Remarkable gains in muscle strength and size result from low-load (<20% of maximum) resistance training coupled with a restriction in blood flow to the active muscle; this challenges traditional theories that suggest that high loads are a prerequisite to muscle hypertrophy. From a practical viewpoint, if the same results could be obtained with lower occlusion pressures, this would improve the comfort of blood flow restriction (BFR) exercise and expand its use to clinical populations.
In this month’s journal, Downs et al. applied different levels of external cuff pressure in a novel approach to characterize the effect of BFR on muscle blood flow, cardiac output, and blood pressure. Their results indicate that local muscle ischemia may stimulate the observed hypertrophic responses. On a systemic level, cardiac output and blood pressure measurements during BFR were within a safe range for cardiac rehabilitation, although further research is warranted prior to prescribing BFR to individuals with cardiac risk factors. In association with this report, we are also featuring an article by Drummond et al. [Human Muscle Gene Expression following Resistance Exercise and Blood Flow Restriction. Med Sci Sports Exerc. 2008;40(4):691-698].
In a second article of special interest in this month’s journal, Laaksonen et al. investigate the effects of endurance training on myocardial vascular function. One would expect that myocardial vascular function would be enhanced after exercise training. However, cross-sectional human studies comparing endurance-trained and untrained subjects and measuring myocardial perfusion using positron emission tomography (the “gold standard” method for this purpose) have not convincingly demonstrated this result. To the contrary, some studies have shown significantly lower myocardial perfusion during a standard adenosine challenge in endurance-trained compared to untrained subjects. In this current study, VO2peak in endurance athletes correlates inversely with myocardial perfusion during adenosine stimulation, an effect that seems to be explained by highly increased left ventricular mass in the athletes. These findings suggest that so-called physiological hypertrophy may not necessarily be positive from all perspectives. However, it must be acknowledged that there does not seem to be any clinical and exercise performance consequences of the somewhat compromised myocardial vascular function. Along with the Laaksonen article, we are providing free access to [Rowley NJ et al. Conduit Diameter and Wall Remodeling in Elite Athletes and Spinal Cord Injury. Med Sci Sports Exerc. 2012;44(5):844-849].
L. Bruce Gladden