Nuclear magnetic resonance transverse relaxation in muscle water.

The origin of the nonexponentiality of proton spin echoes of skeletal muscle has been carefully examined. It is shown that the slowly decaying part of the proton spin echoes is not due to extracellular water. First, for muscle from mice with in vivo deuteration, the deuteron spin echoes were also nonexponential, but the slowly decaying part had a larger weighing factor. Second, for glycerinated muscle in which cell membranes were disrupted, the proton spin echoes were similar to those in intact muscle. Third, the nonexponentiality of the proton spin echoes in intact muscle increased when postmortem rigor set in. Finally, when the lifetimes of extracellular water and intracellular water were taken into account in the exchange, it was found that the two types of water would not give two resolvable exponentials with the observed decay constants. It is suggested that the unusually short T2's and the nonexponential character of the spin echoes of proton and deuteron in muscle water are mainly due to hydrogen exchange between water and functional groups in the protein filaments. These groups have large dipolar or quadrupolar splittings, and undergo hydrogen exchange with water at intermediate rates. The exchange processes and their effects on the spin echoes are pH-dependent. The dependence of transverse relaxation of pH was observed in glycerinated rabbit psoas muscle fibers.     

Characterization of skeletal muscles by MR imaging and relaxation times

Magnetic resonance (MR) images of three major flight muscles of chicks were obtained with surface coils using a 0.3 Tesla whole body imaging system (FONAR Beta 3000). The two fast muscles, pectoralis major (PM) and posterior latissimus dorsi (PLD), and a slow muscle, anterior latissimus dorsi (ALD), were identified in the axial, coronal, and sagittal images. The signal intensity (SI) of each muscle was electronically measured and its ratio to the background noise (S/N) was determined. Although visually the three muscles showed intermediate SI, the slow and fast muscles could be differentiated on the basis of their S/N values. These values were invariably higher in the slow muscles than in the fast muscles. To understand these differences, the muscles were excised and their mono- and multiexponential MR relaxation times (T1 and T2) were determined at 30 MHz. Multiexponential analysis enhanced the differences between the muscle types. With the sole exception of short T2, all relaxation components of the slow muscles were significantly longer than those of the fast muscles. These results suggest that elevation in the S/N, T1 and T2 values of muscles may not necessarily indicate a pathologic event, but may reflect the preponderance of slow fibers.     

MR measurements of muscle damage and adaptation after eccentric exercise.

The purposes of this study were, first, to clarify the long-term pattern of T2 relaxation times and muscle volume changes in human skeletal muscle after intense eccentric exercise and, second, to determine whether the T2 response exhibits an adaptation to repeated bouts. Six young adult men performed two bouts of eccentric biceps curls (5 sets of 10 at 110% of the 1-repetition concentric maximum) separated by 8 wk. Blood samples, soreness ratings, and T2-weighted axial fast spin-echo magnetic resonance images of the upper arm were obtained immediately before and after each bout; at 1, 2, 4, 7, 14, 21, and 56 days after bout 1; and at 2, 4, 7 and 14 days after bout 2. Resting muscle T2 [27.6 +/- 0.2 (SE) ms] increased immediately postexercise by 8 +/- 1 ms after both bouts. T2 peaked 7 days after bout 1 at 47 +/- 4 ms and remained elevated by 2.5 ms at 56 days. T2 peaked lower (37 +/- 4 ms) and earlier (2-4 days) after bout 2, suggesting an adaptation of the T2 response. Peak serum creatine kinase values, pain ratings, and flexor muscle swelling were also significantly lower after the second bout (P < 0.05). Total volume of the imaged arm region increased transiently after bout 1 but returned to preexercise values within 2 wk. The exercised flexor compartment swelled by over 40%, but after 2 wk it reverted to a volume 10% smaller than that before exercise and maintained this volume loss through 8 wk, consistent with partial or total destruction of a small subpopulation of muscle fibers.     

Effects of prior exercise on muscle metabolism during sprint exercise in horses.

The effect of warm-up exercise on energy metabolism and muscle glycogenolysis during sprint exercise (Spr) was examined in six fit Standardbred horses exercised at 115% of maximal O(2) consumption (VO(2 max)) until fatigued, 5 min after each of three protocols: 1) no warm-up (NWU); 2) 10 min at 50% of VO(2 max) [low-intensity warm-up (LWU)]; and 3) 7 min at 50% VO(2 max) followed by 45-s intervals at 80, 90, and 100% VO(2 max) [high-intensity warm-up (HWU)]. Warm-up increased (P < 0.0001) muscle temperature (T(m)) at the onset of Spr in LWU (38.3 +/- 0.2 degrees C) and HWU (40.0 +/- 0. 3 degrees C) compared with NWU (36.6 +/- 0.2 degrees C), and the rate of rise in T(m) during Spr was greater in NWU than in LWU and HWU (P < 0.01). Peak VO(2) was higher and O(2) deficit lower (P < 0. 05) when Spr was preceded by warm-up. Rates of muscle glycogenolysis were lower (P < 0.05) in LWU, and rates of blood and muscle lactate accumulation and anaerobic ATP provision during Spr were lower in LWU and HWU compared with NWU. Mean runtime (s) in LWU (173 +/- 10 s) was greater than HWU (142 +/- 11 s) and NWU (124 +/- 4 s) (P < 0. 01). Warm-up was associated with augmentation of aerobic energy contribution to total energy expenditure, decreased glycogenolysis, and longer run time to fatigue during subsequent sprint exercise, with no additional benefit from HWU vs. LWU.     

Effects of respiratory muscle work on exercise performance.

The normal respiratory muscle effort at maximal exercise requires a significant fraction of cardiac output and causes leg blood flow to fall. We questioned whether the high levels of respiratory muscle work experienced in heavy exercise would affect performance. Seven male cyclists [maximal O(2) consumption (VO(2)) 63 +/- 5 ml. kg(-1). min(-1)] each completed 11 randomized trials on a cycle ergometer at a workload requiring 90% maximal VO(2). Respiratory muscle work was either decreased (unloading), increased (loading), or unchanged (control). Time to exhaustion was increased with unloading in 76% of the trials by an average of 1.3 +/- 0.4 min or 14 +/- 5% and decreased with loading in 83% of the trials by an average of 1.0 +/- 0.6 min or 15 +/- 3% compared with control (P < 0.05). Respiratory muscle unloading during exercise reduced VO(2), caused hyperventilation, and reduced the rate of change in perceptions of respiratory and limb discomfort throughout the duration of exercise. These findings demonstrate that the work of breathing normally incurred during sustained, heavy-intensity exercise (90% VO(2)) has a significant influence on exercise performance. We speculate that this effect of the normal respiratory muscle load on performance in trained male cyclists is due to the associated reduction in leg blood flow, which enhances both the onset of leg fatigue and the intensity with which both leg and respiratory muscle efforts are perceived.     

Effects of inotropic agents on contraction and relaxation of papillary muscle.

The effects of epinephrine and caffeine on isometric rabbit papillary muscle preparations were observed after maximum peak tension was produced by adjustment of initial length and Ca⁺⁺ concentration. Without change in peak tension, epinephrine caused increased positive dP/dt (p < .005), increased negative dP/dt (p < .001) and decreased time to peak tension (TP) (p < .001), while caffeine resulted in decreased positive dP/dt (p < .02), decreased negative dP/dt (p < .005) and prolonged TP (p < .001). Caffeine added to muscles being perfused with epinephrine reversed the epinephrine effects. The data suggest that epinephrine increases the influx of Ca⁺⁺ into the cell and the uptake of Ca⁺⁺ by the sarcoplasmic reticulum, and that caffeine exerts opposite effects on Ca⁺⁺ exchange. However, an additional mechanism not dependent on changes in Ca⁺⁺ flux is suggested. Epinephrine and caffeine may directly effect the rates of actin-myosin interaction, the former agent increasing, the latter decreasing the rates of attachment and detachment of actin-myosin bridges.     

Sidedness of reconstituted calcium channels from muscle transverse tubules as determined by D600 and D890 blockade.

The verapamil-type calcium antagonist, D600, and its charged quaternary derivative, D890, were used to assess the sidedness of blockade in single calcium channels reconstituted from purified transverse tubules of skeletal muscle. Spontaneous single channel openings were induced with the agonist Bay-K8644 and recordings were made in a two-chamber planar bilayer setup so that drugs could be delivered to either side of the channel. Micromolar drug addition resulted in a greater than 10-fold decrease in probability of open channel events (po) without a significant change in single channel currents. Changes in po occurred in parallel with changes in mean open time and both parameters could be titrated with a similar IC50. At pH 7.2, cis or trans D600 blocked with an IC50 of 5 microM but for D890 the IC50 was cis 3 microM and trans greater than 75 microM (cis is the intracellular-equivalent side as defined by the voltage-dependent activation). The asymmetry of D890 blockade indicates that the drug can readily gain access to the blocking site from the aqueous phase adjacent to the inner but not extracellular end of the channel.     

Effects of exercise order on upper-body muscle activation and exercise performance

With the purpose of manipulating training stimuli, several techniques have been employed to resistance training. Two of the most popular techniques are the pre-exhaustion (PRE) and priority system (PS). PRE involves exercising the same muscle or muscle group to the point of muscular failure using a single-joint exercise immediately before a multi-joint exercise (e.g., peck-deck followed by chest press). On the other hand, it is often recommended that the complex exercises should be performed first in a training session (i.e., chest press before peck-deck), a technique known as PS. The purpose of the present study was to compare upper-body muscle activation, total repetitions (TR), and total work (TW) during PRE and PS. Thirteen men (age 25.08 +/- 2.58 years) with recreational weight-training experience performed 1 set of PRE and 1 set of PS in a balanced crossover design. The exercises were performed at the load obtained in a 10 repetition maximum (10RM) test. Therefore, chest press and peck-deck were performed with the same load during PRE and PS. Electromyography (EMG) was recorded from the triceps brachii (TB), anterior deltoids, and pectoralis major during both exercises. According to the results, TW and TR were not significantly different (p > 0.05) between PRE and PS. Likewise, during the peck-deck exercise, no significant (p > 0.05) EMG change was observed between PRE and PS order. However, TB activity was significantly (p < 0.05) higher when chest press was performed after the peck-deck exercise (PRE). Our findings suggest that performing pre-exhaustion exercise is no more effective in increasing the activation of the prefatigued muscles during the multi-joint exercise. Also, independent of the exercise order (PRE vs. PS), TW is similar when performing exercises for the same muscle group. In summary, if the coach wants to maximize the athlete performance in 1 specific resistance exercise, this exercise should be placed at the beginning of the training session.     

Effects of purified recombinant neural and muscle agrin on skeletal muscle fibers in vivo.

Aggregation of acetylcholine receptors (AChRs) in muscle fibers by nerve-derived agrin plays a key role in the formation of neuromuscular junctions. So far, the effects of agrin on muscle fibers have been studied in culture systems, transgenic animals, and in animals injected with agrin--cDNA constructs. We have applied purified recombinant chick neural and muscle agrin to rat soleus muscle in vivo and obtained the following results. Both neural and muscle agrin bind uniformly to the surface of innervated and denervated muscle fibers along their entire length. Neural agrin causes a dose-dependent appearance of AChR aggregates, which persist > or = 7 wk after a single application. Muscle agrin does not cluster AChRs and at 10 times the concentration of neural agrin does not reduce binding or AChR-aggregating activity of neural agrin. Electrical muscle activity affects the stability of agrin binding and the number, size, and spatial distribution of the neural agrin--induced AChR aggregates. Injected agrin is recovered from the muscles together with laminin and both proteins coimmunoprecipitate, indicating that agrin binds to laminin in vivo. Thus, the present approach provides a novel, simple, and efficient method for studying the effects of agrin on muscle under controlled conditions in vivo.     

The relationship between the transverse and longitudinal nuclear magnetic resonance relaxation rates of muscle water.

Whole frog sartorius and gastrocnemius muscles were incubated in Ringer's solutions, either unenriched or enriched with H2 17Oor 2D2O. Subsequently, the rates of transverse (1/T2) and of longitudinal (1/T1) nuclear magnetic relaxation were measured for 17O, 2D, and 1H at room temperature and at 8.1 MHz. The ratio (T1/T2) for 17O was measured to be approximately 1.5-2.0, close to the value roughly estimated from the Larmor frequency dependence of 1/T1 alone over the range 4.3-8.1 MHz. On the other hand (T1/T2) for 2D and 1H were both measured to lie in the range 9-11. Insofar as the entire 17O signal was detected, the data indicate the presence of an exchange mechanism between the major fraction of intracellular water and a minor fraction characterized by enhanced rates of relaxation. Possible molecular mechanisms are presented.     

Effect of acute head-down tilt on skeletal muscle cross-sectional area and proton transverse relaxation time

Conley, Michael S., Jeanne M. Foley, Lori L. Ploutz-Snyder,Ronald A. Meyer, and Gary A. Dudley. Effect of acute head-down tilt on skeletal muscle cross-sectional area and proton transverse relaxation time. J. Appl. Physiol.81(4): 1572-1577, 1996.This study investigated changes inskeletal muscle cross-sectional area (CSA) evoked by fluid shifts thataccompany short-term 6° head-down tilt (HDT) or horizontal bedrest, the time course of the resolution of these changes afterresumption of upright posture, and the effect of altered muscle CSA, inthe absence of increased contractile activity, on proton transverserelaxation time (T₂). Averagemuscle CSA and T₂ were determinedby standard spin-echo magnetic resonance imaging. Analyses wereperformed on contiguous transaxial images of the neck and calf. After aday of normal activity, 24 h of HDT increased neck muscle CSA 19 ± 4 (SE)% (P < 0.05) whilecalf muscle CSA decreased 14 ± 3%(P < 0.05). The horizontal posture(12 h) induced about one-half of these responses: an 11 ± 2%(P < 0.05) increase in neck muscleCSA and an 8 ± 2% decrease (P < 0.05) in the calf. Within 2 h after resumption of upright posture, neckand calf muscle CSA returned to within 0.5% (P > 0.05) of the values assessedafter a day of normal activity, with most of the change occurringwithin the first 30 min. No further change in muscle CSA was observedthrough 6 h of upright posture. Despite these large alterations inmuscle CSA, T₂ was not altered bymore than 1.1 ± 0.6% (P > 0.05)and did not relate to muscle size. These results suggest that posturalmanipulations and subsequent fluid shifts modeling microgravity elicitmarked changes in muscle size. Because these responses were notassociated with alterations in muscleT₂, it does not appear that simple movement of water into muscle can explain the contrast shift observed after exercise.

     

Effects of endurance exercise training on muscle glycogen accumulation in humans.

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 +/- 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher (P < 0.05) in the trained than in the untrained state: 10.5 +/- 0.2 and 4.5 +/- 1.3 mmol. kg wet wt(-1). h(-1), respectively. Muscle glycogen concentration was higher (P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher (P < 0.05) in the trained than in the untrained state (10.7 +/- 1.2 and 4.7 +/- 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise (r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.     

Passive transverse mechanical properties of skeletal muscle under in vivo compression

The objective of the present study is to determine the passive transverse mechanical properties of skeletal muscle. Compression experiments were performed on four rat tibialis anterior muscles. To assess the stress- and strain-distributions in the muscle during the experiment, a plane stress model of the cross section was developed for each muscle. The incompressible viscoelastic Ogden model was used to describe the passive muscle behaviour. The four material parameters were determined by fitting calculated indentation forces on measured indentation forces. The elastic parameters, mu and alpha, were 15.6+/-5.4 kPa and 21.4+/-5.7, respectively. The viscoelastic parameters, delta and tau, were 0.549+/-0.056 and 6.01+/-0.42 s. When applying the estimated material parameters in a three-dimensional finite element model, the measured behaviour can be accurately simulated.     

Interstitial K(+) in human skeletal muscle during and after dynamic graded exercise determined by microdialysis

Interstitial K(+) concentrations were measured during one-legged knee-extensor exercise by use of microdialysis with probes inserted in the vastus lateralis muscle of the subjects. K(+) in the dialysate was measured either by flame photometry or a K(+)-sensitive electrode placed in the perfusion outlet. The correction for fractional K(+) recovery was based on the assumption of identical fractional thallium loss. The interstitial K(+) was 4. 19 +/- 0.09 mM at rest and increased to 6.17 +/- 0.19, 7.48 +/- 1.18, and 9.04 +/- 0.74 mM at 10, 30, and 50 W exercise, respectively. The individual probes demonstrated large variations in interstitial K(+), and values >10 mM were obtained. The observed interstitial K(+) was markedly higher than previously found for venous K(+) concentrations at similar work intensities. The present data support a potential role for interstitial K(+) in regulation of blood flow and development of fatigue.     

Effects of acute hypoxia on cerebral and muscle oxygenation during incremental exercise.

To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% Fi(O2)) and acute hypoxic (Hypox: 12% Fi(O2)) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (microM) changes of oxy- and deoxyhemoglobin (Delta[O2Hb], Delta[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Delta[THb] = Delta[O2Hb] + Delta[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (alpha = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Power(peak); increased (inc) Delta[O2Hb], inc. Delta[HHb], inc. Delta[THb]}, but fell from 75 to 100% Power(peak) {decreased (dec) Delta[O2Hb], inc. Delta[HHb], no change Delta[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Delta[O2Hb], inc. Delta[HHb]), whereas Delta[THb] again rose up to 75% Power(peak) and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Delta[O2Hb], inc. Delta [HHb], inc. Delta[THb]), although Delta[O2Hb] was unchanged between 75 and 100% Power peak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.     

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function.

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca(2+) cycling and whether alterations in SR Ca(2+) cycling are related to the blunted peak mechanical power output (PO(peak)) and peak oxygen consumption (Vo(2 peak)) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 +/- 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of Vo(2 peak) (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca(2+)-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) PO(peak) and Vo(2 peak), respectively. During progressive exercise in N, Ca(2+)-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca(2+) concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca(2+) uptake (before exercise = 357 +/- 29 micromol x min(-1) x g protein(-1); at fatigue = 306 +/- 26 micromol x min(-1) x g protein(-1); P < 0.05) when measured at free Ca(2+) concentration of 2 microM and in phase 2 Ca(2+) release (before exercise = 716 +/- 33 micromol x min(-1) x g protein(-1); at fatigue = 500 +/- 53 micromol x min(-1) x g protein(-1); P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca(2+)-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO(peak) and Vo(2 peak) observed during H.