Regional chest wall impedance during nonrespiratory maneuvers

To assess changes in total and regional chest wall properties during nonrespiratory maneuvers, we measured electromyographic activity of various chest wall muscles, esophageal pressure, and rib cage and abdominal surface displacements in six subjects before and during various static tasks. Subjects were seated at functional residual capacity, and quasi-sinusoidal forcing at the mouth (0.4 Hz, 500 ml) was imposed during the maneuver in the absence of active breathing. Magnitude of total chest wall impedance (magnitude of Zw) increased with effort during all maneuvers; changes in phase were small. Maneuvers involving primarily muscles of the neck and rib cage--holding a 10-kg weight, 10 kg of isometric tension between the arms, and isometric neck flexion--roughly doubled the magnitude of rib cage impedance (magnitude of Zrc) and, to a lesser degree, increased magnitude of diaphragm-abdomen impedance (magnitude of Zd-a). Unilateral and bilateral leg lifts, in addition to increasing magnitude of Zd-a, increased magnitude of Zrc. Passive 90 degrees rotation of the torso caused approximately 25% increases in magnitude of Zrc and magnitude of Zd-a; if the rotation was actively maintained by the trunk muscles, both regional impedances increased over 100%. Increases in magnitude of regional impedance were correlated to increases in regional electromyographic activity; changes in phase were small. Passive restriction of rib cage displacement by strapping increased magnitude of Zrc and magnitude of Zw but not magnitude of Zd-a, whereas abdominal strapping increased magnitude of Zd-a but did not affect magnitude of Zrc or magnitude of Zw.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in muscle coordination with training.

Three core concepts, activity-dependent coupling, the composition of muscle synergies, and Hebbian adaptation, are discussed with a view to illustrating the nature of the constraints imposed by the organization of the central nervous system on the changes in muscle coordination induced by training. It is argued that training invoked variations in the efficiency with which motor actions can be generated influence the stability of coordination by altering the potential for activity-dependent coupling between the cortical representations of the focal muscles recruited in a movement task and brain circuits that do not contribute directly to the required behavior. The behaviors that can be generated during training are also constrained by the composition of existing intrinsic muscle synergies. In circumstances in which attempts to produce forceful or high velocity movements would otherwise result in the generation of inappropriate actions, training designed to promote the development of control strategies specific to the desired movement outcome may be necessary to compensate for protogenic muscle recruitment patterns. Hebbian adaptation refers to processes whereby, for neurons that release action potentials at the same time, there is an increased probability that synaptic connections will be formed. Neural connectivity induced by the repetition of specific muscle recruitment patterns during training may, however, inhibit the subsequent acquisition of new skills. Consideration is given to the possibility that, in the presence of the appropriate sensory guidance, it is possible to gate Hebbian plasticity and to promote greater subsequent flexibility in the recruitment of the trained muscles in other task contexts.     

CCL2 and CCR2 variants are associated with skeletal muscle strength and change in strength with resistance training

Baseline muscle size and muscle adaptation to exercise are traits with high variability across individuals. Recent research has implicated several chemokines and their receptors in the pathogenesis of many conditions that are influenced by inflammatory processes, including muscle damage and repair. One specific chemokine, chemokine (C-C motif) ligand 2 (CCL2), is expressed by macrophages and muscle satellite cells, increases expression dramatically following muscle damage, and increases expression further with repeated bouts of exercise, suggesting that CCL2 plays a key role in muscle adaptation. The present study hypothesizes that genetic variations in CCL2 and its receptor (CCR2) may help explain muscle trait variability. College-aged subjects [n = 874, Functional Single-Nucleotide Polymorphisms Associated With Muscle Size and Strength (FAMUSS) cohort] underwent a 12-wk supervised strength-training program for the upper arm muscles. Muscle size (via MR imaging) and elbow flexion strength (1 repetition maximum and isometric) measurements were taken before and after training. The study participants were then genotyped for 11 genetic variants in CCL2 and five variants in CCR2. Variants in the CCL2 and CCR2 genes show strong associations with several pretraining muscle strength traits, indicating that inflammatory genes in skeletal muscle contribute to the polygenic system that determines muscle phenotypes. These associations extend across both sexes, and several of these genetic variants have been shown to influence gene regulation.     

Human skeletal sarcoplasmic reticulum Ca2+ uptake and muscle function with aging and strength training.

This study investigated the adaptations of skeletal muscle sarcoplasmic reticulum (SR) Ca2+ uptake, relaxation, and fiber types in young (YW) and elderly women (EW) to high-resistance training. Seventeen YW (18-32 yr) and 11 EW (64-79 yr) were assessed for 1) electrically evoked relaxation time and rate of the quadriceps femoris; and 2) maximal rates of SR Ca2+ uptake and Ca2+-ATPase activity and relative fiber-type areas, analyzed from muscle biopsies of the vastus lateralis. EW had significantly slower relaxation rates and times, decreased SR Ca2+ uptake and Ca2+-ATPase activity, and a larger relative type I fiber area than did YW. A subgroup of 9 young (YWT) and 10 elderly women (EWT) performed 12 wk of high-resistance training (8 repetition maximum) of the quadriceps and underwent identical testing procedures pre- and posttraining. EWT significantly increased their SR Ca2+ uptake and Ca2+-ATPase activity in response to training but showed no alterations in speed of relaxation or relative fiber-type areas. In YWT none of the variables was altered after resistance training. These findings suggest that 1) a reduced SR Ca2+ uptake in skeletal muscle of elderly women was partially reversed with resistance training and 2) SR Ca2+ uptake in the vastus lateralis was not the rate-limiting mechanism for the slowing of relaxation measured from electrically evoked quadriceps muscle of elderly women.     

Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training.

Previous studies have shown that low-intensity resistance training with restricted muscular venous blood flow (Kaatsu) causes muscle hypertrophy and strength gain. To investigate the effects of daily physical activity combined with Kaatsu, we examined the acute and chronic effects of walk training with and without Kaatsu on MRI-measured muscle size and maximum dynamic (one repetition maximum) and isometric strength, along with blood hormonal parameters. Nine men performed Kaatsu-walk training, and nine men performed walk training alone (control-walk). Training was conducted two times a day, 6 days/wk, for 3 wk using five sets of 2-min bouts (treadmill speed at 50 m/min), with a 1-min rest between bouts. Mean oxygen uptake during Kaatsu-walk and control-walk exercise was 19.5 (SD 3.6) and 17.2 % (SD 3.1) of treadmill-determined maximum oxygen uptake, respectively. Serum growth hormone was elevated (P < 0.01) after acute Kaatsu-walk exercise but not in control-walk exercise. MRI-measured thigh muscle cross-sectional area and muscle volume increased by 4-7%, and one repetition maximum and maximum isometric strength increased by 8-10% in the Kaatsu-walk group. There was no change in muscle size and dynamic and isometric strength in the control-walk group. Indicators of muscle damage (creatine kinase and myoglobin) and resting anabolic hormones did not change in both groups. The results suggest that the combination of leg muscle blood flow restriction with slow-walk training induces muscle hypertrophy and strength gain, despite the minimal level of exercise intensity. Kaatsu-walk training may be a potentially useful method for promoting muscle hypertrophy, covering a wide range of the population, including the frail and elderly.     

Inheritance of human muscle enzyme adaptation to isokinetic strength training

Five monozygotic twin pairs were submitted to a 10-week isokinetic strength training program and biochemical characteristics measured before and after training to determine the role of heredity in skeletal muscle adaptation, while 5 unrelated sedentary subjects served as control group. Experimental subjects performed twice 3 series of 5 bilateral reciprocal alternating knee flexions and extensions at a velocity of 90 degrees/s 5 times per week. Before and after the training period, for each subject, the peak muscular torque output was measured at the same velocity and the vastus lateralis muscle was biopsied for biochemical determinations. No significant change was observed in the control group. Training increased peak muscular torque output by 24%. The activities of hexokinase, malate dehydrogenase and 3-hydroxyacyl CoA dehydrogenase also increased significantly by 28, 26 and 38%, respectively. Interindividual variations in the response of these variables to training were noted but these were shown to be independent of the genotype. No overall effect of training was observed for oxoglutarate dehydrogenase activity (OGDH). However, changes were seen in individual pairs of twins and these were in opposite directions in some pairs compared to others, thus explaining the absence of a general training effect. Significant intrapair resemblance in the training response was present for OGDH (r = 0.76), indicating that the sensitivity to isokinetic strength training for OGDH was highly variable, not random and probably genetically determined.     

High-volume, heavy-resistance strength training and muscle damage in young and older women.

To determine possible age differences in muscle damage response to strength training, ultrastructural muscle damage was assessed in seven 20- to 30-yr-old and six 65- to 75-yr-old previously sedentary women after heavy-resistance strength training (HRST). Subjects performed unilateral knee-extension exercise 3 days/wk for 9 wk. Bilateral muscle biopsies from the vastus lateralis were assessed for muscle damage via electron microscopy. HRST resulted in a 38 and 25% increase in strength in the young and older women, respectively (P < 0.05), but there were no between-group differences. In the young women, 2-4% of muscle fibers exhibited damage before and after training in both the trained and untrained legs (P = not significant). In contrast, muscle damage increased significantly after HRST, from 5 to 17% of fibers damaged (P < 0.01), in the older women in the trained leg compared with only 2 and 5% of fibers damaged in the untrained leg before and after training, respectively. The present results indicate that older women exhibit higher levels of muscle damage after chronic HRST than do young women.     

Ultrastructural muscle damage in young vs. older men after high-volume, heavy-resistance strength training.

This study assessed ultrastructural muscle damage in young (20-30 yr old) vs. older (65-75 yr old) men after heavy-resistance strength training (HRST). Seven young and eight older subjects completed 9 wk of unilateral leg extension HRST. Five sets of 5-20 repetitions were performed 3 days/wk with variable resistance designed to subject the muscle to near-maximal loads during every repetition. Biopsies were taken from the vastus lateralis of both legs, and muscle damage was quantified via electron microscopy. Training resulted in a 27% strength increase in both groups (P < 0.05). In biopsies before training in the trained leg and in all biopsies from untrained leg, 0-3% of muscle fibers exhibited muscle damage in both groups (P = not significant). After HRST, 7 and 6% of fibers in the trained leg exhibited damage in the young and older men, respectively (P < 0.05, no significant group differences). Myofibrillar damage was primarily focal, confined to one to two sarcomeres. Young and older men appear to exhibit similar levels of muscle damage at baseline and after chronic HRST.     

ACTN3 genotype is associated with increases in muscle strength in response to resistance training in women.

The alpha-actinin 3 (ACTN3) gene encodes a protein of the Z disk of myofibers, and a polymorphism of ACTN3 results in complete loss of the protein. The ACTN3 genotype (R577X) has been found to be associated with performance in Australian elite athletes (Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, and North K. Am J Hum Genet 73: 627-631, 2003). We studied associations between ACTN3 genotype and muscle size [cross-sectional area of the biceps brachii via magnetic resonance imaging (MRI)] and elbow flexor isometric (MVC) and dynamic [1-repetition maximum (1-RM)] strength in a large group of men (N = 247) and women (N = 355) enrolled in a 12-wk standardized elbow flexor/extensor resistance training program of the nondominant arm at one of eight study centers. We found no association between ACTN3 R577X genotype and muscle phenotype in men. However, women homozygous for the ACTN3 577X allele (XX) had lower baseline MVC compared with heterozygotes (P < 0.05) when adjusted for body mass and age. Women homozygous for the mutant allele (577X) demonstrated greater absolute and relative 1-RM gains compared with the homozygous wild type (RR) after resistance training when adjusted for body mass and age (P < 0.05). There was a trend for a dose-response with genotype such that gains were greatest for XX and least for RR. Significant associations were validated in at least one ethnic subpopulation (Caucasians, Asians) and were independent of training volume. About 2% of baseline MVC and of 1-RM strength gain after training were attributable to ACTN3 genotype (likelihood-ratio test P value, P = 0.01), suggesting that ACTN3 is one of many genes contributing to genetic variation in muscle performance and adaptation to exercise.     

Single muscle fiber adaptations with marathon training.

The purpose of this investigation was to characterize the effects of marathon training on single muscle fiber contractile function in a group of recreational runners. Muscle biopsies were obtained from the gastrocnemius muscle of seven individuals (22 +/- 1 yr, 177 +/- 3 cm, and 68 +/- 2 kg) before, after 13 wk of run training, and after 3 wk of taper. Slow-twitch myosin heavy chain [(MHC) I] and fast-twitch (MHC IIa) muscle fibers were analyzed for size, strength (P(o)), speed (V(o)), and power. The run training program led to the successful completion of a marathon (range 3 h 56 min to 5 h 35 min). Oxygen uptake during submaximal running and citrate synthase activity were improved (P < 0.05) with the training program. Muscle fiber size declined (P < 0.05) by approximately 20% in both fiber types after training. P(o) was maintained in both fiber types with training and increased (P < 0.05) by 18% in the MHC IIa fibers after taper. This resulted in >60% increase (P < 0.05) in force per cross-sectional area in both fiber types. Fiber V(o) increased (P < 0.05) by 28% in MHC I fibers with training and was unchanged in MHC IIa fibers. Peak power increased (P < 0.05) in MHC I and IIa fibers after training with a further increase (P < 0.05) in MHC IIa fiber power after taper. These data show that marathon training decreased slow-twitch and fast-twitch muscle fiber size but that it maintained or improved the functional profile of these fibers. A taper period before the marathon further improved the functional profile of the muscle, which was targeted to the fast-twitch muscle fibers.     

Respiratory maneuvers in echocardiography: a review of clinical applications

During echocardiographic examination, respiration induces cyclic physiological changes of intracardiac haemodynamics, causing normal variations of the right and left ventricle Doppler inflows and outflows and physiological variation of extracardiac flows. The respiration related hemodynamic variation in intra and extracardiac flows may be utilized in the echocardiography laboratory to aid diagnosis in different pathological states. Nevertheless, physiologic respiratory phases can cause excessive translational motion of cardiac structures, lowering 2D image quality and interfering with optimal Doppler interrogation of flows or tissue motion. This review focuses on the impact of normal respiratory cycle and provocative respiratory maneuvers in echocardiographic examination, both in physiological and pathological states, emphasizing their applications in specific clinical situations.     

Specificity of resistance training responses in neck muscle size and strength

This study examined hypertrophy after head extension resistance training to assess which muscles of the complicated cervical neuromuscular system were used in this activity. We also determined if conventional resistance exercises, which are likely to evoke isometric action of the neck, induce generalized hypertrophy of the cervical muscle. Twenty-two active college students were studied. [mean (SE) age, weight and height: 21 (1) years, 71 (4) kg and 173 (3) cm, respectively]. Subjects were assigned to one of three groups: RESX (head extension exercise and other resistance exercises), RES (resistance exercises without specific neck exercise), or CON (no training). Groups RESX (n = 8) and RES (n = 6) trained 3 days/week for 12 weeks with large-muscle mass exercises (squat, deadlift, push press, bent row and mid-thigh pull). Group RESX also performed three sets of ten repetitions of a head extension exercise 3 days/week with a load equal to the 3 × 10 repetition maximum (RM). Group CON (n = 8) was a control group. The cross-sectional area (CSA) of nine individual muscles or muscle groups was determined by magnetic resonance imaging (MRI) of the cervical region. The CSA data were averaged over four contiguous transaxial slices in which all muscles of interest were visible. The 3 × 10 RM for the head extension exercise increased for RESX after training [from 17.9 (1.0) to 23.9 (1.4) kg, P < 0.05] but not for RES [from 17.6 (1.4) to 17.7 (1.9)␣kg] or CON [from 10.1 (2.2) to 10.3 (2.1) kg]. RESX showed an increase in total neck muscle CSA after training [from 19.5 (3.0) to 22.0 (3.6) cm², P < 0.05], but RES and CON did not [from 19.6 (2.9) to 19.7 (2.9)␣cm² and 17.0 (2.5) to 17.0 (2.4) cm², respectively]. This hypertrophy for RESX was due mainly to increases in CSA of 23.9 (3.2), 24.0 (5.8), and 24.9 (5.3)% for the splenius capitis, and semispinalis capitis and cervicis muscles, respectively. The lack of generalized neck muscle hypertrophy in RES was not due to insufficient training. For example, the CSA of their quadriceps femoris muscle group, as assessed by MRI, increased by 7 (1)% after this short-term training (P < 0.05). The results suggest that: (1) the splenius capitis, and semispinalis capitis and cervicis muscles are mainly responsible for head extension; (2) short-term resistance training does not provide a sufficient stimulus to evoke neck muscle hypertrophy unless specific neck exercises are performed; and (3) the postural role of head extensors provides modest loading in bipeds. Accepted: 15 October 1996     

Neurophysiological responses after short-term strength training of the biceps brachii muscle

The neural adaptations that mediate the increase in strength in the early phase of a strength training program are not well understood; however, changes in neural drive and corticospinal excitability have been hypothesized. To determine the neural adaptations to strength training, we used transcranial magnetic stimulation (TMS) to compare the effect of strength training of the right elbow flexor muscles on the functional properties of the corticospinal pathway. Motor-evoked potentials (MEPs) were recorded from the right biceps brachii (BB) muscle from 23 individuals (training group; n = 13 and control group; n = 10) before and after 4 weeks of progressive overload strength training at 80% of 1-repetition maximum (1RM). The TMS was delivered at 10% of the root mean square electromyographic signal (rmsEMG) obtained from a maximal voluntary contraction (MVC) at intensities of 5% of stimulator output below active motor threshold (AMT) until saturation of the MEP (MEPmax). Strength training resulted in a 28% (p = 0.0001) increase in 1RM strength, and this was accompanied by a 53% increase (p = 0.05) in the amplitude of the MEP at AMT, 33% (p = 0.05) increase in MEP at 20% above AMT, and a 38% increase at MEPmax (p = 0.04). There were no significant differences in the estimated slope (p = 0.47) or peak slope of the stimulus-response curve for the left primary motor cortex (M1) after strength training (p = 0.61). These results demonstrate that heavy-load isotonic strength training alters neural transmission via the corticospinal pathway projecting to the motoneurons controlling BB and in part underpin the strength changes observed in this study.     

Alterations of mechanical characteristics of human skeletal muscle during strength training

To investigate the influence of strength training on the mechanical characteristics of human skeletal muscle, 14 male subjects went through training of combined heavy concentric and eccentric contractions three times a week for 16 weeks. The strength training program consisted mainly of dynamic exercises for leg extensors with loads of 80 to 120% of one maximum repetition. The force-time curves produced during various vertical jumps were the basis for calculation of various mechanical parameters. In addition to a great increase (p less than 0.001) in maximal isometric force, heavy resistance strength training also caused significant (p less than 0.05-0.01) increases in heights and in various mechanical parameters in positive work phases of vertical and drop jumps. The increase in positive force during a fast dynamic contraction was correlated (p less than 0.01) with the reduced time to produce a certain submaximal force level in isometric condition. No changes in the elastic properties of the muscle were observed as judged from the difference between the counter-movement and squat jumps. When the training was followed by the 8-week detraining period a great decrease (p less than 0.001) in maximal force took place, but only minor changes (ns) were observed in fast force production.     

Hormonal adaptation determines the increase in muscle mass and strength during low-intensity strength training without relaxation

The study was designed to test the hypothesis that, during strength training, a restricted blood supply to the working muscles stimulates the secretion of anabolic hormones and an increase in the muscle mass and strength can be achieved with significantly lower training loads. During eight weeks, three times a week, 18 young, physically active males trained their leg extensor muscles. Nine subjects (group I) worked at 80% of the maximal voluntary contraction (MVC), whereas the rest (group II) performed their exercise without relaxation and at a lower load (50% MVC). The total training load in group II was significantly lower than in group I (77 ± 5 vs. 157 ± 7 kJ, respectively). The eight-week training of both groups significantly increased the mean maximum strength (by 35 and 21% in groups I and II, respectively) and volume (by 17 and 9%, respectively) of the muscles trained (however, the differences between the groups with respect to these changes were nonsignificant). Group I displayed a higher increase in the blood level of creatine phosphokinase than group II, while group II showed a greater increase in the blood concentration of lactate. In contrast to group I, group II displayed a significant increase in the blood concentrations of growth hormone, insulin-like growth factor 1 (IGF-1), and cortisol. Hence, the suggestion that the secretion of metabolic hormones is triggered by a metabolic, rather than mechanical, stimulus from working muscles seems plausible.