The physical demands of riding in National Hunt races

Heart rate (f _c) and post-competition blood lactate concentration ([La⁺]) were studied in seven male professional National Hunt jockeys over 30 races. Thef _c response for individual races followed a similar pattern for all subjects. The mean peakf _c recorded during competition was 184 beats·min^–1 (range 162–198 beats·min^–1) with averagef _c during the races ranging from 136 to 188 beats·min^–1. During consecutive races the recoveryf _c did not return to resting values. The mean [La⁺] was 7.1 mmol·l^–1 (range 3.5–15.0 mmol·l^–1). The conclusions of this study suggest that riding in National Hunt races is a physically demanding occupation. The muscular activity in this profession requires a high metabolic drive and produces a significant cardiorespiratory response.     

Cardiovascular response to static handgrip in trained and untrained men

Summary The influence of aerobic capacity on the cardiovascular response to handgrip exercise, in relation to the muscle mass involved in the effort, was tested in 8 trained men (T) and 17 untrained men (U). The subjects performed handgrip exercises with the right-hand (RH), left-hand (LH) and both hands simultaneously (RLH) at an intensity of 25% of maximal voluntary contraction force. Maximal aerobic capacity was 4.3 l·min^–1 in T and 3.21·min^–1 in U (P<0.01). The endurance time for handgrip was longer in T than in U by 29% (P<0.05) for RH, 38% (P<0.001) for LH and 24% (P<0.001) for RLH. Heart rate (f _c) was significantly lower in T than in U before handgrip exercise, and showed smaller increases (P<0.01) at the point of exhaustion: 89 vs 106 beats·min^–1 for RH, 93 vs 100 beats·min^–1 for LH and 92 vs 108 beats·min^–1 for RLH. Stroke volume (SV) at rest was greater in T than in U and decreased significantly (P<0.05) during handgrip exercise in both groups of subjects. At the point of exhaustion SV was still greater in T than in U: 75 vs 57 ml for RH, 76 vs 54 ml for LH and 76 vs 56 ml for RLH. During the last seconds of handgrip exercise, the left ventricular ejection time was longer in T than in U. Increases in cardiac output (Q _c) and systolic blood pressure did not differ substantially between T and U, nor between the handgrip exercise tests. It was concluded that handgrip exercise caused similar increases inQ _c in both T and U but in T the increased level ofQ _c was an effect of greater SV and lowerf _c than in U. Doubling the muscle mass did not alter the cardiovascular response to handgrip exercise in either T or U.     

Thermal tolerance following artificially induced polycythaemia

Polycythaemia has been shown to improve physical performance, possibly due to increased arterial oxygen transport. Enhanced thermoregulatory function may also accompany this manipulation, since a greater proportion of the cardiac output becomes available for heat dissipation. We further examined this possibility in five trained men, who participated in three-phase heat stress trials (20 min rest, 20 min cycling at 30% peak power W_peak and 20 min at 45% W_peak at 38.3 (SEM 0.7)°C [relative humidity 41.4 (SEM 2.9)%]. Trials were performed during normocythaemia (control) and polycythaemia, obtained by reinfusion of autologous red blood cells and resulting in significant elevation of arterial oxygen transport. During the polycythaemic trials, the subjects demonstrated diminished thermal strain, as evidenced by a significant reduction in cardiac frequency (f _c: 12 beats · min^–1 lower throughout the test;P < 0.05), and reduced auditory canal temperatures (T _ae) during the latter 20-min phase (P < 0.05). Forearm sweat onset was more rapid (363.0 compared to 1083.0 s;P < 0.05), and forearm sweat rate (. _msw) sensitivity was elevated from 1.80 to 2.91 · mg · cm^–2 · min^–1 · °C^–1 (P < 0.05). Foreheadm _sw was depressed during the final 20 min, while forearmm _sw was greater during all test phases, averaging 0.94 and 1.20 mg · cm^–2 · min^–1, respectively, over the 60 min. Skin blood flows for the upper back, upper arm and forearm were reduced (P < 0.05). Polycythaemia enhanced thermoregulation, through an elevation in forearm sweat sensitivity and.m _sw, but not via increased cutaneous blood flow. These modifications occurred simultaneously with decreases inf _c andT _ae, resulting in greater thermal tolerance.     

Maximal heart rates and plasma lactate concentrations observed in middle-aged men and women during a maximal cycle ergometer test

Summary The purpose of this study was to investigate criteria for maximal effort in middle-aged men and women undertaking a maximal exercise test until they were exhausted if no measurements of oxygen uptake are made. A large group of 2164 men and 975 women, all active in sports and aged between 40 and 65 years, volunteered for a medical examination including a progressive exercise test to exhaustion on a cycle ergometer. In the 3rd min of recovery a venous blood sample was taken to determine the plasma lactate concentration ([la^–]_{p, 3min}). Lactate concentration and maximal heart rate (f _{c, max}) were lower in the women than in the men (P<0.001). Multiple regression analyses were performed to assess the contribution of sex to [la^–]_{p, 3 min}, independent of age and f _c max, It was found that [la^–]_{p,3 min} was about 2.5 mmol·l^–1 lower in women than in men of the same age and f _{c, max}. In our population 88% of the men and 85% of the women met a combination of the following f _{c, max} and [la^–]_{p, 3min} criteria: f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 8 mmol·l^–1 in the men and f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 5.5 mmol·1^–1 in the women.     

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity

The calf and forearm blood flows (Q _calf and Q _forearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P₁₀) prior to this combined exercise. The Q _calf and Q _forearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P₁₀ exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times · min^–1 with a load equal to 10% MVC (P₁₀), Q _calf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H₅₀) and P₁₀ were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Q _calf had decreased significantly from 20.6 (SEM 3.0) ml · 100 ml^–1 · min^–1 (10th min during P₁₀ exercise) to 15.3 (SEM) ml · 100 ml^–1 · min^–1 (P = 0.001), whereas Q _forearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml · 100 ml^–1 · min^–1 (10th min of P₁₀ exercise) to 26.2 (SEM 3.2) ml · 100 ml^–1 · min^–1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P₁₀ exercise and increased markedly when H₅₀ was added. The calf vascular conductance during combined exercise decreased significantly (0.001 < P < 0.01) compared with that at the 10th min of P₁₀ alone. Although the MSNA (expressed as burst rate) remained unchanged during P₁₀ exercise for 10 min, it increased markedly when exhausting H₅₀ and P₁₀ exercise were performed simultaneously. These findings indicated that superimposition of exhausting handgrip exercise at 50% MVC caused a vasoconstriction in the exercising calf due to increased MSNA, which counteracted the vasodilatation in this active muscle.     

Effect of pyridostigmine on the exercise-heat response of man

Summary The effect of pyridostigmine on thermoregulatory responses was evaluated during exercise and heat stress. Eight heat acclimated, young adult male subjects received four doses of pyridostigmine (30 mg) or identical placebo tablets every 8 h, in a double blind, randomized, cross-over trial. A 30.3%, SD 4.6% inhibition of the circulating cholinesterase (ChE) activity was induced in the pyridostigmine-treated group. The subjects were exposed to 170-min exercise and heat-stress (dry bulb temperature, 33° C; relative humidity 60%) consisting of 60 min in a sitting position and two bouts of 50-min walking (1.39 m · s^–1, 5% gradient) which were separated by 10-min rest periods. No differences were found between treatments in the physiological responses and heat balance parameters at the end of exposure: heart rate (f _c) was 141 beats · min^–1, SD 16 and 150 beats · min^–1, SD 12, rectal temperature (T _re) was 38.5°C, SD 0.4° and 38.6°C, SD 0.3°, heat storage was 60 W · m^–2, SD 16 and 59 W · m^–2, SD 15 and sweat rate was 678 g · h^–1, SD 184 and 661 g · h^–1, SD 133, in the pyridostigmine and placebo treatments, respectively. The changes in T _re and f _c over the heat-exercise period were parallel in both study and control groups. Pyridostigmine caused a slight slowing of f _c (5 beats·min^–1) which was consistent throughout the entire exposure (P<0.001) but was of no clinical significance. The overall change in f_c was similar for both groups. We have concluded that pyridostigmine administration, in a dose sufficient to induce a moderate degree of ChE inhibition, does not significantly affect performance of exercise in the heat.     

Lung diffusion capacity,oxygen uptake,cardiac output and oxygen transport during exercise before and after an Himalayan expedition

Studies were made of pulmonary diffusion capacity and oxygen transport before and after an expedition to altitudes at and above 4900 m. Maximum power (P _max) and maximal oxygen uptake (VO _2max) were measured in 11 mountaineers in an incremental cycle ergometer test (25W · min^–1) before and after return from basecamp (30 days at 4900 m or higher). In a second test, cardiac output (Q _c) and lung diffusion capacity of carbon monoxide (D _L,CO) were measured by acetylene and CO rebreathing at rest and during exercise at low, medium and submaximal intensities. After acclimatization, VO_2max and P _max decreased by 5.1% [from 61.0 (SD 6.2) to 57.9 (SD 10.2) ml·kg^–1, n.s.] and 9.9% [from 5.13 (SD 0.66) to 4.62 (SD 0.42) W·kg^–1, n.s.], respectively. The maximal cardiac index and DL,co decreased significantly by 15.6% [14.1 (SD 1.41) 1·min^–1 · m^–2 to 11.9 (SD 1.44)1·min^–1 m^–2, P<0.05] and 14.3% [85.9 (SD 4.36)ml·mmHg^–1 min^–t to 73.6 (SD 15.2) ml · mmHg^–1 -min^–1, P<0.05], respectively. The expedition to high altitude led to a decrease in maximal Q _c, oxygen uptake and D_L,CO. A decrease in muscle mass and capillarity may have been responsible for the decrease in maximal Q_c which may have resulted in a decrease of D _L,CO and an increase in alveolar-arterial oxygen difference. The decrease in D _L,CO especially at lower exercise intensities after the expedition may have been due to a ventilation-perfusion mismatch and changes in blood capacitance. At higher exercise intensities diffusion limitation due to reduced pulmonary capillary contact time may also have occurred.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

Summary To find out whether endurance training influences the kinetics of the increases in heart rate (f _c) during exercise driven by the sympathetic nervous system, the changes in the rate off _c adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%–70% of maximal oxygen uptake ( O_2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuousf _c recording. At the completion of the training programme, the subjects' O_2max had increased significantly(39.2 ml·min^–1·kg^–1, SD 4.7 vs 46 ml·min^–1·kg^–1, SD 5.6) and the steady-statef _c at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-statef _c was found at 150 W (146 beats·min^–1, SD 10 vs 169 beats·min^–1, SD 9) but the difference between the steady-statef _c at 150 W and that at 100 W (f _c) did not decrease significantly (26 beats·min^–1, SD 7 vs 32 beats·min^–1, SD 6). The time constant () of thef _c increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P<0.01) and the acceleration index (A=0.63·f _c·^–1) decreased from 0.20 beats·min^–1·s^–1, SD 0.05 to 0.14 beats·min^–1·s^–1, SD 0.04 (P<0.02). The major part of the changes in and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Reduced exercise hyperaemia in calf muscles working at high contraction frequencies

Summary The effects of muscle contraction frequency on blood flow to the calf muscle (Q _calf) were studied in six female subjects, who performed dynamic plantar flexions at frequencies of 20, 40, 60, 80 and 100 contractions · min^–1, in a supine position. TheQ _calf measured by a mercury-in-rubber strain gauge plethysmograph, increased as contraction frequency increased and reached a peak at 60–80 contractions · min^–1. After 100 plantar flexions at 60 contractions · min^–1, the meanQ _calf was 30.95 (SEM 4.52) ml · 100 ml^–1 · min^–1. At 100 contractions · min^–1, however, it decreased significantly compared with that at 60 contractions · min^–1 at a specified time (2 min or exhaustion) or after a fixed amount of work (100 contractions). The contraction frequency at whichQ _calf reached a peak depended on the duration of exercise. The heart rate showed its highest mean value at 60 contractions · min^–1 and decreased significantly at 100 contractions · min^–1. The mean blood pressure was lower at 100 contractions · min^–1 than at 60 contractions · min^–1. The relaxation period between contractions, measured by recording the electromyogram from the gastrocnemius muscles, shortened markedly as the frequency increased; the mean value at 100 contractions · min^–1 was 0.14 (SEM 0.02) s, which corresponded to 35.7% of the contraction time. This shortened relaxation period between contractions should have led to the inhibition of exercise hyperaemia at the higher contraction frequencies.     

Cardiac output during exercise in paraplegic subjects

Summary The purpose of this study was to measure the cardiac output using the CO₂ rebreathing method during submaximal and maximal arm cranking exercise in six male paraplegic subjects with a high level of spinal cord injury (HP). They were compared with eight able bodied subjects (AB) who were not trained in arm exercise. Maximal O₂ consumption ( O_2max) was lower in HP (1.1 1·min^–1, SD 0.1; 17.5 ml·min^–·kg, SD 4) than in AB (2.5 1·min^–1, SD 0.6; 36.7 ml·min^–1·kg, SD 10.7). Maximal cardiac output was similar in the groups (HP, 141·min^–1 SD 2.6; AB, 16.81·min^–1 SD 4). The same result was obtained for maximal heart rate (f _c,max (HP, 175 beats·min^–1, SD 18; AB, 187 beats·min^–, SD 16) and the maximal stroke volume (HP, 82 ml, SD 13; AB, 91 ml, SD 27). The slopes of the relationshipf _c/ O₂ were higher in HP than AB (P<0.025) but when expressed as a % O_2max there were no differences. The results suggests a major alteration of oxygen transport capacity to active muscle mass in paraplegics due to changes in vasomotor regulation below the level of the lesion.     

Effect of very low calorie diet on body composition and exercise response in sedentary women

Summary The effect of very low calorie diet (VLCD) on fat-free mass (FFM) and physiological response to exercise is a topic of current interest. Ten moderately obese women (aged 23–57 years) received VLCD (1695 kJ·day^–1) for 6 weeks. FFM, estimated by four conventional techniques, and heart rate (f _c), blood lactate (la_b), mean arterial pressure (MAP), respiratory exchange ratio (R) and rating of perceived exertion (RPE) were measured during a submaximal cycle ergometry test 1 week bevore, in the 2nd and 6th week, and 1 week after VLCD treatment. Strength and muscular endurance of the quadriceps and hamstrings were tested by isokinetic dynamometry. The 11.5-kg reduction in body mass was approximately 63% fat and 37% FFM. The latter was attributed largely to the loss of water associated with glycogen. Whilst exercise f _c increased by 9–14 beats·min^–1 (P<0.01), there were substantial decreases (P<0.01) in submaximal MAP (1.07–1.73 kPa), lab (0.75–1.00 mmol·1^–1 and R (0.07–0.09) during VLCD. R and f _c returned to normal levels after VLCD. Gross strength decreased (P<0.01) by 9 and 13% at 1.05 rad·s^–1 and 3.14 rad·s^s–1, respectively. Strength expressed relative to body mass (Nm·kg^–1) increased (P<0.01) at the lower contraction velocity, but there was no change at the faster velocity. Muscular endurance also decreased (P<0.01) by 62 and 82% for the hamstrings and quadriceps, respectively: We concluded that the strength decrease was a natural adaptation to the reduction in body mass as the ratio of strength to FFM was maintained. Despite the physiological alterations, subjects could tolerate short-term, steady-state exercise during VLCD, with only slight increases in RPE. However, greater fatigue is associated with long duration strength training exercises during VLCD.     

Kinetics of heart rate and catecholamines during exercise in humans

Summary To elucidate the role of factors other than the nervous system in heart rate (f _c) control during exercise, the kinetics off _c and plasma catecholamine concentrations were studied in ten heart transplant recipients during and after 10-min cycle ergometer exercise at 50 W. Thef _c did not increase at the beginning of the exercise for about 60 s. Then in the eight subjects who completed the exercise it increased following an exponential kinetic with a mean time constant of 210 (SEM 22) s. The two other subjects were exhausted after 5 and 8 min of exercise during whichf _c increased linearly. At the cessation of the exercise,f _c remained unchanged for about 50 s and then decreased exponentially with a time constant which was unchanged from that at the beginning of exercise. In the group of eight subjects plasma noradrenaline concentration ([NA]) increased after 30 s to a mean value above resting of 547 (SEM 124) pg · ml^–1, showing a tendency to a plateau, while adrenaline concentration ([A]) did not increase significantly. In the two subjects who became exhausted an almost linear increase in [NA] occurred up to about 1,300 pg · ml^–1 coupled with a significant increase in [A]. During recovery an immediate decrease in [NA] was observed towards resting values. The values of thef _c increase above resting levels determined at the time of blood collection were linearly related with [NA] increments both at the beginning and end of exercise with a similar slope, i.e. about 2.5 beats · min^–1 per 100 pg · ml^–1 of [NA] change. These findings would seem to suggest that in the absence of heart innervation the increase inf _c depends on plasma [NA].     

Assessment of human knee extensor muscles stress from in vivo physiological cross-sectional area and strength measurements

Summary The physiological cross-sectional areas (CSAp) of the vastus lateralis (VL), vastus intermedius (VI), vastus medialis (VM) and rectus femoris (RF) were obtained, in vivo, from the reconstructed muscle volumes, angles of pennation and distance between tendons of six healthy male volunteers by nuclear magnetic resonance imaging (MRI). In all subjects, the isometric maximum voluntary contraction strength (MVC) was measured at the optimum angle at which peak force occurred. The MVC developed at the ankle was 746.0 (SD 141.8) N and its tendon component (F _t) given by a mechanical advantage of 0.117 (SD 0.010), was 6.367 (SD 1.113) kN. To calculate the force acting along the fibres (F _f) of each muscle, F _t was divided by the cosine of the angle of pennation and multiplied for (CSAp · CSAp^–1), where CSAp was the sum of CSAp of the four muscles. The resulting F _f values of VL, VI, VM and RF were: 1.452 (SD 0.531) kN, 1.997 (SD 0.187) kN, 1.914 (SD 0.827) kN, and 1.601 (SD 0.306) kN, respectively. The stress of each muscle was obtained by dividing these forces for the respective CSAp which was: 6.24 × 10^–3 (SD 2.54 × 10^–3) m² for VL, 8.35 × 10^–3 (SD 1.17 × 10^–3) m² for VI, 6.80 × 10^–3 (SD 2.66 × 10^–3) m² for VM and 6.62 × 10^–3 (SD 1.21 × 10^–3) m² for RE The mean value of stress of VL, VI, VM and RF was 250 (SD 19) kN m²; this value is in good agreement with data on animal muscle and those on human parallel-fibred muscle.     

Heart rate overshoot at the beginning of muscle exercise

Summary A characteristic notch in the heart rate (f _c) on-response at the beginning of square-wave exercise is described in 7 very fit marathon runners and 12 sedentary young men, during cycle tests at 30% and 60% of maximal oxygen consumption (VO_2max). The (f _c) notch revealed af _c overshoot with respect to the (f _c) values predicted from exponential beat-by-beat fitted models. While at 30% of (VO_2max). all subjects showed af _c over-shoot, at 60% of (VO_2max). it occurred in the marathon runners but not in the sedentary subjects. The mean time of occurrence of thef _c overshoot from the onset of the exercise was 16.7 (SD 4.7) s and 12.2 (SD 3.2) s at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 23.8 (SD 8.8) s at 60% of (VO_2max). in the runners. The amplitude of the overshoot, with respect to rest, was 41 (SD 12) beats·min^–1and 31 (SD 4) beats·min^–1 at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 46 (SD 19) beats·min^–1 at 60% of (VO_2max). in the runners. The existence and the amplitude of thef _c overshoot may have been related to central command and muscle heart reflex mechanisms and thus may have been indicators of changes in the balance between sympathetic and parasympathetic activity occurring in fit and unfit subjects.     

Changes in acid-base status of marathon runners during an incremental field test

Summary Four top-class runners who regularly performed marathon and long-distance races participated in this study. They performed a graded field test on an artificial running track within a few weeks of a competitive marathon. The test consisted of five separate bouts of running. Each period lasted 6 min with an intervening 2-min rest bout during which arterialized capillary blood samples were taken. Blood was analysed for pH, partial pressure of oxygen and carbon dioxide (P0₂ and PCO₂) and lactate concentration ([la^–]_b). The values of base excess (BE) and bicarbonate concentration ([HCO₃ ^–]) were calculated. The exercise intensity during the test was regulated by the runners themselves. The subjects were asked to perform the first bout of running at a constant heart rate f _c which was 50 beats · min^–1 below their own maximal f _c. Every subsequent bout, each of which lasted 6 min, was performed with an increment of 10 beats · min^–1 as the target f _c. Thus the last, the fifth run, was planned to be performed with fc amounting to 10 beats · min^–1 less than their maximal f _c. The results from these runners showed that the blood pH changed very little in the bouts performed at a running speed below 100% of mean marathon velocity ( _m). However, once _mwas exceeded, there were marked changes in acid-base status. In the bouts performed at a velocity above the _mthere was a marked increase in [la^–]_b and a significant decrease in pH, [HCO₃ ^–], BE and PCO₂. The average marathon velocity ( _m) was 18.46 (SD 0.32) km·h^–1. The [la^–]_b at a mean running velocity of 97.1 (SD 0.8) % of _mwas 2.33 (SD 1.33) mmol ·l^–1 which, compared with a value at rest of 1.50 (SD 0.60) mmol·l^–1, was not significantly higher. However, when running velocity exceeded the vm by only 3.6 (SD 1.9) %, the [la^–]b increased to 6.94 (SD 2.48) mmol·l-1 (P<0.05 vs rest). We concluded from our study that the highest running velocity at which the blood pH still remained constant in relation to the value at rest and the speed of the run at which [la^–]_b began to increase significantly above the value at rest is a sensitive indicator of capacity for marathon running.     

Pathways of phosphate transport in chick jejunum

The effect of vitamin D₃ on intestinal phosphate (P_i) absorption was studied in everted sacs prepared from jejunum of either vitamin D-deficient (–D) or vitamin D-replete (+D) chicks. Vitamin D₃ stimulates the maximal velocity (V _max) of a mucosal active P_i transport mechanism from 125 to 314 nmol·min^–1·g^–1 tissue.K _m of this process remains virtually unchanged (–D: 0.15 mmol·l^–1; + D: 0.18 mmol·l^–1).Active P_i entry into the epithelium depends on extracellular Na⁺. Reduction of buffer Na⁺ reducesV _max in the + D group to 182 nmol·min^–1·g^–1 tissue but has no significant effect in the –D animals (V _max=105 nmol·min^–1·g^–1 tissue). In this group, the predominant effect of Na⁺ substitution is a shift ofK _m to 1.13 mmol·l^–1, whileK _m in the +D group is changed only to 0.53 mmol·l^–1.Transeptithelial P_i transport in the + D group involves the mucosal phosphate pump and hence an intracellular pathway, proceeding at a rate of 48 nmol·min^–1·g^–1 tissue. This is in contrast to –D P_i transfer (8 nmol·l^–1·g^–1 tissue) which is by a diffusional, Na⁺-insensitive, and presumably paracellular pathway.Transepithelial calcium transport (–D: 3.3 nmol·min^–1·g^–1; + D: 7.6 nmol·min^–1·g^–1 tissue) does not require the presence of extracellular Na⁺ and apparently involves pathways different from those of the P_i absorptive system.Presented in part at the Annual Meeting of the Austrian Biochemical Society, Salzburg, September 1978     

Comparison of mathematically determined blood lactate and heart rate “threshold” points and relationship with performance

Summary The purpose of this study was to investigate the relationship between threshold points for heart rate ( ) and blood lactate (Th_1a) as determined by two objective mathematical models. The models used were the mono-segmental exponential (EXP) model of Hughson et al. and the log-log (LOG) model of Beaver et al. Inter-correlations of these threshold points and correlations with performance were also studied. Seventeen elite runners (mean, SD = 27.5, 6.5 years; 1.73, 0.05 m; 63.8, 7.3 kg; and maximum oxygen consumption of 67.8, 3.7 ml · kg^–1 · min^–1) performed two maximal multistage running field tests on a 183.9-m indoor track with inclined turns. The initial speed of 9 km · h^–1 (2.5 m · s^–1) was increased by 0.5 km · h^–1 (0.14 m · s^–1) every lap for thef _c test and by 1 km · h^–1 (0.28 m · s^–1) every 4 min for the la test. After fitting the la or thef _c data to the two mathematical models, the threshold speed was assessed in the LOG model from the intersection of the two linear segments (LOG-1a; LOG-f _c) and in the EXP model from a tangent point (TI-1a; TI-f _c). Th_1a and speeds computed with the two models were significantly different (P<0.001) and poorly correlated (LOG-1a vs LOG-f _c:r=0.36, TI-1a vs TI-f _c:r=0.13). In general, were less well correlated with performance than Th_1a. With two different objective mathematical models, this study has shown significant differences and poor correlations between Th_1a and . Thus thef _c inflection point with Conconi's protocol is a poor indicator of the la breakpoint with a conventional multistage protocol and a weaker indicator of running performance.     

Stroke volume response to progressive exercise in athletes engaged in different types of training

Summary Using the impedance cardiography method, heart rate ( _c) matched changes on indexed stroke volume (SI) and cardiac output (CI) were compared in subjects engaged in different types of training. The subjects consisted of untrained controls (C), volleyball players (VB) who spent about half of their training time (360 min · week^–1) doing anaerobic conditioning exercises and who had a maximal oxygen uptake ( ) 41% higher than the controls, and distance runners (D) who spent all their training time (366 min·week^–1) doing aerobic conditioning exercises and who had a 26% higher than VB. The subjects performed progressive submaximal cycle ergometer exercise (10 W·min^–1) up to _c of 150 beats·min^–1. In group C, SI had increased significantly (P<0.05) at _c of 90 beats·min^–1 ( + 32%) and maintained this difference up to 110 beats·min^–1, only to return to resting values on reaching 130 beats·min^–1 with no further changes. In group VB, SI peaked (+ 54%) at _c of 110 beats·min^–1, reaching a value significantly higher than that of group C, but decreased progressively to 22010 of the resting value on reaching 150 beats·min^–1. In group D, SI peaked at _c of 130 beats·min^–1 (+ 54%), reaching a value significantly higher than that of group VB, and showed no significant reduction with respect to this peak value on reaching 150 beats·min^–1. As a consequence, the mean CI increase per _c unit was progressively higher in VB than in C (+46%) and in D than in VB (+ 105%). It was concluded that thef _c value at which SI ceased to increase during incremental exercise was closely related to the endurance component in the training programme.     

Myo-electric fatigue manifestations revisited: power spectrum,conduction velocity,and amplitude of human elbow flexor muscles during isolated and repetitive endurance contractions at 30% maximal voluntary contraction

Summary A brief survey of the literature on manifestations of myo-electric fatigue has disclosed a surprisingly sharp conflict between early studies, focusing on neuromotor regulatory mechanisms, and more recent studies which stress the determinant influence of local metabolism and skewed homeostasis. Favoured explanations concerning changes in the electromyographic (EMG) spectrum were synchronization/grouping of motor unit (MU) firing and conduction velocity (CV) decreases of the action potential propagation. The notion of mutual exclusivity interwoven with these theories prompted us to reinvestigate the EMG of moderate level, static endurance contraction. Ten men in their twenties performed isometric elbow flexion (elbow angle 135°) at 30%6 maximal voluntary contraction (MVC), and the surface EMG of the brachioradialis (BR) and biceps brachii (BB) muscles was recorded. Initially the CV — determined by cross-correlation — was 4.3 m · s^–1 (BR) and 4.6 m · s^–1 (BB). At exhaustion the CV of the BR muscle had declined by 33%, roughly twice the decrease of the BB CV. Substantially larger relative median frequency (f _m) reductions of 50% (BR) and 43% (BB) were found. Simultaneously, the root-mean-square amplitudes grew by 150% (BR) and 120% (BB). All changes during contraction reached the same level of significance (P<0.001, both muscles). From the largely uniform relative increases inf _m and CV during the last 4 min of a 5-min recovery period, variations in CV were suggested to produce equivalent shifts inf _m. The gradually increasing discrepancies between relative decreases inf _m and CV during contraction presumably reflected centrally mediated regulation of MU firing patterns (notably synchronization). After the 5-min recovery another 11 endurance contractions at 30% MVC were executed, separated by 5-min intervals. The series of contractions reduced the endurance time to one-third of the 153 s initially sustained, while the terminal CV recordings increased by 1.0 (BR) and 0.6 (BB) m · s^–1, and the terminalf _m increased by 24 (BR) and 14 (BB) Hz. The relative CV decreased in direct proportion to the endurance time and thef _m decreases varied with the CV; the findings did not support a causal link between CV decrease (signifying impaired fibre excitability) and the force failure of exhaustion.     

Regulation of local sweating in sleep-deprived exercising humans

Summary Thermoregulatory sweating [total body (m _sw,b), chest (m _sw,c) and thigh (m _sw,t) sweating], body temperatures [oesophageal (T _oes) and mean skin temperature (T _sk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T _air andT _wall at 35° C. Them _sw,c andm _sw,t were measured under local thermal clamp (T _sk,1), set at 35.5° C. After sleep deprivation, neither the levels of body temperatures (T _oes,T _sk) nor the levels ofm _{sw, b},m _{sw, c} orm _{sw, t} differed from control at rest or during exercise steady state. During the transient phase of exercise (whenT _sk andT _sk,1 were unvarying), them _{sw, c} andm _{sw, t} changes were positively correlated with those ofT _oes. The slopes of them _{sw, c} versusT _oes, orm _{sw, t} versusT _oes relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versusT _oes, relationships (m _{sw, c} andm _{sw, t} sweating data pooled which reached 1.05 (SEM 0.14) mg·cm^–2·min^–1°C^–1 and 1.14 (SEM 0.18) mg·cm^–2·min^–1·°C^–1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased theT _oes threshold for the onset of bothm _{sw, c} andm _{sw, t} (+0.3° C,P<0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.