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Aim: Force expression is characterized by an interplay of biological and molecular determinants that are expected to differentiate males and females in terms of maximal performance. These include muscle characteristics (muscle size, fiber type, contractility), neuromuscular regulation (central and peripheral factors of force expression), and individual genetic factors (miRNAs and gene/protein expression). This research aims to comprehensively assess these physiological variables and their role as determinants of maximal force difference between sexes. Methods: Experimental evaluations include neuromuscular components of isometric contraction, intrinsic muscle characteristics (proteins and fiber type), and some biomarkers associated with muscle function (circulating miRNAs and gut microbiome) in 12 young and healthy males and 12 females. Results: Male strength superiority appears to stem primarily from muscle size while muscle fiber‐type distribution plays a crucial role in contractile properties. Moderate‐to‐strong pooled correlations between these muscle parameters were established with specific circulating miRNAs, as well as muscle and plasma proteins. Conclusion: Muscle size is crucial in explaining the differences in maximal voluntary isometric force generation between males and females with similar fiber type distribution. Potential physiological mechanisms are seen from associations between maximal force, skeletal muscle contractile properties, and biological markers. [ABSTRACT FROM AUTHOR]

The clinical symptoms of chronic obstructive pulmonary disease (COPD) disease are accompanied by severely debilitating extra-pulmonary manifestations, including vascular dysfunction and hypertension. This systematic review evaluated the current evidence for several therapeutic interventions, targeting the nitric oxide (NO) pathway on hemodynamics and, secondarily, exercise capacity in patients with COPD. A comprehensive search on COPD and NO donors was performed on online databases. Of 934 initially found manuscripts, 27 were included in the review, and 16 in the meta-analysis. The analysis indicated inconsistent effects of dietary nitrate supplementation on exercise tolerance in COPD patients. Dietary nitrate supplementation decreased systolic (−3.7 ± 4.3 mmHg; p = 0.10) and diastolic blood pressure (BP; −2.6 ± 3.2 mmHg; p = 0.05) compared with placebo. When restricted to acute studies, a clinically relevant BP lowering effect of nitrate supplementation during diastole was observed (−4.7 ± 3.2 mmHg; n = 5; p = 0.05). In contrast, inhaled NO (iNO) at doses <20 ppm (+9.2 ± 11.3 mmHg) and 25–40 ppm (−5±2 mmHg) resulted in inconsistent effects on PaO 2 (p = 0.48). Data on the effect of iNO on exercise capacity were too limited and inconsistent, but preliminary evidence suggests a possible benefit of iNO on pulmonary vascular resistance during exercise in severe COPD patients. Overall, the effects of acute dietary nitrate supplementation on BP may be of clinical relevance as an adjunct therapy and deserve further investigation in large sample size studies of COPD patients with and without cardiovascular comorbidities. iNO exerted inconsistent physiological effects, with the use of high doses posing safety risks. • This systematic review evaluated therapeutics targeting the nitric oxide pathway in COPD. • Acute dietary nitrate supplementation lowered diastolic blood pressure in COPD patients. • The blood pressure lowering effect of dietary nitrate might be clinically important. • The impact of dietary nitrate on cardiovascular risks should be further explored. • The effects of inhaled nitric oxide is low or even detrimental in some conditions. [ABSTRACT FROM AUTHOR]

Purpose: The involvement of central command in central hemodynamic regulation during exercise is relatively well-known, although its contribution to peripheral hemodynamics at the onset of low-intensity contractions is debated. This study sought to examine central and peripheral hemodynamics during electrically-evoked muscle contractions (without central command) and voluntary muscle activity (with central command).Cyclic quadriceps isometric contractions (1 every second), either electrically-evoked (ES; 200 ms trains composed of 20 square waves) or performed voluntarily (VC), were executed by 10 healthy males (26 ± 3 years). In both trials, matched for force output, peripheral and central hemodynamics were analysed.At exercise onset, both ES and VC exhibited equal peaks of femoral blood flow (1276 ± 849 vs. 1117 ± 632 ml/min, p > 0.05) and vascular conductance (15 ± 11 vs. 13 ± 7 ml/min/mmHg, p > 0.05), respectively. Similar peaks of heart rate (86 ± 16 bpm vs. 85 ± 16 bpm), stroke volume (100 ± 20 vs. 99 ± 27 ml), cardiac output (8.2 ± 2.5 vs. 8.5 ± 2.1 L/min), and mean arterial pressure (113 ± 13 vs. 113 ± 3 mmHg), were recorded (all, p > 0.05). After ~ 50 s, all the variables drifted to lower values. Collectively, the hemodynamics showed equal responses.These results suggest a similar pathway for the initial (first 40 s) increase in central and peripheral hemodynamics. The parallel responses may suggest an initial minimal central command involvement during the onset of low-intensity contractions, likely associated with a neural drive activation delay or threshold.Methods: The involvement of central command in central hemodynamic regulation during exercise is relatively well-known, although its contribution to peripheral hemodynamics at the onset of low-intensity contractions is debated. This study sought to examine central and peripheral hemodynamics during electrically-evoked muscle contractions (without central command) and voluntary muscle activity (with central command).Cyclic quadriceps isometric contractions (1 every second), either electrically-evoked (ES; 200 ms trains composed of 20 square waves) or performed voluntarily (VC), were executed by 10 healthy males (26 ± 3 years). In both trials, matched for force output, peripheral and central hemodynamics were analysed.At exercise onset, both ES and VC exhibited equal peaks of femoral blood flow (1276 ± 849 vs. 1117 ± 632 ml/min, p > 0.05) and vascular conductance (15 ± 11 vs. 13 ± 7 ml/min/mmHg, p > 0.05), respectively. Similar peaks of heart rate (86 ± 16 bpm vs. 85 ± 16 bpm), stroke volume (100 ± 20 vs. 99 ± 27 ml), cardiac output (8.2 ± 2.5 vs. 8.5 ± 2.1 L/min), and mean arterial pressure (113 ± 13 vs. 113 ± 3 mmHg), were recorded (all, p > 0.05). After ~ 50 s, all the variables drifted to lower values. Collectively, the hemodynamics showed equal responses.These results suggest a similar pathway for the initial (first 40 s) increase in central and peripheral hemodynamics. The parallel responses may suggest an initial minimal central command involvement during the onset of low-intensity contractions, likely associated with a neural drive activation delay or threshold.Results: The involvement of central command in central hemodynamic regulation during exercise is relatively well-known, although its contribution to peripheral hemodynamics at the onset of low-intensity contractions is debated. This study sought to examine central and peripheral hemodynamics during electrically-evoked muscle contractions (without central command) and voluntary muscle activity (with central command).Cyclic quadriceps isometric contractions (1 every second), either electrically-evoked (ES; 200 ms trains composed of 20 square waves) or performed voluntarily (VC), were executed by 10 healthy males (26 ± 3 years). In both trials, matched for force output, peripheral and central hemodynamics were analysed.At exercise onset, both ES and VC exhibited equal peaks of femoral blood flow (1276 ± 849 vs. 1117 ± 632 ml/min, p > 0.05) and vascular conductance (15 ± 11 vs. 13 ± 7 ml/min/mmHg, p > 0.05), respectively. Similar peaks of heart rate (86 ± 16 bpm vs. 85 ± 16 bpm), stroke volume (100 ± 20 vs. 99 ± 27 ml), cardiac output (8.2 ± 2.5 vs. 8.5 ± 2.1 L/min), and mean arterial pressure (113 ± 13 vs. 113 ± 3 mmHg), were recorded (all, p > 0.05). After ~ 50 s, all the variables drifted to lower values. Collectively, the hemodynamics showed equal responses.These results suggest a similar pathway for the initial (first 40 s) increase in central and peripheral hemodynamics. The parallel responses may suggest an initial minimal central command involvement during the onset of low-intensity contractions, likely associated with a neural drive activation delay or threshold.Conclusion: The involvement of central command in central hemodynamic regulation during exercise is relatively well-known, although its contribution to peripheral hemodynamics at the onset of low-intensity contractions is debated. This study sought to examine central and peripheral hemodynamics during electrically-evoked muscle contractions (without central command) and voluntary muscle activity (with central command).Cyclic quadriceps isometric contractions (1 every second), either electrically-evoked (ES; 200 ms trains composed of 20 square waves) or performed voluntarily (VC), were executed by 10 healthy males (26 ± 3 years). In both trials, matched for force output, peripheral and central hemodynamics were analysed.At exercise onset, both ES and VC exhibited equal peaks of femoral blood flow (1276 ± 849 vs. 1117 ± 632 ml/min, p > 0.05) and vascular conductance (15 ± 11 vs. 13 ± 7 ml/min/mmHg, p > 0.05), respectively. Similar peaks of heart rate (86 ± 16 bpm vs. 85 ± 16 bpm), stroke volume (100 ± 20 vs. 99 ± 27 ml), cardiac output (8.2 ± 2.5 vs. 8.5 ± 2.1 L/min), and mean arterial pressure (113 ± 13 vs. 113 ± 3 mmHg), were recorded (all, p > 0.05). After ~ 50 s, all the variables drifted to lower values. Collectively, the hemodynamics showed equal responses.These results suggest a similar pathway for the initial (first 40 s) increase in central and peripheral hemodynamics. The parallel responses may suggest an initial minimal central command involvement during the onset of low-intensity contractions, likely associated with a neural drive activation delay or threshold. [ABSTRACT FROM AUTHOR]

The force drop after transcranial magnetic stimulation (TMS) delivered to the motor cortex during voluntary muscle contractions could inform about muscle relaxation properties. Because of the physiological relation between skeletal muscle fibertype distribution and size and muscle relaxation, TMS could be a noninvasive index of muscle relaxation in humans. By combining a noninvasive technique to record muscle relaxation in vivo (TMS) with the gold standard technique for muscle tissue sampling (muscle biopsy), we investigated the relation between TMS-induced muscle relaxation in unfatigued and fatigued states, and muscle fiber-type distribution and size. Sixteen participants (7F/9M) volunteered to participate. Maximal knee-extensor voluntary isometric contractions were performed with TMS before and after a 2-min sustained maximal voluntary isometric contraction. Vastus lateralis muscle tissue was obtained separately from the participants’ dominant limb. Fiber type I distribution and relative cross-sectional area of fiber type I correlated with TMS-induced muscle relaxation at baseline (r = 0.67, adjusted P = 0.01; r = 0.74, adjusted P = 0.004, respectively) and normalized TMS-induced muscle relaxation as a percentage of baseline (r = 0.50, adjusted P = 0.049; r = 0.56, adjusted P = 0.031, respectively). The variance in the normalized peak relaxation rate at baseline (59.8%, P < 0.001) and in the fatigue resistance (23.0%, P = 0.035) were explained by the relative cross-sectional area of fiber type I to total fiber area. Fiber type I proportional area influences TMS-induced muscle relaxation, suggesting TMS as an alternative method to noninvasively inform about skeletal muscle relaxation properties. NEW & NOTEWORTHY Transcranial magnetic stimulation (TMS)-induced muscle relaxation reflects intrinsic muscle contractile properties by interrupting the drive from the central nervous system during voluntary muscle contractions. We showed that fiber type I proportional area influences the TMS-induced muscle relaxation, suggesting that TMS could be used for the noninvasive estimation of muscle relaxation in unfatigued and fatigued human muscles when the feasibility of more direct method to study relaxation properties (i.e., muscle biopsy) is restricted. [ABSTRACT FROM AUTHOR]

Exercise-Associated Muscle Cramps (EAMC) are a common painful condition of muscle spasms. Despite scientists tried to understand the physiological mechanism that underlies these common phenomena, the etiology is still unclear. From 1900 to nowadays, the scientific world retracted several times the original hypothesis of heat cramps. However, recent literature seems to focus on two potential mechanisms: the dehydration or electrolyte depletion mechanism, and the neuromuscular mechanism. The aim of this review is to examine the recent literature, in terms of physiological mechanisms of EAMC. A comprehensive search was conducted on PubMed and Google Scholar. The following terminology was applied: muscle cramps, neuromuscular hypothesis (or thesis), dehydration hypothesis, Exercise-Associated muscle cramps, nocturnal cramps, muscle spasm, muscle fatigue. From the initial literature of 424 manuscripts, sixty-nine manuscripts were included, analyzed, compared and summarized. Literature analysis indicates that neuromuscular hypothesis may prevails over the initial hypothesis of the dehydration as the trigger event of muscle cramps. New evidence suggests that the action potentials during a muscle cramp are generated in the motoneuron soma, likely accompanied by an imbalance between the rising excitatory drive from the muscle spindles (Ia) and the decreasing inhibitory drive from the Golgi tendon organs. In conclusion, from the latest investigations there seem to be a spinal involvement rather than a peripheral excitation of the motoneurons. [ABSTRACT FROM AUTHOR]

Previous studies in animal models showed that exercise-induced metabolites accumulation may sensitize the mechanoreflex-induced response. The aim of this study was to assess whether the magnitude of the central hemodynamic and ventilatory adjustments evoked by isolated stimulation of the mechanoreceptors in humans are influenced by the prior accumulation of metabolic byproducts in the muscle. 10 males and 10 females performed two exercise bouts consisting of 5-min of intermittent isometric knee-extensions performed 10% above the previously determined critical force. Post-exercise, the subjects recovered for 5 min either with a suprasystolic circulatory occlusion applied to the exercised quadriceps (PECO) or under freely-perfused conditions (CON). Afterwards, 1-min of continuous passive leg movement was performed. Central hemodynamics, pulmonary data, and electromyography from exercising/passively-moved leg were recorded throughout the trial. Root mean square of successive differences (RMSSD, index of vagal tone) was also calculated. Δpeak responses of heart rate (ΔHR) and ventilation ( Δ V ˙ E ) to passive leg movement were higher in PECO compared to CON (ΔHR: 6 ± 5 vs 2 ± 4 bpm, p = 0.01; 3.9 ± 3.4 vs 1.9 ± 1.7 L min−1, p = 0.02). Δpeak of mean arterial pressure (ΔMAP) was significantly different between conditions (5 ± 3 vs − 3 ± 3 mmHg, p < 0.01). Changes in RMSSD with passive leg movement were different between PECO and CON (p < 0.01), with a decrease only in the former (39 ± 18 to 32 ± 15 ms, p = 0.04). No difference was found in all the other measured variables between conditions (p > 0.05). These findings suggest that mechanoreflex-mediated increases in HR and V ˙ E are sensitized by metabolites accumulation. These responses were not influenced by biological sex. [ABSTRACT FROM AUTHOR]

R5983 --> 885.8 --> Cardiovascular morbidity and mortality rates are highest among Black Americans (BA), the mechanisms of which are complex and not completely understood. Altered autonomic reflexes or sympathetic transduction could contribute to elevations in baseline blood pressure or an exaggerated exercise pressor response, thereby increasing CVD risk; though no studies have explored whether mechanoreflex sensitivity, a component of the exercise pressor reflex, is altered in BA. PURPOSE: Using passive leg movement (PLM), as model of activating the mechanoreflex and an assessment of lower limb vascular function, the aim of this study was to compare the central and peripheral hemodynamic responses in young healthy Black (BA) and White American (WA) males. METHODS: Young (21±4 yr) healthy BA (n = 9) and WA (n = 10) males, matched for physical activity, were instrumented to continuously monitor central and peripheral hemodynamics using Finger Photoplethysmography (Finometer) and frequency domain multi‐distance near‐infrared spectroscopy (NIRS) of the vastus lateralis (Oxiplex TS), respectively. After 1 minute of baseline, subjects underwent continuous PLM at 1 hz for two minutes, while tissue oxygen saturation (StO2%), cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded. RESULTS: Resting HR (61±3 vs. 62±3 beats/min), SV (89±5 vs. 92±5 mL/beat), CO (5.4±0.4 vs. 4.4±0.5 L/min), and MAP (92±5 vs. 86±3 mmHg) were not different between BA and WA, respectively (all, p>0.05). The individual peak PLM‐induced changes in HR (6±2 vs. 11±3 Δbeats/min, p = 0.06), SV (7.3±1.6 vs. 11.4±1.9 ΔmL/beat, p = 0.04), and CO (0.7±0.2 vs. 1.0±0.2 ΔL/min, p = 0.09) were lower in BA, however the MAP response (5.3±1.4 vs. 6.0±0.8 ΔmmHg, p > 0.05) was not different. The peak PLM‐induced change in StO2 was significantly attenuated in BA (1.6±0.5 vs. 3.8±0.4 Δ%, p=0.01). As a surrogate of nitric oxide, urinary nitrate+nitrate were not different between groups (2.89±1.67 vs. 2.00±1.35 μM, p>0.05). CONCLUSION: A novel insight from the current study reveals that Black American men had an attenuated mechanoreflex response to PLM as compared to White American men. However, Black Americans had a lower peripheral hemodynamic response, perhaps the result of the altered mechanoreflex or suggestive of lower limb vascular dysfunction, which might explain a propensity towards elevated rates of peripheral vascular disease in Black Americans. [ABSTRACT FROM AUTHOR]

L5118 --> Previous work in vitro suggests that capsaicin, the spicy ingredient in peppers, attenuates the vascular response to sympathetic activity ("sympatholysis"), likely mediated through vascular transient receptor potential vanilloid type 1 (TRPV1), and was associated with improved vascular function, though translational studies are needed. Further, given racial disparities in vascular function, and reported racial differences in sensory TRPV1 activity, exploring the potential TRPV1‐related mechanisms underpinning these vascular differences is warranted. Purpose: To determine if racial differences existed in the central hemodynamic responses to sympathetic stimuli, via lower body negative pressure (LBNP) at rest and during exercise. Second, using an acute dose of oral capsaicin, we sought to determine the potential role of TRPV1 receptors in mediating any racial differences in sympatholysis or vascular function. Methods: In a blinded placebo‐controlled crossover design, 23 young healthy black (BM, n=13, 23±5 yrs) and white males (WM, n=10, 19±1 yrs) were given capsules containing either placebo (800mg fiber) or capsaicin (780 mg Chile pepper extract, 2.4±0.04 mg capsaicin, 0.5±0.04 mg dihydrocapsaicin). To assess microvascular responses, frequency‐domain, multi‐distance, near infrared spectroscopy (NIRS) was placed over the muscular medial forearm (i.e. flexor digitorum profundus) providing measure of oxyhemoglobin (HbO, in μM). Central hemodynamics, namely stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and heart rate (HR), were measured continuously using a Finometer. To assess hemodynamic responses and potential differences in sympatholysis, these measures performed at rest, during LBNP (‐20 mmHg), handgrip (HG) exercise (30% MVC), and HG+LBNP. Results: Under placebo conditions, at rest HR, SV, CO, and MAP were not different between BM and WM (p>0.05), and groups were unaffected by capsaicin (p>0.05). The LBNP‐induced changes at rest appeared larger for black males (SV ‐18±4ml vs. ‐8±11ml and MAP 4.6±6 vs. 1.3± 5mmHg, BM vs. WM), which were seemingly reversed with acute capsaicin (SV ‐11±13 vs. ‐9±16ml and MAP ‐2±9 vs. 1.2± 8mmHg, BM vs. WM). At rest, with placebo, the LBNP‐induced ΔHbO, was similar between groups (‐2±6 vs. ‐2±2μM, BM vs WM), and relatively unaffected by capsaicin (‐3±6 vs. ‐1±2 μM, BM vs WM). During HG exercise, the LBNP‐induced ΔHbO was disparate between groups (‐5±7 vs. 1±3 μM, BM vs WM), and this difference was ablated by the capsaicin (1±6 vs. 2±2 μM, BM vs WM). Conclusion: There were racial differences in the central and peripheral hemodynamic response to LBNP at rest and during exercise, suggesting impaired sympatholysis or altered autonomic regulation. Capsaicin, and assumed activation of TRPV1 receptors, seems to affect the hemodynamic response to LBNP, in a relatively race‐specific manner at rest and during exercise, potentially mitigating race‐related differences. Further work is needed to determine whether such differences may be due to altered TRPV1 expression between groups. [ABSTRACT FROM AUTHOR]

R2867 --> The pungent bioactive ingredient in peppers (Capsaicin; CAP) has been widely investigated for its activation of the transient receptor potential vanilloid 1 (TRPV1) channel on sensory neurons. It has been shown to improve mitochondrial biogenesis, adenosine triphosphate (ATP) production and vascular function. In animal models has been demonstrated that increases exercise performance and decreases fatigue development. However, whether acute oral CAP improves endurance performance and the potential underlying mechanisms remains elusive. This study aimed to evaluate the potential ergogenic and anti‐fatigue effects of acute oral CAP supplementation in healthy humans. In a double‐blind, placebo‐controlled, cross‐over design, 10 young healthy males performed constant‐load cycling exercise (294±55W; 85% of peak power output) to exhaustion, after acute ingestion of placebo (PL; 1000mg fiber pill) and CAP (780mg pill) capsules. Fatigue was assessed on the dominant quadriceps with the interpolated twitch technique, via changes in supramaximal electrical stimulation pre‐ vs. post‐exercise, during isometric maximal voluntary contractions (MVC) and at rest. Cardiopulmonary parameters (heart rate, cardiac output, oxygen consumption, ventilation) were assessed throughout the exercise. No statistically significant differences were detected in the muscle contractile functions, despite a trend (P=0.07) for a decreased time to exhaustion during CAP (PL: 369±85 vs. CAP: 296±64 sec). All the values (except muscle voluntary activation (%VMA)) significantly decreased from pre‐ to post‐exercise in both conditions. The exercise‐induced attenuation of the intrinsic muscle contractile properties (Maximal rate of force development (MRFD) and Maximal relaxation rate (MRR) of the resting twitch force) were mitigated, in part, by CAP. Notably, in the PL condition MRR was seemingly reduced by 47±33%, while only of 29±68% in CAP; contrarily, MRFD decreased similarly of 47±23% and of 40±27% in PL and CAP, respectively. In 9 participants, the resting twitch (estimate of peripheral muscle fatigue) pre‐ vs. post‐exercise decreased less with CAP (PL: 44±17 vs. CAP: 37±13%). CAP did not influence the MVC nor %VMA. The cardiopulmonary responses were similar between the conditions (P>0.05). In contrast to prior work, acute oral capsaicin did not improve endurance performance in the present study. CAP did elicit a tendency for faster relaxation rate, which might suggest an enhanced activation of the sarcoendoplasmic reticulum calcium ATPase (SERCA) pumps, thereby increasing the rate of Ca2+ reuptake and relaxation. However, this altered Ca2+ handling might also increase ATP demand. The tendency for CAP to attenuate the exercise‐induced reduction in muscle function, or fatigue, might provide a mechanistic basis for the previously demonstrated beneficial effects of CAP. Further work is needed in larger samples, to further determine the optimal dosing and loading strategies, to better understand the potential ergogenic effects of capsaicin. [ABSTRACT FROM AUTHOR]

Sarcopenia refers to a condition of progressive loss of skeletal muscle mass and function associated with a higher risk of falls and fractures in older adults. Musculoskeletal aging leads to reduced muscle mass and strength, affecting the quality of life in elderly people. In recent years, several studies contributed to improve the knowledge of the pathophysiological alterations that lead to skeletal muscle dysfunction; however, the molecular mechanisms underlying sarcopenia are still not fully understood. Muscle development and homeostasis require a fine gene expression modulation by mechanisms in which microRNAs (miRNAs) play a crucial role. miRNAs modulate key steps of skeletal myogenesis including satellite cells renewal, skeletal muscle plasticity, and regeneration. Here, we provide an overview of the general aspects of muscle regeneration and miRNAs role in skeletal mass homeostasis and plasticity with a special interest in their expression in sarcopenia and skeletal muscle adaptation to exercise in the elderly. [ABSTRACT FROM AUTHOR]

Purpose Given the increased level of fatigue frequently reported by patients with Parkinson's disease (PD), this study investigated the interaction between central and peripheral components of neuromuscular fatigue (NF) in this population compared with healthy peers. Methods Changes in maximal voluntary activation (ΔVA, central fatigue) and potentiated twitch force (Δ Q tw,pot, peripheral fatigue) pre–post exercise were determined via the interpolated twitch technique in 10 patients with PD and 10 healthy controls (CTRL) matched for age, sex, and physical activity. Pulmonary gas exchange, femoral blood flow, and quadriceps EMG were measured during a fatiguing exercise (85% of peak power output [PPO]). For a specific comparison, on another day, CTRL repeat the fatiguing test matching the time to failure (TTF) and PPO of PD. Results At 85% of PPO (PD, 21 ± 7 W; CTRL, 37 ± 22 W), both groups have similar TTF (~5.9 min), pulmonary gas exchange, femoral blood flow, and EMG. After this exercise, the maximal voluntary contraction (MVC) force and Q twpot decreased equally in both groups (−16%, P = 0.483; −43%, P = 0.932), whereas VA decreased in PD compared with CTRL (−3.8% vs −1.1%, P = 0.040). At the same PPO and TTF of PD (21 W; 5.4 min), CTRL showed a constant drop in MVC, and Q twpot (−14%, P = 0.854; −39%, P = 0.540), instead VA decreased more in PD than in CTRL (−3.8% vs −0.7%, P = 0.028). Conclusions In PD, central NF seems exacerbated by the fatiguing task which, however, does not alter peripheral fatigue. This, besides the TTF like CTRL, suggests that physical activity may limit NF and counterbalance PD-induced degeneration through peripheral adaptations. [ABSTRACT FROM AUTHOR]

Aim: Decreased muscle strength has been frequently observed in individuals with Parkinson's disease (PD). However, this condition is still poorly examined in physically active patients. This study compared quadriceps (Q) maximal force and the contribution of central and peripheral components of force production during a maximal isometric task between physically active PD and healthy individuals. In addition, the correlation between force determinants and energy expenditure indices were investigated. Methods: Maximal voluntary contraction (MVC), resting twitch (RT) force, pennation angle (θp), physiological cross‐sectional area (PCSA) and Q volume were assessed in 10 physically active PD and 10 healthy control (CTRL) individuals matched for age, sex and daily energy expenditure (DEE) profile. Results: No significant differences were observed between PD and CTRL in MVC (142 ± 85; 142 ± 47 N m), Q volume (1469 ± 379; 1466 ± 522 cm3), PCSA (206 ± 54; 205 ± 71 cm2), θp (14 ± 7; 13 ± 3 rad) and voluntary muscle‐specific torque (MVC/PCSA [67 ± 35; 66 ± 19 N m cm−2]). Daily calories and MVC correlated (r = 0.56, P =.0099). However, PD displayed lower maximal voluntary activation (MVA) (85 ± 7; 95 ± 5%), rate of torque development (RTD) in the 0‐0.05 (110 ± 70; 447 ± 461 N m s−1) and the 0.05‐0.1 s (156 ± 135; 437 ± 371 N m s−1) epochs of MVCs, whereas RT normalized for PCSA was higher (35 ± 14; 20 ± 6 N m cm−2). Conclusion: Physically active PDs show a preserved strength of the lower limb. This resulted by increasing skeletal muscle contractility, which counterbalances neuromuscular deterioration, likely due to their moderate level of physical activity. [ABSTRACT FROM AUTHOR]

The downward slope during the near‐infrared spectroscopy (NIRS)‐vascular occlusion test (NIRS‐VOT) is purported as a simplified estimate of metabolism. Whether or not the NIRS‐VOT exhibits sex‐ or limb‐specificity or may be acutely altered remains to be elucidated. Thus, we investigated if there is limb‐ or sex specificity in tissue desaturation rates (DeO2) during a NIRS‐VOT, and if acute dietary capsaicin may alter this estimate of muscle metabolism. Young healthy men (n = 25, 21 ± 4 years) and women (n = 20, 20 ± 1 years) ingested either placebo or capsaicin, in a counterbalanced, single‐blind, crossover design after which a simplified NIRS‐VOT was conducted to determine the DeO2 (%/s), as an estimate of oxidative muscle metabolism, in both the forearm (flexors) and thigh (vastus lateralis). There was a significant limb effect with the quadriceps having a greater DeO2 than the forearm (−2.31 ± 1.34 vs. −1.78 ± 1.22%/s, p = 0.007, ηp2 = 0.19). There was a significant effect of sex on DeO2 (p = 0.005, ηp2 = 0.203) with men exhibiting a lesser DeO2 than women (−1.73 ± 1.03 vs. −2.36 ± 1.32%/s, respectively). This manifested in significant interactions of limb*capsaicin (p = 0.001, ηp2 = 0.26) as well as limb*capsaicin*sex on DeO2 (p = 0.013, ηp2 = 0.16) being observed. Capsaicin does not clearly alter O2‐dependent muscle metabolism, but there was apparent limb and sex specificity, interacting with capsaicin in this NIRS‐derived assessment. [ABSTRACT FROM AUTHOR]

Purpose: Heart rate variability (HRV) estimates the autonomic nervous system (ANS) influence on the heart and appears sex-specific. Sensory afferents exhibit sex-specificity; although, it is unknown if Capsaicin, an agonist for transient receptor potential vanilloid channel-1 (TRPV1), alters cardiac ANS activity in a sex-dependent manner, which could be important given the predictive nature of HRV on risk of developing hypertension. Thus, we explored if there was sex-specificity in the effect of capsaicin on estimated cardiac ANS activity. Methods: HRV was measured in 38 young males (M: n = 25) and females (F: n = 13), in a blinded-crossover design, after acute ingestion of placebo or capsaicin. Resting HR, RR-interval, root-mean-square of successive differences (RMSSD), natural log-transformed RMSSD (LnRMSSD), standard deviation of n–n intervals (SDNN), number of pairs of successive n–n intervals differing by > 50 ms (NN50), and percent NN50 (PNN50) were obtained using standard techniques. Results: Significant sex differences were observed in mean HR (M: 59 ± 9.3 vs. F: 65 ± 12 beats/min, p = 0.036, η2 = 0.098), minimum HR (M: 47 ± 8.3 vs. F: 56 ± 12 beats/min, p = 0.014, η2 = 0.124), and NN50 (M: 177 ± 143 vs. F: 29 ± 17, p < 0.001, η2 = 0.249). There was a significant interaction of sex*treatment (p = 0.02, η2 = 0.027) for RMSSD, where males increased (78 ± 55 vs. 91 ± 64 ms), and females decreased (105 ± 83 vs. 76 ± 43 ms), placebo vs. capsaicin. Conclusion: This controlled study recapitulates sex differences in HR and HRV, but revealed a sexual dimorphism in the parasympathetic response to capsaicin, perhaps due to differing TRPV1-afferent sensitivity, highlighting a potential mechanism for differential regulation of hemodynamics, and CVD risk, and should be considered in future studies. [ABSTRACT FROM AUTHOR]

Purpose: Both muscle mass and physical activity are independent mechanisms that play a role in vascular remodeling, however, the direct impact of muscle mass on the structure and function of the vessels is not clear. The aim of the study was to determine the impact of muscle mass alteration on lower limbs arterial diameter, blood flow, shear rate and arterial stiffness. Methods: Nine (33 ± 13 yrs) male individuals with a single-leg amputation were recruited. Vascular size (femoral artery diameter), hemodynamics (femoral artery blood flow and shear rate were measured at the level of the common femoral artery in both amputated (AL) and whole limbs (WL). Muscle mass of both limbs, including thigh for AL and thigh and leg for WL, was measured with a DXA system. Results: AL muscle mass was reduced compared to the WL (3.2 ± 1.2 kg vs. 9.4 ± 2.1 kg; p = 0.001). Diameter of the femoral artery was reduced in the AL (0.5 ± 0.1 cm) in comparison to the WL (0.9 ± 0.2 cm, p = 0.001). However, femoral artery blood flow normalized for the muscle mass (AL = 81.5 ± 78.7ml min−1 kg−1,WL = 32.4 ± 18.3; p = 0.11), and blood shear rate (AL = 709.9 ± 371.4 s−1, WL = 526,9 ± 295,6; p = 0.374) were non different between limbs. A correlation was found only between muscle mass and femoral artery diameter (p = 0.003, R = 0.6561). Conclusion: The results of this study revealed that the massive muscle mass reduction caused by a leg amputation, but independent from the level of physical activity, is coupled by a dramatic arterial diameter decrease. Interestingly, hemodynamics and arterial stiffness do not seem to be impacted by these structural changes. [ABSTRACT FROM AUTHOR]

Purpose: This study evaluated whether central motor drive during fatiguing exercise plays a role in determining performance and the development of neuromuscular fatigue during a subsequent endurance task. Methods: On separate days, 10 males completed three constant-load (80% peak power output), single-leg knee-extension trials to task failure in a randomized fashion. One trial was performed without preexisting quadriceps fatigue (CON), and two trials were performed with preexisting quadriceps fatigue induced either by voluntary (VOL; involving central motor drive) or electrically evoked (EVO; without central motor drive) quadriceps contractions (~20% maximal voluntary contraction (MVC)). Neuromuscular fatigue was assessed via pre–post changes in MVC, voluntary activation (VA), and quadriceps potentiated twitch force (Q tw,pot). Cardiorespiratory responses and rating of perceived exertion were also collected throughout the sessions. The two prefatiguing protocols were matched for peripheral fatigue and stopped when Q tw,pot declined by ~35%. Results: Time to exhaustion was shorter in EVO (4.3 ± 1.3 min) and VOL (4.7 ± 1.5 min) compared with CON (10.8 ± 3.6 min, P < 0.01) with no difference between EVO and VOL. ΔMVC (EVO: −47% ± 8%, VOL: −45% ± 8%, CON: −53% ± 8%), Δ Q tw,pot (EVO: −65% ± 7%, VOL: −59% ± 14%, CON: −64% ± 9%), and ΔVA (EVO: −9% ± 7%, VOL: −8% ± 5%, CON: −7% ± 5%) at the end of the dynamic task were not different between conditions (all P > 0.05). Compared with EVO (10.6 ± 1.7) and CON (6.8 ± 0.8), rating of perceived exertion was higher (P = 0.05) at the beginning of VOL (12.2 ± 1.0). Conclusions: These results suggest that central motor drive involvement during prior exercise plays a negligible role on the subsequent endurance performance. Therefore, our findings indicate that peripheral fatigue–mediated impairments are the primary determinants of high-intensity single-leg endurance performance. [ABSTRACT FROM AUTHOR]

R4530 --> 595.4 --> Purpose: Transcranial magnetic stimulation (TMS) is a noninvasive technique to assess corticospinal excitability and inhibition. TMS over the motor cortex during a voluntary contraction elicits short‐latency excitatory (motor‐evoked potential, MEP) and inhibitory (silent period, SP) responses in the target muscle. However, the technique for searching and determining the optimal site to elicit MEPs ("hotspot"), an essential component in order to correctly place the TMS coil, is not unanimously standardized. This can be a problem since changes in coil position and/or orientation may influence the magnitude of MEP and SP responses. Usually, the "hotspot" is marked either on a swim cap or on the scalp and the investigator holds the coil manually during the entire testing session. However, the capacity to maintain the coil placement within and between sessions may be limited. To reduce variability in coil position and orientation in space and over time, neuronavigated TMS (nTMS) is used. However, no studies investigated the accuracy of the assessment of corticospinal excitability and inhibition using nTMS versus a traditional manual approach for the maintenance of coil positioning. Methods: 18 healthy participants (10W/8M) volunteered in two identical and randomized sessions ~30 days apart. Maximal and submaximal neuromuscular evaluations were performed with TMS six times before (PRE), and at the end (POST) of a 2‐min sustained maximal voluntary isometric contraction (MVIC) (100%, 75%, 50% MVIC and 25%isoEMG). The "hotspot" was maintained either with a grid demarcated on the participants' scalp or with visual feedback provided by nTMS on a computer screen. In both sessions, "hotspot" was considered as the site where the largest MEPs in the rectus femoris were elicited. Results: There were not a "hotspot" technique × contraction intensities × time points interactions for both MEP (P = 0.217) and SP (P = 0.627). Bland‐Altman plots display adequate agreements between the difference in the two "hotspot" techniques and the means of the two "hotspot" techniques. The slopes of the resulting regression lines were not significantly different from zero (horizontal to x‐axis) for both MEP (all r ≤ 0.335, all P ≥ 0.162) and SP (all r ≤ 0.382, all P ≥ 0.131), indicating a uniformity of systematic error at all contraction intensities and time points. Conclusions: Spatial stability of the TMS coil position over the motor cortex did not influence corticospinal excitability and inhibition responses in unfatigued and fatigued knee extensors. This is because the variability in MEP and SP responses is due to spontaneous fluctuations in corticospinal and motoneuron excitability and inhibition; and this variability is not affected by spatial accuracy. Therefore, nTMS or a traditional manual approach could be interchangeably use in order to maintain the TMS coil position in the exact "hotspot". [ABSTRACT FROM AUTHOR]

Fatigue is one of the most disabling symptoms of multiple sclerosis (MS); it influences patients' quality of life. The etiology of fatigue is complex, and its pathogenesis is still unclear and debated. The objective of this review was to describe potential brain structural and functional dysfunctions underlying fatigue symptoms in patients with MS. To reach this purpose, a systematic review was conducted of published studies comparing functional brain activation and structural brain in MS patients with and without fatigue. Electronic databases were searched until 24 February 2021. The structural and functional outcomes were extracted from eligible studies and tabulated. Fifty studies were included: 32 reported structural brain differences between patients with and without fatigue; 14 studies described functional alterations in patients with fatigue compared to patients without it; and four studies showed structural and functional brain alterations in patients. The results revealed structural and functional abnormalities that could correlate to the symptom of fatigue in patients with MS. Several studies reported the differences between patients with fatigue and patients without fatigue in terms of conventional magnetic resonance imaging (MRI) outcomes and brain atrophy, specifically in the thalamus. Functional studies showed abnormal activation in the thalamus and in some regions of the sensorimotor network in patients with fatigue compared to patients without it. Patients with fatigue present more structural and functional alterations compared to patients without fatigue. Specifically, abnormal activation and atrophy of the thalamus and some regions of the sensorimotor network seem linked to fatigue. [ABSTRACT FROM AUTHOR]

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, nonfatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), whereas on the other day, the same KE exercise was repeated following electrically induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to postexercise changes in potentiated twitch force (ΔQtw,pot; peripheral fatigue), and voluntary muscle activation (ΔVA; central fatigue). As reflected by the 57 ± 11% reduction in electrically evoked pulse force, the electrically induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared with No-PreF (4.6 ± 1.2 vs 7.7 ± 2.4 min; P < 0.01). Although ΔQtw,pot was significantly larger in No-PreF compared with PreF (−60% vs −52%, P < 0.05), ΔVA was greater in PreF (−14% vs −10%, P < 0.05). Taken together, electrically induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon. [ABSTRACT FROM AUTHOR]

Purpose: Vascular dysfunction has been demonstrated in patients with Alzheimer's disease (AD). Exercise is known to positively affect vascular function. Thus, the aim of our study was to investigate exercise-induced effects on vascular function in AD. Methods: Thirty-nine patients with AD (79 ± 8 years) were recruited and randomly assigned to exercise training (EX, n = 20) or control group (CTRL, n = 19). All subjects performed 72 treatment sessions (90 min, 3 t/w). EX included moderate–high-intensity aerobic and strength training. CTRL included cognitive stimuli (visual, verbal, auditive). Before and after the 6-month treatment, the vascular function was measured by passive-leg movement test (PLM, calculating the variation in blood flow: ∆peak; and area under the curve: AUC) tests, and flow-mediated dilation (FMD, %). A blood sample was analyzed for vascular endothelial growth factor (VEGF). Arterial blood flow (BF) and shear rate (SR) were measured during EX and CTRL during a typical treatment session. Results: EX group has increased FMD% (+ 3.725%, p < 0.001), PLM ∆peak (+ 99.056 ml/min, p = 0.004), AUC (+ 37.359AU, p = 0.037) and VEGF (+ 8.825 pg/ml, p = 0.004). In the CTRL group, no difference between pre- and post-treatment was found for any variable. Increase in BF and SR was demonstrated during EX (BF + 123%, p < 0.05; SR + 134%, p < 0.05), but not during CTRL treatment. Conclusion: Exercise training improves peripheral vascular function in AD. These ameliorations may be due to the repetitive increase in SR during exercise which triggers NO and VEGF upregulation. This approach might be included in standard AD clinical practice as an effective strategy to treat vascular dysfunction in this population. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction is associated with cardiovascular disease development, nitric oxide (NO) deficiencies, and may be limb or sex-specific. Prior in vitro work indicated that the transient receptor potential vanilloid channel-1 (TRPV 1) is expressed in human arteries and the TRPV 1 agonist capsaicin alters vasodilation in an endothelium-dependent manner; however, it is unknown if this translates in vivo or is limb or sex-dependent. Therefore, we sought to determine if there was limb or sex-specificity in the effect of capsaicin on microvascular function using near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (StO 2) reperfusion slope. In a blinded placebo-controlled crossover design, 45 young males (M: n = 25) and females (F: n = 20), the reperfusion slopes of the forearm and quadriceps were assessed, and a urine sample obtained to assay for nitrate/nitrite (NOx) concentrations and antioxidant capacity after acutely ingesting placebo or capsaicin. Under placebo, females had greater reperfusion rates in both the forearm (M: 0.44 ± 0.24 vs. F: 0.98 ± 0.46 %/ sec ; p = 0.002, d = −1.50) and quadricep (M: 0.86 ± 0.31 vs. F: 1.17 ± 0.43 %/sec; p = 0.010, d = −0.85). Capsaicin decreased microvascular responsiveness in the forearm of females (placebo: 0.98 ± 0.45 vs. capsaicin: 0.84 ± 0.45 %/ sec) as compared to males (placebo: 0.45 ± 0.24 vs. capsaicin: 0.38 ± 0.16 %/sec, interaction p < 0.001, η2 = 0.475). There was a sex*treatment interaction for NOx concentrations, where males increased (placebo: 21.13 ± 12.83 vs. capsaicin: 23.82 ± 13.34 μM), while females decreased (placebo: 22.78 ± 14.40 vs. capsaicin: 14.43 ± 10.01 μM; p = 0.037, η2 = 0.042). Using NIRS to assess microvascular function, there is apparent limb and sex-specificity, and, for the first-time, document that acute oral capsaicin alters reperfusion slope in a sexually divergent manner. • Microvascular function in humans is sex-dependent, especially in the arms. • Capsaicin, spicy component of peppers, alters nitric oxide, depending upon sex. • Capsaicin reduces NO in women might explain reduced microvascular function. • These findings do not appear to be due to differences in antioxidant capacity. • Future researchers should bear these findings in mind when designing studies. [ABSTRACT FROM AUTHOR]

• Transcranial magnetic stimulation (TMS)-induced muscle relaxation demonstrates high within- and between-session reliability in unfatigued and fatigued knee-extensor muscles. • TMS is a useful technique that researchers can use when investigating changes in muscle relaxation rates both in unfatigued and fatigued knee-extensor muscles. • In both healthy individuals and patient groups, TMS-induced muscle relaxation could be used for therapy effect monitoring and diagnostic purposes. Transcranial magnetic stimulation (TMS)-induced relaxation rate reflects intrinsic muscle contractile properties by interrupting the drive from the central nervous system during voluntary muscle contractions. To determine the appropriateness of knee-extensor muscle relaxation measurements induced by TMS, this study aimed to establish both the within- and between-session reliability before and after a fatiguing exercise bout. Eighteen participants (9 females, 9 males, age 25 ± 2 years, height 171 ± 9 cm, body mass 68.5 ± 13.5 kg) volunteered to participate in two identical sessions approximately 30 days apart. Maximal and submaximal neuromuscular evaluations were performed with TMS six times before (PRE) and at the end (POST) of a 2-min sustained maximal voluntary isometric contraction. Within- and between-session reliability of PRE values were assessed with intraclass correlation coefficient (ICC 2,1 , relative reliability), repeatability coefficient (absolute reliability), and coefficient of variation (variability). Test-retest reliability of post-exercise muscle relaxation rates was assessed with Bland-Altman plots. For both the absolute and normalized peak relaxation rates and time to peak relaxation, data demonstrated low variability (e.g. coefficient of variation ≤ 7.8%) and high reliability (e.g. ICC 2,1 ≥ 0.963). Bland-Altman plots showed low systematic errors. These findings establish the reliability of TMS-induced muscle relaxation rates in unfatigued and fatigued knee-extensor muscles, showing that TMS is a useful technique that researchers can use when investigating changes in muscle relaxation rates both in unfatigued and fatigued knee-extensor muscles. [ABSTRACT FROM AUTHOR]

R2447 --> 755.1 --> Heart rate variability (HRV) estimates autonomic nervous system (ANS) influence on the heart and is sex‐specific. Sensory afferents exhibit sex‐specificity; although, there is a paucity of data on the potential effects of Capsaicin, an agonist for transient receptor potential vanilloid channel‐1 (TRPV1), on cardiac ANS activity and if the effect is sex‐dependent. Given the predictive nature of HRV on risk of developing hypertension, understanding the sex differences in factors governing HRV is paramount. PURPOSE: Therefore, this study sought to determine the sex‐specificity in the effect of capsaicin on cardiac autonomic function estimated through HRV. It was hypothesized that females would have lower HRV than the age‐matched males and that capsaicin could attenuate these sex differences. METHODS: HRV was measured in 38 young males (M: n=25) and females (F: n=13), in a blinded crossover design, after acute ingestion of placebo or capsaicin capsules. Resting measurements of HR, RR interval, root mean square of successive differences (RMSSD), natural log‐transformed RMSSD (LnRMSSD), standard deviation of n‐n intervals (SDNN), number of pairs of successive n‐n intervals that differ by more than 50 msec (NN50), and percent NN50 to total n‐n intervals (PNN50) were obtained using standard techniques. RESULTS: Under placebo, males had significantly lower minimum HR (M: 49±9.7 vs. F: 58±16 beats/min, p=0.038, d=‐0.738) and significantly higher NN50 (M: 141±118 vs. F: 33±23, p=0.003, d=‐0.129) than females. There was a main effect of sex on HR (M: 59±9.3 vs. F: 65±12 beats/min, p=0.036, η2=0.098), minimum HR (M: 47±8.3 vs. F: 56±12 beats/min, p=0.014, η2=0.124), and NN50 (M: 177±143 vs. F: 29±17, p<0.001, η2=0.249). There was a significant interaction of sex and treatment (p=0.02, η2=0.027) for RMSSD, where males increased (Placebo: 78±55 vs. Capsaicin: 91±64 ms), and females decreased (Placebo: 105±83 vs. Capsaicin 76±43 ms). CONCLUSION: This study recapitulates previously documented sex differences in HR and HRV. Acute ingestion of capsaicin increased RMSSD in men, but decreased RMSSD in women, suggesting a sexual dimorphism in parasympathetic response, perhaps due to differences in TRPV1‐sensitive afferents or sensitivity. The physiological ramifications of these findings, specifically in the regulation of blood pressure and ultimately cardiovascular disease risk remain to be explored, especially in the transition to menopause in women. [ABSTRACT FROM AUTHOR]

R2504 --> 710.2 --> Previous studies demonstrated that aging, neurodegeneration, and the level of physical activity are associated with vascular alterations. However, in Parkinson's disease (PD) only cerebral vascular function has been investigated; instead, the contribution of PD on systemic vascular function and skeletal muscle circulation remains a matter of debate. In this study, the hyperemic response during the single passive leg movement test (sPLM) was examined at the level of the common femoral artery with an ultrasound Doppler system to assess systemic vascular function in 10 subjects with PD (PDG), compared with 10 aged‐sex and physically active matched healthy elderly (EHG), and 10 physically active young healthy individuals (YHG). Interestingly, femoral blood flow at rest was similar in PDG (64±15 mL min‐1 L‐1), EHG (44±8 mL min‐1 L‐1) and YHG (58±11 mL min‐1 L‐1). Our working hypothesis was that PDG would present an altered blood flow to the skeletal muscle, a reduced vascular function due to the pathology compared with the other groups. However, the sPLM‐hyperemic response appeared markedly lower in PDG and EHG compared to YHG (8.3±0.1 vs 9.8±0.8 vs 17±3 mL min‐1 L‐1; p < 0.05) but the difference between PDG and EHG was negligible (p > 0.05). The results of our study indicate that peripheral circulation and vascular function are not reduced in physically active patients with PD, suggesting that these vascular changes could resemble the physiological adjustments of aging, without any impact from the disease. [ABSTRACT FROM AUTHOR]

R4715 --> 885.5 --> Vascular remodeling refers to the changes in the structure and function of vessels. This adaptability of the arteries is essential to successfully handle vascular distress and arterial disease. Both, skeletal muscle mass and the level of physical activity are independent mechanisms that plays a role in this physiological phenomenon. However, the direct impact of the skeletal muscle mass remodeling on the structure and function of the vessels is not clear. PURPOSE: To determine the impact of skeletal muscle mass remodeling on lower limbs arterial diameter, blood flow and arterial stiffness. METHODS: Nine young (33±13 yrs) physical active individuals with a single‐leg amputation (transtibial amputation) were recruited for the study. Vascular size (femoral artery diameter), hemodynamics (femoral artery blood flow) and arterial stiffness (carotid‐femoral pulse wave velocity) were measure with an ultrasound doppler device at the level of the common femoral artery in both amputee (AL) and whole limbs (WL). Skeletal muscle mass of both limbs was measured with a DEXA system. Both AL and WL were equally utilized by the individuals for ambulation and recreational sports. RESULTS: The skeletal muscle mass of the AL was significantly reduced in comparison to the WL (3.2±1.2 Kg Vs 9.4±2.1 Kg; P=0.0011). Also, the diameter of the femoral artery was significantly reduced in the AL 0.5±0.1 cm in comparison to the WL 0.9±0.2 (p=0.0012). However, femoral artery blood flow normalized for the muscle mass (mean difference 49.07 ml۰min‐1۰kg‐1; p = 0.11) and carotid‐femoral Pulse Wave Velocity (mean difference 0.91 cm۰s‐1; p =0.21) were similar between the two legs. Interestingly, linear regression analysis shows a significant correlation between skeletal muscle mass and femoral artery diameter (p=0.0031). CONCLUSION: The results of this study revealed that the massive skeletal muscle reduction caused by a transtibial amputation, but independent form the level of physical activity, is coupled by a dramatic arterial diameter decrease. Interestingly, local circulation and arterial stiffness seems not impacted by these structural changes. [ABSTRACT FROM AUTHOR]