It is unclear whether blood flow restriction (BFR) accelerates the adaptation of the time constant (τ) of phase II oxygen uptake ($$ {\dot{\text{V}}}{\text{O}}_{2} $$ V ˙ O 2 ) kinetics in the moderate-intensity exercise domain via moderate-intensity aerobic training. Therefore, healthy participants underwent moderate-intensity [45–60% $$ {\dot{\text{V}}}{\text{O}}_{2} $$ V ˙ O 2 Reserve] aerobic cycle training with or without BFR (BFR group, n = 9; CON group, n = 9) for 8 weeks to evaluate $$ {\dot{\text{V}}}{\text{O}}_{2} $$ V ˙ O 2 kinetics during moderate-intensity cycle exercise before (Pre) and after 4 (Mid) and 8 (Post) weeks of training. Both groups trained for 30 min, 3 days weekly. BFR was performed for 5 min every 10 min by applying cuffs to the upper thighs. The τ significantly decreased by Mid in the BFR group (23.7 ± 2.9 s [Pre], 15.3 ± 1.8 s [Mid], 15.5 ± 1.4 s [Post], P < 0.01) and by Post in the CON group (27.5 ± 2.0 s [Pre], 22.1 ± 0.7 s [Mid], 18.5 ± 1.9 s [Post], P < 0.01). Notably, the BFR group’s τ was significantly lower than that of the CON group at Mid (P < 0.01) but not at Post. In conclusion, BFR accelerates the adaptation of the $$ {\dot{\text{V}}}{\text{O}}_{2} $$ V ˙ O 2 kinetics of phase II by moderate-intensity aerobic training.

It is unclear whether blood flow restriction (BFR) accelerates the adaptation of the time constant (τ) of phase II oxygen uptake (VO2) kinetics in the moderate-intensity exercise domain via moderate-intensity aerobic training. Therefore, healthy participants underwent moderate-intensity [45–60% VO2 Reserve] aerobic cycle training with or without BFR (BFR group, n = 9; CON group, n = 9) for 8 weeks to evaluate VO2 kinetics during moderate-intensity cycle exercise before (Pre) and after 4 (Mid) and 8 (Post) weeks of training. Both groups trained for 30 min, 3 days weekly. BFR was performed for 5 min every 10 min by applying cuffs to the upper thighs. The τ significantly decreased by Mid in the BFR group (23.7 ± 2.9 s [Pre], 15.3 ± 1.8 s [Mid], 15.5 ± 1.4 s [Post], P < 0.01) and by Post in the CON group (27.5 ± 2.0 s [Pre], 22.1 ± 0.7 s [Mid], 18.5 ± 1.9 s [Post], P < 0.01). Notably, the BFR group’s τ was significantly lower than that of the CON group at Mid (P < 0.01) but not at Post. In conclusion, BFR accelerates the adaptation of VO2 kinetics at the onset of exercise by moderate-intensity aerobic training.

Chronic stress is known to cause adverse physical and mental effects such as pain, chronic fatigue, and depression, and it is strongly related to many diseases and syndromes (e.g., fibromyalgia, chronic fatigue syndrome, and post‐traumatic stress disorder). Evidence suggests that exercise and physical activity in leisure time are effective in improving stress‐induced symptoms. Repeated cold stress (RCS), in which an animal is repeatedly exposed to alternating room and low temperatures, is one of the chronic stress models that induces chronic pain and depression. Mechanical hyperalgesia through thin muscle afferent fibers has also been reported to occur from RCS exposure. Since the muscle afferents have a dual modulatory function in nociception and cardiovascular reflex, we hypothesized that RCS augments the mechanical component of the exercise pressor reflex (the skeletal muscle mechanoreflex), i.e., skeletal muscle afferents‐mediated increases sympathetic nerve activity (SNA) and arterial blood pressure (AP). [Purpose] The purpose of this study was to clarify the impacts of RCS on sympathetic and cardiovascular responses to stimulation of the skeletal muscle mechanoreflex in decerebrated rats. [Methods] Male Sprague‐Dawley rats (body weight: 410 ± 15 g, age: 12 weeks) were exposed to RCS using a homemade automated RCS device. The rats were alternately moved to room temperature (22°C) and cold temperature (4°C) compartments at 30‐min intervals for 5 days. To assess the skeletal muscle mechanoreflex function, we measured mean AP (MAP), heart rate (HR), and renal SNA (RSNA) responses to 30‐s static passive stretching of the hindlimb muscles by in vivo recording from unanesthetized decerebrated rats. Stretching was performed by tracing the maximum tension curve obtained from 30‐s electrical stimulation. Changes (Δ) from baseline to peak values of the measured parameters between control and RCS rats were compared. [Results] Peak tension during the Achilles tendon stretch from baseline was not significantly different between groups (control: Δ929 ± 63 g [n = 6] vs RCS: Δ765 ± 66 g [n = 4], p = 0.17). Importantly, the peak RSNA response in RCS rats (Δ236.3% and Δ242.7%, n = 2) tended to be greater than that in control rats (Δ37.1% and Δ23.9%, n = 2). Moreover, RCS had a significantly (p < 0.05) greater HR response (RCS: Δ3.7 ± 1.0 bpm [n = 4] vs control: Δ0.6 ± 0.5 bpm [n = 6]), and MAP response tended (P = 0.07) to be higher in the RCS group (Δ23 ± 6 mmHg, n = 4) than in the control group (Δ8 ± 4 mmHg, n = 6). [Conclusions] Our preliminary data demonstrate that RCS augments the skeletal muscle mechanoreflex. These results suggest that chronic stress can potentially cause exaggerated cardiovascular responses during physical activity.