Speed Effects on the Accuracy of Heart Rate as Oxygen-Uptake Indicator in Short-Distance Shuttle Running.

Purpose: Despite the accuracy of heart rate (HR) as an indicator of the aerobic engagement has been evaluated in several intermittent on-court activities, its validity as an oxygen uptake (V˙O2) indicator during shuttle running over short paths remains uncertain. Moreover, it is unclear whether speed may affect such validity. This study evaluated the HR ability in estimating the V˙O2 during 5-m shuttle running at different speeds. Methods: V˙O2 and HR of 12 physically active young men were recorded during an incremental forward running (FW) protocol and a 5-m shuttle test at 50%, 60%, and 75% of maximal aerobic speed (MAS). Slope and intercept of the relationship between HR and V˙O2 (HR/V˙O2) were individually determined, in both protocols. The HR measured during the shuttle test was used in the FW HR/V˙O2 to estimate V˙O2 at each shuttle speed. A paired Student's t-test compared slopes and intercepts of the two HR/V˙O2. A two-way RM-ANOVA and an equality test examined, respectively, the differences and the equality between measured and estimated V˙O2. Lastly, a Bland-Altman plot described the accuracy and precision of the estimated V˙O2 at each shuttle intensity. Results: Slopes and intercepts of the HR/V˙O2 appeared not different between FW and shuttle running. At 50%MAS, HR underestimated the V˙O2 (~7%), whereas returned accurate values at the two higher velocities, although with high variability (±18%). Conclusions: When using HR as V˙O2 indicator during shuttle running over short paths, a separated analysis of the HR validity as V˙O2 indicator is recommended especially when administering different exercise intensities.

Long-Term Passive Leg Stretch Improves Systemic Vascular Responsiveness as Much as Single-Leg Exercise Training.

PURPOSE: The current study compared the local and systemic vascular responsiveness after small muscle mass endurance training or passive stretching training (PST). METHODS: Thirty-six sex-matched healthy participants underwent 8-wk single-leg knee extension (SLKE) (n = 12) training or PST (n = 12), or no intervention (control, n = 12). Before and after the intervention, local and systemic vascular responsiveness was assessed by Doppler ultrasound at the femoral (local effect) and brachial artery (systemic effect) during single passive leg movement and brachial flow-mediated dilation (FMD) test, respectively. RESULTS: After training, delta femoral blood flow (representing the local vascular responsiveness) increased after SLKE and PST by +54 (7)% (effect size, 2.72; P < 0.001) and +20 (2)% (effect size, 2.43; P < 0.001), respectively, albeit with a greater extent in SLKE (post-SLKE vs post-PST: +56 [8]% [effect size, 2.92; P < 0.001]). Interestingly, the %FMD (standing for the systemic effect) increased after SLKE and PST by +12 (2)% (effect size, 0.68; P < 0.001) and +11 (1)% (effect size, 0.83; P < 0.001), respectively, without any between-groups difference (P > 0.05). No changes occurred in control. CONCLUSIONS: The present findings revealed that both active and passive training modalities induced similar improvements in the brachial artery dilatation capacity, whereas the former was more effective in improving femoral artery blood flow. Passive stretching could be used in people with limited mobility to improve vascular responsiveness both at the local and systemic level and in this latter case has similar effects as small muscle mass endurance training.

The effects of 12 weeks of static stretch training on the functional, mechanical, and architectural characteristics of the triceps surae muscle-tendon complex.

PURPOSE: We investigated the effects of 12 weeks of passive static stretching training (PST) on force-generating capacity, passive stiffness, muscle architecture of plantarflexor muscles. METHODS: Thirty healthy adults participated in the study. Fifteen participants (STR, 6 women, 9 men) underwent 12-week plantarflexor muscles PST [(5 × 45 s-on/15 s-off) × 2exercises] × 5times/week (duration: 2250 s/week), while 15 participants (CTRL, 6 women, 9 men) served as control (no PST). Range of motion (ROM), maximum passive resistive torque (PRTmax), triceps surae architecture [fascicle length, fascicle angle, and thickness], passive stiffness [muscle-tendon complex (MTC) and muscle stiffness], and plantarflexors maximun force-generating capacity variables (maximum voluntary contraction, maximum muscle activation, rate of torque development, electromechanical delay) were calculated Pre, at the 6th (Wk6), and the 12th week (Wk12) of the protocol in both groups. RESULTS: Compared to Pre, STR ROM increased (P < 0.05) at Wk6 (8%) and Wk12 (23%). PRTmax increased at Wk12 (30%, P < 0.05), while MTC stiffness decreased (16%, P < 0.05). Muscle stiffness decreased (P < 0.05) at Wk6 (11%) and Wk12 (16%). No changes in triceps surae architecture and plantarflexors maximum force-generating capacity variables were found in STR (P > 0.05). Percentage changes in ROM correlated with percentage changes in PRTmax (ρ = 0.62, P = 0.01) and MTC stiffness (ρ = - 0.78, P = 0.001). In CTRL, no changes (P > 0.05) occurred in any variables at any time point. CONCLUSION: The expected long-term PST-induced changes in ROM were associated with modifications in the whole passive mechanical properties of the ankle joint, while maximum force-generating capacity characteristics were preserved. 12 weeks of PST do not seem a sufficient stimulus to induce triceps surae architectural changes.

Vascular function in continuous-flow left ventricular assist device recipients: effect of a single pulsatility treatment session.

Vascular function is further attenuated in patients with chronic heart failure implanted with a continuous-flow left ventricular assist device (LVAD), likely due to decreased arterial pulsatility, and this may contribute to LVAD-associated cardiovascular complications. However, the impact of increasing pulsatility on vascular function in this population is unknown. Therefore, 15 LVAD recipients and 15 well-matched controls underwent a 45-min, unilateral, arm pulsatility treatment, evoked by intermittent cuff inflation/deflation (2-s duty cycle), distal to the elbow. Vascular function was assessed by percent brachial artery flow-mediated dilation (%FMD) and reactive hyperemia (RH) (Doppler ultrasound). Pretreatment, %FMD (LVAD: 4.0 ± 1.7; controls: 4.2 ± 1.4%) and RH (LVAD: 340 ± 101; controls: 308 ± 94 mL) were not different between LVAD recipients and controls; however, %FMD/shear rate was attenuated (LVAD: 0.10 ± 0.04; controls: 0.17 ± 0.06%/s-1, P < 0.05). The LVAD recipients exhibited a significantly attenuated pulsatility index (PI) compared with controls prior to treatment (LVAD: 2 ± 2; controls: 15 ± 7 AU, P < 0.05); however, during the treatment, PI was no longer different (LVAD: 37 ± 38; controls: 36 ± 14 AU). Although time to peak dilation and RH were not altered by the pulsatility treatment, %FMD (LVAD: 7.0 ± 1.8; controls: 7.4 ± 2.6%) and %FMD/shear rate (LVAD: 0.19 ± 0.07; controls: 0.33 ± 0.15%/s-1) increased significantly in both groups, with, importantly, %FMD/shear rate in the LVAD recipients being restored to that of the controls pretreatment. This study documents that a localized pulsatility treatment in LVAD recipients and controls can recover local vascular function, an important precursor to the development of approaches to increase systemic pulsatility and reduce systemic vascular complications in LVAD recipients.

Neuromuscular versus Mechanical Stretch-induced Changes in Contralateral versus Ipsilateral Muscle.

PURPOSE: Whether or not the homologous contralateral muscle (CM) undergoes stretch-induced force reduction as the stretched muscle (SM) is still unclear. The neuromuscular and mechanical factors underlying the force reduction in CM and SM were investigated. METHODS: Twenty-one participants underwent unilateral knee extensors passive stretching. In both CM and SM, before, immediately after (POST), 5 (POST5), and 10 min (POST10) after passive stretching, maximum voluntary contraction (MVC), peak force (pF), and voluntary activation (VA) were measured. During MVC, the electromyographic and mechanomyographic root mean square (EMG RMS and MMG RMS, respectively) was calculated in rectus femoris, vastus lateralis, and vastus medialis, together with M-wave. The total electromechanical delay (EMD), divided in time delay (Δt) EMG-MMG and Δt MMG-F was calculated. RESULTS: In CM at POST, the decrease in MVC (-11%; 95% confidence interval [CI], -13 to -9; effect size [ES], -2.27) was accompanied by a fall in VA (-7%; 95% CI, -9 to -4; ES, -2.29), EMG RMS (range, -22% to -11%; ES, -3.92 to -2.25), MMG RMS (range, -10% to -8%; ES, -0.52 to -0.39) and an increase in Δt EMG-MMG (≈+10%; ES, 0.73 to 0.93). All changes returned to baseline at POST5. In SM, decrease in MVC (-19%; 95% CI, -24 to -18; ES, -3.08), pF (-25%; 95% CI, -28 to -22; ES, -4.90), VA (-10%; 95% CI, -11 to -9; ES, -5.71), EMG RMS (≈-33%; ES, -5.23 to -3.22) and rise in MMG RMS (range, +25% to +32%; ES, 4.21 to 4.98) and EMD (≈+28%; ES, 1.59 to 1.77) were observed at POST and persisted at POST10. No change in M-wave occurred. CONCLUSIONS: The contralateral central motor drive stretch-induced inhibition seems to account for the force reduction in CM. In SM, both central inhibition and mechanical factors concurred.

Quadriceps and Gastrocnemii Anatomical Cross-Sectional Area and Vastus Lateralis Fascicle Length Predict Peak-Power and Time-To-Peak-Power.

Purpose: The current study investigated the role of quadriceps and gastrocnemii size and vastus lateralis and gastrocnemius medialis muscle architecture in peak-power and time-to-peak-power exerted in an all-out Wingate test. Twenty-one amateur cyclists were recruited. Methods: Quadriceps and gastrocnemii anatomical cross-sectional area (ACSA), and vastus lateralis and gastrocnemius medialis pennation angle and fascicle length were measured using ultrasound. Relative peak-power (normalized per body mass) and time-to-peak-power were measured during a 30s all-out test. Results: Relative peak-power was correlated with quadriceps ACSA (r = 0.896, p < .001), gastrocnemii ACSA (r = 0.811, p < .001), vastus lateralis (r = 0.787, p < .001) and gastrocnemius medialis pennation angle (r = 0.638, p < .003). Multiple regression revealed that quadriceps and gastrocnemii ACSA accounted for 85% (R2= 0.85) of peak-power variance. Time-to-peak-power showed very large (r = -0.868, p < .001) and large correlation (r = -0.680, p = .001) with VL and GM fascicle length, respectively. Multiple regression analysis revealed that VL fascicle length explained 75% (R2= 0.75) of the time-to-peak-power variance. Conclusions: Quadriceps and gastrocnemii ACSA largely explained relative peak-power in an all-out Wingate test. Vastus lateralis fascicle length was the main predictor of the time-to-peak-power. Muscle architecture characteristics seem to be involved in the power generating capacity.

Evidence of Improved Vascular Function in the Arteries of Trained but Not Untrained Limbs After Isolated Knee-Extension Training.

Vascular endothelial function is a strong marker of cardiovascular health and it refers to the ability of the body to maintain the homeostasis of vascular tone. The endothelial cells react to mechanical and chemical stimuli modulating the smooth muscle cells relaxation. The extent of the induced vasodilation depends on the magnitude of the stimulus. During exercise, the peripheral circulation is mostly controlled by the endothelial cells response that increases the peripheral blood flow in body districts involved but also not involved with exercise. However, whether vascular adaptations occur also in the brachial artery as a result of isolated leg extension muscles (KE) training is still an open question. Repetitive changes in blood flow occurring during exercise may act as vascular training for vessels supplying the active muscle bed as well as for the vessels of body districts not directly involved with exercise. This study sought to evaluate whether small muscle mass (KE) training would induce improvements in endothelial function not only in the vasculature of the lower limb (measured at the femoral artery level in the limb directly involved with training), but also in the upper limb (measured at the brachial artery level in the limb not directly involved with training) as an effect of repetitive increments in the peripheral blood flow during training sessions. Ten young healthy participants (five females, and five males; age: 23 ± 3 years; stature: 1.70 ± 0.11 m; body mass: 66 ± 11 kg; BMI: 23 ± 1 kg ⋅ m-2) underwent an 8-week KE training study. Maximum work rate (MWR), vascular function and peripheral blood flow were assessed pre- and post-KE training by KE ergometer, flow mediated dilatation (FMD) in the brachial artery (non-trained limb), and by passive limb movement (PLM) in femoral artery (trained limb), respectively. After 8 weeks of KE training, MWR and PLM increased by 44% (p = 0.015) and 153% (p = 0.003), respectively. Despite acute increase in brachial artery blood flow during exercise occurred (+25%; p < 0.001), endothelial function did not change after training. Eight weeks of KE training improved endothelial cells response only in the lower limb (measured at the femoral artery level) directly involved with training, likely without affecting the endothelial response of the upper limb (measured at the brachial artery level) not involved with training.

Heart and musculoskeletal hemodynamic responses to repetitive bouts of quadriceps static stretching.

The role of sympathetic and parasympathetic activity in relation to the repetitive exposure to static stretching (SS) on heart and musculoskeletal hemodynamics in stretched and resting muscles is still a matter of debate. The aim of the study was to determine cardiac and musculoskeletal hemodynamics to repetitive bouts of unilateral SS. Sympathetic and parasympathetic activity contribution to the central hemodynamics and local difference in circulation of stretched and resting muscles were also investigated. In eight participants, heart rate (HR), cardiac output (CO), mean arterial pressure (MAP), HR variability (HRV), blood pressure variability (BPV), and blood flow in passively stretched limb (SL) and control (CL, resting limb) were measured during five bouts of unilateral SS (45 s of knee flexion and 15 s of knee extension). SS increased sympathetic (~20%) and decreased parasympathetic activity (~30%) with a prevalence of parasympathetic withdrawal. During SS, HR, CO, and MAP increased by ~18 beats/min, ~0.29 l/min, ~12 mmHg, respectively. Peak blood flow in response to the first stretching maneuver increased significantly (+377 ± 95 ml/min) in the SL and reduced significantly (-57 ± 48 ml/min) in the CL. This between-limb difference in local circulation response to SS disappeared after the second SS bout. These results indicate that heart hemodynamic responses to SS are primarily influenced by the parasympathetic withdrawal rather than by the increase in sympathetic activity. The balance between neural and local factors contributing to blood flow regulation was affected by the level of SS exposure, likely associated with differences in the bioavailability of local vasoactive factors throughout the stretching bouts.NEW & NOTEWORTHY Repetitive exposure to static stretching (SS) on heart and musculoskeletal hemodynamics in stretched and remote muscles may be influenced by neural and local factors. We documented that SS-induced heart hemodynamic responses are primarily influenced by parasympathetic withdrawal. The balance between neural and local factors contributing to the regulation of musculoskeletal hemodynamics is dependent on SS exposure possibly because of different local vasoactive factor bioavailability during the subsequent stretching bouts.

Respiratory muscle training positively affects vasomotor response in young healthy women.

Vasomotor response is related to the capacity of the vessel to maintain vascular tone within a narrow range. Two main control mechanisms are involved: the autonomic control of the sympathetic neural drive (global control) and the endothelial smooth cells capacity to respond to mechanical stress by releasing vasoactive factors (peripheral control). The aim of this study was to evaluate the effects of respiratory muscle training (RMT) on vasomotor response, assessed by flow-mediated dilation (FMD) and heart rate variability, in young healthy females. The hypothesis was that RMT could enhance the balance between sympathetic and parasympathetic neural drive and reduce vessel shear stress. Thus, twenty-four women were randomly assigned to either RMT or SHAM group. Maximal inspiratory mouth pressure and maximum voluntary ventilation were utilized to assess the effectiveness of the RMT program, which consisted of three sessions of isocapnic hyperventilation/ week for eight weeks, (twenty-four training sessions). Heart rate variability assessed autonomic balance, a global factor regulating the vasomotor response. Endothelial function was determined by measuring brachial artery vasodilation normalized by shear rate (%FMD/SR). After RMT, but not SHAM, maximal inspiratory mouth pressure and maximum voluntary ventilation increased significantly (+31% and +16%, respectively). Changes in heart rate variability were negligible in both groups. Only RMT exhibited a significant increase in %FMD/SR (+45%; p<0.05). These data suggest a positive effect of RMT on vasomotor response that may be due to a reduction in arterial shear stress, and not through modulation of sympatho-vagal balance.

Sex-Related Responses to Eccentric-Only Resistance Training in Knee-Extensors Muscle Strength and Architecture.

PURPOSE: The present study aimed to investigate whether or not eccentric-only training induced different sex-related adaptations in vastus lateralis muscle architecture and knee extensors strength. METHODS: Thirteen healthy women and 13 healthy men were recruited. Vastus lateralis pennation angle, fascicle length, and muscle thickness, as well as knee extensors eccentric, isometric, and concentric peak torque and one-repetition maximum (1RM) were measured. Both women and men underwent a unilateral iso-load knee-extension eccentric-only training with 120% of the concentric 1RM, consisting of 4 sets × 10 repetitions twice a week for a total of 8 weeks. RESULTS: Pennation angle increased in women (+ 14%, 95% CI [10, 17], effect size [ES] = 1.54) but not in men (+ 5%, 95% CI [-1, 11], ES = 0.28), while fascicle length increased in both women (+ 7%, 95% CI [4, 10], ES = 1.02) and men (+ 12%, 95% CI [8, 16], ES = 1.82) and muscle thickness increased in women (+ 13%, 95% CI [8, 18], ES = 1.11) and men (+ 11%, 95% CI [7, 15], ES = 0.89). In both women and men, eccentric (18%, 95% CI [11, 25], ES = 0.96, and 16%, 95% CI [9, 22], ES = 0.82, respectively), isometric (17%, 95% CI [11, 23], ES = 0.53, and 17%, 95% CI [10, 24], ES = 0.62), concentric (12%, 95% CI [7, 16], ES = 0.49, and 9%, 95% CI [5, 13], ES = 0.42) peak torque and 1RM (10%, 95% CI [6, 14], ES = 0.53, and 10%, 95% CI [5, 15], ES = 0.50) similarly increased after the intervention. CONCLUSIONS: This study showed that the adaptations in strength are not sex-dependent, but the increases in pennation angle only in women suggest that the changes in muscle architecture may depend on sex.

Acute effects of direct inhibitory pressure over the biceps brachii myotendinous junction on skeletal muscle activation and force output.

Force (F) reduction is reported with myotendinous junction (MTJ) manipulation. Autogenic inhibition reflex (AIR) activation is supposed to be the main mechanism. Still, its role remains unclear. The study aimed at assessing the effects of MTJ direct inhibitory pressure (DIP) on neuromuscular activation and F in the elbow flexor (agonist) and extensor (antagonist) muscles. After maximum voluntary contraction (MVC) assessment, thirty-five participants randomly performed submaximal contractions at 20, 40, 60, and 80% MVC. Electromyographic (EMG), mechanomyographic (MMG), and F signals were recorded. Protocol was repeated under (i) DIP (10-s pressure on the biceps brachii MTJ) with the elbow at 120° (DIP120), (ii) DIP with the elbow at 180° (DIP180), and (iii) without DIP (Ctrl). Electromechanical delay (EMD) components, EMG and MMG root mean square (RMS), and rate of force development (RFD) were calculated. Independently from the angle, DIP induced decrements in MVC, RFD, and RMS of EMG and MMG signals and lengthened the EMD components in agonist muscles (P<0.05). The DIP-induced decrease in F output of the agonist muscles seems to be possibly due to a concomitant impairment of the neuromuscular activation and a transient decrease in stiffness. After DIP, the antagonist muscle displayed no changes; therefore, the intervention of AIR remains questionable.

Central and peripheral responses to static and dynamic stretch of skeletal muscle: mechano- and metaboreflex implications.

Passive static stretching (SS), circulatory cuff occlusion (CCO), and the combination of both (SS + CCO) have been used to investigate the mechano- and metaboreflex, respectively. However, the effects of dynamic stretching (DS) alone or in combination with CCO (DS + CCO) on the same reflexes have never been explored. The aim of the study was to compare central and peripheral hemodynamic responses to DS, SS, DS + CCO, and SS + CCO. In 10 participants, femoral blood flow (FBF), heart rate (HR), cardiac output (CO), and mean arterial pressure (MAP) were assessed during DS and SS of the quadriceps muscle with and without CCO. Blood lactate concentration [La-] in the lower limb undergoing CCO was also measured. FBF increased significantly in DS and SS by 365 ± 98 and 377 ± 102 ml/min, respectively. Compared with baseline, hyperemia was negligible during DS + CCO and SS + CCO (+11 ± 98 and +5 ± 87 ml/min, respectively). DS generated a significant, sustained increase in HR and CO (∼40s), while SS induced a blunted and delayed cardioacceleration (∼20 s). After CCO, [La-] in the lower limb increased by 135%. Changes in HR and CO during DS + CCO and SS + CCO were similar to DS and SS alone. MAP decreased significantly by ∼5% during DS and SS, did not change in DS + CCO, and increased by 4% in SS + CCO. The present data indicate a reduced mechanoreflex response to SS compared with DS (i.e., different HR and CO changes). SS evoked a hyperemia similar to DS. The similar central hemodynamics recorded during stretching and [La-] accumulation suggest a marginal interaction between mechano- and metaboreflex. NEW & NOTEWORTHY: Different modalities of passive stretching administration (dynamic or static) in combination with circulatory cuff occlusion may reduce or amplify the mechano- and metaboreflex. We showed a reduced mechanoreflex response to static compared with dynamic stretching. The lack of increase in central hemodynamics during the combined mechano- and metaboreflex stimulation implicates marginal interactions between these two pathways.