scholarly journals Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

2014 ◽  
Vol 15 (4) ◽  
pp. 472-482 ◽  
Author(s):  
Rafael Torres-Peralta ◽  
José Losa-Reyna ◽  
Miriam González-Izal ◽  
Ismael Perez-Suarez ◽  
Jaime Calle-Herrero ◽  
...  
2003 ◽  
Vol 481 (2-3) ◽  
pp. 133-140 ◽  
Author(s):  
Jihua Jiang ◽  
Peter H Backx ◽  
Hwee Teoh ◽  
Michael E Ward

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 58A-58A
Author(s):  
Twan A Mulder ◽  
Caroline A van Goor ◽  
Frits W Prinzen ◽  
Carlos E Blanco
Keyword(s):  

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zbigniew Borysiuk ◽  
Tadeusz Nowicki ◽  
Katarzyna Piechota ◽  
Monika Błaszczyszyn

The objective of the present study was to determine the structure of the movement pattern performed during a wheelchair fencing lunge that is executed in response to visual and sensory stimuli. In addition, a comparison was made between fencers in the categories A and B of disability. In addition, the analysis involved the correlation between the duration of the sensorimotor response and the value of the bioelectric signal recorded in selected muscles. Seven Paralympic team athletes specializing in wheelchair fencing (3 in category A and 4 in category B) participated in the research. The fencers perform at international level competitions and are multiple medalists of the Paralympic Games. In the study, a wireless system for sEMG and accelerometer signal measurement was employed to test the intervals between the initiation of the lunge attack and its termination defined by the touch of the weapon on the coach’s torso. The electrodes were placed on 9 key muscles responsible for the effectiveness of the executed attack: DEL, TRI, BC, ECR FCR, LD, and EAO. The significant intergroup difference in the muscle activation was found to be 0.333 s for category A fencers and 0.522 s for category A fencers at p=0.039 applies to the latissimus dorsi (LD LT) muscle, which demonstrates its significance as a postural muscle in the structure of the examined movement pattern. In terms of the values of EMG, a tendency for higher MVC (%) values in most muscles for category A competitors was recorded. The latissimus dorsi (DL RT) muscle with an intergroup difference of MVC-114.63 for cat. A and 67.50 for cat. B at p=0.039 turned out to play a significant role. The results prove the role of postural muscles: external abdominal oblique and latissimus dorsi on the effectiveness of the attacks executed in wheelchair fencing.


2018 ◽  
Vol 63 (13) ◽  
pp. 139501 ◽  
Author(s):  
Leonard Che Fru ◽  
Erin B Adamson ◽  
David D Campos ◽  
Sean B Fain ◽  
Steven L Jacques ◽  
...  
Keyword(s):  

2001 ◽  
Vol 91 (3) ◽  
pp. 1160-1167 ◽  
Author(s):  
Dawn R. S. Steiner ◽  
Norberto C. Gonzalez ◽  
John G. Wood

Acute systemic hypoxia produces rapid leukocyte adherence in the rat mesenteric microcirculation, although the underlying mechanisms are not fully known. Hypoxia is known to increase reactive oxygen species (ROS) generation, which could result in formation of the lipid inflammatory mediator leukotriene B4 (LTB4). The goal of this study was to examine the role of LTB4 in hypoxia-induced microvascular alterations. Using intravital microscopy, we determined the effect of the LTB4 antagonist, LTB4-dimethyl amide (LTB4-DMA), on ROS generation and leukocyte adherence in mesenteric venules during hypoxia. Exogenous LTB4 increased ROS generation to 144 ± 8% compared with control values and also promoted leukocyte adherence. These responses to LTB4 were blocked by pretreating the mesentery with LTB4-DMA. Leukopenia did not significantly attenuate the LTB4-induced increase in ROS generation (142 ± 12.1%). LTB4-DMA substantially, though not completely, reduced hypoxia-induced ROS generation from 66 ± 18% to 11 ± 4% above control values. Hypoxia-induced leukocyte adherence was significantly attenuated by LTB4-DMA. Our results support a role for LTB4in the mechanism of hypoxia-induced ROS generation and leukocyte adherence in the rat mesenteric microcirculation.


2009 ◽  
Vol 297 (4) ◽  
pp. R978-R987 ◽  
Author(s):  
Aurélien Pichon ◽  
Bai Zhenzhong ◽  
Fabrice Favret ◽  
Guoen Jin ◽  
Han Shufeng ◽  
...  

We assessed ventilatory patterns and ventilatory responses to hypoxia (HVR) in high-altitude (HA) plateau pikas, repetitively exposed to hypoxic burrows, and control rats. We evaluated the role of neuronal nitric oxide synthase (nNOS) and dopamine by using S-methyl-l-thiocitrulline (SMTC) inhibitor and haloperidol antagonist, respectively. Ventilation (V̇i) was measured using a whole body plethysmograph in conscious pikas ( n = 9) and low-altitude (LA) rats ( n = 7) at different PiO2 (56, 80, 111, 150, and 186 mmHg) and in HA acclimatized rats ( n = 9, 8 days at 4,600 m) at two different PiO2 (56 and 80 mmHg). The effects of NaCl, SMTC, and haloperidol on ventilatory patterns were assessed in pikas at PiO2 = 56 and 80 mmHg. We observed a main species effect with larger V̇i, tidal volume (VT), inspiratory time/total time (Ti/Ttot), and a lower expiratory time in pikas than in LA rats. Pikas had also a larger VT and lower respiratory frequency compared with HA rats in hypoxia. HVR of pikas and rats were not statistically different. In pikas, SMTC induced a significant increase in V̇i and VT for a PiO2 of 56 mmHg, but had no effect for a PiO2 of 80 mmHg, i.e., the living altitude of pikas. In pikas, haloperidol injection had no effect on any ventilatory parameter. Long-term ventilatory adaptation in pikas is mainly due to an improvement in respiratory pattern (VT and Ti/Ttot) with no significant improvement in HVR. The sensitivity to severe acute hypoxia in pikas seems to be regulated by a peripheral nNOS mechanism.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Maria V. Vedunova ◽  
Tatiana A. Mishchenko ◽  
Elena V. Mitroshina ◽  
Irina V. Mukhina

The neuroprotective and antihypoxic effects of brain-derived neurotrophic factor (BDNF) on dissociated hippocampal cultures in a hypoxia model were investigated. These experiments demonstrate that 10 minutes of normobaric hypoxia increased the number of dead cells in primary culture, whereas a preventive application of BDNF increased the number of viable cells. Spontaneous bioelectrical and calcium activity in neural networks was analyzed using multielectrode arrays and functional intravital calcium imaging. The results indicate that BDNF affects the functional parameters of neuronal networks in dissociated hippocampal cultures over the 7-day posthypoxic period. In addition, the effects of k252a, an antagonist of tropomyosin-related kinase B (TrkB), on functional bioelectrical activity during and after acute hypoxia were investigated. It was shown that the protective effects of BDNF are associated with binding to the TrkB receptor. Finally, intravital fluorescent mRNA probes were used to study the role of NF-κB1 in the protective effects of BDNF. Our experiments revealed that BDNF application stimulates NF-κB1 mRNA synthesis in primary dissociated hippocampal cells under normal conditions but not in hypoxic state.


2017 ◽  
Vol 312 (6) ◽  
pp. R982-R995 ◽  
Author(s):  
K. Max Coldren ◽  
De-Pei Li ◽  
David D. Kline ◽  
Eileen M. Hasser ◽  
Cheryl M. Heesch

Hypoxia results in decreased arterial Po2, arterial chemoreflex activation, and compensatory increases in breathing, sympathetic outflow, and neuroendocrine secretions, including increased secretion of AVP, corticotropin-releasing hormone (CRH), adrenocorticotropin hormone (ACTH), and corticosterone. In addition to a brain stem pathway, including the nucleus tractus solitarius (nTS) and the rostral ventrolateral medulla (RVLM), medullary pathways to the paraventricular nucleus of the hypothalamus (PVN) contribute to chemoreflex responses. Experiments evaluated activation of specific cell phenotypes within the PVN following an acute hypoxic stimulus (AH; 2 h, 10% O2) in conscious rats. Retrograde tracers (from spinal cord and RVLM) labeled presympathetic (PreS) neurons, and immunohistochemistry identified AVP- and CRH-immunoreactive (IR) cells. c-Fos-IR was an index of neuronal activation. Hypoxia activated AVP-IR (~6%) and CRH-IR (~15%) cells, but not PreS cells in the PVN, suggesting that sympathoexcitation during moderate AH is mediated mainly by a pathway that does not include PreS neurons in the PVN. Approximately 14 to 17% of all PVN cell phenotypes examined expressed neuronal nitric oxide synthase (nNOS-IR). AH activated only nNOS-negative AVP-IR neurons. In contrast ~23% of activated CRH-IR neurons in the PVN contained nNOS. In the median eminence, CRH-IR terminals were closely opposed to tanycyte processes and end-feet (vimentin-IR) in the external zone, where vascular NO participates in tanycyte retraction to facilitate neuropeptide secretion into the pituitary portal circulation. Results are consistent with an inhibitory role of NO on AVP and PreS neurons in the PVN and an excitatory role of NO on CRH secretion in the PVN and median eminence.


1994 ◽  
Vol 76 (4) ◽  
pp. 1528-1532 ◽  
Author(s):  
G. T. De Sanctis ◽  
F. H. Green ◽  
X. Jiang ◽  
M. King ◽  
J. E. Remmers

This study reports experiments designed to evaluate the role of neurokinin-1 (NK1) receptors for substance P (SP) in the ventilatory response to acute hypoxia. Ventilation was measured by indirect plethysmography in eight unanesthetized unrestrained adult rats before and after bolus injection of 1, 5, or 10 mg/kg (ip) of CP-96,345 (Pfizer), a potent nonpeptide competitive antagonist of the SP NK1 receptor. Ventilation was measured while the rats breathed air or 8% O2–92% N2 with and without administration of SP antagonist. Pretreatment with CP-96,345 decreased the magnitude of the hypoxic response in a dose-dependent fashion. Minute ventilation in rats pretreated with CP-96,345 was reduced by 22.1% (P < 0.05) at the highest dose (10 mg/kg), largely because of an attenuation of the frequency component. Although both control and treated rats responded to hypoxia with a decrease in duration of inspiration and expiration rats pretreated with CP-96,345 displayed a smaller decrease in inspiration and expiration than control rats (P < 0.05). We have recently shown that neuropeptide-containing fibers are important for mediating the tachypnic response during acute isocapnic hypoxia in rats. The attenuation in minute ventilation at the highest dose (10 mg/kg) is comparable in magnitude to the attenuation observed with neonatal capsaicin treatment, which permanently ablates neuropeptide-containing unmyelinated fibers. Accordingly, this previously reported role of capsaicin-sensitive nerves in the hypoxic ventilatory response of rats is probably attributable to released SP acting at NK1 receptors. One of the likely sites of action of SP antagonists is the carotid body.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document