SUMMARY1. In dogs anaesthetized with sodium pentobarbitone and artificially ventilated, the gracilis muscles were vascularly isolated and perfused at a constant flow rate of 51-2+9-8 ml min-1 100 g-1 muscle tissue (183+ 17-8% of resting blood flow; mean+S.E.; n = 13).2. Electrical stimulation of the cut peripheral end of the obturator nerve (6 V, 4 Hz) resulted in muscle contraction (658+118 g 100 g-1 force after 5 min), and an immediate decrease in arterial perfusion pressure from 179+15-7 mmHg to 87+10-0 mmHg (514+4-5 % decrease in vascular resistance after 2 min of contraction). Venous oxygen tension decreased from 692 + 51 mmHg to 18-5 + 1-4 mmHg (n = 6). These values did not significantly alter during the remaining period of stimulation (10-20 min).3. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (137 + 23 nM; n = 10). However, the adenosine concentrations in venous plasma showed a significant (P < 0-01) increase from a control value of 164 + 55 nM to 455+77 nM (n = 9) after 5 min of muscle contraction and remained high during the rest of the 20 min contraction. In six of the dogs adenosine concentrations were determined after 1 and 3 min of contraction and showed a smaller but statistically significant (P < 0 05) rise in venous concentration.4. During infusion of adenosine into the artery to give plasma concentrations between 0-3 /LM and 1 mm, 72-6 + 2-1 % (n = 29) of the infused adenosine was taken up by the tissues before it reached the vein. Comparison of vasodilatation and venous adenosine concentrations during adenosine infusion and muscle contractions showed that the released adenosine could contribute about 15 % to the total vasodilatation after 1 min and about 40 % between 5 and 20 min of contractions. Released adenosine could contribute about 80% to the vasodilatation that remained 5 min after the withdrawal of stimulation. Arterial perfusion pressure took 22 min to return to control, whereas adenosine release had fallen to zero within 10 min.5. These data suggest that the released adenosine could contribute to exercise hyperaemia, but is unlikely to be the main factor, particularly in the initial stage.

This supported but unsupervised exercise programme generated improvements in walking distance and leg blood flow without detectable increases in cardiorespiratory work. Exercise compliance is related to MWD and VascuQoL score in a dose-response manner.

Fire fighter breathing apparatus instructors (BAIs) must possess the ability to respond to both the extrinsic stress of a high temperature environment and the intrinsic stress from wearing personal protective equipment (PPE) and self-contained breathing apparatus (SCBA), repeatedly and regularly, whilst training recruits in live fire training exercises (LFTEs). There are few previous investigations on BAIs in hot environments such as LFTEs, since the main research focus has been on regular fire fighters undertaking exercises in temperate or fire conditions at a moderate to high exercise intensity. In this study, the intrinsic cardiovascular stress effects of wearing PPE + SCBA were first investigated using a step test whilst wearing gym kit (control), weighted gym kit (a rucksack weighted to the equivalent of PPE + SCBA) and full PPE + SCBA (weight plus the effects of protective clothing). The extrinsic effects of the very hot environment were investigated in BIAs in LFTEs compared to mock fire training exercises (MFTEs), where the fire was not ignited. There was an increase in heart rate due to the modest workload imposed on the BAIs through carrying out the MFTEs (25.0 (18.7)%) compared to resting. However, when exposed to fire during the LFTEs, heat storage appears to be significant as the heart rate increased by up to 39.8 (+/-20.1)% over that of the mock LFTEs at temperate conditions. Thus, being able to dissipate heat from the PPE is particularly important in reducing the cardiovascular responses for BAIs during LFTEs.

SUMMARY1. A study has been made to see whether active and passive movements of sodium and potassium in human red blood cells are influenced by changing the chloride gradient and hence the potential difference across the cell membrane.2. Chloride distribution was measured between red cells and isotonic solutions with a range of concentrations of chloride and non-penetrating anions (EDTA, citrate, gluconate). The cell chloride concentration was greater than that outside with low external chloride, suggesting that the sign of the membrane potential was reversed. The chloride ratio (internal/ external) was approximately equal to the inverse of the hydrogen ion ratio at normal and low external chloride, and inversely proportional to external pH. These results show that chloride is passively distributed, making it valid to calculate the membrane potential from the chloride ratio.3. Ouabain-sensitive (pump) potassium influx and sodium efflux were decreased by not more than 20 and 40 % respectively on reversing the chloride gradient, corresponding to a change in membrane potential from -9 to +30 mV. In contrast, passive (ouabain-insensitive) movements were reversibly altered -potassium influx was decreased about 60 % and potassium efflux was increased some tenfold. Sodium influx was unaffected by the nature of the anion and depended only on the external sodium concentration, whereas ouabain-insensitive sodium efflux was increased about threefold. When external sodium was replaced by potassium there was a decrease in ouabain-insensitive sodium efflux with normal chloride, but an increase in low-chloride medium.4. Net movements of sodium and potassium were roughly in accord with the unidirectional fluxes.5. The results suggest that reversing the chloride

No abstract