Recovery From 50 Eccentric Biceps Curls in Young, Untrained Men and Women
Condition: Recovery; Muscle Damage; Muscle Stiffness; Cell Structure Alteration; Calcium Cycling
Study type: Interventional

Summary: 
      The purpose of the study is to investigate muscle stiffness in relation to muscle damaging
      work and to investigate how well the change in muscle stiffness correlates with the degree of
      muscle damage (myofibrillar disruption and necrosis). To date, the reduction in
      force-generating capacity is the best non-invasive marker of muscle damage. It is already
      established that muscle stiffness correlates well with the decline in force-generating
      capacity after damaging exercise. However, the correlation between degree of muscle damage
      and muscle stiffness has not yet been investigated. The main focus of the study is therefore
      to investigate the relationship between muscle stiffness and muscle damage. Further, the
      researchers aim to investigate how calcium cycling is affected by damaging work, and if
      impaired calcium cycling may partially explain the observed reduction in force-generating
      capacity.
    

Detailed description: 
      Regardless of whether an individual is in rehabilitation or exercise for general health or
      athletic performance, resistance exercise is an essential form of exercise when the goal is
      to increase muscle mass, strength and function. Although, resistance exercise primarily is
      associated with positive effects it may also result in muscle damage when the exercise is of
      high intensity and/or unaccustomed. This is known as exercise-induced muscle damage (EIMD)
      and is reflected by a substantial decrease in force-generating capacity and often accompanied
      by intracellular swelling and delayed onset muscle soreness. On a cellular level, EIMD
      include myofibrillar disruption, inflammatory response and in severe cases of EIMD; myofibre
      necrosis. While EIMD with its symptoms clearly is evident, its underlying mechanisms are
      still to be fully elaborated.

      One interesting hypothesis regarding the molecular basis of decreased muscle strength as a
      result of EIMD, is related to the strain of this exercise mode causing "popped" sarcomeres.
      When sarcomeres are stretched beyond actin-myosin overlap, some sarcomeres may over-stretch.
      This results in overload of membranes, leading to opening of stretch-activated channels, and
      subsequently influx of Ca2+. High levels of cytoplasmic Ca2+ may cause degradation of
      contractile proteins or Excitation-Contraction coupling proteins mediated through increased
      calpain activity. However, a recent study by Cully and colleagues (2017) suggest a protective
      mechanism post heavy-load strength training related to Ca2+-handling. Cully et al. observed
      formation of vacuoles in longitudinally connecting tubules post exercise when exposing fibers
      to 1.3 μM [Ca2+] in the cytoplasma. These vacuoles provide an enclosed compartment where Ca2+
      can be accumulated, preventing Ca2+ from initiating damage to the muscle. The role of
      Ca2+-regulation in recovery of muscle function warrants further investigation and
      clarification.

      To the best of the investigators knowledge, the most valid method for estimating EIMD is by
      investigating myofibrillar disruption, and in some cases necrosis, in muscle biopsies. This
      requires many resources and is rather expensive. Currently, the best non-invasive marker of
      muscle damage is the force deficit observed at 48 hours post exercise. However, a measurement
      estimating muscle damage immediately post exercise is warranted because force deficit
      immediately post exercise will be confounded by muscle fatigue.

      A novel study performed by Lacourpaille et al. (2017) showed a strong negative correlation
      (-0.80) between stiffness of the muscle tissue, shear modulus, measured 30 minutes post
      exercise and peak isometric force measured at 48 hours post exercise and therefore a strong
      relationship between the decline in force production capacity and increased stiffness post
      exercise, suggesting a possible method to predict EIMD immediately after exercise. However,
      direct evidence of this association is warranted, with measurements of shear modulus and EIMD
      biomarkers, such as the proportion of disrupted fibers and sarcoplasmic Ca2+ regulation.

      The ability to predict EIMD after training is of great interest to athletes, but also
      patients suffering from e.g. muscular dystrophies. Being able to predict EIMD quickly and
      non-invasively after exercise will help employ optimal recovery.

      The aim of this project is to investigate the link between exercise-induced muscle damage
      (EIMD) as changes in shear modulus by ultrasound shear wave elastography, and muscle damage
      as observed in the analysis of muscle biopsies. The hypothesis is that there is a strong
      relationship between muscle stiffness acute post exercise and degree of muscle damage
      observed in muscle biopsies. A secondary aim is to further the understanding of cellular
      mechanisms causing EIMD and the role of Ca2+ in the recovery of muscle function.
    

Intervention name(s): Eccentric biceps curls
Intervention type(s): Other
Intervention description(s): 10 x 5 repetitions of eccentric biceps curls, interspaced by 30 seconds of rest.
Allocation: Randomized
Intervention model: Parallel Assignment
Intervention model description: Participants perform one bout of eccentric exercise with one arm, while the contralateral arm serves as control. Which arm who receives eccentric exercise is randomized between dominant/non-dominant arm.
Masking: Single (Outcomes Assessor)
Primary purpose: Basic Science