The influence of dietary carbohydrate on performance of supramaximal intermittent exercise

Summary The relative contraction force producing a reduction in exercise hyperaemia was studied by superimposing handgrip contraction at different intensities on plantar flexion of low intensity. Ten active women served as subjects. Blood flow to the forearm ( _forearm) and calf ( _calf) was measured with mercury-in-rubber strain gauges by venous occlusion plethysmography immediately after 60 s of rhythmic plantar flexion at 10% of maximum voluntary contraction (MVC), which was expressed as P₁₀H₀, or combined plantar flexion and handgrip contraction. In the combined exercise, handgrip exercise at 30%, 50% or 70% MVC was added to plantar flexion during the last 30 s of exercise (P₁₀H₃₀, P₁₀H₅₀ and P₁₀H₇₀, respectively). The _forearm increases after P₁₀H₃₀, P₁₀H₅₀ and P₁₀ were significantly larger (P<0.01) than that after P₁₀H₀, and the difference between P₁₀H₃₀and P₁₀H₇₀ was also significant (P<0.01) Immediate post-exercise _calf after P₁₀H₀ increased by 7.4 (SEM 0.9) ml·100 ml^–1·min^–1. When handgrip contraction at 70% MVC was added, the _calf increase after exercise [4.5 (SEM 0.7) ml·100 ml^–1·min^–1] was significantly lower than after plantar flexion alone (P<0.05). However, no significant change was found in _calf when the forces of added handgrip contraction were 30% and 50% MVC, although the mean value of _calf increase was lower after P₁₀H₅₀ combined exercise. Calf vascular resistance calculated as / _calf ( mean blood pressure) tended to increase after P₁₀H₇₀ to a nonsignificant extent. Heart rate and oxygen uptake in these exercises increased when handgrip contraction at 30%, 50%, or 70% MVC was added to plantar flexion at 10% MVC. However, the increases were considerably lower than the maximal ones. Thus, a reduction of _calf occurred even when the cardiac demand from the muscle was below its maximum. In conclusion, post-exercise hyperaemia in the active limb working at low intensity was inhibited by superimposition of exercise of another limb at a high contraction force. The critical force producing attenuation of exercise hyperaemia after combined exercise of short duration was found to be higher than 50% MVC in the case of handgrip contraction plus plantar flexion.     

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.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

Summary During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65–70°C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25° C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) ° C at thermo-neutrality, and 37.74 (SEM 0.07) ° C (P<0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats -min^–1 (P<0.01), respectively. At 25° C, handgrip exercise increased blood flow in the exercising forearm above the control forarm by 6.0 (SEM 0.8) ml · 100 ml^–1 · min^–1 during light exercise, and by 17.9 (SEM 2.5) ml · 100 ml^–1 · min^–1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2:2) ml · 100 ml^–1 · min^–1 at the light exercise level (P<0.01), and 32.2 (SEM 5.9) ml · 100 ml^–1·min^–1 (P<0.05) at the moderate exercise level. Skin blood flow was not significantly different in any of the test conditions between the two forearms. These results suggested that hyperthermia of the observed magnitude did not reduce blood flow in active muscles during light or moderate levels of dynamic handgrip exercise.     

Finger and forearm vasodilatatory changes after local cold acclimation

Summary To determine the vascular changes induced by local cold acclimation, post-ischaemia and exercise vasodilatation were studied in the finger and the forearm of five subjects cold-acclimated locally and five non-acclimated subjects. Peak blood flow was measured by venous occlusion plethysmography after 5 min of arterial occlusion (PBF_isc), after 5 min of sustained handgrip at 10% maximal voluntary contraction (PBF_exe), and after 5 min of both treatments simultaneously (PBF_isc+exe). Each test was performed at room temperature (25° C, SE 1 C) (non-cooled condition) and after 5 min of 5'C cold water immersion (cooled condition). After the cold acclimation period, the decrease in skin temperature was more limited in the cold-acclimated compared to the non-acclimated (P<0.01). The PBF_isc was significantly reduced in the cooled condition only in the cold-acclimated subjects (finger: 8.4 ml · 100 ml^–1 · min^–1, SE 1.1,P<0.01; forearm: 5.8 ml · 100 ml^–1 · min^–1, SE 1.5,P<0.01) compared to the non-cooled condition. Forearm PBF_exe was significantly decreased in the cooled condition only in the cold-acclimated subjects (non-cooled: 7.4 ml · 100 ml^–1 · min^–1, SE 1.2; cooled: 3.9 ml · 100 ml^–1 ·min^–1, SE 2.6,P<0.05) indicating that muscle blood flow was also reduced. The application of PBF_isc+exe elicited an increase in peak blood flow only in the forearm of the non-acclimated subjects (non-cooled: 10.4 ml· 100 ml^–1 · min^–1, SE 2.0; cooled: 14.3 ml · 100 ml^–1 · min^–1, SE 2.6,P<0.05) and conversely only in the finger of the cold-acclimated (non-cooled finger: 25.7 ml · 100 ml^–1 · min^–1, SE 4.4; cooled finger: 19.2 ml · 100 ml^–1 · min^–1, SE 3.3,P<0.01). Therefore, subjects cold-acclimated locally showed decreased vasodilatatory responses only when exposed to cold.     

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.     

Cardiac responses to maximal anisotonic isometric contractions during handgrip and leg extension

A group of 14-healthy men performed anisotonic isometric contractions (AIC), for 60 s, at an intensity of 100% maximal voluntary contraction force (MVC) during handgrip (HG) and leg extension (LE). Heart rate (f _c), stroke volume index (SVI) and cardiac output index (Q_cI) were measured during the last 10 s of both AIC by an impedance reography method. Force (F) exerted by the subjects was recorded continuously and reported as a relative force (F _r) (% MVC). The F generated during MVC was greater for LE than for HG (502.I N compared to 374.6 N, P < 0.001). The rate of decrease in F _r was significantly slower for LE than HG for the first 25 s of the exercise (phase 1 of AIC). The F _r developed by the subjects at the end of AIC was 40% MVC for both LE and HG. The increase in f _c was greater for LE (63 beats · min^–1) than for HG (52 beats · min^–1), P < 0.01. The SVI decreased significantly from the resting level by 17.0 ml · m^–2 and by 18.2 ml · m^–2 for LE and HG, respectively. The Q_cI increased insignificantly for HG by 0.091 · min^–1 · m^–2 andsignificantly forLE by 0.561 · min^–1 · m^–2 (P < 0.001). It was concluded that although both AIC caused a significant decrease in SVI, greater increases in f _c and Q_c were observed for LE than for HG. The greater f _c and Q_c reported during LE was probably related to the greater relative force exerted by LE during phase 1 of AIC. It seems, therefore that central command might have dominated for phase 1 of AIC but that the muscle reflex also contributed significantly to the control of the cardiac response to the high intensity AIC.     

Caffeine increases maximal anaerobic power and blood lactate concentration

Summary The aim of this study was to specify the effects of caffeine on maximal anaerobic power (W _max). A group of 14 subjects ingested caffeine (250 mg) or placebo in random double-blind order. TheW _max was determined using a force-velocity exercise test. In addition, we measured blood lactate concentration for each load at the end of pedalling and after 5 min of recovery. We observed that caffeine increasedW _max [964 (SEM 65.77) W with caffeine vs 903.7 (SEM 52.62) W with placebo;P<0.02] and blood lactate concentration both at the end of pedalling [8.36 (SEM 0.95) mmol · l^–1 with caffeine vs 7.17 (SEM 0.53) mmol · l^–1 with placebo;P<0.011 and after 5 min of recovery [10.23 (SEM 0.97) mmol · l^–1 with caffeine vs 8.35 (SEM 0.66) mmol · l^–1 with placebo;P<0.04]. The quotient lactate concentration/power (mmol · l^–1 · W^–1) also increased with caffeine at the end of pedalling [7.6 · 10^–3 (SEM 3.82 · 10^–5) vs 6.85 · 10^–3 (SEM 3.01 · 10^–5);P<0.01] and after 5 min of recovery [9.82·10^–3 (SEM 4.28 · 10^–5) vs 8.84 · 10^–3 (SEM 3.58 · 10^–5);P<0.02]. We concluded that caffeine increased bothW _max and blood lactate concentration.     

Physiological response in the forearm during and after isometric intermittent handgrip

Summary The aim of the present paper was to study the development of fatigue during isometric intermittent handgrip exercise. Using a handgrip dynamometer, four combinations of contraction-relaxation periods were studied (10+10, 10+5, 10+2s and continuous contraction) at three contraction intensities (10, 25 and 40% maximum voluntary contraction, MVC). Local blood flow (BF) in the forearm (venous occlusion plethysmography) was followed before, during and after the exercise period. Electromyography (EMG) (frequency analysis) and the perceived effort and pain were recorded during the exercise period. Forearm BF is insufficient even at isometric contractions of low intensity (10% MVC). The results indicate that vasodilating metabolites play an active role for BF in low-intensity isometric contractions. It is shown that maximal BF in the forearm during relaxation periods (25–30 ml min^–1 · 100 ml^–1) is already reached at 25% MVC. Only intermittent exercise at 10% MVC and (10+5s) and (10+10s) at 25% MVC was considered acceptable with regard to local fatigue, which was defined as a switch of local BF to the post-exercise period, a decrease in the number of zero-crossings (EMG) and marked increases in subjective ratings.     

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.     

Physiological responses to maximal intensity intermittent exercise

Summary Physiological responses to repeated bouts of short duration maximal-intensity exercise were evaluated. Seven male subjects performed three exercise protocols, on separate days, with either 15 (S₁₅), 30 (S₃₀) or 40 (S₄₀) m sprints repeated every 30 s. Plasma hypoxanthine (HX) and uric acid (UA), and blood lactate concentrations were evaluated pre- and postexercise. Oxygen uptake was measured immediately after the last sprint in each protocol. Sprint times were recorded to analyse changes in performance over the trials. Mean plasma concentrations of HX and UA increased during S₃₀ and S₄₀ (P<0.05), HX increasing from 2.9 (SEM 1.0) and 4.1 (SEM 0.9), to 25.4 (SEM 7.8) and 42.7 (SEM 7.5) µmol · l^–1, and UA from 372.8 (SEM 19) and 382.8 (SEM 26), to 458.7 (SEM 40) and 534.6 (SEM 37) µmol · l^–1, respectively. Postexercise blood lactate concentrations were higher than pretest values in all three protocols (P<0.05), increasing to 6.8 (SEM 1.5), 13.9 (SEM 1.7) and 16.8 (SEM 1.1) mmol · l^–1 in S₁₅, S₃₀ and S₄₀, respectively. There was no significant difference between oxygen uptake immediately after S₃₀ [3.2 (SEM 0.1) l · min^–1] and S₄₀ [3.3 (SEM 0.4) l · min^–1], but a lower value [2.6 (SEM 0.1) l · min^–1] was found after S₁₅ (P<0.05). The time of the last sprint [2.63 (SEM 0.04) s] in S₁₅ was not significantly different from that of the first [2.62 (SEM 0.02) s]. However, in S₃₀ and S₄₀ sprint times increased from 4.46 (SEM 0.04) and 5.61 (SEM 0.07) s (first) to 4.66 (SEM 0.05) and 6.19 (SEM 0.09) s (last), respectively (P<0.05). These data showed that with a fixed 30-s intervening rest period, physiological and performance responses to repeated sprints were markedly influenced by sprint distance. While 15-m-sprints could be repeated every 30 s without decreases in performance, 40-m sprint times increased after the third sprint (P<0.05) and this exercise pattern was associated with a net loss to the adenine nucleotide pool.     

The interaction between short-term exercise training and a diuretic-induced hypovolemic stimulus

Nine healthy untrained males [mean (SEM) age, 20.2 (1) years; peak oxygen uptake (VO_2max, 48.2 (2) ml · kg^–1 · min^–1] took part in a study to examine whether short-term exercise training (cycle exercise 2 h · day^–1 for 3 days at 60% ), which normally results in an expansion of plasma volume (PV), can counteract a diuretic-induced hypovolemic stimulus (100 mg triamterene + 50 mg hydrochlorothiazide day^–1 for 5 days concurrent with exercise training) and restore PV to control levels. Resting and exercise responses (90 min, 60% ) in the diuretic plus exercise training condition (D + E) were compared to a control (C) and a diuretic (D) condition in which no exercise was performed. Following the short-term training, PV was still decreased (P < 0.05) below C by –8.3 (3)% in D + E and was similar (P > 0.05) to the reduction in D [–12.4 (2)%]. The reduced PV in response to the diuretic was associated with similar (P > 0.05) elevations in resting aldosterone (ALDO) and norepinephrine (NOREPI) levels (ng · 100 ml^–1) in D [101 (12), 61 (4)] and D + E [85 (16), 60 (10)] above (P < 0.05) C [22 (5), 37 (4)]. During exercise, ALDO levels were increased (P < 0.05) by 66 (5) and 70 (10) ng · 100 ml^–1 in D and D + E, respectively, and the increase was greater (P < 0.05) than C [44 (8) ng · 100 ml^–1]. The rise in NOREPI during exercise was lower (P < 0.05) in D + E [164 (44) ng · 100 ml^–1] than in D [244 (24) ng · 100 ml^–1] with levels similar to C [176 (25) ng · 100 ml^–1]. Thus, the ALDO response to the diuretic was heightened at rest and during exercise but was not additionally affected by the short-term training session. Results suggest that 3 days of exercise training are unable to counteract the hypovolemic effects of a diuretic and restore PV to control levels despite chronic elevations in NOREPI and ALDO.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

Fuel kinetics during intense running and cycling when fed carbohydrate

On two occasions, six well-trained, male competitive triathletes performed, in random order, two experimental trials consisting of either a timed ride to exhaustion on a cycle ergometer or a run to exhaustion on a motor-driven treadmill at 80% of their respective peak cycling and peak running oxygen (VO_2max) uptakes. At the start of exercise, subjects drank 250 ml of a 15 g·100 ml^–1 w/v [U-¹⁴C]glucose solution and, thereafter, 150 ml of the same solution every 15 min. Despite identical metabolic rates [VO₂ 3.51 (0.06) vs 3.51 (0.10) 1·min^–1; values are mean (SEM) for the cycling and running trials, respectively], exercise times to exhaustion were significantly longer during cycling than running [96 (14) vs 63 (11) min; P < 0.05]. The superior cycling than running endurance was not associated with any differences in either the rate of blood glucose oxidation [3.8 (0.1) vs 3.9 (0.4) mmol· min^–1], or the rate of ingested glucose oxidation [2.0 (0.1) vs 1.7 (0.2) mmol· min^–1] at the last common time point (40 min) before exhaustion, despite higher blood glucose concentrations at exhaustion during running than cycling [7.0 (0.9) vs 5.8 (0.5) mmol·1^–1; P < 0.05]. However, the final rate of total carbohydrate (CHO) oxidation was significantly greater during cycling than running [24.0 (0.8) vs 21.7 (1.4) mmol C₆·min^–1; P < 0.01]. At exhaustion, the estimated contribution to energy production from muscle glycogen had declined to similar extents in both cycling and running [68 (3) vs 65 (5)%]. These differences between the rates of total CHO oxidation and blood glucose oxidation suggest that the direct and/or indirect (via lactate) oxidation of muscle glycogen was greater in cycling than running.     

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.     

Atrial natriuretic peptide response to endurance physical training in the rat

Summary The effect of an endurance physical training programme on the plasma and atrial natriuretic peptides (ANP) and on renal glomerular ANP receptors was evaluated in male normotensive Wistar rats. Maximal O₂ uptake was significantly greater in the endurance trained (117.1 Ml O₂ · kg^–1 · min^–1, SEM 6.18 versus the control rats 84.2 ml O₂ · kg^–1 · min^–1, SEM 4.88, P<0.01. In addition, various muscle oxidative enzymes were also significantly higher in endurance trained animals. An increase in resting plasma [ANP] was observed after 11 weeks of physical training (40.02 pg · ml^–1, SEM 7.07 vs 22.8 pg.ml^–1, SEM 3.83, P<0.05). Glomerular ANP receptor density was lower in trained rats (272 fmol · mg^–1 protein, SEM 3.1 vs 380 fmol · mg^–1 protein, SEM 6.1, P < 0.05), whereas atrial tissue [ANP] was not significantly different between controls and trained animals. However, in trained rats, circulating [ANP] was closely correlated with left atrial [ANP] (r = –0.92, P<0.05). Resting systolic blood pressure had not changed at the end of this physical training programme. It is considered that under physiological conditions ANP may be involved in long-term extracellular fluid volume homeostasis through the regulation of renal glomerular ANP receptors, and that the left atrium might play a significant role in this long term fluid volume control.     

Effects of exercise during normoxia and hypoxia on the growth hormone—insulin-like growth factor I axis

The response of plasma insulin-like growth factor I (IGF I) to exercise-induced increase of total human growth hormone concentration [hGH_tot] and of its molecular species [hGH_20kD] was investigated up to 48 h after an 1-h ergometer exercise at 60% of maximal capacity during normoxia (N) and hypoxia (H) (inspiratory partial pressure of oxygen = 92 mmHg (12.7 kPa);n = 8). Lactate and glucose concentrations were differently affected during both conditions showing higher levels under H. Despite similar maximal concentrations, the increase of human growth hormone (hGH) was faster during exercise during H than during N[hGH_tot after 30 min: 8.6 (SD 11.4) ng · ml^–1 (N); 16.2 (SD 11.6) ng · ml^–1 (H);P < 0.05]. The variations in plasma [hGH_20kD] were closely correlated to those of [hGH_tot], but its absolute concentration did not exceed 3% of the [hGH_tot]. Plasma IGF I concentration was significantly decreased 24 h after both experimental conditions [N from 319 (SD 71) ng · ml^-1 to 228 (SD 72) ng · ml^–1,P < 0.05; H from 253 (SD 47) to 200 (SD 47) ng · ml^–1,P < 0.01], and was still lower than basal levels 48 h after exercise during H [204 (SD 44) ng · ml^–1,P < 0.01]. Linear regression analysis yielded no significant correlation between increase in plasma [hGH_tot] or [hGH_20kD] during exercise and the plasma IGF I concentration after exercise. It was concluded that the exercise-associated elevated plasma [hGH] did not increase the hepatic IGF I production. From our study it would seem that the high energy demand during and after the long-lasting intensive exercise may have overridden an existing hGH stimulus on plasma IGH I, which was most obvious during hypoxia.     

Influence of angiotensin II blockade during exercise in the heat

The effect of the blockade of the renin angiotensin system (RAS) on thermorgulatory, cardiovascular and renal function during moderate exercise in a hot [mean (SEM) 34.4 (0.1)°C] environment was evaluated. Six men and three women cycled at 60% peak oxygen uptake for 45 min following acute administration of a placebo (PLAC) or enalapril (ENAL), an angiotensin converting enzyme inhibitor (ACE-I). Resting mean arterial pressure (MAP) was reduced by ENAL, but the pressor response to exercise was unaffected [MAP = 7.8 (1.4) mmHg for both trials (P > 0.05)]. Peak esophageal temperature [T _es = 38.7 (1.0)°C (PLAC) vs 38.4 (0.2)°C (ENAL)] and mean skin temperatures [ _sk = 36.5 (0.1)°C (PLAC) vs 36.6 (0.1)°C (ENAL)] were similar for both drug treatments during the exercise. Both aldosterone and plasma renin activity (PRA) increased five fold above resting values during exercise; however, only the PRA response [16.7 (3.2) ng angiotensin I (Ang I) · ml^–1 · h^–1 (ENAL) vs 7.4 (1.2) ng Ang I · ml^–1 · h^–1 (PLAC)] was significantly altered by ENAL treatment (P < 0.05). Urine flow, sodium excretion and glomerular filtration rates, determined from creatinine clearance, were similarly reduced following exercise for both ENAL and PLAC treatments. These results suggest acute administration (5 mg) of ACE-I does not impair thermoregulatory, cardiovascular or renal responses during moderate exercise in the heat.     

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].     

Changes in muscle sympathetic nerve activity and calf blood flow during combined leg and forearm exercise

In order to examine efferent sympathetic nerve control of the peripheral circulation during exercise, muscle sympathetic nerve activity (MSNA), calf blood flow (CBF), heart rate (HR), blood pressure (BP) and oxygen uptake were measured during combined foot and forearm exercise. An initial period of rhythmic foot exercise (RFE) (60 min^-1 at 10% of maximal voluntary contraction (MVC) was followed by the addition of rhythmic handgrip exercise (RFE+OCCL) (60 min at 30% of MVC) and by forearm ischaemia after handgrip exercise while continuing RFE (RFE + OCCL). During RFE, CBF in the working leg, HR and oxygen increased respectively by 560%, 121% and 144% when compared with the control rest period, but MSNA (burst rate) was reduced by 13% (P > 0.05) and BP was unchanged. During RFE+RHG, HR, BP and oxygen uptake were greater than during RFE alone. There was no change in CBF, but a significant increase occurred in calf vascular resistance (CVR) and MSNA increased to 121% of the control level. During RFE + OCCL, MSNA, CVR and BP were all higher than during RFE alone, whereas HR and oxygen uptake decreased slightly, although they remained higher than the control values. The increase in CVR in the working leg and the rise in BP during RFE+RHG or RFE+OCCL might be linked to enhancement of MSNA, which may have been reflexly evoked by input from muscle metabolic receptors in the working forearm.     

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min^–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO_{2 peak}). During exercise the subjects ingested either a 15 g · 100 ml^–1 U-¹⁴C labelled glucose solution or H₂O labelled with a U-¹⁴C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma¹⁴C glucose and¹⁴CO₂ specific activities, and respiratory gas exchange. Simultaneously, 2-³H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l^–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l^–1; infusion 5.0 (0.09) mmol · l^–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l^–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min^–1 kg fat free mass^–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min^–1 kg FFM^–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min^–1 kg FFM^–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.