Blunting of sympathetic vasoconstriction in exercising muscle is well-established. Whether it persists during the early post-exercise period is unknown. This study tested the hypothesis that it persists in human skeletal muscle during the first 10 min of recovery from exercise. Eight healthy young males (21.4 ± 0.8 yrs, SE) performed 7 min of forearm rhythmic isometric handgrip exercise at 15% below forearm critical force (fCF). In separate trials, a cold pressor test (CPT) of 2 min duration was used to evoke forearm sympathetic vasoconstriction in each of Rest (R), Steady State Exercise (Ex), 2–4 min Post-Exercise (PEearly), and 8–10 min Post-Exercise (PElate). A 7 min control exercise trial with no CPT was also performed. Exercising forearm brachial artery blood flow, arterial blood pressure, cardiac output (CO), heart rate (HR), forearm deep venous catecholamine concentration, and arterialized venous catecholamine concentration were obtained immediately prior to and following the CPT in each trial. CPT resulted in a significant increase in forearm venous plasma norepinephrine concentration in all trials (P = 0.007), but no change in arterialized plasma norepinephrine (P = 0.32). CPT did not change forearm venous plasma epinephrine (P = 0.596) or arterialized plasma epinephrine concentration (P = 0.15). As assessed by the %reduction in forearm vascular conductance (FVC) the CPT evoked a robust vasoconstriction at rest that was severely blunted in exercise (R = −39.9 ± 4.6% vs. Ex = 5.5 ± 7.4%, P < 0.001). This blunting of vasoconstriction persisted at PEearly (-12.3 ± 10.1%, P = 0.02) and PElate (-18.1 ± 8.2%, P = 0.03) post-exercise. In conclusion, functional sympatholysis remains evident in human skeletal muscle as much as 10 min after the end of a bout of forearm exercise. Persistence of functional sympatholysis may have important implications for blood pressure regulation in the face of a challenge to blood pressure following exercise.

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Mammalian skeletal muscle cells have the ability to regulate volume in response to increases or decreases in extracellular osmolarity. In the present study we measured the time course of change in single fibre intracellular calcein fluorescence (volume indicastor) and width in response to varied 200 mosmol/L increase in extracellular osmolarity using NaCl or sucrose. Adult mouse EDL single fibres were isolated using collagenase and incubated in DMEM prior to and during experimentation. Fibres were loaded with calcein‐AM for 30 min, and triple‐rinsed with calcein‐free DMEM. After obtaining baseline images NaCl or sucrose solution was added. Fibre images were obtained at 3–6 s intervals for up to 60 min. Fibre images were analyzed for intensity and width at 2–3 sites. Increased osmolarity resulted in a rapid increase in fibre fluorescence and decrease in fibre width. Both variables gradually recovered to baseline values within ~45 min. Bumetanide, an inhibitor of the sodium‐potassium‐2 chloride cotransporter (NKCC) impaired recovery. There was a linear relationship between increases in fibre fluorescent intensity and decreases in fibre width. It is concluded that the NKCC is involved in regulatory volume increase in skeletal muscle, and that changes in fluorescence intensity can be used as an indicator of changes in cell volume.Supported by NSERC of Canada.

PURPOSEWe tested the hypothesis that manipulating perfusion pressure (PP) impacts forearm critical power (fCP).METHODS9 healthy young (23 ± 2.6 yrs) males completed 10 min fCP tests in each of arm above (A) and below (B) heart level (forearm PP A < B by ~30 mmHg). fCP (average of force impulse in last 30 s of test), forearm blood flow (FBF; echo and Doppler ultrasound), arterial pressure (MAP; finger photoplethysmography), O2 consumption (VO2; venous blood samples, Fick eqn) were measured during exercise.RESULTSmean ± SD. Responders (all with compromised fCP in A vs. B; 21 ± 7 vs. 30 ± 6 kg·s, p=0.01) and non‐responders (no compromise to fCP in A vs. B; 29 ± 17 vs. 27 ± 16 kg·s, P=0.14) were identified. Responders exhibited O2D compromise in A vs. B (164 ± 60 vs. 178 ± 65 ml O2/min, p=0.04), and all had lower VO2 in A vs. B but this was not statistically significant (VO2 88 ± 30 ml/min vs. 104 ± 40 ml/min, p=0.12). Non‐responders had no compromise to O2D in A vs. B (153 ± 26 vs. 164 ± 28 ml O2/min, p=0.53), nor any compromise to VO2 (99 ± 21 ml/min vs. 106 ± 28 ml/min, p=0.58). No clear pattern regarding pressor or vasodilatory compensation to protect O2D was found (Responders A vs. B, ΔFVC p=0.01, ΔMAP p=0.12; Non‐responders A vs. B ΔFVC p=0.22, ΔMAP p=0.37).CONCLUSIONSReductions in perfusion pressure can reduce forearm critical power in individuals who cannot defend O2D. These data highlight the importance of O2D to fCP. NSERC