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Profiling skeletal muscle loss during leg immobilisation and a reduced energy diet

Effect of reduced energy availability on skeletal muscle loss during leg immobilisation in healthy male adults

Status
Not yet recruiting
Phases
Unknown
Study type
Interventional
Source
ANZCTR
Registry ID
ACTRN12617001391369
Enrollment
12
Registered
2017-09-29
Start date
2017-10-02
Completion date
2018-01-29
Last updated
2017-10-09

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

None listed

Brief summary

The nature of training and competition in the majority of popular sports dictates that debilitating injury is not uncommon when individuals engage in high musculoskeletal loading patterns and/or high impact collisions. A consequence of such injuries is that repair and remodelling of tissues and joints often requires significant periods of limb immobilisation. During immobilisation a reduction in the normal mechanical loading of skeletal muscle results in muscle wasting (atrophy). A challenge for individuals during periods of reduced physical activity (e.g. bed rest) or immobilisation is the management of body composition. The muscle unloading interaction with dietary intake has the capacity to modulate the effects of immobilisation on mechanisms regulating skeletal muscle mass. We (Areta et al. 2014) and others (Pasiakos et al. 2013) have shown that reduced total energy intake (30-40% below energy balance requirements) decreases muscle protein synthesis and results in a loss of fat mass but also muscle mass. However, higher protein intakes (>1.6 g/kg) during energy deficit may attenuate losses in lean mass (Pasiakos et al. 2013), despite an increased expression of genes associated with muscle protein breakdown (Carbone et al. 2013). How these dietary-muscle protein interactions change during periods of immobilisation is unknown. Decreased energy expenditure from cessation of physical activity with immobilisation necessitates restriction of energy intake to prevent undesirable gains in fat mass. However, whether implementing an energy deficit, despite higher protein intakes, exacerbates muscle wasting experienced during muscle unloading is unknown. Importantly, the effect of an energy deficit on the magnitude of muscle loss and the associated underlying molecular profile during immobilisation is currently unknown. The aim of this study is to determine changes in inducible gene/protein expression and skeletal muscle mass in the acute (3 d) and early (14 d) immobilisation period while under a moderate (30%) energy restriction with sufficient protein intake (1.4-1.5 g/kg). We will compare the effect of this energy deficit on muscle mass with immobilised participants in energy balance, a study previously completed in our laboratory. We hypothesize that 14 d of limb immobilisation with energy deficit will result in greater losses of total body fat, immobilised limb mass and gene expression for protein breakdown compared to immobilised limbs in energy balance.

Interventions

14 days of limb (leg) immobilisation will be undertaken using a Donjoy X-ACT ROM Universal leg brace worn 24 h per day. This intervention will be combined with a 30% energy restriction over the 14 day immobilisation period. All foods will be provided to participants and supplied by a commercial provider (Lite 'n' easy, Brisbane, Australia). For the seven days prior to knee brace immobilisaton, participants will be provided a diet to achieve expected energy balance as calculated by the Schofield

14 days of limb (leg) immobilisation will be undertaken using a Donjoy X-ACT ROM Universal leg brace worn 24 h per day. This intervention will be combined with a 30% energy restriction over the 14 day immobilisation period. All foods will be provided to participants and supplied by a commercial provider (Lite 'n' easy, Brisbane, Australia). For the seven days prior to knee brace immobilisaton, participants will be provided a diet to achieve expected energy balance as calculated by the Schofield equation with an activity factor of 1.5. Macronutrient contributions will be ~17/66/17% for protein, carbohydrate and fat, respectively; protein will be clamped at 1.4-1.5 g/kg. At the commencement of the immobilisation period, an energy deficit of 30% (based on Schofield equation and activity factor of 1.5) will be implemented by reducing carbohydrate (primarily) and fat intake; protein will remain clamped at 1.4-1.5 g/kg. The resulting macronutrient contributions will be ~23/57/20% for protein, carbohydrate and fat, respectively, Adherence to diet will be monitored via daily food diaries that require participants to check off all foods consumed. Adherence to immobilisation will be monitored through actigraph accelerometers to determine physical activity levels and a unique identifier tape wrapped around to the brace will determine if/when a brace is removed. Muscle biopsies will be obtained on day 0, 3 and 14.

Sponsors

Bond University
Lead SponsorUniversity

Study design

Allocation
Non-randomised trial
Intervention model
Single group
Primary purpose
Treatment
Masking
Open (masking not used)

Eligibility

Sex/Gender
Male
Age
20 Years to 40 Years
Healthy volunteers
Yes

Inclusion criteria

Physically active individuals undertaking ~4 exercise sessions per week of moderate-vigorous exercise.

Exclusion criteria

Recent (<6 months) injury requiring immobilsation, medical conditions that would place participants at increased risk during resistance exercise (strength testing), currently taking medications known to affect body composition, dietary allergies, employment requiring physical labour.

Outcome results

None listed

Source: ANZCTR · Data processed: Feb 4, 2026