The effect of range of motion and isometric pre-activation on isokinetic torques

Summary The effect of an increased angle of excursion and isometric pre-activation on isokinetic torques of knee extensors was investigated in five male subjects, mean age 35.0 years, SD 9.6. Peak torque and isoangular torque at 0.52 rad from full knee extension (FKE) were measured when contractions were carried out at 3.14, 4.19 and 5.24 rad·s^–1 starting: 1) from a standard knee angle (SA) of 1.57 rad from FKE, 2) from the same starting angle as SA, plus an isometric preload (P) equivalent to 25% of isometric maximal voluntary contraction and 3) from an increased angle of knee flexion (1A), 2.09 rad from FKE plus P. Surface integrated electromyograms (iEMG) of the vastus lateralis muscle in SA and IA+P were also recorded. The IA+P had the effect of increasing peak torque, as compared to SA, on average by 12.0%, SD 7.5% (P<0.001) at 3.14 rad·s^–1, 19.5%, SD 5.5% (P<0.001) at 4.19 rad·s^–1, 21.6%, SD 10.7% (P<0.001) at 5.24 rad·s^–1 and of increasing mean iEMG by 15.7%, SD 7.0% (P<0.001) at 5.24 rad·s^–1. The IA+P also had the effect of increasing the angle from FKE at which peak torque occurred: from means of 0.80 rad, SD 0.11 to 1.00 rad, SD 0.07 at 3.14 rad·s^–1, from 0.65 rad, SD 0.11 to 0.92 rad, SD 0.09 at 4.19 rad·s^–1 and from 0.60 rad, SD 0.11 to 0.88 rad, SD 0.11 at 5.24 rad·s^–1 (P<0.0001). Mean isoangular torque rose by 12.6%, SD 5.1% at 5.24 rad·s^–1 (P<0.01); mean iEMG values by 8.5%, SD 5.2% (P<0.02) and 11.6%, SD 6.4%(P<0.02) at 4.19 and 5.24 rad·s^–1, respectively. The mean time for both peak and isoangular torque development was significantly increased (P<0.0001). The effect of SA+P on peak torque was smaller than that of IA+P, a mean increment of 3.4%, SD 6% (P<0.02) only being observed at 5.24 rad·s^–1. The increase in isoangular torque was of the same magnitude as that of IA+P. It was concluded that when isokinetic contractions were carried out from a standard position of the knee at a right angle, neuromuscular activation at high angular velocities (>4.19 rad·s^–1) was submaximal. The underestimation of torque seemed to be counteracted by starting the contraction from a flexed position and by utilizing a submaximal P.     

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.     

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.     

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.     

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.     

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.     

Effects of hypotension on cutaneous and subcutaneous blood flow in anaesthetized humans

Summary The aim of this study was to determine the effect of controlled hypotension on subcutaneous and cutaneous haemodynamics in humans. Moderate hypotension was achieved with nitroglycerin (NTG) and sodium nitroprusside (SNP) infusion during narconeuroleptanalgesia in seven patients. Subcutaneous and cutaneous blood flow were measured by a superficial and deep heat clearance (HC) technique. The mean arterial pressure ( ) decreased by 23%–30% and heart rate (f _c) increased but only during NTG infusion (+22%; P < 0.02). Subcutaneous and cutaneous blood flows remained unchanged despite a significant decrease in calculated cutaneous resistance (NTG: –26%, P < 0.01; SNP: –34%, P < 0.02)) and subcutaneous vascular resistance changed only with SNP (–31%, P < 0.02). After hypotension was discontinued the subcutaneous blood flow decreased (–13%, P = 0.05), whereas subcutaneous vascular resistance returned to its control values. An inverse relationship was found between f _c and (NTG: r = –0.525, P < 0.01; SNP: r = –0.622, P < 0.01) as well as with subcutaneous blood flow (NTG: r = –0.653, P < 0.001; SNP: r = –0.573, P < 0.01). In addition, we found oscillatory changes in deep HC values which differed in magnitudes (NTG 0.22 (SEM 0.09) W · m^–1 · °C^–1 vs SNP 0.42 (SEM 0.1) W · m^t–1 · °C^–1, P< 0.01) and frequencies (NTG 0.02 (SEM 0.006) Hz vs SNP 0.01 (SEM 0.002) Hz, P < 0.01). Despite unchanged blood flow, the effects of controlled hypotension on cutaneous and subcutaneous haemodynamics were different depending on the type of drug. These differences may have been related to counterregulatory responses and/or to direct vascular effects.     

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.     

The acute effect of 30 min of moderate exercise on high density lipoprotein cholesterol in untrained middle-aged men

Summary Fifteen middle-aged, untrained (defined as no regular exercise) men (mean age 49.9 years, range 42–67) cycled on a cycle ergometer at 50 rpm for 30 min at an intensity producing 60% predicted maximum heart rate [(f _c,max), wheref _{c, max} = 220 - age]. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (Tg) concentrations were measured from fasting fingertip capillary blood samples collected at rest, after 15 and 30 min of exercise, and at 15 min post-exercise. The mean HDL-C level increased significantly from the resting level of 0.85 mmol · l^–1 to 0.97 mmol · 1^–1 (P<0.05) after 15 min of exercise, increased further to 1.08 mmol · 1^–1 (P<0.01) after 30 min of exercise and remained elevated at 1.07 mmol · 1^–1 (P<0.01) at 15 min post-exercise. These increases represented changes above the mean resting level of 14.1%, 27.1% and 25.9% respectively. The HDL-C/LDL-C ratio increased significantly from a resting ratio of 0.20 to 0.26 after 30 min of exercise (P < 0.01) and to 0.24 at 15 min post-exercise (P<0.05). The mean Tg level increased significantly from a resting level of 0.88 mmol · 1^–1 to 1.05 mmol · 1^–1 after 15 min, and to 1.06 mmol · I^–1 after 30 min of exercise (P<0.05 at each time). The TC/HDL-C ratio decreased significantly (P=0.05) after 30 min of exercise and at 15 min post-exercise by 18.8% and 14%, respectively. No significant changes were observed in the levels of TC or LDL-C over time. These results indicate that 30 min of moderate exercise elicits significant changes in HDL-C concentration during and up to 15 min after the exercise in untrained middle-aged men with low mean resting levels of HDL-C (0.85 mmol · 1^–1).     

Effect of hand paddle aids on oxygen uptake during arm-stroke-only swimming

Summary Cardiorespiratory responses during armstroke-only swimming with and without the aid of paddle were compared in seven trained swimmers. Water flow rate was started at 0.80 m · s^–1 and was increased by 0.05 m · s^–1 every 2 min up to 1.00 m · s^–1 Subsequently, the flow rate was increased by 0.05 m · s^–1 every minute until exhaustion. At given submaximal water flow rates, oxygen uptake, heart rate (f _c), pulmonary ventilation ( _E) and respiratory frequency (f _R) during swimming using hands alone (H) were significantly higher than when aided by paddles (P). There were no significant differences in tidal volume (V _T) between H and P. The subjects were able to swim significantly faster using paddles (P<0.05); however, no significant differences between H and P were found in peak oxygen uptake ( O_2peak,f _c, _E,f _R,V _T and the blood lactate concentration at which O_2peak was obtained (P>0.05). These results would suggest that the ability to swim faster with paddles does not depend on higher energy production but may be attributed to higher propelling efficiency.     

Heart rate and oxygen uptake relationship: a comparison of loaded marching and running in women

Heart rate (beats · min^–1;f _c) measured during marching with a load is often used to predict the oxygen cost (1·min^–1; VO₂) of the activity. The prediction comes from thef _c/VO₂ relationship determined from laboratory measures off _c and VO₂ during treadmill running. Studies in men have suggested that this may not be appropriate although this has yet to be examined in women. This study, therefore, compared thef _c/VO₂ relationship between loaded marching and maximal running protocols in women. Sixteen female subjects [mean (SD), age 21.9 (2.3) years, height 6 (0.06) m, weight 62.6 (7.6) kg] had theirf _c (from three-lead chest electrodes) and VO₂ measured first during standard treadmill run protocols, and again 1 week later during loaded marching protocols. The slopes and intercepts determined from linear regression off _c on VO₂ for each individual for each protocol were compared as were the maximalf _c(f _cmax), VO₂ and ratings of perceived exertion (RPE) from the last work period of each protocol in pairedt-tests. The VO₂ slopes (P < 0.01) and intercepts (P < 0.05) differed significantly between loaded marching and running.f _cmax for loaded marching were 90% off _cmax for running (P < 0.01) and VO₂ for loaded marching were 80% of those for running (P < 0.01). However, RPE at the final levels for the two protocols were not significantly different. The data suggest that in women the VO₂ relationships for loaded marching and for running are different. This difference is similar to that found in men when speed is held constant and the load and gradient are varied. The results suggest that it would be erroneous to usef _c and VO₂ measured during running protocols in the laboratory to estimate energy expenditure and work intensity during loaded marching in the filed.     

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.     

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].     

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.     

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.     

Water balance during and after marathon running

To describe the time course of plasma volume alterations and the changes in the plasma concentrations of hormones regulating water balance in relation to a marathon race, six experienced marathon runners (five men, one women) aged 28 (SD 6) years were studied during and for the 3 days following a treadmill marathon run at 68 (SD 5)% of maximal oxygen consumption. Haematocrit, haemoglobin, plasma protein (Prot) and electrolyte (Na⁺, K⁺) concentration, osmolality (osm), plasma concentrations of renin (Ren), aldosterone (Ald) and atrial natriuretic peptide (ANP) were determined at rest in a sitting position (T_–30), and then after 30 min in an upright posture (R₀), while running a marathon at 10 km (R₁₀), 30 km (R₃₀) and 42.2 km (R_end), and after the marathon at 30 min (T₃₀), 60 min (T₆₀), 120 min (T₁₂₀) and 24 h (TD₊₁), 48 h (TD₊₂) and 72 h (TD₊₃). The changes in plasma volume (PV), Prot, osm and Na⁺ observed during the race were nonsignificant. Significant increases in plasma concentration of K⁺ [4.8 (SD 0.6) vs 5.5 (SD 0.6) mmol·l^–1; P < 0.01], Ren [38 (SD 57) vs 197 (SD 145) pmol·l^–1; P < 0.02] and Ald [175 (SD 142) vs 1632 (SD 490) pmol·^–1; P < 0.01] were observed at R_end. A significant increase of ANP (P < 0.05) was only found after R₁₀. Body mass significantly decreased by 2.0 kg (P < 0.01) during the race in spite of the ingestion of 1.46 (SD 0.34) 1 of a 5% glucose solution. Urinary volume and Na⁺ excretion dropped significantly after the completion of the marathon in comparison with the day before [2600 vs 1452 ml·day^–1 (P < 0.02) and 161.3 vs 97.1 mmol·l^–1 (P < 0.05)]. At TD₊₁ and TD₊₂ a significant increase in PV was noted, compared to T_–30. The lack of a decrease in PV during the marathon may have been due to the production of 402 g of metabolic water and by the release of 1280 g of water stored in glycogen complexes in muscle and liver. Thus, the hormone response during the marathon may have been due to the effects of the exercise itself and not to the effects of dehydration. The postmarathon PV expansion may be explained by a protein shift to the intravascular space and by renal sodium retention.     

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.     

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.     

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.     

Changes in carotid blood flow and electrocardiogram in humans during and after walking on a treadmill

Blood flow velocity in the common carotid artery and the electrocardiogram were measured simultaneously by telemetry in seven male subjects during 20-min walking on a treadmill at an exercise intensity corresponding to a mean oxygen uptake of 26.0 (SD 2.9) ml · kg ^–1 · min ^–1. The mean cardiac cycle was shortened from 0.814 (SD 0.103) s to 0.452 (SD 0.054) s during this exercise. Of this shortening, 73% was due to shortening of the diastolic period and 27% to shortening of the systolic period. In the relatively small shortening of the mean systolic period [from 0.377 (SD 0.043) s to 0.268 (SD 0.029) s], the isovolumetric contraction time was shortened by 56%. During exercise, the heart rate (f _c) increased by 79.4% [from 74.3 (SD 9.3) beats · min ^–1 to 133.3 (SD 14.8) beats · min ^–1], and the peak blood velocity (S₁) in the common carotid artery increased by 56.1% [from 0.82 (SD 0.10) m · s^–1 to 1.28 (SD 0.11) m · s^–1]. After exercise, the S₁ decreased rapidly to the resting level. The f _c decreased more slowly, still being higher than the initial resting level 5 min after exercise. The diastolic velocity wave and the end-diastolic foot decreased during exercise. The blood flow rate in the carotid artery increased transiently by 13.5% at the beginning of exercise [from 5.62 (SD 0.63) ml · s^–1 to 6.38 (SD 0.85) ml · s^–1] and by 26.5% at the end of the exercise period [from 5.62 (SD 0.63) ml · s^–1 to 7.11 (SD 1.34) ml · s^–1]. The increase of blood flow in the carotid artery at the onset of exercise may have been mainly related to cerebral activation, and partly to an increase of blood flow to the skin of the head. The physiological significance for cerebral function of the increase of blood flow in the artery after the end of exercise is unknown.