Decompression to altitude: assumptions, experimental evidence, and future directions

2009 ◽  
Vol 106 (2) ◽  
pp. 678-690 ◽  
Author(s):  
Philip P. Foster ◽  
Bruce D. Butler

Although differences exist, hypobaric and hyperbaric exposures share common physiological, biochemical, and clinical features, and their comparison may provide further insight into the mechanisms of decompression stress. Although altitude decompression illness (DCI) has been experienced by high-altitude Air Force pilots and is common in ground-based experiments simulating decompression profiles of extravehicular activities (EVAs) or astronauts' space walks, no case has been reported during actual EVAs in the non-weight-bearing microgravity environment of orbital space missions. We are uncertain whether gravity influences decompression outcomes via nitrogen tissue washout or via alterations related to skeletal muscle activity. However, robust experimental evidence demonstrated the role of skeletal muscle exercise, activities, and/or movement in bubble formation and DCI occurrence. Dualism of effects of exercise, positive or negative, on bubble formation and DCI is a striking feature in hypobaric exposure. Therefore, the discussion and the structure of this review are centered on those highlighted unresolved topics about the relationship between muscle activity, decompression, and microgravity. This article also provides, in the context of altitude decompression, an overview of the role of denitrogenation, metabolic gases, gas micronuclei, stabilization of bubbles, biochemical pathways activated by bubbles, nitric oxide, oxygen, anthropometric or physiological variables, Doppler-detectable bubbles, and potential arterialization of bubbles. These findings and uncertainties will produce further physiological challenges to solve in order to line up for the programmed human return to the Moon, the preparation for human exploration of Mars, and the EVAs implementation in a non-zero gravity environment.

1977 ◽  
Vol 54 (1) ◽  
pp. 148-171 ◽  
Author(s):  
P.-A. Lavoie ◽  
B. Collier ◽  
A. Tenenhouse

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 789.1-790 ◽  
Author(s):  
M. Wieczorek ◽  
C. Rotonda ◽  
J. Sellam ◽  
F. Guillemin ◽  
A. C. Rat

Background:Many trials investigated the beneficial effect of physical activity (PA) on physical function (PF) in people with osteoarthritis (OA), but factors involved in this relationship are poorly understood. Considering the link between OA and obesity and obesity-related disorders, body composition (BC) could be one of these factors.Objectives:To examine the relationships between baseline components of PA and 5-year PF scores, considering BC variables measured at 3 years as potential mediators in theses associations (Figure).Methods:We used data from the KHOALA cohort, a French population-based multicenter cohort of 878 patients with symptomatic knee and/or hip OA, aged between 40 and 75 years old. Baseline PA intensity (Metabolic Equivalent of Task, MET), frequency (times/week), duration (hours/week) and type (weight-bearing or not) were assessed by the Modifiable Activity Questionnaire. PF was measured with the WOMAC questionnaire at 5 years (higher scores = greater functional limitations).Skeletal muscle mass (grams) and fat mass (grams) were measured by dual X-ray absorptiometry (DXA) in 358 patients at 3 years. Fat mass index (kg/m2), appendicular fat mass (kg), % of fat mass, lean mass index (kg/m2), appendicular muscle mass (kg), skeletal muscle mass index (kg/m2or %) were calculated based on DXA data. Sarcopenia was defined according to the FNIH Sarcopenia Project recommendations.A causal mediation analysis was used to highlight the mediating role of BC variables. Bivariate analyses (multiple linear and logistic regressions) were performed to select the variables of interest. Separate generalized linear models were used to describe the relationships between PA components, PF and selected BC variables. Unadjusted and adjusted for baseline confounders (age, gender, number of comorbidities, disease duration, mental health and vitality scores) models were ran.Results:A 1-MET increase in baseline PA intensity was significantly associated with an improvement in PF at 5 years (-3 points). Weight-bearing PA was also significantly associated with better PF scores (-5 points).A 1-MET-increase in PA intensity at baseline was associated with a subsequent decrease at 3 years in fat mass index (-0.86 k/m2), an increase in skeletal muscle mass index (≥ 6%), and a decrease in % of fat mass (-2%). Non-weight-bearing PA was significantly associated with a decrease in fat mass index (-2.5 kg/m2).A 1-point increase in PF score was associated with a reduction in skeletal muscle mass index (calculated from body mass index, -0.3%) and an increase in skeletal muscle mass index (calculated from height, +3 kg/m2). The presence of sarcopenia was significantly associated with a degradation of PF (+7 points).Crude analyses indicated that 20.4% of the effect of baseline PA intensity on PF scores at 5 years was mediated by skeletal muscle mass index (calculated from height), 23.2% by fat mass index and 26.6% by % of fat mass. Similarly, 19.3% of the effect of baseline PA type on PF scores at 5 years was mediated by fat mass index and 15.1% by % of fat mass. After adjustment, we found no longer evidence of a mediating role of BC variables in these associations.Conclusion:We found significant associations between a 1-MET increase in PA intensity, weight-bearing PA at baseline and improvement in PF at 5 years, without any mediating role of BC variables. Further studies are needed to better understand the factors involved in these associations, especially psychosocial variables.Disclosure of Interests:Maud Wieczorek: None declared, Christine Rotonda: None declared, Jérémie SELLAM: None declared, Francis Guillemin Grant/research support from: Francis Guillemin received a grant from Expanscience paid to his institution., Anne-Christine Rat: None declared


2011 ◽  
Vol 138 (1) ◽  
pp. 73-93 ◽  
Author(s):  
Thomas H. Pedersen ◽  
Christopher L.-H. Huang ◽  
James A. Fraser

Skeletal muscle activation requires action potential (AP) initiation followed by its sarcolemmal propagation and tubular excitation to trigger Ca2+ release and contraction. Recent studies demonstrate that ion channels underlying the resting membrane conductance (GM) of fast-twitch mammalian muscle fibers are highly regulated during muscle activity. Thus, onset of activity reduces GM, whereas prolonged activity can markedly elevate GM. Although these observations implicate GM regulation in control of muscle excitability, classical theoretical studies in un-myelinated axons predict little influence of GM on membrane excitability. However, surface membrane morphologies differ markedly between un-myelinated axons and muscle fibers, predominantly because of the tubular (t)-system of muscle fibers. This study develops a linear circuit model of mammalian muscle fiber and uses this to assess the role of subthreshold electrical properties, including GM changes during muscle activity, for AP initiation, AP propagation, and t-system excitation. Experimental observations of frequency-dependent length constant and membrane-phase properties in fast-twitch rat fibers could only be replicated by models that included t-system luminal resistances. Having quantified these resistances, the resulting models showed enhanced conduction velocity of passive current flow also implicating elevated AP propagation velocity. Furthermore, the resistances filter passive currents such that higher frequency current components would determine sarcolemma AP conduction velocity, whereas lower frequency components excite t-system APs. Because GM modulation affects only the low-frequency membrane impedance, the GM changes in active muscle would predominantly affect neuromuscular transmission and low-frequency t-system excitation while exerting little influence on the high-frequency process of sarcolemmal AP propagation. This physiological role of GM regulation was increased by high Cl− permeability, as in muscle endplate regions, and by increased extracellular [K+], as observed in working muscle. Thus, reduced GM at the onset of exercise would enhance t-system excitation and neuromuscular transmission, whereas elevated GM after sustained activity would inhibit these processes and thereby accentuate muscle fatigue.


2020 ◽  
Vol 7 ◽  
Author(s):  
Paul T. Morgan ◽  
Benoit Smeuninx ◽  
Leigh Breen

Sarcopenia is of important clinical relevance for loss of independence in older adults. The prevalence of obesity in combination with sarcopenia (“sarcopenic-obesity”) is increasing at a rapid rate. However, whilst the development of sarcopenia is understood to be multi-factorial and harmful to health, the role of obesity from a protective and damaging perspective on skeletal muscle in aging, is poorly understood. Specifically, the presence of obesity in older age may be accompanied by a greater volume of skeletal muscle mass in weight-bearing muscles compared with lean older individuals, despite impaired physical function and resistance to anabolic stimuli. Collectively, these findings support a potential paradox in which obesity may protect skeletal muscle mass in older age. One explanation for these paradoxical findings may be that the anabolic response to weight-bearing activity could be greater in obese vs. lean older individuals due to a larger mechanical stimulus, compensating for the heightened muscle anabolic resistance. However, it is likely that there is a complex interplay between muscle, adipose, and external influences in the aging process that are ultimately harmful to health in the long-term. This narrative briefly explores some of the potential mechanisms regulating changes in skeletal muscle mass and function in aging combined with obesity and the interplay with sarcopenia, with a particular focus on muscle morphology and the regulation of muscle proteostasis. In addition, whilst highly complex, we attempt to provide an updated summary for the role of obesity from a protective and damaging perspective on muscle mass and function in older age. We conclude with a brief discussion on treatment of sarcopenia and obesity and a summary of future directions for this research field.


1990 ◽  
Vol 24 (2) ◽  
pp. 261-267 ◽  
Author(s):  
Justin Kenardy ◽  
Tian P. S. Oei ◽  
Larry Evans

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.


1960 ◽  
Vol 199 (2) ◽  
pp. 301-310 ◽  
Author(s):  
H. S. Louckes ◽  
J. P. Quigley ◽  
J. Kersey

The inductograph method for registering in vivo muscle activity under physiological conditions is described. The method is applied to a study of the physiology of the pyloric sphincter region of well-trained, unanesthetized dogs, but is readily applicable for similar studies of the heart, uterus, skeletal muscle, etc. The motor activity of the pyloric sphincter and the pyloric antrum during fasting, feeding and gastric evacuation; the response of these regions to parasympatheticomimetic and sympatheticomimetic stimulation; and the role of the sphincter in gastric evacuation is presented. These studies show that the pyloric sphincter and the pyloric antrum are either quiescent and relaxed or the pyloric sphincter contracts momentarily in a rhythmic manner four to six times a minute in response to each propagated antral peristaltic wave. The inherent rhythm of the pyloric sphincter region is almost impossible to alter, but one or more contraction cycles may be inhibited by excitement, epinephrine, atropine, etc. or the inherent rhythm in a quiescent sphincter may be made manifest by feeding, pilocarpine, etc.


1994 ◽  
Vol 127 (5) ◽  
pp. 1435-1445 ◽  
Author(s):  
E A Connor ◽  
K Qin ◽  
H Yankelev ◽  
D DeStefano

Denervation of skeletal muscle results in dramatic remodeling of the cellular and molecular composition of the muscle connective tissue. This remodeling is concentrated in muscle near neuromuscular junctions and involves the accumulation of interstitial cells and several extracellular matrix molecules. Given the role of extracellular matrix in neurite outgrowth and synaptogenesis, we predict that this remodeling of the junctional connective tissue directly influences the regeneration of the neuromuscular junction. As one step toward understanding the role of this denervation-induced remodeling in synapse formation, we have begun to look for the signals that are involved in initiating the junctional accumulations of interstitial cells and matrix molecules. Here, the role of muscle inactivity as a signal was examined. The distributions of interstitial cells, fibronectin, and tenascin were determined in muscles inactivated by presynaptic blockade of muscle activity with tetrodotoxin. We found that blockade of muscle activity for up to 4 wk produced neither the junctional accumulation of interstitial cells nor the junctional concentrations of tenascin and fibronectin normally present in denervated frog muscle. In contrast, the muscle inactivity induced the extrajunctional appearance of two synapse-specific molecules, the acetylcholine receptor and a muscle fiber antigen, mAb 3B6. These results demonstrate that the remodeling of the junctional connective tissue in response to nerve injury is a unique response of muscle to denervation in that it is initiated by a mechanism that is independent of muscle activity. Thus connective tissue remodeling in denervated skeletal muscle may be induced by signals released from or associated with the nerve other than the evoked release of neurotransmitter.


Author(s):  
Bruno Rocha de Avila Pelozin ◽  
◽  
Larissa Ferreira-Santos ◽  
Luis Felipe Rodrigues ◽  
Edilamar Menezes de Oliveira ◽  
...  

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