Desmin increases with high-intensity concentric contractions in humans

Abstract

To investigate the role desmin may play in muscular adaptation to exercise, we measured desmin protein content in the vastus lateralis muscle of seven untrained men in response to 8 weeks of high-intensity cycle training. Training involved 15-s sprints separated by rest for 5 min. Subjects began with four sprints twice per week, and progressed to six sprints three times per week. Peak power was measured before and after training with a 30-s maximal sprint test. Mean power during the first 15 s increased significantly after training (P < 0.05). Desmin and actin protein levels were determined by immunoblotting, from pretraining and posttraining muscle biopsies. Desmin protein levels were increased by 60% after training (P < 0.01), whereas actin protein levels did not change with training. We conclude that the cytoskeletal protein desmin increases in response to a high-tension, concentric-only load consequent to sprint training. Desmin appears to increase as the force generating capacity of the muscle increases. A reinforced desmin cytoskeleton may be necessary for increased force generation by the muscle.

Temporal response of desmin and dystrophin proteins to progressive resistance exercise in human skeletal muscle

“…Desmin and actin immunoblotting. Desmin and actin were measured using immunoblotting procedures as previously reported (40). Briefly, aliquots of the homogenate sample (7 g of total protein) were loaded onto a 12% polyacrylamide minigel.…”

“…Blots were incubated with the secondary antibody, anti-mouse IgG labeled with horseradish peroxidase (1:1,500; Vector Laboratories, Burlingame, CA) for 1 h at room temperature. Protein bands were detected with chemiluminescence (Amersham Pharmacia Biotech, Piscataway, NJ) (40), and quantified with densitometry (Un-Scan-It gel software, version 4.3, Silk Scientific, Orem, UT). A representative sample from each time point was included on each blot.…”

“…The response of desmin to a progressive resistance training regimen is unknown; however, two studies indicate that an increase in desmin protein content occurs after a chronic stimulus. For instance, after 8 wk of sprint cycle training, desmin protein content was increased by 60% (40); and in rabbits exposed to several weeks of chronic low-frequency stimulation, desmin levels increased after 1 and 2 wk and reached a plateau by 3 wk of stimulation (4). Furthermore, eccentric exercise plays an important role in the strength and hypertrophy adaptations to resistance training (12,18,21), and desmin cytoskeletal alterations have been shown to occur after a single bout of severe eccentric exercise.…”

Subcellular movement and expression of HSP27, αB-crystallin, and HSP70 after two bouts of eccentric exercise in humans

“…Yu et al (49,50) suggested desmin as a central player in the remodeling process (sarcomerogenesis) after eccentric exercise. Moreover, rather than being a one-time response to unaccustomed exercise, the upregulation of cytoskeletal proteins, such as desmin, appears to be a continuing adaptation to repeated bouts of high-force exercise [i.e., training (24,47,48)]. It is plausible that the strengthening of cytoskeletal/myofibrillar structures requires a concomitant upregulation of certain HSPs, especially ␣Bcrystallin, which is a part of these structures (6).…”

Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy

“…In the healthy heart, desmin forms a filamentous lattice in the interfibrillar space to anchor myofibers at the Z-discs and maintain their alignment within myocytes (Ganote and Vander Heide, 1987;Huang et al, 2002). The desmin scaffolding stabilizes myocyte architecture transversely and longitudinally, reinforcing the sarcomere during cardiac contraction and preventing slippage, enabling force generation (Schaper et al, 1991;Woolstenhulme et al, 2005). Desmin is one of the major stress-bearing elements supporting the sarcomere and is speculated to have a role in diastolic dysfunction .…”