Mechanical deficit persists during long-term muscle hypertrophy

1990 ◽  
Vol 69 (3) ◽  
pp. 861-867 ◽  
Author(s):  
S. C. Kandarian ◽  
T. P. White

Hypotheses were tested that the deficit in maximum isometric force normalized to muscle cross-sectional area (i.e., specific Po, N/cm2) of hypertrophied muscle would return to control value with time and that the rate and magnitude of adaptation of specific force would not differ between soleus and plantaris muscles. Ablation operations of the gastrocnemius and plantaris muscles or the gastrocnemius and soleus muscles were done to induce hypertrophy of synergistic muscle left intact in female Wistar rats (n = 47) at 5 wk of age. The hypertrophied soleus and plantaris muscles and control muscles from other age-matched rats (n = 22) were studied from days 30 to 240 thereafter. Po was measured in vitro at 25 degrees C in oxygenated Krebs-Ringer bicarbonate. Compared with control values, soleus muscle cross-sectional area increased 41-15% from days 30 to 240 after ablation, whereas Po increased 11 and 15% only at days 60 and 90. Compared with control values, plantaris muscle cross-sectional area increased 52% at day 30, 40% from days 60 through 120, and 15% at day 240. Plantaris muscle Po increased 25% from days 30 to 120 but at day 240 was not different from control value. Changes in muscle architecture were negligible after ablation in both muscles. Specific Po was depressed from 11 to 28% for both muscles at all times. At no time after the ablation of synergistic muscle did the increased muscle cross-sectional area contribute fully to isometric force production.

1994 ◽  
Vol 76 (2) ◽  
pp. 974-978 ◽  
Author(s):  
J. A. Taylor ◽  
S. C. Kandarian

When maximum isometric force (Po) is normalized to muscle cross-sectional area (CSA), intrinsic differences in force production among muscles may be masked by alterations in myofibrillar protein concentration or extracellular space. We tested the hypothesis that there is a greater deficit in Po when normalized to the average whole muscle CSA than when normalized to the myofibrillar protein CSA under conditions known to alter the concentration of myofibrils or connective tissue protein or interstitial fluid volume. Rats underwent either hindlimb unweighting (HU) to induce atrophy in the soleus muscle, sciatic nerve denervation to induce atrophy in the soleus and extensor digitorum longus (EDL) muscles, or ablation of gastrocnemius and plantaris muscles to induce hypertrophy in the soleus muscle. Po of the soleus muscle normalized to the muscle CSA (specific Po) was 58, 25, and 72% of control muscles with HU, denervation, and hypertrophy, respectively, whereas denervated EDL muscle specific Po was 60% of control muscles (P < 0.05). Soleus muscle Po normalized to the myofibrillar CSA was 80, 53, and 75% of control muscles with HU, denervation, and hypertrophy, respectively, whereas the denervated EDL muscle value was 82% of control muscles (P < 0.05). Both approaches to normalizing Po show force deficits, but normalization to the average myofibrillar protein in the muscle cross section gives values substantially closer to control values for HU and denervated muscles only. Data support the hypothesis because myofibrillar protein concentration is decreased in HU and denervation and interstitial space is increased in HU but neither parameter is altered with hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)


2010 ◽  
Vol 298 (1) ◽  
pp. C149-C162 ◽  
Author(s):  
Nadège Zanou ◽  
Georges Shapovalov ◽  
Magali Louis ◽  
Nicolas Tajeddine ◽  
Chiara Gallo ◽  
...  

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.


1985 ◽  
Vol 58 (4) ◽  
pp. 1354-1359 ◽  
Author(s):  
S. G. Kelsen ◽  
M. Ference ◽  
S. Kapoor

The present study examined the effect of prolonged undernutrition on diaphragmatic structure and force-generating ability. Studies were performed on 58 Syrian hamsters in which the feed was reduced by 33% for a 4-wk period. Sixty animals fed a similar diet ad libitum served as controls. Diaphragm muscle structure was assessed from its mass (wet and dry weight), thickness, fiber composition, and fiber size. Isometric force produced in vitro by isolated muscle strips in response to electrical stimulation of the phrenic nerve was examined over a range of muscle lengths (length-tension relationship). In undernourished animals, body weight decreased 25 +/- 5%. Diaphragm wet and dry weight, muscle thickness, and the cross-sectional area of fast-glycolytic (FG) and fast-oxidative (FO) fibers were significantly less in undernourished than control animals and correlated with reductions in body weight. The cross-sectional area of slow-oxidative (SO) fibers was the same in the two groups. The percentage of FG fibers in undernourished animals was decreased slightly and the percentage of SO fibers increased. Maximum isometric tension was reduced in undernourished animals as compared with controls, but the position and shape of the length-tension relationship was the same in the two groups. Reductions in muscle force appeared to be explained by decreases in muscle mass, since tension corrected for cross-sectional area or tissue weight was the same in the two groups. Therefore muscle mechanical efficiency appeared to be unaffected by undernutrition. These data indicate that prolonged undernutrition causes deleterious changes in diaphragm muscle structure that impair its ability to generate force.


1995 ◽  
Vol 79 (5) ◽  
pp. 1796-1802 ◽  
Author(s):  
K. S. McDonald ◽  
R. H. Fitts

The purpose of this study was to examine the time course of change in soleus muscle fiber peak force (N), tension (Po, kN/m2), elastic modulus (Eo), and force-pCa and stiffness-pCa relationships. After 1, 2, or 3 wk of hindlimb unloading (HU), single fibers were isolated and placed between a motor arm and a transducer, and fiber diameter, peak absolute force, Po, Eo, and force-pCa and stiffness-pCa relationships were characterized. One week of HU resulted in a significant reduction in fiber diameter (68 +/- 2 vs 57 +/- 1 microns), force (3.59 +/- 0.15 vs. 2.19 +/- 0.12 x 10(-4) N), Po (102 +/- 4 vs. 85 +/- 2 kN/m2), and Eo (1.96 +/- 0.12 vs. 1.37 +/- 0.13 x 10(7) N/m2), and 2 wk of HU caused a further decline in fiber diameter (45 +/- 1 microns), force (1.31 +/- 0.06 x 10(-4) N), and Eo (0.96 +/- 0.09 x 10(7) N/m2). Although the mean fiber diameter and absolute force continued to decline through 3 wk of HU, Po recovered to values not significantly different from control. The Po/Eo ratio was significantly increased after 1 (5.5 +/- 0.3 to 7.1 +/- 0.6), 2, and 3 wk of HU, and the 2-wk (9.5 +/- 0.4) and 3-wk (9.4 +/- 0.8) values were significantly greater than the 1-wk values. The force-pCa and stiffness-pCa curves were shifted rightward after 1, 2, and 3 wk of HU. At 1 wk of HU, the Ca2+ sensitivity of isometric force, assessed by Ca2+ concentration required for half-maximal force, was increased from the control value of 1.83 +/- 0.12 to 2.30 +/- 0.10 microM. In conclusion, after HU, the decrease in soleus fiber Po can be explained by a reduction in the number of myofibrillar cross bridges per cross-sectional area. Our working hypothesis is that the loss of contractile protein reduces the number of cross bridges per cross-sectional area and increases the filament lattice spacing. The increased spacing reduces cross-bridge force and stiffness, but Po/Eo increases because of a quantitatively greater effect on stiffness.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Chong Liu ◽  
Jiang Xue ◽  
Jingjing Liu ◽  
Gang Ma ◽  
Abu Moro ◽  
...  

Abstract Background The purpose of the study is to investigate the correlation between upper lumbar disc herniation (ULDH) and multifidus muscle degeneration via the comparison of width, the cross-sectional area and degree of fatty infiltration of the lumbar multifidus muscle. Methods Using the axial T2-weighted images of magnetic resonance imaging as an assessment tool, we retrospectively investigated 132 patients with ULDH and 132 healthy individuals. The total muscle cross-sectional area (TMCSA) and the pure muscle cross-sectional area (PMCSA) of the multifidus muscle at the L1/2, L2/3, and L3/4 intervertebral disc levels were measured respectively, and in the meantime, the average multifidus muscle width (AMMW) and degree of fatty infiltration of bilateral multifidus muscle were evaluated. The resulting data were analyzed to determine the presence/absence of statistical significance between the study and control groups. Multivariate logistical regression analyses were used to evaluate the correlation between ULDH and multifidus degeneration. Results The results of the analysis of the two groups showed that there were statistically significant differences (p < 0.05) between TMCSA, PMCSA, AMMW and degree of fatty infiltration. The multivariate logistic regression analysis indicated that the TMCSA, PMCSA, AMMW and the degree of fatty infiltration of multifidus muscle were correlated with ULDH, and the differences were statistically significant (P < 0.05). Conclusions A correlation could exist between multifidus muscles degeneration and ULDH, that may be a process of mutual influence and interaction. Lumbar muscle strengthening training could prevent and improve muscle atrophy and degeneration.


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