SarcopeniaNCT03326648
The Role of Muscle Protein Breakdown in the Regulation of Muscle Quality in Frail Elderly Individuals
A study testing Strength training and Protein supplementation in people with Sarcopenia, run by Truls Raastad at 1 site in Norway.
Trial summary
The purpose of this study is to investigate mechanisms underlying the reduction in muscle quality (the ratio between muscle strength and muscle size) with aging, and to investigate how these factors are affected by strength training and protein supplementation. Read more about this study
- Who is it for?
- Ages 65 years and olderHealthy volunteers can take part
- Conditions the study is for
- Sarcopenia
- What is being tested?
- Strength training and Protein supplementation
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 34 participants
- Where
- 1 siteNorway
- Study dates
- 1 Sep 2016to 1 Mar 2018
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 65 years and older
- All sexes
- Healthy volunteers accepted
- Older adult
Who may be able to join
- Age > 65
- Frail or pre-frail according to the Fried Frailty Criteria or Short Physical Performance Battery (SPPB) score <6.
- Mini Mental State Examination score > 18
Who cannot join
- Diseases or injuries contraindicating participation
- Lactose intolerance
- Allergy to milk
- Allergy towards local anesthetics (xylocain)
- Use of anticoagulants that cannot be discontinued prior to the muscle biopsy
Trial locations and contacts
1 site in 1 country.
About this study
The purpose of this study is to investigate mechanisms underlying the reduction in muscle quality (the ratio between muscle strength and muscle size) with aging, and to investigate how these factors are affected by strength training and protein supplementation. It is already established that muscle quality defined as the ratio between the strength and the size of a muscle is improved with strength training, even in frail elderly individuals. However, the relative contribution of factors such as activation level, fat infiltration, muscle architecture and single fiber function is unknown. The main focus of this study is to investigate the relationship between muscle quality and muscle protein breakdown, as insufficient degradation of proteins is hypothesized to negatively affect muscle quality.
Read the detailed description
Aging is associated with impaired skeletal muscle function. This is evident not only by a reduced capacity to generate force and power at the whole muscle level, but also by a decline in individual muscle fiber contraction velocity and force generation. Combined with muscle atrophy, these changes lead to reduced muscle strength and quality and loss off physical function with age. Clinically, muscle quality may be a better indicator of overall functional capacity than absolute muscle strength. Thus, identifying the mechanisms underlying the age-related loss of muscle quality is of high relevance for the prevention of functional impairment with aging. The explanation for the loss of muscle quality with aging seems to be multifactorial, with alterations in voluntary muscle activation, muscle architecture, fat infiltration and impaired contractile properties of single muscle fibers being likely contributors. Single fiber specific force seems to be related to myosin heavy chain (MHC) content, which is thought to reflect the number of available cross-bridges. The reduction of single fiber specific force with aging may thus be a consequence of reduced synthesis of MHC and/or increased concentration of non-contractile tissue (e.g. intramyocellular lipids).
Some studies in mice also indicate attenuated activity in some of the pathways responsible for degradation of muscle proteins with aging (especially autophagy). As a result, damaged proteins and organelles are not removed as effectively as they should, which could ultimately compromise the muscle's ability to produce force. In addition, reduced efficiency of mitophagy and lipophagy (two specific forms of autophagy), may indirectly affect single fiber specific force, through oxidative damage by reactive oxygen species (ROS) and increased levels of intramyocellular lipids, respectively. Although animal studies indicate attenuated autophagic function, exercise seems to restore the activity in this pathway. Whether this also is the case in humans is unknown. Thus, the purpose of this study is to investigate how the different factors contributing to reduced muscle quality in frail elderly individuals, with emphasis on the relationship between muscle quality and autophagy, may be counteracted by a specific strength training program targeting muscle quality and muscle mass.
In this randomized controlled trial the investigators will aim to recruit frail elderly individuals, as muscle quality is shown to be low in this population. As a consequence, the potential for improved muscle quality is expected to be large. Subjects will be randomized to two groups; one group performing strength training twice a week for 10 weeks in addition to receiving daily protein supplementation. The other group will only receive the protein supplement. Several tests will be performed before and after the intervention period, including a test day where a biopsy is obtained both at rest, and 2.5 hours following strength training + protein supplementation or protein supplementation only. This will provide information about the regulation of muscle protein breakdown in a resting state, following protein intake and following strength training in combination with protein intake. As this will be done both before and after the training period, it will also provide information on how long-term strength training affects the activity in these systems.
- Conditions
- Sarcopenia
- Being tested
- Strength training, Protein supplementation
- Keywords
- Sarcopenia, Frailty, Strength training, Autophagy
- Medical subject headings
- Sarcopenia, Frailty
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Strength trainingOther
Also called Resistance training
Heavy load strength training performed twice a week for 10 weeks.
Protein supplementationDietary supplement
Dietary protein supplement (protein-enriched milk with 0,2 % fat). 0,33 l each day for 10 weeks.
| Study group | Role | What they receive |
|---|---|---|
| Strength training + protein supplement | Experimental | Two sessions of strength training each week in addition to daily protein supplementation for 10 weeks. Receives: Other: Strength training; Dietary Supplement: Protein supplementation |
| Protein supplement | Experimental | Daily protein supplementation for 10 weeks. Receives: Dietary Supplement: Protein supplementation |
What is being measured
The primary outcome is the main question the study is designed to answer.
Single fiber specific force
A measure of muscle quality at the single fiber level. Biopsies obtained from m. Vastus Lateralis
Measured: Change from baseline at 10 weeks
Secondary outcomes (51)
Lean mass
Measured by a Dual-energy X-ray absorptiometry (DXA) scan
Measured: Change from baseline at 10 weeks
Fat mass
Measured by a Dual-energy X-ray absorptiometry (DXA) scan
Measured: Change from baseline at 10 weeks
Bone mineral density
Measured by a Dual-energy X-ray absorptiometry (DXA) scan
Measured: Change from baseline at 10 weeks
Muscle strength of m. quadriceps
Maximal isometric and dynamic muscle strength of m. quadriceps
Measured: Change from baseline at 10 weeks
Muscle size of m. quadriceps
Cross-sectional area of m. quadriceps measured by a Computed Tomography scan
Measured: Change from baseline at 10 weeks
Fat infiltration of m. quadriceps
Fat infiltration of m. quadriceps measured by a Computed Tomography scan
Measured: Change from baseline at 10 weeks
Muscle activation
Voluntary activation level during a maximal isometric knee extension using the interpolated twitch technique
Measured: Change from baseline at 10 weeks
Fractional Breakdown Rate
Measurement of fractional breakdown rate by the use of orally provided Deuterium Oxide, biopsies and blood samples
Measured: Measured over the last 14 days of the intervention period
m. Vastus Lateralis thickness
Measured by ultrasound
Measured: Change from baseline at 10 weeks
Chair stand performance
Time (sec) to stand up from a chair five times
Measured: Change from baseline at 10 weeks
Habitual gait velocity
Time (sec) to walk 6 meters at habitual gait velocity
Measured: Change from baseline at 10 weeks
Maximal gait velocity
Time (sec) to walk 6 meters as fast as possible
Measured: Change from baseline at 10 weeks
Level/cellular location of Microtubule-associated protein 1A/1B-light chain 3 (LC3)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of p62/Sequestosome-1
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of Lysosome-associated membrane glycoprotein 2 (LAMP2)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of forkhead box O3 (FOXO3a)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of ribosomal protein S6 kinase beta-1(P70S6K)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of eukaryotic elongation factor 2 (eEF-2)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of eukaryotic translation initiation factor 4E-binding protein 1 (4EBP-1)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of muscle RING-finger protein-1 (Murf-1)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of ubiquitin (Ub)
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Blood serum glucose
Fasted
Measured: Change from baseline at 10 weeks
Blood serum insulin
Fasted
Measured: Change from baseline at 10 weeks
Blood plasma Hemoglobin A1c (HbA1c)
Fasted
Measured: Change from baseline at 10 weeks
Blood serum Triglycerides
Fasted
Measured: Change from baseline at 10 weeks
Blood serum High-density lipoproteins (HDL)
Fasted
Measured: Change from baseline at 10 weeks
Blood serum Low-density lipoproteins (LDL)
Fasted
Measured: Change from baseline at 10 weeks
Blood serum C-reactive protein (CRP)
Fasted
Measured: Change from baseline at 10 weeks
forkhead box protein O3 (FOXO3A) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
forkhead box protein O1 (FOXO1) mRNA mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
hepatocyte growth factor (HGF) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
insulin-like growth factor I (IGF1) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
myostatin (MSTN) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
E3 ubiquitin-protein ligase TRIM63 (TRIM63) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
p62/Sequestosome-1 mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
muscle RING-finger protein-1 (Murf-1) protein 1 (4EBP-1) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Atrogin1 mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Microtubule-associated protein 1A/1B-light chain 3 (LC3) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
BCL2/adenovirus E1B interacting protein 3 (BNIP3) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
PTEN-induced putative kinase 1 (PINK1) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
TNF receptor associated factor 6 (TRAF6) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
transcription factor EB (Tfeb) mRNA
Biopsies from m. Vastus Lateralis analyzed by western blot
Measured: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Intramyocellular lipids
Oil-Red-O staining of muscle sections. Biopsy from m. Vastus Lateralis analyzed by immunohistochemistry
Measured: Change from baseline at 10 weeks
Muscle fiber type distribution
Biopsy from m. Vastus Lateralis analyzed by immunohistochemistry
Measured: Change from baseline at 10 weeks
Muscle fiber cross-sectional area
Biopsy from m. Vastus Lateralis analyzed by immunohistochemistry
Measured: Change from baseline at 10 weeks
Muscle satellite cells
Biopsy from m. Vastus Lateralis analyzed by immunohistochemistry
Measured: Change from baseline at 10 weeks
Myonuclei
Biopsy from m. Vastus Lateralis analyzed by immunohistochemistry
Measured: Change from baseline at 10 weeks
Myonuclei number
Biopsy from m. Vastus Lateralis analyzed by confocal microscopy
Measured: Change from baseline at 10 weeks
Myonuclei location
Biopsy from m. Vastus Lateralis analyzed by confocal microscopy
Measured: Change from baseline at 10 weeks
Amount of mitochondria
Biopsy from m. Vastus Lateralis analyzed by confocal microscopy
Measured: Change from baseline at 10 weeks
Location of mitochondria
Biopsy from m. Vastus Lateralis analyzed by confocal microscopy
Measured: Change from baseline at 10 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted31 Oct 2017
- Study start1 Sep 2016
- Primary completion20 Dec 2017
- Study completion1 Mar 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for SarcopeniaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Single blind
- Who is masked
- Outcomes assessor
- Enrolment
- 34 participants (actual)
Sponsor and investigators
- Lead sponsor
- Truls Raastad
- Sponsor type
- University, hospital or other
- Collaborators
- University of Padova, University of Copenhagen, Tine
- Responsible party
- Sponsor-investigator, Truls Raastad, Norwegian School of Sport Sciences
- Investigators
- Truls Raastad, Prof., Principal investigator, Norwegian School of Sport Sciences
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03326648
- Sponsor's protocol ID
- STAS
- Status last verified
- Apr 2018
- First submitted
- 5 May 2017
- Last updated
- 11 Apr 2018
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 11 Apr 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Role of Muscle Protein Breakdown in the Regulation of Muscle Quality in Frail Elderly Individuals
- ClinicalTrials.gov ID
- NCT03326648
- Acronym / sponsor ID
- STAS
- Conditions
- Sarcopenia
- Keywords
- Sarcopenia, Frailty, Strength training, Autophagy
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 34 participants (actual)
- Lead sponsor
- Truls RaastadUniversity, hospital or other
- Collaborators
- University of Padova, University of Copenhagen, Tine
- Study start
- 1 Sep 2016 (actual)
- Primary completion
- 20 Dec 2017 (actual)
- Study completion
- 1 Mar 2018 (actual)
- First posted
- 31 Oct 2017 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The purpose of this study is to investigate mechanisms underlying the reduction in muscle quality (the ratio between muscle strength and muscle size) with aging, and to investigate how these factors are affected by strength training and protein supplementation. It is already established that muscle quality defined as the ratio between the strength and the size of a muscle is improved with strength training, even in frail elderly individuals. However, the relative contribution of factors such as activation level, fat infiltration, muscle architecture and single fiber function is unknown. The main focus of this study is to investigate the relationship between muscle quality and muscle protein breakdown, as insufficient degradation of proteins is hypothesized to negatively affect muscle quality.
Detailed description
Aging is associated with impaired skeletal muscle function. This is evident not only by a reduced capacity to generate force and power at the whole muscle level, but also by a decline in individual muscle fiber contraction velocity and force generation. Combined with muscle atrophy, these changes lead to reduced muscle strength and quality and loss off physical function with age. Clinically, muscle quality may be a better indicator of overall functional capacity than absolute muscle strength. Thus, identifying the mechanisms underlying the age-related loss of muscle quality is of high relevance for the prevention of functional impairment with aging. The explanation for the loss of muscle quality with aging seems to be multifactorial, with alterations in voluntary muscle activation, muscle architecture, fat infiltration and impaired contractile properties of single muscle fibers being likely contributors. Single fiber specific force seems to be related to myosin heavy chain (MHC) content, which is thought to reflect the number of available cross-bridges. The reduction of single fiber specific force with aging may thus be a consequence of reduced synthesis of MHC and/or increased concentration of non-contractile tissue (e.g. intramyocellular lipids).
Some studies in mice also indicate attenuated activity in some of the pathways responsible for degradation of muscle proteins with aging (especially autophagy). As a result, damaged proteins and organelles are not removed as effectively as they should, which could ultimately compromise the muscle's ability to produce force. In addition, reduced efficiency of mitophagy and lipophagy (two specific forms of autophagy), may indirectly affect single fiber specific force, through oxidative damage by reactive oxygen species (ROS) and increased levels of intramyocellular lipids, respectively. Although animal studies indicate attenuated autophagic function, exercise seems to restore the activity in this pathway. Whether this also is the case in humans is unknown. Thus, the purpose of this study is to investigate how the different factors contributing to reduced muscle quality in frail elderly individuals, with emphasis on the relationship between muscle quality and autophagy, may be counteracted by a specific strength training program targeting muscle quality and muscle mass.
In this randomized controlled trial the investigators will aim to recruit frail elderly individuals, as muscle quality is shown to be low in this population. As a consequence, the potential for improved muscle quality is expected to be large. Subjects will be randomized to two groups; one group performing strength training twice a week for 10 weeks in addition to receiving daily protein supplementation. The other group will only receive the protein supplement. Several tests will be performed before and after the intervention period, including a test day where a biopsy is obtained both at rest, and 2.5 hours following strength training + protein supplementation or protein supplementation only. This will provide information about the regulation of muscle protein breakdown in a resting state, following protein intake and following strength training in combination with protein intake. As this will be done both before and after the training period, it will also provide information on how long-term strength training affects the activity in these systems.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Single blind (outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Strength training + protein supplement | Experimental | Other: Strength training, Dietary Supplement: Protein supplementationTwo sessions of strength training each week in addition to daily protein supplementation for 10 weeks. |
| Protein supplement | Experimental | Dietary Supplement: Protein supplementationDaily protein supplementation for 10 weeks. |
Who may qualify
- Ages
- 65 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Older adult
Key inclusion criteria (3 listed)
- Age > 65
- Frail or pre-frail according to the Fried Frailty Criteria or Short Physical Performance Battery (SPPB) score <6.
- Mini Mental State Examination score > 18
Key exclusion criteria (5 listed)
- Diseases or injuries contraindicating participation
- Lactose intolerance
- Allergy to milk
- Allergy towards local anesthetics (xylocain)
- Use of anticoagulants that cannot be discontinued prior to the muscle biopsy
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Strength trainingAlso: Resistance trainingHeavy load strength training performed twice a week for 10 weeks. | Other | Strength training + protein supplement |
| Protein supplementationDietary protein supplement (protein-enriched milk with 0,2 % fat). 0,33 l each day for 10 weeks. | Dietary supplement | Protein supplement, Strength training + protein supplement |
Primary outcome
Single fiber specific force
Time frame: Change from baseline at 10 weeks
A measure of muscle quality at the single fiber level. Biopsies obtained from m. Vastus Lateralis
51 secondary outcomes
Lean mass
Time frame: Change from baseline at 10 weeks
Fat mass
Time frame: Change from baseline at 10 weeks
Bone mineral density
Time frame: Change from baseline at 10 weeks
Muscle strength of m. quadriceps
Time frame: Change from baseline at 10 weeks
Muscle size of m. quadriceps
Time frame: Change from baseline at 10 weeks
Fat infiltration of m. quadriceps
Time frame: Change from baseline at 10 weeks
Muscle activation
Time frame: Change from baseline at 10 weeks
Fractional Breakdown Rate
Time frame: Measured over the last 14 days of the intervention period
m. Vastus Lateralis thickness
Time frame: Change from baseline at 10 weeks
Chair stand performance
Time frame: Change from baseline at 10 weeks
Habitual gait velocity
Time frame: Change from baseline at 10 weeks
Maximal gait velocity
Time frame: Change from baseline at 10 weeks
Level/cellular location of Microtubule-associated protein 1A/1B-light chain 3 (LC3)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of p62/Sequestosome-1
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of Lysosome-associated membrane glycoprotein 2 (LAMP2)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of forkhead box O3 (FOXO3a)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of ribosomal protein S6 kinase beta-1(P70S6K)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of eukaryotic elongation factor 2 (eEF-2)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Phosphorylation status and total level of eukaryotic translation initiation factor 4E-binding protein 1 (4EBP-1)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of muscle RING-finger protein-1 (Murf-1)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Level/cellular location of ubiquitin (Ub)
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Blood serum glucose
Time frame: Change from baseline at 10 weeks
Blood serum insulin
Time frame: Change from baseline at 10 weeks
Blood plasma Hemoglobin A1c (HbA1c)
Time frame: Change from baseline at 10 weeks
Blood serum Triglycerides
Time frame: Change from baseline at 10 weeks
Blood serum High-density lipoproteins (HDL)
Time frame: Change from baseline at 10 weeks
Blood serum Low-density lipoproteins (LDL)
Time frame: Change from baseline at 10 weeks
Blood serum C-reactive protein (CRP)
Time frame: Change from baseline at 10 weeks
forkhead box protein O3 (FOXO3A) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
forkhead box protein O1 (FOXO1) mRNA mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
hepatocyte growth factor (HGF) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
insulin-like growth factor I (IGF1) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
myostatin (MSTN) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
E3 ubiquitin-protein ligase TRIM63 (TRIM63) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
p62/Sequestosome-1 mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
muscle RING-finger protein-1 (Murf-1) protein 1 (4EBP-1) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Atrogin1 mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Microtubule-associated protein 1A/1B-light chain 3 (LC3) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
BCL2/adenovirus E1B interacting protein 3 (BNIP3) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
PTEN-induced putative kinase 1 (PINK1) mRNA
Time frame: Before and 2.5 hours after acute training session both at baseline and after 10 weeks
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 11 Apr 2018.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Truls Raastad, Prof. principal investigator
Norwegian School of Sport Sciences
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Strength training and Protein supplementation in people with Sarcopenia, run by Truls Raastad at 1 site in Norway.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 5 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 11 Apr 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Norway. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Single fiber specific force (time frame: Change from baseline at 10 weeks). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 11 Apr 2018.