking whether they often felt severe coldness even in an air-conditioned environment (20–26°C) and compared with women not suffering from coldness (N, n = 6). Experiments were conducted twice for each subject: 120-min exposure at 23.5°C or 29.5°C after a 40-min baseline at 29.5°C. Mean skin temperature decreased ( P < 0.05) from 33.6 ± 0.1°C (mean ± SE) to 31.1 ± 0.1°C and from 33.5 ± 0.1°C to 31.1 ± 0.1°C in C and N during the 23.5°C exposure. Fingertip temperature in C decreased more than in N ( P < 0.05; from 35.2 ± 0.1°C to 23.6 ± 0.2°C and from 35.5 ± 0.1°C to 25.6 ± 0.6°C). Those temperatures during the 29.5°C exposure remained at the baseline levels. Rectal temperature during the 23.5°C exposure was maintained at the baseline level in both groups (from 36.9 ± 0.2°C to 36.8 ± 0.1°C and 37.1 ± 0.1°C to 37.0 ± 0.1°C in C and N). The rating scores of cold discomfort for both the body and extremities were greater ( P < 0.05) in C than in N. Thus the augmented thermal sensitivity of the body to cold and activated vasoconstriction of the extremities during cold exposure could be the mechanism for the severe coldness felt in C.
Exercise training normalizes altered calcium-handling proteins during development of heart failure
Authors: Lu Lu , Mei Dan Feng , Gu An-Guo , Wang Su , Lentzner Benjamin , Gutstein David E. , Zwas Donna , Homma Shunichi , Yi Geng-Hua , Wang Jie
Published: March 2015

The cardiac sarcoplasmic reticulum calcium-ATPase (SERCA2a), Na+/Ca2+exchanger (NCX1), and ryanodine receptor (RyR2) are proteins involved in the regulation of myocyte calcium. We tested whether exercise training (ET) alters those proteins during development of chronic heart failure (CHF). Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent 4 wk of cardiac pacing (210 beats/min for 3 wk and 240 beats/min for the 4th wk), whereas five dogs underwent the same pacing regimen plus daily ET (5.1 ± 0.3 km/h, 2 h/day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction. ET preserved resting hemodynamics and ejection fraction. Left ventricular samples were obtained from all dogs and another five normal dogs for mRNA (Northern analysis, band intensities normalized to glyceraldehyde-3-phosphate dehydrogenase) and protein level (Western analysis, band intensities normalized to tubulin) measurements. In failing hearts, SERCA2a was decreased by 33% ( P < 0.05) and 65% ( P < 0.05) in mRNA and protein level, respectively, compared with normal hearts; there was only an 8.6% reduction in mRNA and a 32% reduction in protein in exercised animals ( P < 0.05 from CHF). mRNA expression of NCX1 increased by 44% in paced-only dogs compared with normal ( P < 0.05) but only by 22% in trained dogs ( P < 0.05 vs. CHF); protein level of NCX1 was elevated in paced-only dogs (71%, P < 0.05) but partially normalized by ET (33%, P < 0.05 from CHF). RyR2 was not altered in any of the dogs. In conclusion, long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium-handling proteins.
Validity of pulse oximetry during maximal exercise in normoxia, hypoxia, and hyperoxia
Authors: Yamaya Yoshiki , Bogaard Harm J. , Wagner Peter D. , Niizeki Kyuichi , Hopkins Susan R.
Published: March 2015

During exercise, pulse oximetry is problematic due to motion artifact and altered digital perfusion. New pulse oximeter technology addresses these issues and may offer improved performance. We simultaneously compared Nellcor N-395 (Oxismart XLTM) pulse oximeters with an RS-10 forehead sensor (RS-10), a D-25 digit sensor (D-25), and the Ivy 2000 (Masimo SETTM)/LNOP-Adt digit sensor (Ivy) to arterial blood oxygen saturation (SaO2 ) by cooximetry. Nine normal subjects, six athletes, and four patients with chronic disease exercised to maximum oxygen consumption (V˙o 2 max) under various conditions [normoxia, hypoxia inspired oxygen fraction (Fi O2 ) = 0.125; hyperoxia, Fi O2 = 1.0]. Regression analysis for normoxia and hypoxic data was performed ( n = 161 observations, SaO2 = 73–99.9%), and bias (B) and precision (P) were calculated. RS10 offered greater validity than the other two devices tested ( y = 1.009 x − 0.52, R 2 = 0.90, B±P = 0.3 ± 2.5). Finger sensors had low precision and a significant negative bias (D-25: y = 1.004 x − 2.327, R 2 = 0.52, B±P = −2.0 ± 7.3; Ivy: y = 1.237 x − 24.2, R 2 = 0.78, B±P = −2.0 ± 5.2). Eliminating measurements in which heart rate differed by >10 beats/min from the electrocardiogram value improved precision minimally and did not affect bias substantially (B±P = 0.5 ± 2.0, −1.8 ± 8.4, and −1.25±4.33 for RS-10, D-25, and Ivy, respectively). Signal detection algorithms and pulse oximeter were identical between RS-10 and D-25; thus the improved performance of the forehead sensor is likely because of sensor location. RS-10 should be considered for exercise testing in which pulse oximetry is desirable.
Selected Contribution: Limiting Na+transport rate in airway epithelia from α-ENaC transgenic mice: a model for pulmonary edema
Authors: Olivier Reynald , Scherrer Urs , Horisberger Jean-Daniel , Rossier Bernard C. , Hummler Edith
Published: March 2015

The amiloride-sensitive epithelial Na+channel (ENaC) is essential for fluid clearance from the airways. An experimental animal model with a reduced expression of ENaC, the α-ENaC transgenic rescue mouse, is prone to develop edema under hypoxia exposure. This strongly suggests an involvement of ENaC in the pathogenesis of pulmonary edema. To investigate the pathogenesis of this type of edema, primary cultures of tracheal cells from these mice were studied in vitro. An ∼60% reduction in baseline amiloride-sensitive Na+transport was observed, but the pharmacological characteristics and physiological regulation of the channel were similar to those observed in cells from wild-type mice. Aprotinin, an inhibitor of serine proteases, blocked 50–60% of the basal transepithelial current, hypoxia induced downregulation of Na+transport, and β-adrenergic stimulation was effective to stimulate Na+transport after the hypoxia-induced decrease. When downregulation of ENaC activity (such as observed under hypoxia) is added to a low “constitutive” ENaC expression, the resulting reduced Na+transport rate may be insufficient for airway fluid clearance and favor pulmonary edema.
Elevation in resting blood flow attenuates exercise hyperemia
Authors: Valic Zoran , Naik Jay S. , Ruble Stephen B. , Buckwalter John B. , Clifford Philip S.
Published: March 2015

These experiments tested the hypothesis that elevating muscle blood flow before exercise would wash out vasoactive substances produced by muscle contraction and reduce the magnitude of exercise hyperemia and/or delay the response. In chronically instrumented dogs ( n = 7), hindlimb blood flow was measured with chronically implanted flow probes during mild treadmill exercise. In an anesthetized preparation ( n = 8), arterial and venous blood flows of a single hindlimb were obtained during 1-s tetanic contractions evoked by electrical stimulation of the cut sciatic nerve. Elevation of blood flow by intra-arterial infusion of adenosine attenuated the increase in flow during exercise and tetanic contraction by 48 and 47%, respectively. No delay was observed in the latency to peak flow. The attenuated hyperemic response to exercise or contraction is best explained by washout of vasoactive substance(s) produced by contracting muscle, but the residual response suggests that a metabolic mediator may not be the sole explanation for exercise hyperemia.
Effects of training frequency on the dynamics of performance response to a single training bout
Authors: Busso Thierry , Benoit Henri , Bonnefoy Régis , Feasson Léonard , Lacour Jean-René
Published: March 2015

The aim of this study was to analyze the effect of an increase in training frequency on exercise-induced fatigue by using a systems model with parameters free to vary over time. Six previously untrained subjects undertook a 15-wk training experiment composed of 1) an 8-wk training period with three sessions per week (low-frequency training), 2) 1 wk without training, 3) a 4-wk training period with five sessions per week [high frequency training (HFT)], and 4) 2 wk without training. The systems input ascribed to training loads was computed from interval exercises and expressed in arbitrary units. The systems output ascribed to performance was evaluated three times each week using maximal power sustained over 5 min. The time-varying parameters of the model were estimated by fitting modeled performances to the measured ones using a recursive least squares method. The variations over time in the model parameters showed an increase in magnitude and duration of fatigue induced by a single training bout. The time needed to recover performance after a training session increased from 0.9 ± 2.1 days at the end of low-frequency training to 3.6 ± 2.0 days at the end of HFT. The maximal gain in performance for a given training load decreased during HFT. This study showed that shortening recovery time between training sessions progressively yielded a more persistent fatigue induced by each training.
Percent body fat via DEXA: comparison with a four-compartment model
Authors: van der Ploeg Grant E. , Withers Robert T. , Laforgia Joe
Published: March 2015

This study compared body composition by dual-energy X-ray absorptiometry (DEXA; Lunar DPX-L) with that via a four-compartment (4C; water, bone mineral mass, fat, and residual) model. Relative body fat was determined for 152 healthy adults [30.0 ± 11.1 (SD) yr; 75.10 ± 14.88 kg; 176.3 ± 8.7 cm] aged from 18 to 59 yr. The 4C approach [20.7% body fat (%BF)] resulted in a significantly ( P < 0.001) higher mean %BF compared with DEXA (18.9% BF), with intraindividual variations ranging from −2.6 to 7.3% BF. Linear regression and a Bland and Altman plot demonstrated the tendency for DEXA to progressively underestimate the %BF of leaner individuals compared with the criterion 4C model (4C %BF = 0.862 × DEXA %BF + 4.417; r 2 = 0.952, standard error of estimate = 1.6% BF). This bias was not attributable to variations in fat-free mass hydration but may have been due to beam-hardening errors that resulted from differences in anterior-posterior tissue thickness.
Age-related changes in the mitotic and metabolic characteristics of muscle-derived cells
Authors: Barani Aude E. , Durieux Anne-Cécile , Sabido Odile , Freyssenet Damien
Published: March 2015

Age-related sarcopenia could partly result from cumulative repeated episodes of incomplete repair and regeneration. We hypothesized that mitotic and metabolic events associated with satellite cell activation and proliferation could be altered with aging. Muscle-derived cells (mdc) were isolated from gastrocnemius and quadriceps muscles of young (3 wk old), adult (9 mo old), and old (24 mo old) Sprague-Dawley male rats ( n = 10/group). The mdc from young growing rats started to proliferate earlier compared with adult and old animals. Cell cycle duration was significantly reduced with aging from 36.5 ± 3.2 to 28.0 ± 2.2 h. However, the proportion of noncycling (G0phase) and cycling (G1+ S + G2+ M phases) cultured mdc was statistically unchanged among the three age groups. Significantly lower increase in c-met and proliferating cell nuclear antigen expression were observed in cultured mdc of old rats upon serum stimulation. Major changes in the expression of citrate synthase, lactate dehydrogenase, proteasome, caspase 3, plasminogen activators (PAs), and matrix metalloproteinase 2-9 (MMP2-9) were observed upon serum stimulation, but no age-related difference was noted. However, when measured on crushed muscle extracts, PAs and MMP2-9 enzyme activities were significantly decreased with aging. Our results show that cellular and biochemical events associated with the control of mdc activation and proliferation occur with aging. These alterations may participate in the accumulation of repeated episodes of incomplete repair and regeneration throughout the life span, thus contributing to the loss of skeletal muscle mass and function with aging.
Deficiency of SP-B reveals protective role of SP-C during oxygen lung injury
Authors: Ikegami Machiko , Weaver Timothy E. , Conkright Juliana J. , Sly Peter D. , Ross Gary F. , Whitsett Jeffrey A. , Glasser Stephan W.
Published: March 2015

Although the surface properties of surfactant protein (SP)-B and SP-C are similar, the contributions that either protein may make to lung function have not been identified in vivo. Mutations in SP-B cause lethal respiratory failure at birth; however, SP-B null mice are deficient in both SP-B and SP-C. To identify potential contributions of SP-C to lung function in vivo, the following transgenic mice were generated and exposed to 95% O2for 3 days: (SP-B+/+,SP-C+/+), (SP-B+/+, SP-C−/−), (SP-B+/−,SP-C+/+), (SP-B+/−,SP-C+/−), and (SP-B+/−,SP-C−/−). Hyperoxia altered pressure-volume curves in mice that were heterozygous for SP-B, and these values were further decreased in (SP-B+/−,SP-C−/−) mice. Likewise, alveolar interleukin (IL)-6 and IL-1β were maximally increased by O2exposure of (SP-B+/−,SP-C−/−) mice compared with the other genotypes. Lung hysteresivity was lower in the (SP-B+/−,SP-C−/−) mice. Surfactant isolated from (SP-B+/+,SP-C−/−) and (SP-B+/−,SP-C−/−) mice failed to stabilize the surface tension of microbubbles, showing that SP-C plays a role in stabilization or recruitment of phospholipid films at low bubble radius. Genetically decreased levels of SP-B combined with superimposed O2-induced injury reveals the distinct contribution of SP-C to pulmonary function in vivo.
Impaired leg vasodilation during dynamic exercise in healthy older women
Authors: Proctor David N. , Koch Dennis W. , Newcomer Sean C. , Le Khoi U. , Leuenberger Urs A.
Published: March 2015

The purpose of the present study was to test the hypothesis that leg blood flow responses during leg cycle ergometry are reduced with age in healthy non-estrogen-replaced women. Thirteen younger (20-27 yr) and thirteen older (61-71 yr) normotensive, non-endurance-trained women performed both graded and constant-load bouts of leg cycling at the same absolute exercise intensities. Leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), mean femoral venous pressure, cardiac output (acetylene rebreathing), and blood O2 contents were measured. Leg blood flow responses at light workloads (20-40 W) were similar in younger and older women. However, at moderate workloads (50-60 W), leg blood flow responses were significantly attenuated in older women. MAP was 20-25 mmHg higher ( P < 0.01) in the older women across all work intensities, and calculated leg vascular conductance (leg blood flow/estimated leg perfusion pressure) was lower ( P < 0.05). Exercise-induced increases in leg arteriovenous O2 difference and O2 extraction were identical between groups ( P > 0.6). Leg O2 uptake was tightly correlated with leg blood flow across all workloads in both subject groups ( r2 = 0.80). These results suggest the ability of healthy older women to undergo limb vasodilation in response to submaximal exercise is impaired and that the legs are a potentially important contributor to the augmented systemic vascular resistance seen during dynamic exercise in older women.
Sympathetic activity and the heterogenous blood pressure response to exercise training in hypertensives
Authors: Brown Michael D. , Dengel Donald R. , Hogikyan Robert V. , Supiano Mark A.
Published: March 2015

To test whether changes in sympathetic nervous system (SNS) activity or insulin sensitivity contribute to the heterogeneous blood pressure response to aerobic exercise training, we used compartmental analysis of [3H]norepinephrine kinetics to determine the extravascular norepinephrine release rate (NE2) as an index of systemic SNS activity and determined the insulin sensitivity index (SI) by an intravenous glucose tolerance test, before and after 6 mo of aerobic exercise training, in 30 (63 ± 7 yr) hypertensive subjects. Maximal O2consumption increased from 18.4 ± 0.7 to 20.8 ± 0.7 ml · kg−1· min−1( P = 0.02). The average mean arterial blood pressure (MABP) did not change (114 ± 2 vs. 114 ± 2 mmHg); however, there was a wide range of responses (−19 to +17 mmHg). The average NE2did not change significantly (2.11 ± 0.15 vs. 1.99 ± 0.13 μg · min−1· m−2), but there was a significant positive linear relationship between the change in NE2and the change in MABP ( r = 0.38, P = 0.04). SIincreased from 2.81 ± 0.37 to 3.71 ± 0.42 μU × 10−4· min−1· ml−1( P = 0.004). The relationship between the change in SIand the change in MABP was not statistically significant ( r = −0.03, P = 0.89). When the changes in maximal O2consumption, percent body fat, NE2, and SIwere considered as predictors of the change in MABP, only NE2was a significant independent predictor. Thus suppression of SNS activity may play a role in the reduction in MABP and account for a portion of the heterogeneity of the MABP response to aerobic exercise training in older hypertensive subjects.
Damage to different motor units from active lengthening of the medial gastrocnemius muscle of the cat
Authors: Brockett C. L. , Morgan D. L. , Gregory J. E. , Proske U.
Published: March 2015

Slow-twitch motor units in the medial gastrocnemius muscle of the anesthetized cat were found to have an average optimum length for active tension that was 0.8 ± 0.5 (SE) mm longer than the whole muscle optimum. For fast-twitch units (time to peak < 50 ms), the average optimum was 1.3 ± 0.3 mm shorter than the whole muscle optimum. After the muscle had been subjected to 10 stretches while maximally activated, beginning at the whole muscle optimum length, the optimum lengths of the 27 fast-twitch motor units shifted significantly further in the direction of longer muscle lengths (mean 4.3 ± 0.3 mm) than for the eight slow-twitch units (2.1 ± 0.4 mm). A shift in the muscle's length-tension relation was interpreted as being due to sarcomere disruption. Statistical analysis showed that a motor unit's optimum length for a contraction, relative to the whole muscle optimum, was a better indicator of the unit's susceptibility to damage from active lengthenings than was motor unit type.
Postnatal maturation of vagal respiratory reflexes in preterm and full-term lambs
Authors: Arsenault Julie , Moreau-Bussière François , Reix Philippe , Niyonsenga Théophile , Praud Jean-Paul
Published: March 2015

The postnatal development of ventilatory reflexes originating from bronchopulmonary receptors was assessed in preterm vs. full-term lambs. Ventilation and arterial pressure were repeatedly measured in 10 preterm (gestational age, 132 days) and 7 full-term lambs without sedation from day 1 to day 42. The Hering-Breuer inhibitory reflex (slowly adapting stretch receptors) was assessed by the increase in expiratory time during end-inspiratory occlusion. The pulmonary chemoreflex (C-fiber endings) was assessed by the initial apnea + bradycardia + systemic hypotension and the secondary tachypnea after capsaicin intravenous injection. Results show the following. 1) Premature birth did not modify the maturation of the Hering-Breuer reflex. 2) Whereas a classic pulmonary chemoreflex was observed in the very first hours of life in preterm lambs, the tachypneic component of this reflex was weaker than in full-term lambs on day 1. 3) Premature birth led to a reversed postnatal maturation of this tachypneic response (tendency to increase with postnatal age). Our findings suggest that premature birth in lambs modifies postnatal maturation of the pulmonary chemoreflex.
Amelioration of depressed cardiopulmonary reflex control of sympathetic nerve activity by short-term exercise training in male rabbits with heart failure
Authors: Pliquett R. U. , Cornish K. G. , Patel K. P. , Schultz H. D. , Peuler J. D. , Zucker I. H.
Published: March 2015

The reflex regulation of sympathetic nerve activity has been demonstrated to be impaired in the chronic heart failure (CHF) state compared with the normal condition (Liu JL, Murakami H, and Zucker IH. Circ Res 82: 496–502, 1998). Exercise training (Ex) appears to be beneficial to patients with CHF and has been shown to reduce sympathetic outflow in this disease state (Hambrecht R, Hilbrich L, Erbs S, Gielen S, Fiehn E, Schoene N, and Schuler G. J Am Coll Cardiol 35: 706–713, 2000). We tested the hypothesis that Ex corrects the reduced cardiopulmonary (CP) reflex response to volume expansion in the CHF state. Normal, normal with Ex, CHF, and CHF with Ex (CHF-Ex) groups ( n = 10–21) of male New Zealand White rabbits were studied. CHF was induced by chronic ventricular pacing. Rabbits were instrumented to record left ventricular end-diastolic pressure (LVEDP), left ventricular end-diastolic diameter (LVEDD), and renal sympathetic nerve activity (RSNA). Experiments were carried out with the animals in the conscious state. Volume expansion was performed with 6% dextran in normal saline at a rate of 5 ml/min to ∼20% of estimated plasma volume without any significant effect on mean arterial pressure being exhibited. The relationships between RSNA and LVEDP and between RSNA and LVEDD were determined by linear regression; the slopes served as an index of CP reflex sensitivity. Normal rabbits exhibited a CP reflex sensitivity of -8.4 ± 1.5%Δ RSNA/mmHg. This value fell to 0.0 ± 1.3%Δ RSNA/mmHg in CHF rabbits ( P < 0.001). Ex increased CP reflex sensitivity to -5.0 ± 0.7%Δ RSNA/mmHg in CHF-Ex rabbits ( P < 0.05 compared with CHF). A similar trend was seen when related to the change in LVEDD. Furthermore, resting RSNA expressed as a percentage of maximum RSNA in response to cigarette smoke was also normalized by Ex in rabbits with CHF. Ex had no effect on these parameters in normal rabbits. These data confirm an impairment of CP reflex sensitivity and sympathoexcitation in CHF vs. normal animals. Ex substantially restored both CP reflex sensitivity and baseline RSNA in CHF animals. Thus Ex beneficially affects reflex regulation in CHF, thereby lowering resting sympathetic nerve activity.
Distribution and reproducibility of spirometric response to ozone by gender and age
Authors: Hazucha Milan J. , Folinsbee Lawrence J. , Bromberg Philip A.
Published: March 2015

Subjects were healthy nonsmoking men ( n = 146) and women ( n = 94) 18-60 yr old. Initially, each subject was exposed for 1.5 h to 0.42 ppm O3. Forty-seven individuals were later reexposed twice, 1 wk to several months apart, to 0.4 ppm O3. Intermittent exercise utilized in all exposures was adjusted to produce an O3 dose of 560 ppm × l/m2 body surface area. The post-O3 percent change in forced-expiratory volume in 1 s (Δ%FEV1) decrements of young (18-35 yr) and middle-aged (36-60 yr) men and women differed significantly ( P < 0.05) from normal distribution with values skewed toward larger decrements in younger subjects. The mean Δ%FEV1 rates were -16.3%, -16.6%, -11.6%, and -6.4%, respectively. The rate of decline with age was 2.5 times higher in young women compared with young men ( P < 0.05). This pattern was reversed in the middle-age cohort. Our data support earlier reports of no significant difference in spirometric response to O3 between young men and women. The data also confirm that large FEV1 decrements after O3 exposure are mostly confined to younger individuals that also show much greater variance in response to repeated exposures than the middle-aged subjects. The majority of subjects remained in their initial category of O3 sensitivity on retesting after various time lapses. The r value (Spearman) between the first and second and first and third exposure response ranged from 0.544 to 850, depending on classification. However, the mean Δ%FEV1 differed by as much as six percentage points between exposure days. The yearly loss of responsiveness (0.2% to 0.7%/year) with progressing age determined by cross-sectional analyses was substantially smaller.
Acid-base balance during repeated cycling sprints in boys and men
Authors: Ratel S. , Duche P. , Hennegrave A. , Van Praagh E. , Bedu M.
Published: March 2015

The aim of this study was to investigate the acid-base balance during repeated cycling sprints in children and adults. Eleven boys (9.6 ± 0.7 yr) and ten men (20.4 ± 0.8 yr) performed ten 10-s sprints on a cycle ergometer separated by 30-s passive recovery intervals. To measure the time course of lactate ([La]), hydrogen ions ([H+]), bicarbonate ions ([HCO[Formula: see text]]), and base excess concentrations and the arterial partial pressure of CO2, capillary blood samples were collected at rest and after each sprint. Ventilation and CO2output were continuously measured. After the 10th sprint, concentrations of boys vs. men were as follows: [La], 8.5 ± 2.1 vs. 15.4 ± 2.0 mmol/l; [H+], 43.8 ± 1.3 vs. 66.9 ± 9.9 nmol/l ( P < 0.001). Significant correlations showed that, for a given [La], [H+] was lower in the boys compared with the men ( P < 0.001). Significant relationships also indicated that, for a given [La], [HCO[Formula: see text]] and base excess concentration were similar in the boys compared with the men. Moreover, significant relationships revealed that, for a given [H+] or [HCO[Formula: see text]], arterial partial pressure of CO2was lower in the boys compared with the men ( P < 0.001). The ventilation-to-CO2output ratio was higher in the boys during the first five rest intervals and was then higher in the men during the last five sprints. To conclude, during repeated sprints, the ventilatory regulation related to the change in acid-base balance induced by lactic acidosis was more important during the first rest intervals in the boys compared with the men.
Combined intervention of exercise and genistein prevented androgen deficiency-induced bone loss in mice
Authors: Wu Jian , Wang Xin Xiang , Chiba Hiroshige , Higuchi Mitsuru , Takasaki Misao , Ohta Atsutane , Ishimi Yoshiko
Published: March 2015

There is evidence that estrogen plays an important role in skeletal tissue in males as well as females. We have reported that phytoestrogens, such as genistein, selectively act on bone and exhibit cooperative effects on bone mass when combined with exercise in ovariectomized mice. In this study, we examined whether both interventions exhibit cooperative effects on bone loss in androgen-deficient mice similar to those in estrogen-deficient mice. Male mice aged 7 wk were either sham operated or orchidectomized (ORX) and divided into six groups: 1) sham; 2) ORX; 3) ORX and treated with genistein (0.4 mg/day) subcutaneously; 4) ORX, exercised on a treadmill daily for 30 min/day at 12 m/min; 5) ORX, given genistein, and exercised (ORX+ExG); and 6) ORX and treated with 17β-estradiol (E2). Four weeks after the intervention, seminal vesicle weight strikingly decreased in ORX mice, and it was not affected by administration of genistein or E2. Bone mineral density of whole femur was significantly reduced by ORX, and bone loss was prevented by the combined intervention. Histomorphometric analysis showed that bone volume and trabecular thickness in the distal femoral cancellous bone were significantly lower in the ORX group than in the Sham group, and they were completely restored in the ORX+ExG group, as in the ORX with E2 group. These results indicate that the combined intervention of moderate exercise and a low dose of genistein administration shows an additive effect in preventing bone loss in ORX mice similar to that in ovariectomized mice.
Ventilatory and metabolic responses to hypoxia in the smallest simian primate, the pygmy marmoset
Authors: Tattersall Glenn J. , Blank James L. , Wood Stephen C.
Published: March 2015

The pygmy marmoset ( Cebuella pygmaea) is the smallest New World Monkey (average body mass of 120–130 g). As such, it faces possible challenges to thermoregulation. Small mammals (e.g., rats) are well known to lower body temperature and metabolism in response to hypoxia; however, small primates have not been studied in this respect nor have, in general, the interactions between metabolism and ventilation. Because little is known about these responses in small primates, it seemed of great interest to assess the hypoxia-induced metabolic depression and drop in body temperature and the associated ventilatory requirements in this species under hypoxic conditions. Exposure to graded hypoxia (30 min at each of 18, 16, 14, 12, and 10% O2) caused body temperature to drop from the normoxic value of 39 to 37°C. This was accompanied by a marked metabolic depression (O2consumption was ∼68% of the normoxic value, implying a suppression of metabolism greater than that predicted from a typical value of the effect of 10°C change on metabolism of 2–3 times). Minute ventilation declined in parallel to metabolism, maintaining a constant air-convection requirement during hypoxia; thus this species did not show the typical mammalian hyperventilation. Acute exposure to 10% O2led to a similar overall decline in metabolism and body temperature and qualitative differences in the timing of these changes. The pygmy marmoset shares some similarities in its hypoxic metabolic response with other mammals of similar size yet appears to be unique in its much diminished ventilatory response to hypoxia.
Selected Contribution: Identification of differentially expressed genes between young and old rat soleus muscle during recovery from immobilization-induced atrophy
Authors: Pattison J. Scott , Folk Lillian C. , Madsen Richard W. , Booth Frank W.
Published: March 2015

After cessation of hindlimb immobilization, which resulted in a 27-37% loss in soleus mass, the atrophied soleus muscle of young but not old rats regrows to its mass before treatment. We hypothesized that during remobilization the mRNA levels of growth potentiating factor(s) would be present in the soleus muscle of young (3- to 4-mo-old) but absent in old (30- to 31-mo-old) Fischer 344 × Brown Norway rats or that mRNAs for growth inhibitory factor(s) would be absent in young but present in old. Gene expression levels of >24,000 transcripts were determined by using Affymetrix RGU34A-C high-density oligonucleotide microarrays in soleus muscles at 3, 6, 10, and 30 days of remobilization after cessation of a 10-day period of hindlimb immobilization. Each muscle sample was applied to an independent set of arrays. Recovery-related differences were determined by using a three-factor ANOVA with a false discovery rate-adjustment of P = 0.01, which yielded 64 significantly different probe sets. Elfin, amphiregulin, and clusterin mRNAs were selected for further confirmation by real-time PCR. Elfin mRNA levels were less in old than in young rats at 6, 10, and 30 days of remobilization. Amphiregulin expression exhibited a unique spike on the 10th day of successful regrowth in young rats but remained unchanged old. Clusterin mRNA was unchanged in young muscles but was elevated on the 3rd, 6th, and 10th days of recovery in old soleus muscles. The mRNAs identified as differentially expressed between young and old recovery may modulate muscle growth that could highlight new candidate mechanisms to explain the failure of old soleus muscle to recover lost muscle mass.
L-Arginine protects from ischemia-reperfusion-induced endothelial dysfunction in humans in vivo
Authors: Pernow John , Böhm Felix , Beltran Emma , Gonon Adrian
Published: March 2015

It has been shown that nitric oxide (NO) protects from myocardial ischemia-reperfusion injury in animal models. The present study investigated whether administration of the NO substrate l-arginine protects against ischemia-reperfusion-induced endothelial dysfunction in humans. Forearm blood flow was measured with venous occlusion plethysmography in 16 healthy male subjects who were investigated on two occasions. Forearm ischemia was induced for 20 min followed by 60-min reperfusion. With the use of a crossover protocol, the subject received a 15-min intrabrachial artery infusion of l-arginine (20 mg/min) and vehicle (saline, n = 12 or d-arginine, n = 4) starting at 15 min of ischemia on two separate occasions. Compared with preischemia, endothelium-dependent increase in forearm blood flow induced by intra-arterial acetylcholine (3–30 μg/min) was significantly impaired at 15 and 30 min of reperfusion when the subjects received saline ( P < 0.001). When the subjects received l-arginine, the acetylcholine-induced increase in forearm blood flow was not significantly affected by ischemia-reperfusion. The recovery of endothelium-dependent vasodilatation at 15- and 30-min reperfusion was significantly greater after administration of l-arginine than after saline ( P < 0.05). d-Arginine did not affect the response to acetylcholine. Endothelium-independent vasodilatation to nitroprusside was not affected during reperfusion. These results demonstrate that the NO substrate l-arginine significantly attenuates ischemia-reperfusion-induced endothelial dysfunction in humans in vivo. This suggests that l-arginine may be useful as a therapeutic agent in the treatment of ischemia-reperfusion injury in humans.
Structure and function of the ankle dorsiflexor muscles in young and moderately active men and women
Authors: Holmbäck Anna Maria , Porter Michelle M. , Downham David , Andersen Jesper L. , Lexell Jan
Published: March 2015

The aim was to investigate determinants of ankle dorsiflexor muscle (DF) strength and size in moderately active young men and women ( n = 30; age 20–31 yr). Concentric (Con) and eccentric (Ecc) strength were measured isokinetically. Magnetic resonance imaging was used to determine the muscle cross-sectional area (CSA). Multiple biopsies were obtained from the tibialis anterior muscle to determine total numbers, areas (Area I and II) and proportions (Prop I and II) of type I and II fibers, respectively, and relative contents of myosin heavy chain (MHC) isoforms MHC1, MHC2a, and MHC2x. Women had lower Con and Ecc strength (24 and 27%; P < 0.01), smaller CSA (19%; P < 0.001), lower Ecc DF specific strength (strength/CSA) (10%; P < 0.01), and smaller Area I and Area II (21 and 31%; P < 0.01) than men. Prop I, MHC1, estimated total number of fibers, and Con DF specific strength were similar for both sexes. Con DF strength was up to 72% determined by CSA and Prop I, and Ecc DF strength was up to 81% determined by CSA, Prop I, and sex; variables other than CSA explained at most 9%. Body weight and fiber areas explained >50% of the variation in CSA. In conclusion, CSA was the predominant determinant of DF strength, CSA was to a great extent determined by the body weight and the sizes of muscle fibers, and sex differences in Ecc specific strength require further study.
Exercise-induced elevation of HSP70 is intensity dependent
Authors: Milne Kevin J. , Noble Earl G.
Published: March 2015

Exercise induces expression of the protective heat shock protein, HSP70, in striated muscle. To characterize the relationship between induction of this protein and exercise intensity in muscles exhibiting different recruitment patterns, male Sprague-Dawley rats were assigned to a sedentary control or one of seven exercise groups for which treadmill running speed varied between 15 and 33 m/min ( n = 8/group). Twenty-four hours after a single 60-min exercise bout, hearts, red and white portions of the vastus (RV and WV, respectively) muscles, and soleus (Sol) muscles were harvested and analyzed for both relative and absolute HSP70 content. Cardiac HSP70 was significantly elevated only when animals were exercised at 24 m/min and beyond. Similarly, HSP70 was elevated in RV at running speeds above 24 m/min but did not increase in WV until 27 m/min. In contrast, HSP70 content was initially elevated in the Sol but subsequently declined at the highest running speeds. The observed patterns of HSP70 expression in skeletal muscle were in general accordance with known muscle recruitment patterns and suggest that alterations in muscle loading, resulting from changes in exercise intensity, are an important component of exercise-induced increases in HSP70 content.
A high-fat, refined-carbohydrate diet affects renal NO synthase protein expression and salt sensitivity
Authors: Roberts Christian K. , Vaziri Nosratola D. , Sindhu Ram K. , Barnard R. James
Published: March 2015

Chronic consumption of a high-fat, refined-carbohydrate (HFS) diet causes hypertension. In an earlier study, we found increased nitric oxide (NO) inactivation by reactive oxygen species (ROS) and functional NO deficiency in this model. Given the critical role of NO in renal sodium handling, we hypothesized that diet-induced hypertension may be associated with salt sensitivity. Female Fischer rats were fed an HFS or a standard low-fat, complex-carbohydrate (LFCC) rat chow diet starting at 2 mo of age for 2 yr. Arterial blood pressure, renal neuronal NO synthase (nNOS), endothelial NO synthase (eNOS), and inducible NO synthase (iNOS) protein and nitrotyrosine abundance (a marker of NO inactivation by ROS), and urinary NO metabolite excretion were measured. To assess salt sensitivity, the blood pressure response to a high-salt (4%) diet for 1 wk was determined. After 2 yr, renal nNOS and urinary NO metabolite excretion were significantly depressed, whereas arterial pressure, eNOS, iNOS, and nitrotyrosine were elevated in the HFS group but remained virtually unchanged in the LFCC group. Consumption of the high-salt diet resulted in a significant rise in arterial pressure in the HFS, but not in the LFCC, group. Thus chronic consumption of an HFS diet results in hypertension and salt sensitivity, which may be in part due to a combination of ROS-mediated NO inactivation and depressed renal nNOS protein expression.