This study was undertaken to explore the nature of impaired postural stability following physical exercise. Nine healthy subjects (aged 24 +/- 3 years) were subjected to 30 min of treadmill walking or running on two separate occasions. Walking and running speeds (1.9 to 2.2 m/s) were chosen to induce equal energy expenditure. During treadmill exercise, kinematic analysis of head movement was performed. Prior to and immediately following exercise, postural sway was evaluated as mean velocity of centre of pressure (VCOP), measured on a force plate during 30 s quiet stance with eyes open or eyes closed. The results indicate that exercise increased two-dimensional postural sway by 9 - 19 % in eyes open, but not in the eyes closed condition. The deteriorating effect of exercise was both evident in the sagittal and in the frontal plane, although the effect on the former was slightly more transient. Post-exercise sway values were significantly higher after running than after walking. Kinematic analysis of head movement confirmed larger vertical displacement and acceleration pattern in running compared to walking. It is concluded that exercise of moderate intensity deteriorates visual contribution to postural stability. The effect is evident as an initial destabilisation in the sagittal direction and a less transient loss of latero-lateral stability. Running tends to disturb postural stability more than walking, possibly due to more excessive head movement and disturbance of vestibular and visual information centres.

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

The aim of this study was to investigate the effects of exercise-induced and thermal dehydration on postural balance. Eight male subjects cycled for 2 h at a power output equal to 57-63% VO2max on two different occasions: once without drinking (NF) and once with intake of 1.9 l of a carbohydrate-electrolyte solution (FR). Before and after the exercise test, the velocity of the centre of pressure (COP) excursion was measured on a force platform during 30-s bipedal standing in normal position, feet side by side, and tandem position, feet heel to toe. On another occasion, eight subjects underwent seven consecutive sauna sessions (85 degrees C, 50% rh) of 15 min duration with no fluid replacement (S) to induce thermal dehydration. Mean fluid loss was 2.7 (+/- 0.4)%, 0.5 (+/- 0.5)% and 3.0 (+/- 0.6)% of body mass after NF, FR and S, respectively. Mean velocity of COP excursion after the exercise test was significantly higher in the NF than in the FR trial (p < 0.05). Postural stability was not influenced by S. In conclusion, prolonged exercise without fluid ingestion seems to negatively affect postural stability, whereas no effect is observed after exercise with fluid replacement or after thermal dehydration.

To study the change in soil organic carbon (SOC) since it was recorded during the Belgian National Soil Survey some 40 years ago, we recently revisited 939 locations still under use as arable land. The study area comprised almost the entire province of West Flanders (about 3000 km2) characterized by profound changes in its arable land management.'raking the increased ploughing depth (by 9.8 cm on average) into account, a significant (P = 0.001) increase of the SOC content by 0.2% on average was found. Expressed as an amount, the SOC in the topsoil rose by 9.3 t/ha on average, representing an increase of 25'Yo. This is comparable with the conversion of arable land into grassland for 2 to 3 decades.Geostatistical tools were used to map the SOC at the two times of observation. These showed that most of the spatial variation occurred within about 4 km. Since the community level is the smallest spatial resolution on which agricultural statistics are gathered officially, a detailed modelling of the change in SOC was impossible. llowever, by selecting communities with extreme changes in SOC, we found indications that the major source of increase in SOC was due to the large increase in pig breeding.

This study investigated the effects of pre-exercise branched-chain amino acid (BCAA) administration on blood ammonia levels and on time to exhaustion during treadmill exercise in rats. Adult female Wistar rats were trained on a motor driven treadmill. After a 24-h fast, rats were injected intraperitoneally (i.p.) with 1 mL of placebo or BCAA (30 mg), 5 min before performing 30 min of submaximal exercise (N = 18) or running to exhaustion (N = 12). In both cases, rats were sacrificed immediately following exercise, and blood was collected for the measurement of glucose, nonesterified fatty acid (NEFA), lactic acid, BCAA, ammonia, and free-tryptophan (free-TRP) levels. Control values were obtained from sedentary rats that were subjected to identical treatments and procedures (N = 30). Plasma BCAA levels increased threefold within 5 min after BCAA administration. Mean run time to exhaustion was significantly longer (P < 0.01) after BCAA administration (99 +/- 9 min) compared with placebo (76 +/- 4 min). During exercise, blood ammonia levels were significantly higher (P < 0.01) in the BCAA treated compared with those in the placebo treated rats both in the 30-min exercise bout (113 +/- 25 mumol.L-1 (BCAA) vs 89 +/- 16 mumol.L-1) and following exercise to exhaustion (186 +/- 44 mumol.L-1 (BCAA) vs 123 +/- 19 mumol.L-1). These data demonstrate that BCAA administration in rats results in enhanced endurance performance and an increase in blood ammonia during exercise.