scholarly journals Age-Related Changes in Muscle Fatigue Resistance in Humans

Author(s):  
K. Ming Chan ◽  
Asim J. Raja ◽  
Fay J. Strohschein ◽  
Katherine Lechelt

Objective:The goal of this study was to compare the relative contributions from the muscle and the central nervous system to muscle fatigue resistance in aging.Methods:Each subject carried out 90 s of sustained maximal voluntary isometric contraction (MVC) of the thumb using the thenar and forearm thumb muscles. Contractile capacity of the thenar muscles was assessed through tetanic stimulation of the median nerve. Interpolated doublets delivered during an MVC represented the overall voluntary activation level while transcranial cortical stimulation with an electromagnetic stimulator was used to assess motor output upstream from the corticomotoneuronal pathway.Results:Nine elderly subjects [four females and five males, 70±9 years old (mean±SD)] and 10 younger subjects (five females and five males, 30±6 years old) were tested. After the fatiguing exercise, the elderly group's MVC declined by 29% as opposed to 47% in the younger group (p<0.01). The elderly group's greater fatigue resistance was accounted for by increased fatigue resistance at the muscle level as well as in the central nervous system. At least some of the decline in the central motor drive was upstream from the corticomotoneuronal pathway.Conclusion:The higher muscle fatigue resistance in the elderly group was attributable to differences in both the peripheral and central nervous systems.

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1256
Author(s):  
Andrea Tinnirello ◽  
Silvia Mazzoleni ◽  
Carola Santi

Background: Chronic pain is a major issue affecting more than 50% of the older population and up to 80% of nursing homes residents. Research on pain in the elderly focuses mainly on the development of clinical tools to assess pain in patients with dementia and cognitive impairment or on the efficacy and tolerability of medications. In this review, we searched for evidence of specific pain mechanisms or modifications in pain signals processing either at the cellular level or in the central nervous system. Methods: Narrative review. Results: Investigation on pain sensitivity led to conflicting results, with some studies indicating a modest decrease in age-related pain sensitivity, while other researchers found a reduced pain threshold for pressure stimuli. Areas of the brain involved in pain perception and analgesia are susceptible to pathological changes such as gliosis and neuronal death and the effectiveness of descending pain inhibitory mechanisms, particularly their endogenous opioid component, also appears to deteriorate with advancing age. Hyperalgesia is more common at older age and recovery from peripheral nerve injury appears to be delayed. In addition, peripheral nociceptors may contribute minimally to pain sensation at either acute or chronic time points in aged populations. Conclusions: Elderly subjects appear to be more susceptible to prolonged pain development, and medications acting on peripheral sensitization are less efficient. Pathologic changes in the central nervous system are responsible for different pain processing and response to treatment. Specific guidelines focusing on specific pathophysiological changes in the elderly are needed to ensure adequate treatment of chronic pain conditions.


2020 ◽  
Vol 9 (3) ◽  
pp. 741 ◽  
Author(s):  
Riccardo Borzuola ◽  
Arrigo Giombini ◽  
Guglielmo Torre ◽  
Stefano Campi ◽  
Erika Albo ◽  
...  

Ageing is accompanied by a severe muscle function decline presumably caused by structural and functional adaptations at the central and peripheral level. Although researchers have reported an extensive analysis of the alterations involving muscle intrinsic properties, only a limited number of studies have recognised the importance of the central nervous system, and its reorganisation, on neuromuscular decline. Neural changes, such as degeneration of the human cortex and function of spinal circuitry, as well as the remodelling of the neuromuscular junction and motor units, appear to play a fundamental role in muscle quality decay and culminate with considerable impairments in voluntary activation and motor performance. Modern diagnostic techniques have provided indisputable evidence of a structural and morphological rearrangement of the central nervous system during ageing. Nevertheless, there is no clear insight on how such structural reorganisation contributes to the age-related functional decline and whether it is a result of a neural malfunction or serves as a compensatory mechanism to preserve motor control and performance in the elderly population. Combining leading-edge techniques such as high-density surface electromyography (EMG) and improved diagnostic procedures such as functional magnetic resonance imaging (fMRI) or high-resolution electroencephalography (EEG) could be essential to address the unresolved controversies and achieve an extensive understanding of the relationship between neural adaptations and muscle decline.


1994 ◽  
Vol 74 (1) ◽  
pp. 49-94 ◽  
Author(s):  
R. H. Fitts

Fatigue, defined as the failure to maintain the required or expected power output, is a complex problem, since multiple factors are clearly involved, with the relative importance of each dependent on the fiber type composition of the contracting muscles(s), and the intensity, type, and duration of the contractile activity. The primary sites of fatigue appear to be within the muscle cell itself and for the most part do not involve the central nervous system or the neuromuscular junction. The major hypotheses of fatigue center on disturbances in the surface membrane, E-C coupling, or metabolic events. The cell sites most frequently linked to the etiology of skeletal muscle fatigue are shown in Figure 1. Skeletal muscles are composed of at least four distinct fiber types (3 fast twitch and 1 slow twitch), with the slow type I and fast type IIa fibers containing the highest mitochondrial content and fatigue resistance. Despite fiber type differences in the degree of fatigability, the contractile properties undergo characteristic changes with the development of fatigue that can be observed in whole muscles, single motor units, and single fibers. The Po declines, and the contraction and relaxation times are prolonged. Additionally, there is a decrease in the peak rate of tension development and decline and a reduced Vo. Changes in Vo are more resistant to fatigue than Po and are not observed until Po has declined by at least 10% of its initial prefatigued value. However, the reduced peak power by which fatigue is defined results from both a reduction in Vo and Po. In the absence of muscle fiber damage, the prolonged relaxation time associated with fatigue causes the force-frequency curve to shift to the left, such that peak tensions are obtained at lower frequencies of stimulation. In a mechanism not clearly understood, the central nervous system senses this condition and reduces the alpha-motor nerve activation frequency as fatigue develops. In some cases, selective LFF develops that displaces the force-frequency curve to the right. Although not proven, it appears likely that this condition is associated with and likely caused by muscle injury, such that the SR releases less Ca2+ at low frequencies of activation. Alternatively, LFF could result from a reduced membrane excitability, such that the sarcolemma action potential frequency is considerably less than the stimulation frequency.(ABSTRACT TRUNCATED AT 400 WORDS)


1993 ◽  
Vol 8 (6) ◽  
pp. 285-291 ◽  
Author(s):  
M Bourin ◽  
A Couetoux du Tertre ◽  
R Payeur

SummaryAs with other drugs it is necessary to look for changes induced by anxiolytics on vital signs, laboratory parameters and adverse events. In return, in a more specific way for anxiolytics, we will look at side effects at the central nervous system level with psychological and physiological battery tests. We will also assess the safety of use of anxiolytics in certain specific conditions, such as overdose or withdrawal and in certain populations such as the elderly, neonates and children. The assessment of safety and side effects, whatever the drug type studied, must come early in the developing process of a drug (phases I, II and III).


1998 ◽  
Vol 8 (1) ◽  
pp. 31-43
Author(s):  
Linda M Luxon

The cochleovestibular system is unique in that the peripheral labyrinth subserves two senses, hearing and balance, while the central auditory and vestibular connections diverge within the central nervous system and interact with a multiplicity of information from other sensory inputs. During the seventh decade of life, approximately 40% of people in Great Britain have a significant hearing impairment while in the eighth decade of life this figure rises to 60%. By the age of 65, 35% of people have experienced episodes of dizziness and by the age of 80, two-thirds of women and one-third of men have suffered episodes of vertigo. The elderly population is reported to be increasing by approximately 30% every 20 years and the prevalence of vertigo and hearing loss has been reported to rise in parallel with advancing age.


Antioxidants ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 46 ◽  
Author(s):  
Rafael Franco ◽  
Gemma Navarro ◽  
Eva Martínez-Pinilla

Differential antioxidant action is found upon comparison of organ/tissue systems in the human body. In erythrocytes (red blood cells), which transport oxygen and carbon dioxide through the circulatory system, the most important issue is to keep hemoglobin in a functional state that requires maintaining the haem group in ferrous (Fe2+) state. Conversion of oxidized Fe3+ back into Fe2+ in hemoglobin needs a special mechanism involving a tripeptide glutathione, glucose-6-phosphate dehydrogenase, and glucose and NADPH as suppliers of reducing power. Fava beans are probably a good resource to make the detox innate system more robust as the pro-oxidant molecules in this food likely induce the upregulation of members of such mechanisms. The central nervous system consumes more oxygen than the majority of human tissues, i.e., 20% of the body’s total oxygen consumption and, therefore, it is exposed to a high level of oxidative stress. This fact, together with the progressive age-related decline in the efficiency of the antioxidant defense system, leads to neuronal death and disease. The innate mechanism operating in the central nervous system is not well known and seems different to that of the erythrocytes. The strategies of antioxidant intervention in brain will be reviewed here.


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