Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Factors in delayed muscle soreness

W M Abraham

    Medicine and Science in Sports
    |January 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    Delayed muscle soreness after exercise may stem from connective tissue damage, not muscle spasms or cell damage alone. Research indicates a link between exercise-induced soreness and disruptions in muscle connective tissues.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    NVP-QBE170: an inhaled blocker of the epithelial sodium channel with a reduced potential to induce hyperkalaemia.

    British journal of pharmacology·2015
    Same author

    A prostaglandin D2 receptor antagonist modifies experimental asthma in sheep.

    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2009
    Same author

    Camostat attenuates airway epithelial sodium channel function in vivo through the inhibition of a channel-activating protease.

    The Journal of pharmacology and experimental therapeutics·2009
    Same author

    L-454,560, a potent and selective PDE4 inhibitor with in vivo efficacy in animal models of asthma and cognition.

    Biochemical pharmacology·2007
    Same author

    Elevated tissue kallikrein activity in airway secretions from patients with tracheobronchitis associated with prolonged mechanical ventilation.

    Lung·2004
    Same author

    Pharmacology of INS37217 [P(1)-(uridine 5')-P(4)- (2'-deoxycytidine 5')tetraphosphate, tetrasodium salt], a next-generation P2Y(2) receptor agonist for the treatment of cystic fibrosis.

    The Journal of pharmacology and experimental therapeutics·2002

    Area of Science:

    • Exercise Physiology
    • Biochemistry
    • Sports Medicine

    Background:

    • Delayed onset muscle soreness (DOMS) is a common post-exercise phenomenon.
    • Existing hypotheses attribute DOMS to muscle spasms, cell damage, or connective tissue issues.

    Purpose of the Study:

    • To investigate the underlying causes of delayed muscle soreness occurring 24-48 hours after exercise.
    • To differentiate between muscle spasm, muscle cell damage, and connective tissue involvement.

    Main Methods:

    • Surface electromyograms (EMG) assessed muscle spasm.
    • Myoglobinuria monitored for muscle cell damage.
    • Hydroxyproline/creatinine (OHP/Cr) ratio in urine measured connective tissue changes.

    Main Results:

    Related Experiment Videos

    • EMG showed no change in sore muscles, ruling out spasm as the primary cause.
    • Myoglobinuria was present in most subjects with and without soreness, indicating it's not solely linked to soreness.
    • Increased OHP/Cr ratio post-exercise, especially on days of maximal soreness, suggests connective tissue disruption.

    Conclusions:

    • Muscle spasm and general muscle cell damage (indicated by myoglobinuria) are unlikely primary causes of DOMS.
    • Findings support the hypothesis that exercise-induced soreness is related to the disruption of muscle connective tissue elements.