Serial effects of high-resistance and prolonged endurance training on Na+–K+ pump concentration and enzymatic activities in human vastus lateralis

The purpose of this study was to compare two contrasting training models, namely high-resistance training and prolonged submaximal training on the expression of Na⁺–K+ ATPase and changes in the potential of pathways involved in energy production in human vastus lateralis. The high-resistance training group (VO _2peak = 45.3 ± 1.9 mL kg^?1 min^?1, mean ± SE, n = 9) performed three sets of six to eight repetitions maximal, each of squats, leg presses and leg extensions, three times per week for 12 weeks, while the prolonged submaximal training group (VO _2peak = 44.4 ± 6.6 mL kg^?1 min^?1, n = 7) cycled 5–6 times per week for 2 h day^?1 at 68% VO _2peak for 11 weeks. In the HRT group, Na⁺–K⁺ ATPase (pmol g^?1 wet wt), measured with the ³H-ouabain binding technique, showed no change from 0 (289 ± 22) to 4 weeks (283 ± 15), increased (P < 0.05) by 16% at 7 weeks and remained stable until 12 weeks (319 ± 19). For prolonged submaximal training, a 22% increase (P < 0.05) was observed from 0 (278 ± 31) until 3 weeks (339 ± 29) with no further changes observed at either 9 weeks (345 ± 25) or 11 weeks (359 ± 34). In contrast to high-resistance training, where a 15% increase (P < 0.05) was observed, only in the maximal activity of phosphorylase, prolonged submaximal training resulted in increases in malate dehydrogenase, β-hydroxyl-CoA dehydrogenase, hexokinase and phosphofructokinase. In contrast to high-resistance training which failed to result in an increase in VO _2peak, prolonged submaximal training increased VO _2peak by ≈15%. Only for prolonged exercise training was a relationship observed for VO _2peak and Na⁺–K⁺-ATPase (r = 0.59; P < 0.05). Correlations between VO _2peak and mitochondrial enzyme activities were not significant (P > 0.05) for either training programme. It is concluded that although both training programmes stimulate an up-regulation in Na⁺–K⁺ ATPase concentration, only the prolonged submaximal training programme enhances the potential for β-oxidation, oxidative phosphorylation and glucose phosphorylation.     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Cardiac output but not stroke volume is similar in a Wingate and \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} test in young men

Wingate test (WT) training programmes lasting 2?C3?weeks lead to improved peak oxygen consumption. If a single 30?s WT was capable of significantly increasing stroke volume and cardiac output, the increase in peak oxygen consumption could possibly be explained by improved oxygen delivery. Thus, we investigated whether a single WT increases stroke volume and cardiac output to similar levels than those obtained at peak exercise during a graded cycling exercise test (GXT) to exhaustion. Fifteen healthy young men (peak oxygen consumption 45.0?±?5.3?ml?kg^?1?min^?1) performed one WT and one GXT on separate days in randomised order. During the tests, we estimated cardiac output using inert gas rebreathing (nitrous oxide and sulphur hexafluoride) and subsequently calculated stroke volume. We found that cardiac output was similar (18.2?±?3.3 vs. 17.9?±?2.6?l?min^?1; P?=?0.744), stroke volume was higher (127?±?37 vs. 94?±?15?ml; P?<?0.001), and heart rate was lower (149?±?26 vs. 190?±?12 beats?min^?1; P?<?0.001) at the end (27?±?2?s) of a WT as compared to peak exercise during a GXT. Our results suggest that a single WT produces a haemodynamic response which is characterised by similar cardiac output, higher stroke volume and lower heart rate as compared to peak exercise during a GXT.     

Muscle fatigue and excitation-contraction coupling responses following a session of prolonged cycling

Aim: The mechanisms underlying the fatigue that occurs in human muscle following sustained activity are thought to reside in one or more of the excitation–contraction coupling (E–C coupling) processes. This study investigated the association between the changes in select E–C coupling properties and the impairment in force generation that occurs with prolonged cycling. Methods: Ten volunteers with a peak aerobic power () of 2.95 ± 0.27 L min^?1 (mean ± SE), exercised for 2 h at 62 ± 1.3%. Quadriceps function was assessed and tissue properties (vastus lateralis) were measured prior to (E1‐pre) and following (E1‐post) exercise and on three consecutive days of recovery (R1, R2 and R3). Results: While exercise failed to depress the maximal activity (V_max) of the Na⁺,K⁺‐ATPase (P = 0.10), reductions (P < 0.05) were found at E1‐post in V_max of sarcoplasmic reticulum Ca²⁺‐ATPase (?22%), Ca²⁺‐uptake (?26%) and phase 1(?33%) and 2 (?38%) Ca²⁺‐release. Both V_max and Ca²⁺‐release (phase 2) recovered by R1, whereas Ca²⁺‐uptake and Ca²⁺‐release (phase 1) remained depressed (P < 0.05) at R1 and at R1 and R2 and possibly R3 (P < 0.06) respectively. Compared with E1‐pre, fatigue was observed (P < 0.05) at 10 Hz electrical stimulation at E1‐post (?56%), which persisted throughout recovery. The exercise increased (P < 0.05) overall content of the Na⁺,K⁺‐ATPase (R1, R2 and R3) and the isoforms β2 (R1, R2 and R3) and β3 (R3), but not β1 or the α‐isoforms (α1, α2 and α3). Conclusion: These results suggest a possible direct role for Ca²⁺‐release in fatigue and demonstrate a single exercise session can induce overlapping perturbations and adaptations (particularly to the Na⁺,K⁺‐ATPase).     

Substrate utilization in sea level residents during exercise in acute hypoxia and after 4 weeks of acclimatization to 4100 m

To investigate the effect of acclimatization to hypoxia on substrate utilization, eight sea level residents were studied during exercise at the same relative (rel) and absolute (abs) work rate as at sea level (SL), under acute (AH), and after 4 weeks exposure to 4100 m altitude (CH). Carbohydrate (CHO) and fat oxidation during exercise at SL were 2.0 ± 0.2 and 0.3 ± 0.0 g min^?1, respectively. At AH_abs and CH_abs CHO oxidation increased (P < 0.05) to 2.5 ± 0.2 and 2.3 ± 0.1 for CHO, and fat oxidation decreased (P < 0.05) to 0.2 ± 0.01 and 0.2 ± 0.01 g min^?1, respectively. Exercise in AH_rel and CH_rel did not cause a change in the relative CHO and fat oxidation compared with SL, the absolute rate of CHO oxidized being 1.7 ± 0.1 and 1.7 ± 0.02 g min^?1, respectively, and fat oxidation was 0.2 ± 0.02 g min^?1 in AC_rel and 0.3 ± 0.02 g min^?1 in CH_rel. In conclusion, substrate utilization is unaffected by AH and CH, when the work rate is matched to the same relative intensity as at SL.     

Exercise thermoregulatory responses following a 28-day sleep-high train-low regimen

The potentiated exercise-sweating rate observed during acute hypoxia is diminished after a sleep-high train-low (SH-TL) regimen. We tested the hypothesis that this attenuation of the sweating response after SH-TL is compensated for by an increase in heat loss via vasodilatation. Nine male subjects participated in a 28-day SH-TL regimen. Before (pre-), and after (post-) the SH-TL protocol, they performed an $ \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} $ test under normoxia and hypoxia. Additionally, pre- and post-SH-TL they completed three 30-min constant-work rate trials on a cycle ergometer. In one trial, the subjects inspired room air while exercising at 50?% of normoxic $ \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} $ (CT). In the remaining trials, subjects exercised in hypoxia (F_IO₂ 12.5?%), either at the same absolute (HAT) or relative (50?% of hypoxic $ \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} $ ) work rate (HRT) as in CT. Despite similar exercise core temperature responses between pre- and post-SH-TL trials, sweating rate was potentiated in HAT pre-SH-TL [CT: 1.97 (0.42); HRT: 1.86 (0.31); HAT: 2.55 (0.53)?mg?cm^?2?min^?1; p?<?0.05]. Post-SH-TL exercise sweating rate was increased for CT, and remained unchanged in HRT and HAT [CT: 2.42 (0.76); HRT: 2.01 (0.33); HAT: 2.59 (0.30)?mg?cm^?2?min^?1]. Pre-SH-TL, the forearm-fingertip skin temperature difference (Tsk_f?f) was higher in HAT than in CT and HRT by ~3.5°C (p?<?0.05). The inter-condition differences in Tsk_f?f were diminished post-SH-TL. In conclusion, the decrease in sweating rate during hypoxic exercise, following a SH-TL regimen, was countered by an increase in vasodilatation (reduced Tsk_f?f), whereas SH-TL enhanced the sweating response during normoxic exercise. The mechanisms underlying these SH-TL-induced alterations in thermoregulatory responses remain to be settled.     

Effects of high-intensity training and acute exercise on in vitro function of rat sarcoplasmic reticulum

To evaluate the effects of high-intensity training and/or a single bout of exercise on in vitro function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of interval running program (final training: 2.5-min running × 4 sets per day, 50 m/min at 10% incline). Following training, SR function, i.e., Ca²⁺-ATPase activity and Ca²⁺-uptake and release rates, was examined in homogenates of the superficial region of the vastus lateralis muscle from rats subjected to a single bout of treadmill running (50 m/min at 10% incline) for 2.5 min or to exhaustion. Training brought about a 12.4% increase (P < 0.05) in SR Ca²⁺-uptake rate in rested muscles. This change was not accompanied by alterations in Ca²⁺-ATPase activity, Ca²⁺-release rate, Ca²⁺ dependence of enzyme and protein contents of Ca²⁺-ATPase and ryanodine receptor. A single bout of high-intensity exercise to exhaustion evoked significant reductions (P < 0.05) in SR function, irrespective of whether or not the animals were trained. For 2.5-min run and exhausted rats, no differences existed between SR functions of untrained and trained muscles. These data suggest that high-intensity training may be capable of enhancing SR Ca²⁺-sequestering ability, and may not protect against decreasing SR function with high-intensity exercise.     

Rate of oxidative phosphorylation in isolated mitochondria from human skeletal muscle: effect of training status

Muscle oxidative function has been investigated in subjects with various training status (VO _{2 max}, 41–72 mL O₂ kg^?1 body wt min^?1, n=10). Mitochondria were isolated from biopsies taken from m. vastus lateralis. Maximal mitochondrial oxygen consumption (QO ₂) and ATP production (MAPR) were measured with polarographic and bioluminometric techniques, respectively. The yield of mitochondria, calculated from the fractional activity of citrate synthase (CS), averaged 26%. With pyruvate + malate, the respiratory control ratio was 5.7 ± 0.4 (X ± SE) and the P/O ratio was 2.83 ± 0.02, which demonstrates that the isolated mitochondria were functionally intact. QO ₂ was significantly correlated to aerobic training status expressed as muscle CS activity (r=0.86), VO _{2 max} (r=0.84) and lactate threshold (r=0.83) but not to the fibre type composition. A highly significant correlation (r=0.93) was observed between ATP production calculated from QO ₂ and MAPR, but ATP production derived from QO ₂ was higher than MAPR both for pyruvate + malate (255%) and for α-ketoglutarate (23%). QO ₂ extrapolated to a temperature of 38 °C averaged 68 mL O₂ min^?1 kg^?1 wet wt, which is similar to previous findings in vitro and in vivo during the post-exercise period. However, calculated muscle O₂ utilization during exercise was three- to fivefold higher than QO ₂ measured on isolated mitochondria. It is suggested that additional factors exist for activation of mitochondrial respiration during exercise. It is concluded that muscle oxidative function can be quantitatively assessed from the respiration of mitochondria isolated from needle biopsy specimens and that QO ₂ is closely correlated to whole-body VO _{2 max}.     

The contribution of the sarcoplasmic reticulum Ca2+-transport ATPase to caffeine-induced Ca2+ transients of murine skinned skeletal muscle fibres

The present study was carried out to investigate the contribution of the Ca²⁺-transport ATPase of the sarcoplasmic reticulum (SR) to caffeine-induced Ca²⁺ release in skinned skeletal muscle fibres. Chemically skinned fibres of balb-C-mouse EDL (extensor digitorum longus) were exposed for 1 min to a free Ca²⁺ concentration of 0.36 μM to load the SR with Ca²⁺. Release of Ca²⁺ from the SR was induced by 30 mM caffeine and recorded as an isometric force transient. For every preparation a pCa/force relationship was constructed, where pCa = −log₁₀ [Ca²⁺]. In a new experimental approach, we used the pCa/force relationship to transform each force transient directly into a Ca²⁺ transient. The calculated Ca²⁺ transients were fitted by a double exponential function: Y ₀ + A ₁⋅exp (−t/t ₁) + A ₂⋅exp(t/t ₂), with A ₁ < 0 < A ₂, t ₁ < t ₂ and Y ₀, A ₁, A ₂ in micromolar. Ca²⁺ transients in the presence of the SR Ca²⁺-ATPase inhibitor cyclopiazonic acid (CPA) were compared to those obtained in the absence of the drug. We found that inhibition of the SR Ca²⁺-ATPase during caffeine-induced Ca²⁺ release causes an increase in the peak Ca²⁺ concentration in comparison to the control transients. Increasing CPA concentrations prolonged the time-to-peak in a dose-dependent manner, following a Hill curve with a half-maximal value of 6.5 ± 3 μM CPA and a Hill slope of 1.1 ± 0.2, saturating at 100 μM. The effects of CPA could be simulated by an extended three-compartment model representing the SR, the myofilament space and the external bathing solution. In terms of this model, the SR Ca²⁺-ATPase influences the Ca²⁺ gradient across the SR membrane in particular during the early stages of the Ca²⁺ transient, whereas the subsequent relaxation is governed by diffusional loss of Ca²⁺ into the bathing solution. Received: 2 February 1996/Accepted: 1 April 1996     

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

We examined the influence of hyperoxia on peak oxygen uptake (V˙O _2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O₂ (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O₂ tension (P_aO ₂) increased from 13.5 ± 0.3 (x ± SE) to 41.6 ± 0.3 kPa, O₂ saturation (S_aO ₂) from 98 ± 0.1 to 100 ± 0.1%, and O₂ concentration (C_aO ₂) from 177 ± 4 to 186 ± 4 mL L^–1 (all P < 0.01). Peak exercise femoral venous PO ₂ (P_vO ₂) was also higher in HiOX (3.68 ± 0.06 vs. 3.39 ± 0.7 kPa; P < 0.05), indicating a higher O₂ diffusion driving pressure. HiOX femoral venous O₂ saturation averaged 36.8 ± 2.0% as opposed to 33.4 ± 1.5% in NOX (P < 0.05) and O₂ concentration 63 ± 6 vs. 55 ± 4 mL L^–1 (P < 0.05). Peak exercise quadriceps blood flow (Q˙_leg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 ± 0.5 vs. 7.3 ± 0.9 L min^–1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O₂ delivery to the limb (Q˙_leq times C_aO ₂) was not significantly different in HiOX and NOX. V˙O _2peak of the exercising limb averaged 890 mL min^–1 in NOX and 801 mL min^–1 in HiOX (n.s.) corresponding to 365 and 330 mL min^–1 per kg active muscle, respectively. The V˙O _2peak-to-P_vO ₂ ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O₂ conductance. We conclude that the similar V˙O _2peak values despite higher O₂ driving pressure in HiOX indicates a peripheral limitation for V˙O _2peak. This may relate to saturation of the rate of O₂ turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O₂ conductance.     

Influence of ingested fluid volume on physiological responses during prolonged exercise

The effect of different rates of fluid ingestion on heart rate, rectal temperature, plasma electrolytes, hormones and performance was examined during prolonged strenuous exercise conducted at 21 °C. Seven well-trained males (24 ± 1 yr; 68.6 ± 2.9 kg; Vo ₂ peak = 4.69 ± 0.17 L min^?1; mean ± SEM) cycled for 2 h at 69 ± 1% Vo ₂ peak while receiving either no fluid replacement (NF), a volume of water estimated to prevent body weight loss (FR-100 = 2.32 ± 0.10 L 2 h^?1) or 50% of this volume (FR-50 = 1.16 ± 0.05 L 2 h^?1). The 2-h exercise bout was followed by a ride to exhaustion at a workload estimated to be 90% Vo ₂ peak. After 2 h of exercise, NF was associated with a 3.2 ± 0.1% weight loss, while FR-50 and FR-100 resulted in losses of 1.8 ± 0.1 and 0.1 ± 0.1%, respectively. Compared with FR-100, heart rate and rectal temperature were elevated (P < 0.05) during the second hour of exercise in NF, with FR-50 intermediate. Reductions in plasma volume during exercise were greater in NF and FR-50, compared with FR-100 and plasma sodium concentration was elevated in NF, decreased slightly in FR-100, with FR-50 intermediate. Plasma renin activity, aldosterone and atrial natriuretic peptide increased to similar extents in the three trials. Plasma vasopressin remained unchanged for FR-100, increased for NF, with intermediate values for FR-50. Exercise time to exhaustion at 90% Vo ₂ peak was longer in FR-100 (328 ± 93 s) than NF (171 ± 75 s) with FR-50 (248 ± 107 s) not significantly different from either FR-100 or NF. In conclusion, the responses of heart rate, rectal temperature, plasma sodium, and vasopressin during, and performance following, prolonged cycling exercise conducted at 21 °C are related to the amount of fluid ingested (i.e. the degree of dehydration).     

Central and peripheral cardiovascular adaptations to exercise in endurance‐trained children

Stroke volume (SV) response to exercise depends on changes in cardiac filling, intrinsic myocardial contractility and left ventricular afterload. The aim of the present study was to identify whether these variables are influenced by endurance training in pre‐pubertal children during a maximal cycle test. SV, cardiac output (Doppler echocardiography), left ventricular dimensions (time–movement echocardiography) as well as arterial pressure and systemic vascular resistances were assessed in 10 child cyclists (VO_2max: 58.5 ± 4.4 mL min^?1 kg^?1) and 13 untrained children (UTC) (VO_2max: 45.9 ± 6.7 mL min^?1 kg^?1). All variables were measured at the end of the resting period, during the final minute of each workload and during the last minute of the progressive maximal aerobic test. At rest and during exercise, stroke index was significantly higher in the child cyclists than in UTC. However, the SV patterns were strictly similar for both groups. Moreover, the patterns of diastolic and systolic left ventricular dimensions, and the pattern of systemic vascular resistance of the child cyclists mimicked those of the UTC. SV patterns, as well as their underlying mechanisms, were not altered by endurance training in children. This result implied that the higher maximal SV obtained in child cyclists depended on factors influencing resting SV, such as cardiac hypertrophy, augmented myocardium relaxation properties or expanded blood volume.     

Increased finger arterial blood pressure after exercise detraining in women with parental hypertension: autonomic tasks

The effects of exercise detraining on resting finger arterial blood pressure (BP), the carotid-cardiac vagal baroreflex, and BP and heart rate (HR) responses to mental arithmetic and forehead cold exposure were studied in young (19 ± 1.1 years) normotensive women with parental history of hypertension. Following 8 weeks of aerobic exercise for 25 min, 3 days week^?1 at an intensity of 60% V˙O _{2 peak}, subjects ceased training for 6–8 weeks. After detraining, V˙O _{2 peak} (mL kg^?1 min^?1) was reduced by 11.5% (41.1 ± 6.9 to 36.4 ± 4.8) coincident with an ≈ 10 %increase in submaximal exercise heart rate. Responses to the laboratory tasks were then compared. Detraining was accompanied by increases (P <0.05) in resting systolic (SBP) (113.6 ± 8.9 to 121.2 ± 9.0), diastolic (DBP) (63.0 ± 8.4 to 68.3 ± 6.8), and mean arterial (MAP) (78.7 ±8.4 to 84.2 ± 7.3) BP (mmHg). None of the above changes occurred in sedentary matched-control subjects. Systolic blood pressure was elevated during forehead cold exposure and MAP was elevated during mental arithmetic after detraining, but the rates of response and recovery for SBP, DBP and MAP were not altered by detraining. Despite higher submaximal exercise HR after detraining, HR responses to autonomic challenges, including the carotid-cardiac vagal baroreflex, were unchanged between training and detraining. Our results indicate that exercise detraining increases resting finger arterial BP in young normotensive women at risk for hypertension with no effects on the rate of response or recovery of heart rate and BP during autonomic tasks known to elicit sympathetic and carotid-cardiac vagal activities in this population. The use of auscultatory brachial artery pressures in a similar study of women diagnosed with hypertension will clarify the clinical meaning of our findings.     

Enhancement of the finger cold-induced vasodilation response with exercise training

Cold-induced vasodilatation (CIVD) is a cyclical increase in finger temperature that has been suggested to provide cryoprotective function during cold exposures. Physical fitness has been suggested as a potential factor that could affect CIVD response, possibly via central (increased cardiac output, decreased sympathetic nerve activity) and/or peripheral (increased microcirculation) cardiovascular and neural adaptations to exercise training. Therefore, the purpose of this study was to investigate the effect of endurance exercise training on the CIVD response. Eighteen healthy males trained 1 h d⁻¹ on a cycle ergometer at 50% of peak power output, 5 days week⁻¹ for 4-weeks. Pre, Mid, Post, and 10 days after the cessation of training and on separate days, subjects performed an incremental exercise test to exhaustion (\mathop V ^· \textO_2\textpeak ), (\mathop V\limits^{ \cdot }\!\! {\text{O}}_{{2{\text{peak}}}} ), and a 30-min hand immersion in 8°C water to examine their CIVD response. The exercise-training regimen significantly increased \mathop V ^·\textO_2\textpeak \mathop V\limits^{ \cdot }\!\!{\text{O}}_{{2{\text{peak}}}} (Pre: 46.0 ± 5.9, Mid: 52.5 ± 5.7, Post: 52.1 ± 6.2, After: 52.6 ± 7.6 ml kg⁻¹ min⁻¹; P < 0.001). There was a significant increase in average finger skin temperature (Pre: 11.9 ± 2.4, After: 13.5 ± 2.5°C; P < 0.05), the number of waves (Pre: 1.1 ± 1.0, After: 1.7 ± 1.1; P < 0.001) and the thermal sensation (Pre: 1.7 ± 0.9, After: 2.5 ± 1.4; P < 0.001), after training. In conclusion, the aforementioned endurance exercise training significantly improved the finger CIVD response during cold-water hand immersion.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

Diabetes affects blood pressure and heart rate responses during acute hypothermia

Many diabetics are cold-intolerant and experience dramatic changes in normal systemic function during hypothermia. Little is known of the cardiovascular adjustments in diabetics exposed to an acute cold stress. In an effort to identify the alterations in mean arterial blood pressure (MAP) and heart rate (HR) in the diabetic during environmental cooling (10 ± 2 °C), we compared the in vivo MAP and HR responses of urethane-anaesthetized (1.5 g kg^?1), streptozotocin-diabetic (STZ, 65 mg kg^?1, n = 12) and control (CON, n = 10) rats during acute hypothermia. MAP was measured directly via an indwelling carotid artery cannula and HR was calculated from the peak systolic pressure waves. Overall, the STZ rats were more cold-intolerant than CON as evidenced by the greater rate of decline in colonic temperature (T_c) from 36 to 28 °C (STZ, 0.16 °C min^?1 vs. CON, 0.06 °C min^?1; P < 0.05). Prior to cooling, HR was significantly lower (P < 0.05) in STZ (282 ± 9 beats min^?1) than in CON rats (399 ± 24 beats min^?1); however, during the acute hypothermic period, HR displayed a similar rate of decline in both groups. With respect to MAP, both groups demonstrated similar pre-experimental pressor responses (CON, 81.7 ± 5.4 vs. STZ, 83.2 ± 5.1 mmHg, P > 0.05). During progressive hypothermia, MAP gradually increased (P < 0.05) in the CON group from baseline (T_c = 36 °C) and reached peak values (118.4 ± 2.5 mmHg) at T_c = 30 °C, while the STZ group failed to exhibit any cold pressor response. At the conclusion of the experiment (T_c = 28 °C), the STZ group pressor response to hypothermia was not different from baseline (T_c = 36 °C, 83.2 ± 5.1 vs. T_c = 28 °C, 77.4 ± 3.4 mmHg; P > 0.05). The absence of any pressor response in the diabetic group during progressive hypothermia reflects the poor overall vasoconstrictive capacity to cooling and could partially explain the rapid decline of core temperature in this group.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

Effects of intensified endurance training on the concentration of Na,K-ATPase and Ca-ATPase in human skeletal muscle

Thirty-nine moderately endurance trained males increased their normal training programme of 2.2 h week^-1 with an average training intensity of 65 % of maximum heart rate (HR_max) to 2.7 h week^-1 and a mean intensity of 78% of HR_max. Performance tests and measurements of the total concentrations of Na,K-ATPase (³H-ouabain binding) and Ca-ATPase, fibre type distribution and fibre area were performed in biopsies from the vastus lateralis muscle before and after increased training. The 6 weeks of training elevated Vo_2max from 54.9 + 3.1 to 58.3±3.0 ml 0₂ min^-1 kg^-1 (P < 0.0001). Exercise time to exhaustion at 86% of Fo_2max (pre-training) increased from 35 ±8 to 61 + 17 min (P < 0.0001). The concentration of Ca-ATPase was unaffected by the intensified training (6.74 ± 1.03 vs. 6.68+ 1.07 nmol g wet wt^-1), but the concentration of Na,K-ATPase increased from 307±43 to 354 + 59 pmol g wet wt ' (P < 0.0001). The relative distribution of FT-fibres was correlated with the concentration of Ca-ATPase (r = 0.72, P < 0.0001). The data support the view that intensive training induces an upregulation of the concentration of skeletal muscle Na,K-ATPase, but no change in the total capacity for reaccumulation of Ca²⁺ into the SR. There was no correlation between the concentrations of Na,K-ATPase, Ca-ATPase and indices of endurance performance.     

Effect of endurance training on muscle microvascular filtration capacity and vascular bed morphometry in the elderly

Aim: Exercise training is a strong stimulus for vascular remodelling and could restore age‐induced vascular alterations. The purpose of the study was to test the hypothesis that an increase in vascular bed filtration capacity would corroborate microvascular adaptation with training. Methods: We quantified (1) microvascularization from vastus lateralis muscle biopsy to measure the capillary to fibre interface (LC/PF) and (2) the microvascular filtration capacity (K_f) in lower limbs through a venous congestion plethysmography procedure. Twelve healthy older subjects (74 ± 4 years) were submitted to a 14‐week training programme during which lower‐limbs were trained for endurance exercise. Results: The training programme induced a significant increase in the aerobic exercise capacity of lower limbs (+11%Vo _2peak; P < 0.05; +28% Citrate Synthase Activity; P < 0.01). K_f was largely increased (4.3 ± 0.9 10^?3 mL min^?1 mmHg^?1 100 mL^?1 post‐training vs. 2.4 ± 0.8 pre‐training, mean ± SD; P < 0.05) and microvascularization developed as shown by the rise in LC/PF (0.29 ± 0.06 post‐ vs. 0.23 ± 0.06 pre‐training; P < 0.05). Furthermore, K_f and LC/PF were correlated (r = 0.65, P < 0.05). Conclusion: These results demonstrated the microvascular adaptation to endurance training in the elderly. The increase in K_f with endurance training was probably related to a greater surface of exchange with an increased microvessel/fibre interface area. We conclude that measurement of the microvascular filtration rate reflects the change in the muscle exchange area and is influenced by exercise training.     

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 ± 2.7 min (mean, SE) (fatigue) and oxygen uptake (Vo₂) increased to 1.90 ± 0.13 1 min^-1. Compared with voluntary exercise at the same Vo₂, increases in heart rate (HR) (135 ± 7 vs. 130 ± 9 beats min^-1) and cardiac output (16.9 ± 1.1 vs. 17.3 ± 0.9 1 min^-1) were similar, and ventilation (54 ± 5 vs. 45 ± 4 1 min^-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 ± 4 (rest) to 119 ± 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 ± 3 (rest) to 95 ± 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.