Venous blood lactate increase after vertical jumping in volleyball athletes

The aim of this study was to test the hypothesis that venous blood lactate concentrations ([La^–]) would vary from the beginning of brief exercise. Maximal vertical jumping was used as a model of brief intense exercise. Eleven healthy male volleyball players, aged [mean (SE)] 18.5 (0.7) years, performed three exercise tests with different protocols, each separated by quiet seated recovery periods of 45 min. After the first test, consisting of a single maximal jump [lasting ≅0.6 s for the pushing phase, and in which the subjects jumped 64 (2.2) cm], forearm venous [La^–] increased significantly with respect to rest at 1 min (t ₁), 3 min (t ₃), and 5 min (t ₅) of recovery. The second test, comprising six maximal jumps, each separated by 20-s recovery periods, resulted in an unchanged [La^–] with respect to the baseline value. After the third test [i.e., six consecutive maximal jumps that lasted a total of 7.36 (0.33) s], [La^–] increased significantly at t ₃ and t ₅ with respect to the pre-test value (F=10.3, P<0.001). We conclude that a significant venous [La^–] increase occurs after vertical jumping. This result may be explained by the activation of lactic anaerobic metabolism at the very onset of exercise, which participates in energy production and/or in the resynthesis of the phosphocreatine that was used during such brief exercise. Electronic Publication     

Potassium kinetics in human muscle interstitium during repeated intense exercise in relation to fatigue

Accumulation of K⁺ in skeletal muscle interstitium during intense exercise has been suggested to cause fatigue in humans. The present study examined interstitial K⁺ kinetics and fatigue during repeated, intense, exhaustive exercise in human skeletal muscle. Ten subjects performed three repeated, intense (61.6±4.1 W; mean±SEM), one-legged knee extension exercise bouts (EX1, EX2 and EX3) to exhaustion separated by 10-min recovery periods. Interstitial [K⁺] ([K⁺]_interst) in the vastus lateralis muscle were determined using microdialysis. Time-to-fatigue decreased progressively (P<0.05) during the protocol (5.1±0.4, 4.2±0.3 and 3.2±0.2 min for EX1, EX2 and EX3 respectively). Prior to these bouts, [K⁺]_interst was 4.1±0.2, 4.8±0.2 and 5.2±0.2 mM, respectively. During the initial 1.5 min of exercise the accumulation rate of interstitial K⁺ was 85% greater (P<0.05) in EX1 than in EX3. At exhaustion [K⁺]_interst was 11.4±0.8 mM in EX1, which was not different from that in EX2 (10.4±0.8 mM), but higher (P<0.05) than in EX3 (9.1±0.3 mM). The study demonstrated that the rate of accumulation of K⁺ in the muscle interstitium declines during intense repetitive exercise. Furthermore, whilst [K⁺]_interst at exhaustion reached levels high enough to impair performance, the concentration decreased with repeated exercise, suggesting that accumulation of interstitial K⁺ per se does not cause fatigue when intense exercise is repeated.     

Evidence for interference of vitamin D with PTH/PTHrP receptor expression in opossum kidney cells

 Vitamin D counters the phosphaturic action of parathyroid hormone (PTH) in rats in vivo. The present study was undertaken to examine this interaction using monolayers of Opossum kidney (OK) cells. ³²P uptake, cAMP generation, PTH/PTHrP receptor mRNA expression and intracellular Ca²⁺ [Ca²⁺]_i were measured in (1) control cells, (2) cells exposed to PTH, (3) cells pretreated with 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], and (4) 1,25(OH)₂D₃-pretreated cells exposed to PTH. ³²P uptakes were in (1) 5.00±0.20 (mean ±SE), in (2) 2.30±0.14 (P<0.001 versus group 1), in (3) 4.80±0.24 (P NS versus group 1) and in (4) 3.70±0.20 (P<0.001 versus group 2) nmol P_i/(mg·prot 10 mm). cAMP levels were in (1) 10±3, in (2) 210±8, in (3) 12±4, and in (4) 122±12 pmol cAMP/mg protein (P<0.001 versus group 2). PTH/PTHrP receptor mRNA expression was in relative units: (1) 100±0, (2) 99.5±6.2, (3) 68.7±2.6 (P<0.001 versus group 1), and (4) 34.8±3.3 (P<0.001 versus group 1). In groups 2 and 4 PTH induced equal transient increments in [Ca²⁺]_i. These experiments demonstrate that the effect of vitamin D on phosphate transport is associated with a commensurate diminution in PTH/PTHrP receptor gene expression and PTH-induced cAMP formation but not with Ca²⁺ transients. Vitamin D per se does not affect ³²P uptake or cAMP generation while it slightly decreased PTH/PTHrP receptor gene expression. These observations demonstrate that: (1) 1.25(OH)₂D₃ directly antagonizes the effects of PTH on ³²P uptake in OK cells, (2) this effect is mediated via inhibition of PTH-induced activation of AC/cAMP system, (3) the diminution in PTH-induced cAMP formation may stem at least in part from a decrease in the expression of PTH/PTHrP receptor mRNA. Received: 2 December 1997 / Received after revision: 19 January 1998 / Accepted: 28 January 1998     

Effects of brief leg cooling after moderate exercise on cardiorespiratory responses to subsequent exercise in the heat

We investigated the effects of brief leg cooling after moderate exercise on the cardiorespiratory responses to subsequent exercise in the heat. Following 40 min of ergometer cycling [65% peak oxygen uptake (O_2peak)] at 35°C (Ex. 1), seven male subjects [21.9 (1.1) years of age; 170.9 (1.9) cm height; 66.0 (2.0) kg body mass; 46.7 (2.0) ml kg^–1 min^–1 O_2peak] immersed their legs in 35°C (control condition, CONT) or 20°C (cooling condition, COOL) water for 5 min and then repeated the cycling (as before, but for 10 min) (Ex. 2). Just before Ex. 2, esophageal temperature (T _es) was lower in COOL than in CONT [36.9 (0.2) vs 37.5 (0.1)°C] (P<0.01), as also were both mean skin temperature [33.9 (0.2) vs 35.2 (0.2)°C] (P<0.01), and heart rate (HR) [93.2 (6.0) vs 102.7 (4.9) beats min^–1] (P<0.05). During Ex. 2, no differences between CONT and COOL were observed in oxygen uptake, arterial blood pressure, blood lactate concentration, or ratings of perceived exertion; however, T _es, skin temperature, and HR were lower in COOL than in CONT. Further, during the first 5 min of Ex. 2, minute ventilation was significantly lower in COOL than in CONT [50.3 (2.0) vs 53.4 (2.6) l min^–1] (P<0.01). These results suggest that brief leg cooling during the recovery period may be effective at reducing thermal and cardiorespiratory strain during subsequent exercise in the heat.     

Heart rate variability dynamics during early recovery after different endurance exercises

Since heart rate variability (HRV) during the first minutes of the recovery after exercise has barely been studied, we wanted to find out HRV dynamics immediately after five different constant-speed exercises. Thirteen sedentary women performed two low-intensity (3,500 m [3,500_LI] and 7,000 m [7,000_LI] at 50% of the velocity of VO_2max [vVO_2max]), two moderate-intensity (3,500 m [3,500_MI] and 7,000 m [7,000_MI] at ∼63% vVO_2max) and one high-intensity (3,500 m at ∼74% vVO_2max [3,500_HI]) exercises on a treadmill. HRV was analyzed with short-time Fourier transform method during the 30-min recovery. High frequency power (HFP) was for the first time higher than at the end of the exercise after the first minute of the recovery (3,500_LI and 7,000_LI, P < 0.001), after the fourth (3,500_MI, P < 0.05) and the fifth (7,000_MI, P < 0.05) minute of the recovery and at the end of the 30-min recovery (3,500_HI, P < 0.01). There were no differences in HRV between 3,500_LI and 7,000_LI or between 3,500_MI and 7,000_MI during the recovery. The levels of HFP and TP were higher during the whole recovery after 3,500_LI compared to 3,500_MI and 3,500_HI. We found increased HFP, presumably caused by vagal reactivation, during the first 5 min of the recovery after each exercise, except for 3,500_HI. The increased intensity of the exercise resulted in slower recovery of HFP as well as lower levels of HFP and TP when compared to low-intensity exercise. Instead, the doubled running distance had no influence on HRV recovery.     

Effects of laboratory versus field exercise on leukocyte subsets and cell adhesion molecule expression in children

In adults, exercise is a powerful and natural stimulator of immune cells and adhesion molecules. Far less is known about these exercise responses during childhood and whether or not exercise in real-life activities of healthy children might influence immune responses. We compared laboratory exercise (10×2 min periods of heavy, constant intensity, cycle ergometer exercise with 1 min rests between exercise in nine subjects, aged 9–15 years) with field exercise (90 min soccer practice in nine different subjects, aged 9–11 years). Blood was sampled before both protocols, 5 min after the 30 min laboratory protocol, and 10–15 min after the 90 min field protocol. Both field and laboratory exercise protocols led to significant (P<0.05) increases in granulocytes, monocytes, and all lymphocyte subpopulations. The mean (SEM) increases were similar for the two protocols except for the significantly greater increase in laboratory compared with field protocols for natural killer cells [142 (39)% vs 12 (16)%, P<0.001] and monocytes [64 (22)% vs 32 (19)%, P<0.001]. Both protocols significantly influenced adhesion molecules (such as CD54) which have not been previously studied in children. However, the adhesion molecule CD8⁺CD62L^– increased to a significantly (P<0.001) greater extent in the laboratory [101 (25)%] versus field [34 (25)%] protocol. Finally, the density of CD62L on lymphocytes significantly decreased with laboratory exercise but showed no change in the field protocol [–20 (3)% vs –3 (3)%, P<0.001]. The rapid and substantial immune response in both laboratory and field protocols suggests that exercise stimulation of the immune system occurs commonly in the real lives of children and may play a role in their overall immune status. Electronic Publication     

Parathyroid function in cardiac transplant patients: evaluation during physical exercise

The survival rate of heart transplant patients has increased considerably since the development of new immunosuppressive drugs. In the long term, however, cardiac transplantation results in a high incidence of osteoporosis which represents a major functional handicap. To examine whether patients in the early stages have impaired phosphocalcic metabolism, intact parathyroid hormone (PTH 1–84), native osteocalcin, ionized Ca⁺⁺ and pH were measured at rest and during muscular exercises a dynamic test used to override circadian and ultradian PTH variations. A group of 12 patients receiving the usual immunosuppressive therapy, which is mainly an association of cyclosporin and prednisolone, and 8 sedentary control subjects performed a square-wave endurance test at the same relative intensity for 30 min. No patient had previous bone disease and the period since transplantation was 12.2 ± 2.7 months. For the transplant patients, initial PTH concentrations and responses to exercise were higher (P < 0.01) compared to the control subjects with a dramatic increase after 10 min of recovery. From higher (P < 0.001) resting concentrations, osteocalcin further increased during exercise (P < 0.01) in the heart transplant group but not in the control subjects. In both groups pH showed the same time-course with a rapid fall during exercise (P < 0.05) and Ca⁺⁺ concentrations increased during the exercise period. (P < 0.01 for patients;P < 0.05 for controls) with a significant fall in both groups after 10 min of recovery (P < 0.01). Despite a tendency for initial Ca⁺⁺ concentrations to be lower in the patients (P < 0.07), there were no significant differences between both groups either for pH or for Ca⁺⁺. These results show that in the early stage of transplantation, the patients under immunosuppressive therapy have moderate hyperparathyroidism which precedes the serious complications of bone loss in long-term transplant patients.     

Influence of glucose ingestion by humans during recovery from exercise on substrate utilisation during subsequent exercise in a warm environment

Carbohydrate (CHO) ingestion during short-term recovery from prolonged running has been shown to increase the capacity for subsequent exercise in a warm environment. The aim of this study was to examine the effects of the amount of glucose given during recovery on substrate storage and utilisation during recovery and subsequent exercise in a warm environment. A group of 11 healthy male volunteers took part in two experiments in a controlled warm environment (35°C, 40% relative humidity), 1 week apart. On each occasion the subjects completed two treadmill runs (T1 and T2) at a speed equivalent to 60% of maximal oxygen uptake, for 90 min, until they were fatigued, or until aural temperature (T _aur) reached 39°C. The two runs were separated by a 4 h recovery period (REC), during which subjects consumed 55 g of naturally enriched [U-¹³C]-glucose in the form of a 7.5% carbohydrate-electrolyte solution (CES, mass of solution 667 g) immediately after T1. The subjects then consumed either: the same quantity of CES, or an equivalent volume of an electrolyte placebo, at 60, 120 and 180 min during REC, providing a total of 220 g (C220) or 55 g (C55) of [U-¹³C]-glucose, respectively. Expired gases were collected at 15 min intervals during exercise and 60 min intervals during REC, for determination of total CHO and fat oxidation by indirect respiratory calorimetry, and orally ingested [U-¹³C]-glucose oxidation, estimated from the ¹³C:¹²C ratio of expired CO₂. Substrate metabolism did not differ between conditions during T1. Despite the fact that total CHO (P<0.05) and ingested glucose oxidation (P<0.01) were greater during REC of the C220 condition, glycogen synthesis was estimated to be approximately fivefold greater (P<0.01) than in the C55 condition. During T2 the rate of total CHO oxidation was higher (P<0.01) and total fat oxidation lower (P<0.01) at all times during the C220 compared to the C55 condition. The greater CHO oxidation during C220 appeared to be met from ingested sources, as the rate of [U-¹³C]-glucose oxidation was greater (P<0.01) at all times during T2, compared to C55. Whilst more of the ingested substrate remained unoxidised on completion of T2 during C220, exercise duration was similar in the two experimental conditions, and was limited by thermoregulatory incapacity (T _aur>39°C) rather than substrate availability per se. Electronic Publication     

A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise

In this study we compared substrate oxidation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise with similar overall (i.e. work and recovery) oxygen consumption (V˙O₂). Physically active subjects (n?=?7) completed 90?min of an intermittent intense (12?s work:18?s recovery) and a continuous submaximal treadmill running protocol on separate days. In another experiment (n?=?5) we compared oxygen availability in the vastus lateralis muscle between these two exercise protocols using near-infrared spectroscopy. Initially, overall V˙O₂ (i.e. work and recovery) was matched, and from 37.5?min to 67.5?min of exercise was similar, although slightly higher during continuous exercise (8%; P??1?·?kg^?1] and continuous submaximal [0.85 (0.01)?kJ?·?min^?1?·?kg^?1] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (V˙O_2peak), was 68.1 (2.5)% V˙O_2peak and 71.8 (1.8)% V˙O_2peak for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P?P?P?P?P?r?=?0.72; P?V˙O₂ and identical energy expenditure.     

Effect of catecholamines on the ventricular myocyte action potential in raised extracellular potassium

We describe the relationship between catecholamines and raised extracellular potassium ([K⁺]_o) on action potential parameters and calcium currents in isolated ventricular myocytes of the guinea-pig and relate these findings to the problem of understanding how the heart is protected from exercise-induced hyperkalaemia ([K⁺]_a up to 8.5 mm ). Action potential duration (APD₉₀), amplitude and upstroke velocity were recorded in stimulated (2Hz) guinea-pig ventricular myocytes using whole-cell patch electrode recordings (37 ±C). Cells were superfused with normal K⁺Tyrode and with raised K⁺Tyrode in the presence of either noradrenaline, adrenaline or raised calcium. Inward calcium current was measured using voltage clamp. Raised K⁺(8, 12, 16 mm K⁺Tyrode) caused a significant (P < 0.01) depolarisation, shortened the APD₉₀ and decreased the action potential amplitude and upstroke velocity. In raised K⁺Tyrode addition of noradrenaline (0.08–0.1 μm ) or adrenaline (0.1–0.2 μm ) increased action potential amplitude (P < 0.01), APD₉₀ (P < 0.01) and upstroke velocity (P < 0.01) (measured only in 16 mm K⁺Tyrode). In 12 mm K⁺Tyrode raised Ca²⁺(5–6 mm ) increased action potential amplitude (P < 0.05) and shortened APD₉₀ (P < 0.05). Addition of NA (0.08–0.1 μm ) increased the inward Ca²⁺current. All effects were fully reversible. In raised [K⁺]_o increases in catecholamines and [Ca²⁺]_o cause changes in action potential parameters that would be expected to maintain propagation of the cardiac action potential in the whole heart. Thus, in the ventricular myocyte the increase in conductance to Ca²⁺caused by catecholamines may be one factor that is important in minimising the potentially adverse effects of exercise-induced hyperkalaemia.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Effects of substrate-free anoxia and veratridine on intracellular calcium concentration in isolated rat ventricular cardiomyocytes

Cytosolic free Ca²⁺ concentration ([Ca²⁺]_i) was measured in freshly isolated rat ventricular cardiomyocytes during substrate-free anoxia. Cardiomyocytes were loaded with fura-2 and incubated in an anoxic chamber in which a pO₂ equal to 0 mmHg was realized by inclusion of Oxyrase. [Ca²⁺]_i was measured in individual cells using digital imaging fluorescence microscopy. During anoxia, the shape of cardiomyocytes changed from a relaxed-elongated form into a rigor configuration within 15 min after the onset of anoxia. After the cells had developed the rigor state, a delayed rise in [Ca²⁺]_i reached a stable maximal level within 45 min. The mean values for the pre-anoxic and maximal anoxic [Ca²⁺ _i were 52±3 nM (N=42) and 2115±59 nM (N=45), respectively. The purported Na⁺ overload blocker R 56865, significantly reduced maximal anoxic [Ca²⁺]_i to 553±56 nM (P<0.05), implicating a role of elevated intracellular Na⁺ in the anoxia-induced increase in [Ca²⁺]_i. Veratridine (30 M), which induces Na⁺ overload, increased [Ca²⁺]_i to 787±39 nM. The compound R 56865 reduced veratridine-induced increases in [Ca²⁺]_i to 152±38 nM. Upon reperfusion, after 45 min of anoxia, two distinct responses were observed. Most often, [Ca²⁺]_i decreased upon reperfusion without a change in morphology or viability, while in the minority of cases, [Ca²⁺]_i increased further followed by hypercontraction and loss of cell viability. The mean value for [Ca²⁺]_i 10 min after reperfusion of the former group, was 752±46 nM (N=38). The cardiomyocyte cell shape could be followed by monitoring changes in the total fura-2 fluorescence (340+380 nm signal). Within 15 min after the onset of anoxia, the total fluorescence signal increased suddenly, before [Ca²⁺]_i started to rise, coinciding with the onset of rigor contraction induced by ATP depletion.     

The relationship between plasma potassium concentration and muscle torque during recovery following intense exercise

The present study investigated the relationship between plasma potassium ion concentration ([K⁺]) and skeletal muscle torque during three different 15-min recovery periods after fatigue induced by four 30-s sprints. Four males and one female completed the multiple sprint exercise on three separate days; recovery was passive, i.e. no cycling exercise (PRec), active cycling at 30% peak oxygen consumption $\dot V$ O_2peak (30% Rec) and active cycling at 60% $\dot V$ O_2peak (60% Rec). Plasma [K⁺] was measured from blood sampled from an antecubital vein of subjects at rest and at 0, 3, 5, 10 and 15 min into each recovery. Isokinetic leg strength was measured at rest and at 1, 6, 11 and 16 min during each recovery. Following the exhaustive sprints, [K⁺] increased significantly from an average mean (SEM) resting value of 3.81 (0.07) mmol?·?l^?1 to 4.48 (0.19) mmol?·?l^?1 (P?+] returned to resting levels within 3 min following the fourth sprint. However, in the two active recovery conditions plasma [K⁺] increased over the remainder of the recovery periods to 4.36 (0.12) mmol?·?l^?1 in the 30% Rec condition and 4.62 (0.12) mmol?·?l^?1 in the 60% Rec condition, the latter being significantly higher than the former (P?P?P?+] across all three recovery conditions, muscle torque recovery was significantly different in only the 30% Rec condition. In summary, recovery of peak levels of muscle torque following fatiguing exercise does not appear to follow changes in plasma [K⁺].     

Lactate uptake by forearm skeletal muscles during repeated periods of short-term intense leg exercise in humans

We investigated the role of the forearm skeletal muscles in the removal of lactate during repeated periods of short-term intensive leg exercise, i.e. a force-velocity (FV) test known to induce a marked accumulation of lactate in the blood. The leg FV test was performed by seven untrained male subjects. Arterial and venous blood samples for determination of arterial ([la^–]_a) and venous ([la^–]_v) plasma lactate concentrations were concomitantly taken at rest before the test, during the FV test at the end of each period of intensive exercise just before the 5-min between-sprint recovery period, and after the completion of the test at 2, 4, 6, 8, 10, 15, and 20 min of the final recovery. The arteriovenous difference in concentration for plasma lactate ([la^–]_a–v) was determined for each blood sample. During the test, [la^–]_a and [la^–]_v increased significantly (P < 0.001;P < 0.001) with significantly higher values for [la^–]_a (P < 0.001). At the onset of the test, [la^–]_a–v became positive and increased up to a braking force of 6 kg, correlating significantly with [la^–]_a (r = 0.61,P < 0.001) with power (r = 0.58,P < 0.001) during the test. At the end of the test, [la^–]_a, [la^–]_v and [la^–]_a–v decreased (P < 0.001;P < 0.001;P < 0.001 respectively) but were still higher than the basal values after 20-min of passive recovery. In conclusion, forearm skeletal muscles would seem to have been involved in the removal of lactate from the blood during the leg FV test, with an increase in lactate uptake proportional to the increase in plasma lactate concentration and power.     

Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition,potassium and lactate

Summary Six healthy men performed sustained static handgrip exercise for 2 min at 40% maximal voluntary contraction followed by a 6-min recovery period. Heart rate (f _c), arterial blood pressures, and forearm blood flow were measured during rest, exercise, and recovery. Potassium ([K⁺]) and lactate concentrations in blood from a deep forearm vein were analysed at rest and during recovery. Mean arterial pressure (MAP) andf _c declined immediately after exercise and had returned to control levels about 2 min into recovery. The time course of the changes in MAP observed during recovery closely paralleled the changes in [K⁺] (r=0.800,P<0.01), whereas the lactate concentration remained elevated throughout the recovery period. The close relationship between MAP and [K⁺] was also confirmed by experiments in which a 3-min arterial occlusion period was applied during recovery to the exercised arm by an upper arm cuff. The arterial occlusion affected MAP whilef _c recovered at almost the same rate as in the control experiment. Muscle biopsies were taken from the brachioradialis muscle and analysed for fibre composition and capillary supply. The MAP at the end of static contraction and the [K⁺] appearing in the effluent blood immediately after contraction were positively correlated to the relative content of fast twitch (% FT) fibres (r=0.886 for MAP vs %FT fibres,P<0.05 andr=0.878 for [K⁺] vs %FT fibres,P<0.05). Capillary to fibre ratio showed an inverse correlation to % FT fibres (r=–0.979,P<0.01). These results indicated that activation of FT rather than slow twitch fibres during static contraction induced a more marked arterial pressure reflex. It was concluded that the arterial pressure reflex would seem to be mediated through stimulation of unmyelinized free nerve endings in the contracted muscle. The [K⁺] would appear to be a more likely candidate than lactate as a mediator for this pressure reflex.     

Haemolysis caused by alterations of α- and β-spectrin after 10 to 35 min of severe exercise

The pathophysiology of exercise related haemolysis is not thoroughly understood. We investigated whether exercise related haemolysis (1) is associated with alterations of red blood cell (RBC) membrane proteins similar to those found in inherited anaemic diseases, (2) can be induced with a non-running exercise mode, (3) is related to exercise intensity, and (4) coincides with indicators of oxidative stress. In ten triathletes [median (P25/P75-percentiles) age: 28.0 (26.3/28.5) years, height: 1.84 (1.78/1.87) m, body mass: 78.5 (74.8/80.8) kg, maximal oxygen uptake: 60.0 (57.3/64.8) ml kg⁻¹ min⁻¹], haptoglobin, α- and β-spectrin bands, malondialdehyde (MDA) and H₂O₂-induced chemiluminescence (H₂O₂-Chem) were determined immediately pre- and post-both, a 35 min low intensity and a high intensity cycling exercise [240 (218/253) vs 290 (270/300) W, P<0.05) requiring similar amounts of metabolic energy [28.3 (25.9/29.9) vs 24.9 (18.4/30.5) kJ kg⁻¹, P>0.05]. At high exercise intensity haptoglobin [1.10 (0.81/2.53) vs 1.01 (0.75/2.00) g l⁻¹] decreased (P<0.05) whilst MDA [2.80 (2.65/3.20) vs 3.13 (2.78/3.31) nmol ml⁻¹] and H₂O₂-Chem [29.70 (22.55/37.10) vs 37.25 (35.20/52.63) rel. U min] increased (P<0.05), coinciding with the disappearance of the spectrin bands in six out of ten gels. No corresponding changes were found at low intensity exercise. Ten to 35 min of non-running exercise in a regularly used intensity domain causes intra-vascular haemolysis associated with alterations in the RBC membrane proteins similar to those found after in vitro oxidative stress and in inherited anaemic diseases like Sphaerocytosis and Fanconi’s anaemia.     

Effect of O2 availability on neuroendocrine variables at rest and during exercise: O2 breathing increases plasma prolactin

Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O₂ (HE), 14% O₂ (HO) or normoxic gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH₃), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA⁻], partial pressure of oxygen (PO₂), oxygen saturation (SO₂), partial pressure of carbon dioxide and pH in capillary blood. ThePO₂ andSO₂ were augmented in HE and decreased in HO (P ≤ 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P ≤ 0.01). Heart rate (HR) and [LA⁻] were higher during exercise in HO (P ≤ 0.01). In all trials, NH₃, NA, A, T, GH and ACTH increased during exercise (P ≤ 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA⁻] and HR. Responses of plasma NH₃, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in bloodSO₂ during hyperoxia. Deceased     

Effect of water ingestion on cardiovascular and thermal responses to prolonged cycling and running in humans: a comparison

The aim of this investigation was to examine the effect of water ingestion on physiological responses to prolonged cycling (CYC) and running (RUN). A group of 11 men with mean (SEM) maximal oxygen uptake (V˙O_2max) 48.5 (1.8) ml·kg^–1·min^–1 on a cycle-ergometer and 52.1 (2.2) ml·kg^–1·min^–1 on a treadmill (P<0.01) exercised for 90 min on four occasions, twice on each ergometer, at 60% of mode specific V˙O_2max. No fluid was taken (D) in one trial on each ergometer, whereas 60% of fluid losses were replaced by drinking water in the other trial (W). In CYC, water ingestion attenuated the change in cardiac output ( ) and the reduction in stroke volume (ΔSV) [ΔSV: –22.7 (3.8) in D, –10.7 (2.9) ml·beat^–1 in W, P<0.01; : –1.9 (0.5) in D, –0.2 (0.4) l·min^–1 in W at 85 min, P<0.01], but did not affect rectal temperature [T _re at 90 min: 38.8 (0.1)°C in D, 38.7 (0.1)°C in W]. In contrast, fluid replacement reduced hyperthermia in RUN [T _re at 90 min: 39.6 (0.2) in D, 39.1 (0.2)°C in W, P<0.01], and this was linked with a higher skin blood flow [RUN-W 88.9 (8.5), RUN-D 70.7 (8.4)%, P<0.05]. The and ΔSV were also attenuated with water ingestion in this mode of exercise (P<0.05). It is concluded that water ingestion improves physiological function in both cycling and running, but that the underlying mechanism is different in the two modes of exercise. Electronic Publication     

Contribution of pH,diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip

The relative importance of pH, diprotonated phosphate (H₂PO₄^?) and potassium (K⁺) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K⁺] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L^?1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H₂PO₄^?] increased 8.4 ± 2 mmol kg^?1 and the venous [H₂PO₄^?] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L^?1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H₂PO₄^?] as well as a low intracellular and venous pH. However, venous [K⁺] and [H₂PO₄^?] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K⁺] to 5.8 ± 0.2 mmol L^?1, the intracellular and extracellular [H₂PO₄^?] by 20 ± 5 mmol kg^?1 and to 0.20 ± 0.02 mmol L^?1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.     

Change in post-exercise vagal reactivation with exercise training and detraining in young men

We studied the effects of aerobic exercise training and detraining in humans on post-exercise vagal reactivation. Ten healthy untrained men trained for 8 weeks using a cycle ergometer [70% of initial maximal oxygen uptake ( ) for 1 h, 3–4 days·week^–1] and then did not exercise for the next 4 weeks. Post-exercise vagal reactivation was evaluated as the time constant of the beat-by-beat decrease in heart rate during the 30 s (t₃₀) immediately following 4 min exercise at 80% of ventilatory threshold (VT). The and the oxygen uptake at VT had significantly increased after the 8 weeks training programme (P<0.0001, P<0.001, respectively). The t₃₀ had shortened after training, and values after 4 weeks and 8 weeks of training were significantly shorter than the initial t₃₀ (P<0.05, P<0.01, respectively). The change in the t₃₀ after 8 weeks of training closely and inversely correlated with the initial t₃₀ (r=–0.965, P<0.0001). The reduced t₃₀ was prolonged significantly after 2 weeks of detraining, and had returned almost to the baseline level after a further 2 weeks of detraining. These results suggest that aerobic exercise training of moderate intensity accelerates post-exercise vagal reactivation, but that the accelerated function regresses within a few weeks of detraining. Electronic Publication