Trial reportThe Journal of physiology2002
Contraction-induced muscle damage in humans following calcium channel blocker administration.
Trial report in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exercise-Induced Muscle Damage after a High-Intensity Interval Exercise Session: Systematic Review.International journal of environmental research and public health · 2023Pooled it
- A low dose of alcohol does not impact skeletal muscle performance after exercise-induced muscle damage.European journal of applied physiology · 2011Trial
- Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes.PloS one · 2010Trial
- Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Trial
- Thromboxane signalling links immune activation to enhanced glucose uptake in skeletal muscle.Diabetologia · 2026Article
- Integrated cross-species translation and biophysical multi-scale modeling links molecular signatures and locomotory phenotypes in spaceflight-induced sarcopenia.NPJ microgravity · 2026Article
- Integrated Cross-Species Translation and Biophysical Multi-Scale Modeling Links Molecular Signatures and Locomotory Phenotypes in Spaceflight-Induced Sarcopenia.bioRxiv : the preprint server for biology · 2025Article
- Recycle, repair, recover: the role of autophagy in modulating skeletal muscle repair and post-exercise recovery.Bioscience reports · 2025Review
- Skeletal Muscle Damage and Inflammation.Advances in experimental medicine and biology · 2025Review
- Skeletal muscle myosin heavy chain fragmentation as a potential marker of protein degradation in response to resistance training and disuse atrophy.Experimental physiology · 2024Article
- Skeletal muscle myosin heavy chain protein fragmentation as a potential marker of protein degradation in response to resistance training and disuse atrophy.bioRxiv : the preprint server for biology · 2024Article
- Newly Synthesized Creatine Derivatives as Potential Neuroprotective and Antioxidant Agents on In Vitro Models of Parkinson's Disease.Life (Basel, Switzerland) · 2023Article
- Role of macrophages during skeletal muscle regeneration and hypertrophy-Implications for immunomodulatory strategies.Physiological reports · 2022Review
- Circulating Concentration of Chemical Elements During Exercise-Induced Muscle Damage and the Repeated Bout Effect.Biological trace element research · 2022Article
- Nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage and accelerate recovery in athletes: current knowledge, practical application and future perspectives.European journal of applied physiology · 2020Review
- Immunohistochemical Identification of Human Skeletal Muscle Macrophages.Bio-protocol · 2018Article
- The General Adaptation Syndrome: A Foundation for the Concept of Periodization.Sports medicine (Auckland, N.Z.) · 2018Review
- The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis.European journal of applied physiology · 2018Review
- Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage.The Journal of physiology · 2016Article
- The serine protease, dipeptidyl peptidase IV as a myokine: dietary protein and exercise mimetics as a stimulus for transcription and release.Physiological reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following contraction-induced damage of skeletal muscle there is a loss of calcium homeostasis. Attenuating the damage-induced rise in myocellular calcium concentration may reduce proteolytic activation and attenuate other indices of damage; calcium channel blockers have been shown to be effective in this regard. The effect of administration of a calcium channel blocker (CCB), amlodipine, on indices of muscle damage following a unilateral 'damage protocol', during which subjects performed 300 maximal isokinetic (0.52 rad s(-1)) eccentric contractions with the knee extensors was investigated. The design was a randomized, double-blind crossover. On one occasion, prior to the damage protocol, subjects consumed CCB for 7 days prior to and for 7 days following the damage protocol. Biopsies were taken from the vastus lateralis prior to (baseline) and following the damage protocol at 4 h and 24 h post-damage. Isometric peak knee extensor torque was reduced (P < 0.05) immediately post-, 24 h post- and 48 h post-damage protocol compared to pre-exercise values with no effect of treatment. Desmin disruption was attenuated (P < 0.05) with CCB versus placebo at 4 h post-damage. Z-band streaming was significantly (P < 0.05) elevated compared to baseline at both times post-damage, but was lower with CCB at 4 h (P < 0.05). Damage resulted in increased inflammatory cell (macrophage) infiltration into skeletal muscle at both 4 h and 24 h post-damage, with no effect of CCB. Neutrophil number was elevated by the damage protocol, but was higher at 24 h post-damage in the CCB condition (P < 0.05). Creatine kinase (CK) activity was higher (P < 0.05) at 24 h and 48 h following the damage protocol compared to baseline, with no effect of treatment. In conclusion, the reduction in desmin disruption and Z-band streaming indicates that CCB attenuated, or delayed, the contraction-induced damage to sarcomeric proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.