External load can alter the energy cost of prolonged exercise

Summary The present study was undertaken to examine the energy cost of prolonged walking while carrying a backpack load. Six trained subjects were tested while walking for 120 min on a treadmill at a speed of 1.25 m · s^–1 and 5% elevation with a well fitted backpack load of 25 and 40 kg alternately. Carrying 40 kg elicited a significantly higher (p<0.01) enery cost than 25 kg. Furthermore, whereas carrying 25 kg resulted in a constant energy cost, 40 kg yielded a highly significant (p<0.05) increase in energy cost over time. The study implies that increase in load causes physical fatigue, once work intensity is higher than 50% maximal work capacity. This is probably due to altered locomotion biomechanics which in turn lead to the increase in energy cost. Finally, the prediction model which estimates energy cost while carrying loads should be used with some caution when applied to heavy loads and long duration of exercise, since it might underestimate the acutal enery cost.     

AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)‐activated protein kinase (AMPK)‐activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol‐3‐phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5‐aminoimidazole 4‐carboxamide‐riboside (AICAR), further indicating that the exercise‐induced alterations in these enzymes were AMPK‐mediated. Conclusions: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post‐exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

Significance of skin temperature changes in surface electromyography

Summary Differing results have been reported concerning the direction and quantity of the electromyogram (EMG) amplitude response to changes in tissue temperature. The EMG signals from the soleus muscle of six healthy human subjects were therefore recorded during dynamic exercise (concentric contractions) at ambient temperatures of 30°C and 14°C. The mean skin temperature above the muscle investigated was 32.9° C and 21.7° C, respectively. The core temperature, estimated by rectal temperature, was unchanged. The cooling of the superficial tissues caused approximately a doubling of the EMG amplitude. For the probability level 0.9 in the amplitude probability distribution function, the average signal level increased from 73 V to 135 V (P=0.02). The average mean power frequency of the EMG signal was reduced from 142 Hz to 83 Hz (P=0.004). The amplitude increase was not due to shivering but other possible explanations are presented. As the changes in T _sk investigated were within the range which may occur normally during the working hours, it was concluded that T _sk should be carefully controlled in vocational EMG studies.     

Increase in the ratio of serum levels of apolipoproteins A-I and A-II during prolonged physical strain and calorie deficiency

Summary Effects of four days of intense physical activity on serum concentrations of total triglycerides, total cholesterol and apolipoproteins A-I, A-II, and B were studied in 35 well-trained young men. Serum total triglyceride levels decreased to 70% of baseline levels after 24 h, and fell further to 50% of baseline levels after 4 days. Serum levels of total cholesterol fell steadily to about 80% of baseline levels on the 4th day. Apo-B levels fell to 85% of baseline levels after 24 h, and remained at that level. Apo A-I fell to about 90%, and apo A-II to about 80% of baseline levels, causing a significant increase in the ratio of apo A-I to apo A-II. The intraindividual changes in apo B were positively correlated to changes in cholesterol during the first day (r=0.60). The changes in apo A-I and apo A-II had no significant correlation with changes in total cholesterol or triglycerides, or with one another, suggesting that apo A-I and apo A-II are metabolized independently during conditions of hard physical exercise.     

The effect on immunity of long-term intensive training in elite swimmers

The impact of long-term training on systemic and mucosal immunity was assessed prospectively in a cohort of elite swimmers over a 7-month training season in preparation for national championships. The results indicated significant suppression (P < 0.05) of serum IgA. IgG and IgM and salivary IgA concentration in athletes associated with long-term training at an intensive level. There was also a trend towards lower IgG2 subclass levels in serum in athletes compared with controls (P= 0.07). There were no significant changes in numbers or percentages of B or T cell subsets, but there was a significant fall in natural killer (NK) cell numbers and percentages in athletes over the training season (P < 0.05). After individual training sessions there was a significant decrease in salivary IgA levels for athletes compared with controls (P= 0.02). In athletes there was a downward trend in salivary IgA levels over the 7-month training period in both the pre-exercise (P= 0.06) and post-exercise samples (P= 0.04). There were no significant trends in salivary IgG levels over the study period in either athletes or controls. The only significant change in salivary IgM levels was an increase in detection rate in the pre-competition phase in athletes (P= 0.03). The study suggests that training of elite athletes at an intensive level over both short- and long-time frames suppresses both systemic and mucosal immunity. Protracted immune suppression linked with prolonged training may determine susceptibility to infection, particularly at times of major competitions.     

Antimicrobial resistance of Escherichia coli and therapeutic implications

Widespread antibiotic resistance has been recognized in Escherichia coli isolates from human, animal and environmental sources. Although prevalence rates for resistant E. coli strains are significantly distinct for various populations and environments, the impact of resistance to antimicrobial drugs is ubiquitous. This article provides information about the epidemiology, mechanisms and molecular principles of resistance, shows consequences for the antiinfective treatment of selected infections and describes measures to control the spread of antibiotic-resistant E. coli.     

Beta-adrenergic blockade and training in healthy men—effects on central circulation

The effect of chronic β-adrenergic blockade on central circulatory adaptations to physical training was investigated. 16 healthy sedentary males (20–31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks at a work load that during the last 5 weeks corresponded to 75% of the pretraining VO₂ max. In a single blind way, 8 subjects were during the training period treated with the β-adrenergic receptor blocker propranolol (160 mg/day), while the remaining 8 received placebo tablets. Pretraining tests were performed before the start of medication and posttraining tests were performed 6 days after the last day of training and medication. The training program resulted in a similar increase (8%) in VO₂ max in both groups (p<0.01). The resting heart rate (-4 beats/min; p<0.05) as well as the exercise heart rate at a moderate work load (120 W: -11 beats/min; p<0.01) decreased with training, and no significant difference was seen between the 2 groups. At a high work load (180 W), however, the heart rate decreased significantly more with training in the placebo group as compared with the β-blockade group (-19 vs.-7 beats/min; p<0.05). The oxygen pulse (VO₂/HR) increased in both groups at 120 W (+6%; p<0.01). At 180 W the oxygen pulse increased only in the placebo group (+8%; p<0.05). The estimated stroke volume at 120 and 180 W, as determined by impedance cardiography, did not change significantly with training although there was a tendency towards an increase in the placebo group only. The resting left ventricular wall thickness and diameter, as determined by echocardiography, did not change significantly with training in either group.—In conclusion, the present study indicates that a moderate degree of β-adrenergic blockade does not prevent or impair the training-induced increase in the maximal oxygen uptake. During submaximal work, however, the circulatory adaptation may be less apparent if training has been performed during partial blockade of the sympathoadrenal system.     

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective β₁ adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 ± 13 vs. 260 ± 16%), heart rate (114 ± 3 vs. 135 ± 7 beats min^?1) and mean arterial pressure (103 ± 3 vs.112 ± 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 ± 3 to 66 ± 3 vs. 60 ± 2 to 72 ± 3 cm s^?1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest; ?4.8 ± 1.8 vs. 1.2 ± 1.7 μmol L^?1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.     

Muscle strength, volume and activation following 12-month resistance training in 70-year-old males

In elderly males muscle plantar flexor maximal voluntary contraction (MVC) torque normalised to muscle volume (MVC/VOL) is reduced compared to young males as a result of incomplete muscle activation in the elderly. The aim of the present study was to determine the influence of a 12-month resistance training programme on muscle volume, strength, MVC/VOL, agonist activation and antagonist coactivation of the plantarfexors in elderly males. Thirteen elderly males aged 70 years and over (range 70–82 years), completed a 12-month whole body resistance-training programme (TRN), training three times a week. Another eight males (range 18–30 years), who maintained their habitual physical activity for the same 12-month period as the TRN group acted as controls (CTRL). Isometric plantarflexor maximal voluntary contraction (MVC) torque increased in the TRN group by 20% (P<0.01), from 113.1±22.0 Nm to 141.5±19.2 Nm. Triceps surae volume (TS VOL) assessed using MRI, increased by 12%, from 796.3±78.9 cm³ to 916.8±144.4 cm³ . PF activation, measured using supramaximal double twitch interpolation, increased from 83.6±11.0% pre training, to 92.1±7.6% post training (P<0.05). Dorsiflexion MVC and antagonist coactivation (assessed using surface electromyography) did not change with training. Plantarflexor MVC torque normalized for triceps surae muscle volume (MVC/VOL) was 142.6±32.4 kN m^–2 before training and 157.0± 27.9 kN m^–2 after training (a non-significant increase of 8%). No significant change in any measurement was observed in the CTRL group. This study has shown that the gain in muscle strength in response to long-term (12-month) training in older men is mostly accounted for by an increased muscle volume and activation.     

Human temperature regulation during cycling with moderate leg ischaemia

The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2)°C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3)°C) and Absolute (2.4 (0.7)°C) trials, but was substantially lower (P<0.01) in the Relative trial (1.4 (0.8)°C). Ischaemia potentiated (P<0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m^–2 min^–1) compared to the Control trial (13.4 (6.2) g m^–2 min^–1), concomitant with an attenuated (P<0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex.