Mitochondrial and Muscle Endurance Changes with BFR


Adding to the list of clinical implications with BFR, mitochondrial change or biogenesis is emerging as a potential target. Mitochondria play a vital role in fuel production for muscle function. "Skeletal muscle performance is limited by either oxygen supply to or oxygen consumption through mitochondrial oxidative phosphorylation (MOP)." (Frisbee 2018) Traditionally, mitochondrial changes are attributed to endurance training but recent studies have shown mitochondrial changes with high-load resistance. A study that was just published in Frontiers in Physiology by Groennebaek et al, aimed to determine if light load with BFR would be as effective as high load in eliciting mitochondrial changes. 

The study was carried out with a frequency of 3 days per week over 6 weeks. The BFR group used 50% Limb Occlusion Pressure (LOP) and performed unilateral knee extension at 30% of a 1RM for 4 sets to volitional fatigue. The high load group performed 4 sets of 12 knee extensions at a 70% of 1RM without BFR. Both groups significantly increased mitochondrial protein fractional synthetic rates and respiratory function compared to a non-exercising group. Additionally, both groups significantly increased maximal knee extension strength, with high-load demonstrating a greater change than BFR (33% vs 10.7% respectively). However, the BFR group significantly increased muscle strength-endurance capacity (28.3%) while the high-load group didn't show change.

These changes in muscle endurance and mitochondrial function along with previously shown angiogenic changes have implications for occlusion training with aging or clinical populations and long-term health and muscle function. Aging is associated with reduced mitochondrial function and this decline is directly linked to many age associated diseases. Furthermore, loss of muscle endurance possibly via a reduction in vascularity has been linked to the atrophy seen after ACL surgery.

The ischemic or hypoxic state of occlusion training exercise may be the driver for angiogenic and mitochondrial responses. Increasing capillary beds (oxygen transport) and mitochondrial respiration (oxygen utilization for ATP production) is a huge value regardless of the population and may help explain some of the positive VO2 changes seen with BFR. In addition, the ability to significantly increase muscular endurance and create a strength change may be a more important combination than a greater 1RM for a large part of the clinical population. Perhaps we should begin to turn our attention to muscle endurance, angiogenesis and mitochondrial biogenesis to optimize athletic and geriatric function. The simple addition of a tourniquet during low-level exercise seems to accomplish this. As always, more research is needed to determine the best populations and parameters for application.

Bibliography:

Frisbee, Jefferson C., et al. “Skeletal Muscle Performance in Metabolic Disease: Microvascular or Mitochondrial Limitation or Both?” Microcirculation , Nov. 2018, p. e12517.

Groennebaek, Thomas, Nichlas Jespersen, Jesper Jakobsgaard, Peter Sieljacks, Jakob Wang, Emil Rindom, Robert Musci, et al. 2018. “Skeletal Muscle Mitochondrial Protein Synthesis and Respiration Increase with Low-Load Blood Flow Restricted as Well as High-Load Resistance Training.” Frontiers in Physiology 9: 1796.

Seo, Dae Yun, et al. "Age-related changes in skeletal muscle mitochondria: the role of exercise." Integrative medicine research 5.3 (2016): 182-186.

Grapar Žargi, T., Matej Drobnič, Renata Vauhnik, Jadran Koder, and Alan Kacin. 2017. “Factors Predicting Quadriceps Femoris Muscle Atrophy during the First 12weeks Following Anterior Cruciate Ligament Reconstruction.” The Knee 24 (2): 319–28.

Russell, Aaron P., et al. "Skeletal muscle mitochondria: a major player in exercise, health and disease." Biochimica et biophysica acta (BBA)-general subjects 1840.4 (2014): 1276-1284.