CoChat
Sign Up
Cited by 108Muscle activation and electromyography studiesPain Mechanisms and TreatmentsMuscle Physiology and Disorders

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Immobilization induces changes in presynaptic control of group Ia afferents in healthy humans

Open access
Lundbye‐Jensen, Jesper, Nielsen, Jens Bo·2008·The Journal of Physiology
DOI 10.1113/jphysiol.2008.156547PMC PMC2652189
Open this paper in CoChat — free accountOpen PDF

Abstract

Neural plasticity occurs throughout adult life in response to maturation, use and disuse. Recent studies have documented that H‐reflex amplitudes increase following a period of immobilization. To elucidate the mechanisms contributing to the increase in H‐reflex size following immobilization we immobilized the left foot and ankle joint for 2 weeks in 12 able‐bodied subjects. Disynaptic reciprocal inhibition of soleus (SOL) motoneurons and presynaptic control of SOL group Ia afferents was measured before and after the immobilization as well as following 2 weeks of recovery. Following immobilization, maximal voluntary plantar‐ and dorsiflexion torque (MVC) was significantly reduced and the maximal SOL H‐reflex amplitude increased with no changes in the maximal compound motor response (M max). Decreased presynaptic inhibition of the Ia afferents probably contributed to the increase of the H‐reflex size, since we observed a significant decrease in the long‐latency depression of the SOL H‐reflex evoked by peroneal nerve stimulation (D2 inhibition) and an increase in the size of the monosynaptic Ia facilitation of the SOL H‐reflex evoked by femoral nerve stimulation. These two measures provide independent evidence of changes in presynaptic inhibition of SOL Ia afferents and taken together suggest that GABAergic presynaptic inhibition of the SOL Ia afferents is decreased following 2 weeks of immobilization. The depression of the SOL H‐reflex when evoked at intervals shorter than 10 s (homosynaptic post‐activation depression) also decreased following immobilization, suggesting that the activity‐dependent regulation of transmitter release from the afferents was also affected by immobilization. We observed no significant changes in disynaptic reciprocal Ia inhibition. Two weeks after cast removal measurements returned to pre‐immobilization levels. Together, these observations suggest that disuse causes plastic changes in spinal interneuronal circuitries responsible for presynaptic control of sensory input to the spinal cord. This may be of significance for the motor disabilities seen following immobilization as well as the development of spasticity following central motor lesions.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1113/jphysiol.2008.156547

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Neuronal factors have been specified by increased coactivation of antagonistic muscles in voluntary movement, increasing the vector force that counteracts movement direction, as well as adaptations on the spinal circuitries and supraspinal level within the central nervous system.

    “However, the neuronal factors have been specified by an increased coactivation of antagonistic muscles in voluntary movement (92) increasing the vector force, which counteracts the movement direction as well as adaptations on the spinal circuitries and supraspinal level within the central nervous system (93, 94).”

    From Nonuniform loss of muscle strength and atrophy during bed rest: a systematic review (2021) · cites this paper as [93]

    Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

  • Sensory input is processed and integrated differently into motor programs after periods of disuse, and the excitability of interneurons of the motor cortex and spinal alpha motoneurons is modulated in response to immobilization.

    “Sensory input is processed and integrated differently into motor programs after periods of disuse (93), and the excitability of interneurons of the motor cortex and spinal alpha motoneurons is modulated in response to immobilization (94).”

    From Nonuniform loss of muscle strength and atrophy during bed rest: a systematic review (2021) · cites this paper as [93]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 75

  1. Anderson J, 1999, Reflex and muscular adaptations in rat soleus muscle after hindlimb suspension, J Exp Biol, 202, 2701, 10.1242/jeb.202.19.2701 · DOI
  2. 10.1093/brain/123.8.1688 · DOI
  3. Baldissera F, 1981, Handbook of Physiology, section 1, The Nervous System, 509
  4. 10.1523/JNEUROSCI.5692-07.2008 · DOI
  5. 10.1523/JNEUROSCI.06-05-01308.1986 · DOI
  6. 10.1152/jn.1995.73.1.411 · DOI
  7. 10.1152/japplphysiol.01402.2005 · DOI
  8. 10.1152/japplphysiol.01404.2005 · DOI
  9. 10.1113/jphysiol.2005.091835 · DOI
  10. 10.1113/jphysiol.1987.sp016652 · DOI
  11. 10.1007/BF00230098 · DOI
  12. 10.1007/BF00230683 · DOI
  13. 10.1113/jphysiol.1989.sp017759 · DOI
  14. 10.1113/jphysiol.1960.sp006393 · DOI
  15. 10.1007/BF00690897 · DOI
  16. 10.1152/jn.1998.79.3.1329 · DOI
  17. Duchateau J, 1995, Bed rest induces neural and contractile adaptations in triceps surae, Med Sci Sports Exerc, 27, 1581
  18. 10.1152/jappl.1987.62.6.2168 · DOI
  19. 10.1016/S0079-6123(08)60618-4 · DOI
  20. 10.1152/jn.2002.88.4.1664 · DOI
  21. 10.1007/BF00229628 · DOI
  22. 10.1093/brain/117.6.1449 · DOI
  23. Frank K, 1957, Presynaptic and postsynaptic inhibition of monosynaptic reflexes, Federation Proceeding, 39
  24. 10.1113/jphysiol.1979.sp012807 · DOI
  25. 10.1007/s00421-004-1225-z · DOI · Paper page
  26. 10.1007/s00221-007-1142-6 · DOI
  27. 10.3200/JMBR.39.1.68-78 · DOI
  28. Hultborn H, 2004, Key mechanisms for setting the input‐output gain across the motoneuron pool, Prog Brain Res, 143, 77
  29. 10.1007/BF00227268 · DOI
  30. 10.1113/jphysiol.1987.sp016680 · DOI
  31. Hultborn H, 1998, Presynaptic Inhibition and Neural Control, 178
  32. 10.1113/jphysiol.1996.sp021207 · DOI
  33. 10.1136/jnnp.49.8.937 · DOI
  34. 10.1016/0006-8993(84)90967-3 · DOI
  35. Kandel ER, 2000, Principles of Neural Science
  36. 10.1093/brain/111.2.417 · DOI
  37. 10.1007/s004210000330 · DOI · Paper page
  38. 10.1016/0006-8993(90)90542-J · DOI
  39. 10.1007/PL00005765 · DOI
  40. 10.1113/jphysiol.1992.sp018996 · DOI
  41. 10.1007/BF00232189 · DOI
  42. 10.1152/japplphysiol.00687.2007 · DOI
  43. Manabe T, 1989, Disuse‐induced enhancement of Ia synaptic transmission in spinal motoneurons of the rat, J Neurosci, 9, 2455, 10.1523/JNEUROSCI.09-07-02455.1989 · DOI
  44. 10.1113/jphysiol.2006.122911 · DOI
  45. 10.1113/jphysiol.1989.sp017896 · DOI
  46. 10.1007/s002210050357 · DOI
  47. 10.1007/BF00234121 · DOI
  48. 10.1152/jn.1971.34.6.1010 · DOI
  49. 10.1007/s002210050388 · DOI
  50. 10.1111/j.1748-1716.1993.tb09515.x · DOI
  51. 10.1113/jphysiol.1993.sp019652 · DOI
  52. 10.1007/BF00228827 · DOI
  53. 10.1093/brain/118.4.995 · DOI
  54. 10.1016/S1050-6411(02)00023-8 · DOI
  55. 10.1016/S0079-6123(00)28007-2 · DOI
  56. 10.1152/jn.00988.2007 · DOI
  57. 10.1113/jphysiol.2005.089904 · DOI
  58. 10.1016/S0165-0270(98)00044-2 · DOI
  59. 10.1016/0301-0082(96)00002-0 · DOI
  60. 10.1007/BF00237499 · DOI
  61. Pinco M, 1993, Modulation of monosynaptic excitation in the neonatal rat spinal cord, J Neurophysiol, 70, 1151, 10.1152/jn.1993.70.3.1151 · DOI
  62. 10.1016/0166-2236(90)90084-N · DOI
  63. 10.1016/S0079-6123(02)36033-3 · DOI
  64. 10.1007/s002210050933 · DOI
  65. 10.1146/annurev.neuro.23.1.393 · DOI
  66. 10.1007/BFb0047741 · DOI
  67. 10.1016/j.jelekin.2005.10.008 · DOI
  68. 10.1111/j.1469-7793.2001.0507k.x · DOI
  69. 10.1111/j.1469-7793.2001.0521k.x · DOI
  70. 10.1046/j.1365-201X.2001.00853.x · DOI
  71. 10.1002/(SICI)1097-4598(199808)21:8<1006::AID-MUS4>3.0.CO;2-C · DOI
  72. 10.1113/expphysiol.1984.sp002860 · DOI
  73. 10.1111/j.1748-1716.2006.01656.x · DOI
  74. 10.1152/jn.1983.50.6.1296 · DOI
  75. 10.1016/0006-8993(83)91059-4 · DOI

Cited by

Sorted by citations

Metadata

Authors
Lundbye‐Jensen, J., & Nielsen, J. B.
Affiliations
University of Copenhagen (DK)
ORCID
Venue
The Journal of Physiology
Publisher
Wiley
Published
2008-09
Volume
586
Issue
17
Pages
4121-4135
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.2008.156547
PMC
PMC2652189
OpenAlex
W1866755470
Cited by
108
References
2
Citations by year
2026: 2 · 2025: 7 · 2024: 5 · 2023: 10 · 2022: 7 · 2021: 5 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 5 · 2015: 4 · 2014: 7 · 2013: 8 · 2012: 6
FWCI
4.63
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 9 d)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Funders
  • Novo Nordisk
  • Elsass Fonden
  • Kulturministeriet
Topics
  • Physical Sciences › Engineering › Biomedical Engineering › Muscle activation and electromyography studies
  • Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
immobilization, disuse, Ia afferents, presynaptic inhibition, GABAergic inhibition, H-reflex, post-activation depression, neuroplasticity, spasticity
MeSH terms
Adult, Afferent Pathways, Ankle, Electric Stimulation, Female, Femoral Nerve, Foot, Humans, Male, Muscle Contraction, Neural Inhibition, Synaptic Transmission, Neuronal Plasticity, Neurons, Afferent, Peroneal Nerve, Restraint, Physical, Spinal Cord, Presynaptic Terminals, Muscle, Skeletal

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review