In this month’s MSSE, I am highlighting three articles from different areas: one concerning muscle aponeurosis size, another on fatty infiltration into muscle in chronic obstructive pulmonary disease (COPD), and a third on human immunity in vivo.
Evangelidis et al. investigated whether the anatomical structure of the biceps femoris long head (BFlh) muscle–tendon unit including the proximal aponeurosis size was a risk factor for hamstring injury. The authors report that the BFlh proximal aponeurosis area exhibited large variability (4.5-fold) and was not related to the size of the BFlh muscle maximal anatomical cross-sectional area, which also varied considerably (1.8-fold) in 30 healthy, young men. Additionally, the aponeurosis size was unrelated to knee flexor isometric or eccentric strength. This variability between proximal aponeurosis and muscle size/strength raises the possibility that individuals with a small aponeurosis relative to muscle size (i.e. low aponeurosis:muscle area ratio) may experience greater mechanical strains in the muscle tissue adjacent to the aponeurosis and be at greater risk of hamstrings injury.
The muscle weakness observed in patients having COPD is not fully explained by muscle atrophy. In other chronic diseases such as diabetes, spinal cord injury and neuromuscular conditions, fatty infiltration of the muscle is often associated with atrophy and resultant weakness, but the degree of fat infiltration into muscles of persons having COPD had not been investigated. The study by Robles et al. uses a novel, noninvasive technique of magnetic resonance spectroscopy to demonstrate that people with COPD have greater intramuscular fat infiltration of the soleus and vastus lateralis muscles than their healthy counterparts. Interestingly, walking capacity and muscle strength deficits were more highly correlated with muscle fat infiltration than with muscle cross-sectional area in these individuals. The effect of exercise training on muscle fat infiltration in COPD patients is an area for future study.
Finally, Diment et al. report data challenging the concept that short-lasting, high-intensity exercise decreases immunity. These authors examined the effects of running at different intensities and durations on immunity in humans in vivo using a simple and practical skin patch test with a novel antigen. They show impaired immunity after prolonged, moderate-intensity running (2 h at 60% VO2peak) but not after shorter-duration (30 min), high-intensity (80% VO2peak) or moderate-intensity (60% VO2peak) running. These findings suggest that athletes might replace some of their long-duration, moderate-intensity training bouts with shorter spike sessions to limit training-induced immune impairments. Further, the work may help explain lower respiratory infection incidence in high-level swimmers during the taper period when overall training volume is reduced but intensity remains high [Hellard et al. Training-Related Risk of Common Illnesses in Elite Swimmers over a 4-yr Period. Med Sci Sports Exerc. 2015;47(4):698-707].
L. Bruce Gladden