Soleus muscle stability in wild hibernating black bears.

Based on studies of fast skeletal muscles, hibernating black and brown bears resist skeletal muscle atrophy during months of reduced physical activity and not feeding. The present study examined atrophy sparing in the slow soleus muscle, known to be highly prone to disuse atrophy in humans and other mammals. We demonstrated histochemically that the black bear soleus is rich in slow fibers, averaging 84.0 ± 6.6%. The percentages of slow fibers in fall (87.3 ± 4.9%) and during hibernation (87.1 ± 5.6%) did not differ ( P = 0.3152) from summer. The average fiber cross-sectional area to body mass ratio (48.6 ± 11.7 µm2/kg) in winter hibernating bears was not significantly different from that of summer (54.1 ± 11.8 µm2/kg, P = 0.4186) and fall (47.0 ± 9.7 µm2/kg, P = 0.9410) animals. The percentage of single hybrid fibers containing both slow and fast myosin heavy chains, detected biochemically, increased from 2.6 ± 3.8% in summer to 24.4 ± 24.4% ( P = 0.0244) during hibernation. The shortening velocities of individual hybrid fibers remained unchanged from that of pure slow and fast fibers, indicating low content of the minority myosins. Slow and fast fibers in winter bears exhibited elevated specific tension (kN/m2; 22%, P = 0.0161 and 11%, P = 0.0404, respectively) and maintained normalized power. The relative stability of fiber type percentage and size, fiber size-to-body mass ratio, myosin heavy chain isoform content, shortening velocity, power output, and elevated specific tension during hibernation validates the ability of the black bear to preserve the biochemical and performance characteristics of the soleus muscle during prolonged hibernation.

Skeletal muscle plasticity with marathon training in novice runners.

The purpose of this study was to investigate leg muscle adaptation in runners preparing for their first marathon. Soleus and vastus lateralis (VL) biopsies were obtained from six recreational runners (23 ± 1 years, 61 ± 3 kg) before (T1), after 13 weeks of run training (T2), and after 3 weeks of taper and marathon (T3). Single muscle fiber size, contractile function (strength, speed, and power) and oxidative enzyme activity [citrate synthase (CS)] were measured at all three time points, and fiber type distribution was determined before and after the 16-week intervention. Training increased VO(2max) ∼9% (P<0.05). All soleus parameters were unchanged. VL MHC I fiber diameter increased (+8%; P<0.05) from T1 to T2. VL MHC I V(o) (-12%), MHC I power (-22%) and MHC IIa power (-29%) were reduced from T1 to T2 (P<0.05). No changes in VL single fiber contractile properties were observed from T2 to T3. No change was observed in soleus CS activity, whereas VL CS activity increased 66% (P<0.05). Our observations indicate that modest marathon training elicits very specific skeletal muscle adaptations that likely support the ability to perform 42.2 km of continuous running - further strengthening the existing body of evidence for skeletal muscle specificity.

Single muscle fiber contractile properties during a competitive season in male runners.

The purpose of this investigation was to examine the contractile properties of individual myofibers in response to periodized training periods throughout a collegiate cross-country season in male runners. Muscle biopsies of the gastrocnemius were taken after a summer base training phase (T1), an 8-wk intense training period (T2), and a 4-wk taper phase (T3). Five runners (n = 5; age = 20 +/- 1 yr; wt = 65 +/- 4 kg; ht = 178 +/- 3 cm) completed all three time points. A total of 328 individual muscle fibers [myosin heavy chain (MHC) I = 66%; MHC IIa = 33%; hybrids = 1%] were isolated and studied at 15 degrees C for their contractile properties. Diameter of MHC I fibers was 3% smaller (P < 0.05) at T2 compared with T1 and an additional 4% smaller (P < 0.05) after the taper. Cell size was unaltered in the MHC IIa fibers. MHC I and IIa fiber strength increased 18 and 11% (P < 0.05), respectively, from T1 to T2. MHC I fibers produced 9% less force (P < 0.05) after the taper, whereas MHC IIa fibers were 9% stronger (P < 0.05). Specific tension increased 38 and 26% (P < 0.05) for MHC I and IIa fibers, respectively, from T1 to T2 and was unchanged with the taper. Maximal shortening velocity (Vo) of the MHC I fibers decreased 23% (P < 0.05) from T1 to T2 and 17% (P < 0.05) from T2 to T3, whereas MHC IIa Vo was unchanged. MHC I peak power decreased 20% (P < 0.05) from T1 to T2 and 25% (P < 0.05) from T2 to T3, whereas MHC IIa peak power was unchanged. Power corrected for cell size decreased 15% (P < 0.05) from T2 to T3 and was 24% (P < 0.05) lower at T3 compared with T1 for the MHC I fibers only. These data suggest that changes in run training alter myocellular physiology via decreases in fiber size, Vo, and power of MHC I fibers and through increases in force per cross-sectional area of slow- and fast-twitch muscle fibers.