Peripheral Fatigue: High‐Energy Phosphates and Hydrogen Ions

Keyser, Randall E.

doi:10.1016/j.pmrj.2010.04.009

Cited by 49 publications

(41 citation statements)

References 59 publications

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“…Overweight is universally associated with a loss of insulin sensitivity in muscle, which reduces the efficiency of mitochondria, 33 leading to early fatigue. 34 Of course, the string in this argument remains speculative until the trial has been done, but primary weight reduction could improve metabolic health in two waysFdirectly by improving insulin sensitivity, and permissively by rendering the child more tolerant to physical exercise.…”

Section: Discussionmentioning

confidence: 99%

Can we modulate physical activity in children?

Wilkin

2011

Int J Obes

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Intuition tells us that physical activity is central to weight reduction in obese children. Evidence, on the other hand, suggests that increases in physical activity are difficult to achieve in the short term, and may not be possible in the long term. One explanation could be an 'activitystat', a feedback loop in the child's brain that controls physical activity according to a set point. This brief article, which argues that it may not be possible to modulate the activity of children, reviews the principles of feedback control as they apply to physical activity, discusses evidence for its central control, and demonstrates how a physical activity control loop might operate to defend the set point. Studies restricted to objective measurement suggest that the physical activity of children varies in a systematic, rather than random manner. It varies little from environment to environment, from year to year or from place to place. Where children undertake more activity at one time of day, they appear to compensate at another. Systematic variation of this kind implies control, and the control of physical activity appears to lie with the child, not with his environment. Perturbation (temporary change in response to disturbance) during short-term physical activity interventions may be mistaken for modulation (permanent change in set point), a fundamentally different response. Perturbation lasts no longer than the disturbance that causes it, and there is little evidence that interventions raise activity long term, if at all.

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Section: Discussionmentioning

confidence: 99%

Can we modulate physical activity in children?

Wilkin

2011

Int J Obes

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“…Although murine nNOSμ deficiency substantially increased type IIx fiber number at the expense of more oxidative type IIa fibers, this had no impact on muscle fatigue (Percival et al 2010). Importantly, in contrast to mice, human type IIx fibers are the most prone to fatigue, leading to the prediction that human muscle lacking normal nNOSμ expression would be highly susceptible to fatigue (Keyser 2010). There was a 50% increase in fatigable type IIb fibers in murine muscles lacking both nNOSμ and nNOSβ, again at the expense of type IIa fibers that may contribute to fatigue (Percival et al 2010).…”

Section: Mechanisms By Which Nnos Splice Variants Regulate Skeletal Mmentioning

confidence: 99%

nNOS regulation of skeletal muscle fatigue and exercise performance

Percival

2011

Biophys Rev

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Neuronal nitric oxide synthases (nNOS) are Ca 2+ /calmodulin-activated enzymes that synthesize the gaseous messenger nitric oxide (NO). nNOSμ and the recently described nNOSβ, both spliced nNOS isoforms, are important enzymatic sources of NO in skeletal muscle, a tissue long considered to be a paradigmatic system for studying NO-dependent redox signaling. nNOS is indispensable for skeletal muscle integrity and contractile performance, and deregulation of nNOSμ signaling is a common pathogenic feature of many neuromuscular diseases. Recent evidence suggests that both nNOSμ and nNOSβ regulate skeletal muscle size, strength, and fatigue resistance, making them important players in exercise performance. nNOSμ acts as an activity sensor and appears to assist skeletal muscle adaptation to new functional demands, particularly those of endurance exercise. Prolonged inactivity leads to nNOS-mediated muscle atrophy through a FoxO-dependent pathway. nNOS also plays a role in modulating exercise performance in neuromuscular disease. In the mdx mouse model of Duchenne muscular dystrophy, defective nNOS signaling is thought to restrict contractile capacity of working muscle in two ways: loss of sarcolemmal nNOSμ causes excessive ischemic damage while residual cytosolic nNOSμ contributes to hypernitrosylation of the ryanodine receptor, causing pathogenic Ca 2+ leak. This defect in Ca 2+ handling promotes muscle damage, weakness, and fatigue. This review addresses these recent advances in the understanding of nNOS-dependent redox regulation of skeletal muscle function and exercise performance under physiological and neuromuscular disease conditions.

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“…Whereas central fatigue involves higher-level neurological control mechanisms as described in the Introduction, 6 peripheral fatigue results from a decline in extraocular muscle function associated with increased physical activity derived from non-central nervous system mechanisms. 7 The long-standing debate as to the actual site of this fatigue appears to have been only recently resolved. This critical question was addressed in a recent study for saccades, 45 but which we believe can be extended to the vergence system.…”

Section: Fatigue Vs Oculomotor Learningmentioning

confidence: 99%

“…Central and peripheral mechanisms have been found to be involved in the manifestation of fatigue. 6,7 Centrallybased fatigue is defined as the failure to initiate and/or sustain attentional tasks and physical activities requiring self-motivation. 6 The basal ganglia and their interconnected regions have been identified as the primary neural region for central fatigue.…”

Section: Introductionmentioning

confidence: 99%