The aim of this study was to examine the effect of skeletal muscle stretching on peripheral, central, and autonomic cardiovascular responses in humans. Twelve healthy males completed a controlled passive stretch of the plantar flexors for 4 min at three different intensities. Doppler ultrasound velocimetry and imaging techniques assessed mean leg blood flow (MLBF), antegrade blood flow, and retrograde blood flow of the popliteal artery. Near-infrared spectroscopy assessed the concentration of deoxygenated hemoglobin + myoglobin ([HHb]) and the sum of its deoxygenated and oxygenated forms [i.e., blood volume ([Hbtot])]. Heart rate (HR) and mean arterial pressure were measured simultaneously to peripheral hemodynamic responses. During stretch there was an increase (P < 0.05) in antegrade and retrograde blood flow along with [HHb] and [Hbtot] relative to baseline, whereas MLBF was not altered. HR increased (P < 0.01) in a stretch intensity- and time-dependent manner, suggesting a threshold tension must be met that results in a mechanoreflex-mediated increase in HR. After stretch there was an increase (P < 0.05) in [Hbtot] and MLBF in each condition, suggesting that stretch creates a poststretch hyperemic response. Furthermore, retrograde blood flow was decreased (P < 0.05) after stretch in each stretch condition. Mean arterial pressure was decreased (P < 0.05) after moderate-intensity stretching. Collectively, our data provide novel mechanistic evidence on cardiovascular responses to skeletal muscle stretching in humans. Moreover, the reductions in MAP and retrograde blood flow suggest that stretch transiently reduces myogenic vascular tone in a poststretch resting period.

The purpose of the investigation was to observe how varying occlusion durations affected neuromuscular activation and microvascular oxygenation during low-volume isometric knee extension exercise. Healthy, recreationally active males performed isometric knee extension at a variety of submaximal intensities under different blood flow restriction (BFR) occlusion durations. The occlusion pressure (130% SBP) was applied either 5 min prior to exercise (PO), immediately prior to exercise (IO) or not during exercise (CON). Surface electromyography (sEMG) and near-infrared spectroscopy (NIRS) was used to record the neuromuscular activation and microvascular oxygenation of the knee extensors during exercise. No difference in sEMG was observed in the vastus lateralis or vastus medialis during any exercise condition or any submaximal intensity. PO elicited greater microvascular deoxygenation (deoxy-[Hb + Mb]) compared to CON (P≤0·05) at all submaximal intensities and also compared to IO at 20% maximal voluntary contraction (MVC). IO resulted in a greater deoxy-[Hb + Mb] response during low-intensity exercise (20% and 40% MVC) compared to CON (P≤0·05). These findings suggest that applying BFR 5 min before exercise can enhance the exercise-induced metabolic stress (i.e. deoxy-[Hb + Mb]), measured via NIRS, during low-intensity exercise (20% MVC) compared to applying BFR immediately prior to exercise. Furthermore, the increased metabolic stress observed during IO is attenuated during high-intensity (60% MVC, 80% MVC) exercise when compared to CON conditions. Knowledge of the changes in exercise-induced metabolic stress between the various occlusion durations may assist in developing efficient BFR exercise programmes.

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An individual typically experiences a wide range of metabolic demands during a normal day. Rarely does a person perform abrupt changes in physical activity nor does the demand last for a long period of time at that same intensity. However, much of the research into the control of oxygen uptake (VO2) kinetics has utilized square wave, constant load exercise to understand the underlying physiological responses to exercise. This study examined the integrated response of pulmonary VO2, microvascular oxygenation measured using near‐infrared spectroscopy (NIRS) and muscle activation using surface electromyography (sEMG) techniques during sinusoidal cycling where the exercise intensity continuously changes. Ten male subjects (age, 30 ± 9 yrs (±SD); height, 179 ± 8 cm; weight, 89.9 ± 18.7 kg) completed a maximal exercise test to determine the lactate threshold (LaT) and peak VO2 (VO2pk). Each subject completed 2 trials consisting of 4 min of cycling at 20 W followed by 4 bouts of sinusoidal cycling transitions. The work rate transitioned between 30 W and a work rate corresponding to 70% of the difference between the LaT and VO2pk (Δ70) as a sinewave function. Pulmonary VO2 was measured breath‐by‐breath using a metabolic cart, interpolated to 1 s and ensemble averaged to yield a single sinewave for analysis. Changes in hemoglobin oxygenation ([HHb]) and total hemoglobin concentrations [(THC)] were measured from VL using NIRS. Data were collected at 1 Hz and ensemble averaged to yield a single sinewave for analysis. Muscle activation (vastus medialis (VM), vastus lateralis (VL)) was assessed using sEMG and reported as the root mean square (RMS). The RMS of the VL and VM were divided into 5 s bins and compared at each crest (CR) and trough (TR) during the 4 sinewaves. The group mean transition in work rate from the TR to the crest CR of each sinewave was 208 ± 27 W. No difference in muscle activation was observed at the CR of each sinewave as shown by the similar RMS for VL and VM. Compared to baseline (1064 ± 136 ml/min), there was a significant (p<0.05) increase in VO2 (2567 ± 322 ml/min) that was 220 ml lower (p<0.05) than the predicted VO2 (assuming 10 ml/min/W) for the work rate (2788 ± 271 ml/min). VO2 did not return to baseline values during the TR (1806 ± 223 ml/min, p<0.05) resulting in an lower gain for VO2 than expected (4.7 ± 1.0 ml/min/W). A significant phase lag was observed for VO2 of 64.9 ± 14.0 deg. Mean [HHb] increased (p<0.05) from baseline (12.4 ± 2.9 μM) to the CR of the sinewave (17.7 ± 7.8 μM). Similar to VO2, there was a significant phase lag observed for [HHb] of 56.9 ± 16.0 deg. The difference in phase lag responses between VO2 and [HHb] was not different. These findings are consistent with previous studies reporting a lower gain and a significant phase lag for VO2 during sinewave exercise. Compared to studies utilizing square wave exercise which have shown [HHb] to adapt much faster than VO2, the similar phase lag for VO2 and [HHb] observed in the present study suggests that VO2 and [HHb] respond similarly to the increase in exercise intensity during sinewave exercise. Further investigations into the integration of VO2 and [HHb] during exercise that is continuously changing intensities are warranted.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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