Previous research has shown that short periods of both bed rest and leg immobilisation result in a reduction in muscle size and strength, particularly of the quadriceps and hamstring muscles. Furthermore, longer term bed rest studies lasting months have shown in more detail how individual muscles of the thigh atrophy over a longer time period. However, there were no data available on how individual muscles of the thigh atrophy during short term disuse (i.e. up to one week). Therefore, in Chapter 2 we assessed how the individual muscles of the thigh respond to one week of unilateral leg immobilisation. We report in this study that thigh muscle atrophy occurs rapidly (within just 2 days) and at a sustained rate (by approximately 0.8% per day) during one week of immobilisation. The atrophy is mainly attributed to the loss of M. quadriceps tissue mass. Furthermore, the constituent muscles of the thigh atrophy during immobilisation at markedly differing rates (~0.4 – 1.0% per day) with the M. vastus lateralis experiencing the most and M. gracilis the least atrophy. The preponderance towards M. quadriceps rather than hamstrings atrophy during immobilisation is accompanied by functional declines manifesting distinctly within leg extension movements.

Extensive research has shown that muscle disuse lowers both post-absorptive and post-prandial muscle protein synthesis rates over a short term period (i.e. one week) and after long term disuse (i.e. more than 1 month), however these measurements have only been made using stable isotope labelled amino acid tracers which only allow for the investigation of muscle protein synthesis after a period of disuse. Thus there were no data on how muscle protein synthesis rates changes over time throughout the entire period of muscle disuse. Recently, the application of deuterated water (2H2O) has re-emerged in the field as an approach to assess muscle protein synthesis rates over multiple days or weeks in vivo in humans. In chapter 3, 13 healthy young males underwent one week of unilateral leg immobilisation. Muscle disuse induced a rapid decline in muscle volume (within 2 days) that was further increased with prolonged disuse (up to 7 days). The decline in muscle volume was accompanied by a ~36% decline in daily myofibrillar protein synthesis rates in healthy young men over one week of disuse. These data highlight the key role that declining myofibrillar protein synthesis rates play in the development of skeletal muscle disuse atrophy in vivo in humans. A small but growing body of research has highlighted how higher protein/amino acid intakes may act to reduce muscle atrophy during a period of disuse. These research studies generally assessed the impact of consuming animal based protein sources. In Chapter 4 we assessed the bioavailability of mycoprotein in an attempt to gain more insight into the potential anabolic properties of more sustainable, non-animal protein sources. Mycoprotein is a sustainable non-animal derived protein source that is produced by the continuous fermentation of the filamentous fungus Fusarium venenatum. Based on the observed bioavailability, we speculate that the ingestion of 40 g mycoprotein (i.e. 18 g total protein) would be sufficient to mount a robust muscle protein synthetic response, with the ingestion of 60 g mycoprotein (i.e. 27 g total protein) likely necessary to provide an optimal anabolic response. It is unlikely that consuming an excess of 60 g would confer any further benefits in healthy individuals. We conclude that mycoprotein represents a bioavailable and insulinotropic, non-animal derived dietary protein source. Consumed in sufficient quantities, mycoprotein would be expected to support skeletal muscle anabolism and reconditioning.

In Chapters 2, 3 and 4 we identified that skeletal muscle atrophy occurs rapidly in just 2 days of disuse, which is attributed, at least partly, to a rapid reduction in muscle protein synthesis rates. Although some research studies investigated the effects of increased amino acid or protein intake on muscle atrophy during disuse, there were no studies that assessed this while consuming different amounts of protein. Thus, in Chapter 5 we investigated how graded protein intakes of 0.15, 0.5 and 1.6 g·kg bm·d-1 may modulate muscle atrophy and muscle protein synthesis rates during a short period of disuse. We found that graded dietary protein intakes of 0.15, 0.5 or 1.6 g·kg bm·d-1 did not attenuate the rapid decline in myofibrillar protein synthesis rates, muscle mass, or function during 3 days of unilateral leg immobilisation. This study is the first to evaluate the role of dietary protein intake per se under controlled dietary conditions on the rate of skeletal muscle deconditioning during short-term muscle disuse.

Defence date: 25/09/2023

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Kilroe, R. J.
Kilroe, R. J.
Post doctoral researcher, University of Texas Health San Antonio