Regional Cross-sectional Area Research Articles

Equalization of Training Protocols by Time Under Tension Determines the Magnitude of Changes in Strength and Muscular Hypertrophy.

Martins-Costa, HC, Lacerda, LT, Diniz, RCR, Lima, FV, Andrade, AGP, Peixoto, GH, Gomes, MC, Lanza, MB, Bemben, MG, and Chagas, MH. Equalization of training protocols by time under tension determines the magnitude of changes in strength and muscular hypertrophy. J Strength Cond Res 36(7): 1770-1780, 2022-The aim of this study was to investigate the effects of 2 training protocols equalized by tension (TUT) on maximal strength (1 repetition maximum [RM]), regional cross-sectional areas (proximal, middle, and distal), and total cross-sectional areas (sum of the regional cross-sectional areas) of the pectoralis major and triceps brachii muscles. Thirty-eight men untrained in resistance training participated in the study and were allocated under 3 conditions: Protocol 3s (n = 11; 12 repetitions; 3s repetition duration), Protocol 6s (n = 11; 6 repetitions; 6s repetition duration), and Control (n = 11; no training). Training protocols (10 weeks; bench press exercise) were equated for TUT (36 seconds per set), number of sets (3-4), intensity (50-55% of 1RM), and rest between sets (3 minutes). Analysis of variance was used to examine a percentage change in variables of interest across the 3 groups with an alpha level of 0.05 used to establish statistical significance. Protocols 3s and 6s showed no differences in the increase of total and regional muscle cross-sectional areas. There were no differences in regional hypertrophy of the pectoralis major muscle. In the triceps brachii muscle, the increase in distal cross-sectional area was greater when compared with the middle and proximal regions. Both experimental groups had similar increases in the 1RM test. In conclusion, training protocols with the same TUT promote similar strength gains and muscle hypertrophy. Moreover, considering that the protocols used different numbers of repetitions, the results indicate that training volumes cannot be considered separately from TUT when evaluating neuromuscular adaptations.

The Free Achilles Tendon Is Shorter, Stiffer, Has Larger Cross-Sectional Area and Longer T2* Relaxation Time in Trained Middle-Distance Runners Compared to Healthy Controls

Tendon geometry and tissue properties are important determinants of tendon function and injury risk and are altered in response to ageing, disease, and physical activity levels. The purpose of this study was to compare free Achilles tendon geometry and mechanical properties between trained elite/sub-elite middle-distance runners and a healthy control group. Magnetic resonance imaging (MRI) was used to measure free Achilles tendon volume, length, average cross-sectional area (CSA), regional CSA, moment arm, and T2* relaxation time at rest, while freehand three-dimensional ultrasound (3DUS) was used to quantify free Achilles tendon mechanical stiffness, Young’s modulus, and length normalised mechanical stiffness. The free Achilles tendon in trained runners was significantly shorter and the average and regional CSA (distal end) were significantly larger compared to the control group. Mechanical stiffness of the free Achilles tendon was also significantly higher in trained runners compared to controls, which was explained by the group differences in tendon CSA and length. T2* relaxation time was significantly longer in trained middle-distance runners when compared to healthy controls. There was no relationship between T2* relaxation time and Young’s modulus. The longer T2* relaxation time in trained runners may be indicative of accumulated damage, disorganised collagen, and increased water content in the free Achilles tendon. A short free Achilles tendon with large CSA and higher mechanical stiffness may enable trained runners to rapidly transfer high muscle forces and possibly reduce the risk of tendon damage from mechanical fatigue.

Regional Muscle Activity During Strength & Power Exercises

Previous studies have linked regional muscle activity during exercise to increases in regional cross-sectional area (CSA). While both strength (Heavy Squat: HS) and power (Jump Squat: JS) training have been shown to increase CSA in untrained individuals, differences in regional hypertrophy have been observed. In a previous study we observed that in response to HS and JS training, HS resulted in greater proximal hypertrophy while JS resulted in greater distal hypertrophy. However, it is presently unclear if observed regional differences in hypertrophy are a result of selective regional muscle activation. PURPOSE: To compare muscle activity of the VL in proximal (p-), mid (m-), and distal (d-) thigh regions during HS and JS exercises. We hypothesize that regional muscle activity will reflect previous observations of regional specific hypertrophy. METHODS: Three subjects had their one repetition maximum (1RM) determined for HS. On a following day VL-EMG was obtained at 33% (p-), 50% (m-) and 67% (d-) thigh length during unloaded JS and HS performed with 80% 1RM. Knee angle and bar depth were matched between movements using videography and a tensiometer while EMG signals were normalized to a maximal voluntary isometric contraction. Significant differences between HS and JS were determined using paired t-test and regional differences using repeated measures ANOVAs and Bonferroni adjustments (p < 0.05). RESULTS: Across all regions, muscle activity was significantly greater in HS than JS (p < 0.00). Furthermore, p-EMG was significantly greater than m-EMG and d-EMG (p = 0.005, 0.007). Regional differences between movements showed a non-significant trend with greater muscle activity in the distal regions during HS than JS (p-EMG = 6.0 ± 3.4%, m-EMG = 13.1 ± 6.9%, d-EMG = 19.0 ± 16.7%). CONCLUSION: Results show that p-EMG is greatest across both exercises and HS-EMG is greatest across all regions. However, results do not support our hypothesis that HS would experience greater muscle activation in the p-thigh and that JS in the d-thigh. In fact, results show that the opposite may be true. Suggesting that factors other than selective regional activation are driving the previously observed inhomogeneous hypertrophy. Presented data is preliminary and more subjects will be tested to explore this relationship.

Three-dimensional morphology and strain of the human Achilles free tendon immediately following eccentric heel drop exercise.

Our understanding of the immediate effects of exercise on Achilles free tendon transverse morphology is limited to single site measurements acquired at rest using 2D ultrasound. The purpose of this study was to provide a detailed 3D description of changes in Achilles free tendon morphology immediately following a single clinical bout of exercise. Freehand 3D ultrasound was used to measure Achilles free tendon length, and regional cross-sectional area (CSA), medio-lateral (ML) diameter and antero-posterior (AP) diameter in healthy young adults (N=14) at rest and during isometric muscle contraction, immediately before and after 3×15 eccentric heel drops. Post-exercise reductions in transverse strain were limited to CSA and AP diameter in the mid-proximal region of the Achilles free tendon during muscle contraction. The change in CSA strain during muscle contraction was significantly correlated to the change in longitudinal strain (r=-0.72) and the change in AP diameter strain (r=0.64). Overall findings suggest the Achilles free tendon experiences a complex change in 3D morphology following eccentric heel drop exercise that manifests under contractile but not rest conditions, is most pronounced in the mid-proximal tendon and is primarily driven by changes in AP diameter strain and not ML diameter strain.

Peripharyngeal tissue deformation, stress distributions, and hyoid bone movement in response to mandibular advancement.

Mandibular advancement (MA) increases upper airway (UA) patency and decreases collapsibility. Furthermore, MA displaces the hyoid bone in a cranial-anterior direction, which may contribute to MA-associated UA improvements via redistribution of peripharyngeal tissue stresses (extraluminal tissue pressure, ETP). In the present study, we examined effects of MA on ETP distributions, deformation of the peripharyngeal tissue surface (UA geometry), and hyoid bone position. We studied 13 supine, anesthetized, tracheostomized, spontaneously breathing adult male New Zealand White rabbits. Graded MA was applied from 0 to ∼4.5 mm. ETP was measured at six locations distributed throughout three UA regions: tongue, hyoid, and epiglottis. Axial computed tomography images of the UA (nasal choanae to glottis) were acquired and used to measure lumen geometry (UA length; regional cross-sectional area) and hyoid displacement. MA resulted in nonuniform decreases in ETP (greatest at tongue region), ranging from -0.11 (-0.15 to -0.06) to -0.82 (-1.09 to -0.54) cmH2O/mm MA [linear mixed-effects model slope (95% confidence interval)], across all sites. UA length decreased by -0.5 (-0.8 to -0.2) %/mm accompanied by nonuniform increases in cross-sectional area (greatest at hyoid region) ranging from 7.5 (3.6-11.4) to 18.7 (14.9-22.5) %/mm. The hyoid bone was displaced in a cranial-anterior direction by 0.42 (0.36-0.44) mm/mm MA. In summary, MA results in nonuniform changes in peripharyngeal tissue pressure distributions and lumen geometry. Displacement of the hyoid bone with MA may play a pivotal role in redistributing applied MA loads, thus modifying tissue stress/deformation distributions and determining resultant UA geometry outcomes.

Peripharyngeal tissue deformation and stress distributions in response to caudal tracheal displacement: pivotal influence of the hyoid bone?

Caudal tracheal displacement (TD) leads to improvements in upper airway (UA) function and decreased collapsibility. To better understand the mechanisms underlying these changes, we examined effects of TD on peripharyngeal tissue stress distributions [i.e., extraluminal tissue pressure (ETP)], deformation of its topographical surface (UA lumen geometry), and hyoid bone position. We studied 13 supine, anesthetized, tracheostomized, spontaneously breathing, adult male New Zealand white rabbits. Graded TD was applied to the cranial tracheal segment from 0 to ∼ 10 mm. ETP was measured at six locations distributed around/along the length of the UA, covering three regions: tongue, hyoid, and epiglottis. Axial images of the UA (nasal choanae to glottis) were acquired with computed tomography and used to measure lumen geometry (UA length; regional cross-sectional area) and hyoid bone displacement. TD resulted in nonuniform decreases in ETP (generally greatest at tongue region), ranging from -0.07 (-0.11 to -0.03) [linear mixed-effects model slope (95% confidence interval)] to -0.27 (-0.31 to -0.23) cmH2O/mm TD, across all sites. UA length increased by 1.6 (1.5-1.8)%/mm, accompanied by nonuniform increases in cross-sectional area (greatest at hyoid region) ranging from 2.8 (1.7-3.9) to 4.9 (3.8-6.0)%/mm. The hyoid bone was displaced caudally by 0.22 (0.18-0.25) mm/mm TD. In summary, TD imposes a load on the UA that results in heterogeneous changes in peripharyngeal tissue stress distributions and resultant lumen geometry. The hyoid bone may play a pivotal role in redistributing applied caudal tracheal loads, thus modifying tissue deformation distributions and determining resultant UA geometry outcomes.

Region-specific corpus callosum atrophy correlates with the regional pattern of cortical glucose metabolism in Alzheimer disease.

Positron emission tomographic studies of patients with Alzheimer disease (AD) suggest a loss of metabolic functional interactions between different cortical regions. Atrophy of the corpus callosum as the major tract of intracortical connective fibers may reflect decreased cortical functional integration in AD. To investigate whether regional atrophy of the corpus callosum is correlated with regional reductions of cortical glucose metabolism, as shown by positron emission tomography, and whether primary white matter degeneration is a possible cofactor of corpus callosum atrophy in AD. We measured total and regional cross-sectional areas of the corpus callosum on midsagittal magnetic resonance imaging scans from 12 patients with AD and 15 age-matched control subjects. Regional cerebral metabolic rates for glucose in cortical lobes were measured by positron emission tomography using fludeoxyglucose F 18. White matter hyperintensities were rated in T2-weighted magnetic resonance imaging scans. The total cross-sectional area of corpus callosum was significantly reduced in patients with AD, with the most prominent changes in the rostrum and splenium and relative sparing of the body of the corpus callosum. Frontal and parietal lobe metabolism was correlated with the truncal area of the corpus callosum in AD. The ratios of frontal to parietal and of frontal to occipital metabolism were correlated with the ratio of anterior to posterior corpus callosum area in the group with AD. White matter hyperintensities did not correlate with corpus callosum atrophy in the patients with AD. The regional pattern of corpus callosum atrophy correlated with reduced regional glucose metabolism independently of primary white matter degeneration in the patients with AD.

Gp120, a human immunodeficiency virus-1 coat protein, augments excitotoxic hippocampal injury in perinatal rats.

Recent data suggest that gp120, a human immunodeficiency virus-1 (HIV-1) coat glycoprotein that is secreted by HIV-infected cells, is neurotoxic, and that this toxicity is mediated, at least in part, by activation of N-methyl-D-aspartate-type excitatory amino acid receptors. To test this hypothesis in vivo, we examined the neurotoxicity of gp120 injected intrahippocampally, alone or co-injected with the selective excitatory amino acid agonist N-methyl-D-aspartate, in seven-day-old rats. Severity of injury in the lesioned hippocampus was assessed five days later, using three outcome measures: histopathology, hippocampal atrophy (derived from regional cross-sectional area measurements) and loss of [3H]glutamate receptor binding (based on in vitro autoradiography assays). To confirm that any observed effects were attributable to gp120 bioactivity, each group of experiments included controls that received equal amounts of heat-treated gp120. Gp120 (200 ng) elicited minimal focal pyramidal cell loss immediately adjacent to the injection track; there was no hippocampal atrophy or loss of [3H]glutamate binding. Co-injection of 50 ng gp120 with N-methyl-D-aspartate (5 nmol, threshold excitotoxic dose) increased the severity of hippocampal injury; hippocampal atrophy was greater in animals that received injections of 5 nmol N-methyl-D-aspartate in combination with 50 ng gp120 than in those that received either N-methyl-D-aspartate alone (5 nmol) or 5 nmol N-methyl-D-aspartate+50 ng heat-treated gp120 (mean+/-S.E.M. percentage reduction in injected hippocampal volume vs contralateral: N-methyl-D-aspartate, -19+/-3; N-methyl-D-aspartate+gp120, -26.8+/-2.1; N-methyl-D-aspartate+heat-treated gp120, -14.0+/-2.2; P<0.001, ANOVA). Treatment with the competitive N-methyl-D-aspartate antagonist 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (20mg/kg) markedly reduced the severity of injury elicited by the combination of gp120 with N-methyl-D-aspartate. These data support the hypothesis that locally secreted gp120 could exert neurotoxic effects, mediated by N-methyl-D-aspartate receptor activation, in vivo in the immature brain.

The platelet-activating factor antagonist BN 52021 attenuates hypoxic-ischemic brain injury in the immature rat.

Platelet-activating factor (PAF) is overproduced in ischemic brain. Although postischemic PAF antagonist administration protects the mature brain in some models, little is known about the effects of PAF antagonists in the immature brain. We hypothesized that the PAF antagonist BN 52021 would attenuate perinatal cerebral hypoxic-ischemic injury. To elicit focal hypoxic-ischemic brain injury, 7-d-old (P7) rats (n = 111) underwent right carotid ligation, followed by 2.5-3.25 h of hypoxia (fractional concentration of inspired O2 = 0.08). BN 52021 neuroprotection was evaluated in three groups of experiments: 1) 25 mg/kg/dose, 0 and 2 h posthypoxia; 2), 25 mg/kg/dose immediately before and 1 h after hypoxia; and 3) posthypoxia-ischemia treatment with BN 52021 12.5, 25, or 50 mg/kg/dose in 2 doses 0 and 2 h after hypoxia. All experiments included concurrent vehicle-injected controls. To quantitate severity of injury, bilateral regional cross-sectional areas (groups 1 and 2) or hemisphere weights (group 3) were evaluated on P12. Both pre- and posthypoxic treatment with BN 52021 (25 mg/kg/dose, two serial doses) decreased the incidence of cerebral infarction from 90% to about 30% (p < 0.02, Fisher's exact test). Measurement of cross-sectional areas confirmed neuroprotection and indicated some benefit of pre- over posthypoxic-ischemic treatment in hippocampus and cortex. Over the dose range tested, the neuroprotective effect of BN 52021 administration was not dose-dependent. In contrast, BN 52021 did not attenuate N-methyl-D-aspartate-induced hippocampal excitotoxic injury in P7 rats. Either prophylactic or "rescue" administration of PAF antagonists decreases the incidence and severity of brain injury associated with an episode of perinatal cerebral hypoxia-ischemia.

Gp120, an HIV-1 protein, increases susceptibility to hypoglycemic and ischemic brain injury in perinatal rats

Recent data suggest that gp120, a glycoprotein secreted by HIV-1-infected macrophages, is neurotoxic, and that toxicity is mediated, at least in part, by overactivation of NMDA-type excitatory amino acid receptors. In experimental animals, considerable evidence indicates that hypoglycemic and ischemic neuronal injury are mediated by endogenous excitatory amino acids. We hypothesized that in the presence of gp 120 the severity of brain injury resulting from hypoglycemia and cerebral ischemia would increase. To test this hypothesis in vivo, we evaluated the influence of gp120 on the extent of brain injury resulting from these two clinically relevant pathophysiological insults in 7-day-old (P7) rats, the developmental stage of peak susceptibility to NMDA neurotoxicity. We compared the severity of hippocampal injury resulting from right intrahippocampal injections of gp120 (50 ng) in P7 rats rendered markedly hypoglycemic ( n = 10) and in controls ( n = 12). We also determined the influence of gp120 administration on the severity of hypoxic-ischemic injury, using a perinatal rat stroke model. P7 rats received intrahippocampal injections of gp120 (50 ng) ( n = 23) or saline ( n = 18) and then underwent right carotid ligation, followed by 2 h exposure to 8% oxygen. Brain injury was evaluated 5 days later, based on neuropathology evaluation and measurements of bilateral regional cross-sectional areas. The severity of hippocampal injury, based on cross-sectional area measurements, was considerably greater in animals from the hypoglycemic group than in litter-mate gp120-injected controls. Among the animals that underwent hypoxic-ischemic lesioning, the severity of injury, based on histopathology scoring and regional volume measurements, was considerably greater in animals that received gp120 than in those that received saline. These results provide support for the hypothesis that locally secreted HIV peptides, such as gp120, may potentiate the neurotoxicity of endogenous excitatory amino acid neurotransmitters in HIV-infected brain.

Changes in regional myocardial cross-sectional area during brief coronary occlusion and reperfusion in conscious dogs

The effect of a brief period of coronary occlusion on a regional myocardial cross-sectional area was studied in 6 conscious dogs. Subendocardial segment length and wall thickness were continuously measured with a sonomicrometer in the central ischemic area perfused by the left circumflex coronary artery during a 2-min circumflex occlusion and subsequent reperfusion. Measurements were repeated before and after collateral development induced by 180 ± 30 (SEM) 2-min circumflex occlusions (20 ± 3 days). In order to evaluate the changes in regional myocardial volume, end-diastolic regional cross-sectional area was calculated as a product of end-diastolic segment length and wall thickness. Before collateral development, end-diastolic regional cross-sectional area transiently decreased 1.4 ± 0.6% (NS) at 10 sec following sudden coronary occlusion, thereafter gradually increased to 3.7 ± 1.0% ( P < 0.05) at the end of a 2-min occlusion. At 10 sec of reperfusion, end-diastolic regional cross-sectional area further increased to 7.0 ± 1.1% ( P < 0.05) probably due to increased intravascular volume. Increase in end-diastolic regional cross-sectional area was still 2.5 ± 0.6% (NS) at 3 min after the release of occlusion. After collateral development, the changes in end-diastolic regional cross-sectional area were 0.1 ± 0.1% (NS), 0.4 ± 0.3% (NS), 1.0 ± 0.6% (NS) and 0.2 ± 0.4% (NS), respectively. Thus, a significant increase in the regional myocardial cross-sectional area occurs during a brief period of coronary occlusion and reperfusion.

Regional myocardial volume alterations induced by brief repeated coronary occlusion in conscious dogs

The purpose of this study was to evaluate whether brief repeated coronary occlusions induce changes in regional myocardial geometry at rest. Five conscious dogs were instrumented for the measurement of subendocardial segment length and transmural wall thickness in the ischemic area, subendocardial segment length in the normally perfused area, coronary flow and left ventricular pressure. After recovery from surgery, 180 (mean) 2 min coronary occlusions were given over a period of 20 days. The heart rate at rest, left ventricular peak systolic and end-diastolic pressures and peak positive first derivative of left ventricular pressure (dP/dt) remained unchanged throughout the experiment.In the normal area, the end-diastolic segment length at rest did not change significantly. By contrast, in the ischemic area, at 14 days after the initiation of repeated coronary occlusion, the end-diastolic regional crosssectional area (product of segment length and wall thickness) at rest had increased by 9.7% (p < 0.05); thereafter it decreased to 6.5% (p < 0.05) above the value at rest before repeated occlusion despite an additional 6 days of coronary occlusions. At 10 days after the Interruption of repeated occlusion, this value had regressed to 4.3% (p = NS) above control. These findings suggest the occurrence of regional myocardial hypertrophy confined to the ischemic area in response to the periodic ischemic stimulus.

Architecture of the masticatory apparatus in eastern raccoons (Procyon lotor lotor).

The structure and function of the masticatory apparatus of raccoons resemble those found in carnivores. In this study, the architecture of the skull, dentition, and masticatory apparatus is described, and a model is proposed that suggests a mechanism used by raccoons to reduce different foods. The model suggests that jaw movements are similar to those of cats, the posterior regions of the superficial and deep parts of the temporalis and the anterior region of the medial pterygoid generate horizontal jaw movements, and the anterior portions of the superficial and deep temporalis as well as portions of the masseteric complex generate vertical closing movement. The distributions of slow, fast fatigable, and fast fatigue-resistant fibers for the temporalis and masseteric complex are related to the possible actions of these muscles during mastication, as are the regional cross-sectional areas of the masticatory muscles.

Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.

The human aorta and its terminal branches were investigated in normal subjects during elective cardiac catheterization to evaluate regional wave travel and arterial wave reflections. A specially designed catheter with six micromanometers equally spaced at 10 cm intervals was positioned with the tip sensor in the distal external iliac artery and the proximal sensor in the aortic arch. Simultaneous pressures were obtained and analyzed for foot-to-foot wave velocity, and Fourier analysis was used to derive apparent phase velocity. These quantities were assessed during control (n = 9), during Valsalva (n = 8) and Müller (n = 4) maneuvers, and during femoral artery occlusion by bilateral manual compression (n = 8). During control, regional cross-sectional areas, determined from aortography, and regional foot-to-foot pulse wave velocities were used to calculate the local reflection coefficient in the proximal descending aorta (gamma = 0.05), at the junction of the renal arteries (gamma = 0.43), and at the terminal aortic bifurcation (gamma = 0.13). To test the hypothesis that significant reflections originate in the aorta, at the level of the renal arteries, aortograms were used to design a latex tube model with geometric properties similar to the descending aorta. Velocities and reflection characteristics in the model and in vivo were compared. Inspection of thoracic aortic pressures under control conditions revealed a reflected wave originating from the region of the aorta at the level of the renal arterial branches while abdominal pressures exhibited reflection from a site peripheral to the terminal aortic bifurcation. In the low frequency range, apparent phase velocity was found to be higher proximal to the renal arteries as compared with at the distal sites. In addition, the minimum value occurred at a higher frequency in the lower thoracic aorta than at more distal sites. The effects of reflection on apparent wave velocity in the tube model were consistent with data obtained in vivo. The Valsalva maneuver diminished the reflection from the aortic region of the renal arteries, thus allowing the distal reflected wave to become more evident on the thoracic pressure waveforms. Bilateral femoral artery occlusion usually enhanced the distal reflection and the Müller maneuver usually resulted in small increases in reflections. In conclusion, the geometric and elastic nonuniformity of the aorta results in two major sites of arterial wave reflection that influence the aortic pressure waveforms in man.(ABSTRACT TRUNCATED AT 400 WORDS)