Sympathetic control of the forearm blood flow in man during brief isometric contractions

Summary Experiments were performed to assess the possible neurally mediated constriction in active skeletal muscle during isometric hand-grip contractions. Forearm blood flow was measured by venous occlusion plethysmography on 5 volunteers who exerted a series of repeated contractions of 4 s duration every 12 s at 60% of their maximum strength of fatigue. The blood flows increased initially, but then remained constant at 20–24 ml·min⁻¹·100 ml⁻¹ throughout the exercise even though mean arterial blood pressure reached 21–23 kPa (160–170 mm Hg). When the same exercise was performed after arterial infusion of phentolamine, forearm blood flow increased steadily to near maximal levels of 38.7±1.4 ml·min⁻¹·100 ml⁻¹. Venous catecholamines, principally norepinephrine, increased throughout exercise, reaching peak values of 983±258 pg·ml⁻¹ at fatigue. Of the vasoactive substances measured, the concentration of K⁺ and osmolarity in venous plasma also increased initially and reached a steady-state during the exercise but ATP increased steadily throughout the exercise. These data indicate a continually increasing α-adrenergic constriction to the vascular beds in active muscles in the human forearm during isometric exercise, that is only partially counteracted by vasoactive metabolites.     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

Summary The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21%±2.8%, 43%±2.1% and 65%±2.3% of respectively (mean±SE). The HR decreased mono-exponentially withτ values of 13.6±1.6 s, 32.7±5.6 s and 55.8±8.1s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (Δ[NE]=207.7±22.5 pg·ml⁻¹ and 521.3±58.3 pg·ml⁻¹ respectively); (b) after a time lag of 1 min [NE] decreased exponentially (τ=87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats · min⁻¹; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg·ml⁻¹ Δ[NE]5 beats ·min⁻¹). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Oxidative stress, inflammation and recovery of muscle function after damaging exercise: effect of 6-week mixed antioxidant supplementation

There is no consensus regarding the effects of mixed antioxidant vitamin C and/or vitamin E supplementation on oxidative stress responses to exercise and restoration of muscle function. Thirty-eight men were randomly assigned to receive either placebo group (n = 18) or mixed antioxidant (primarily vitamin C & E) supplements (n = 20) in a double-blind manner. After 6 weeks, participants performed 90 min of intermittent shuttle-running. Peak isometric torque of the knee flexors/extensors and range of motion at this joint were determined before and after exercise, with recovery of these variables tracked for up to 168 h post-exercise. Antioxidant supplementation elevated pre-exercise plasma vitamin C (93 ± 8 μmol l⁻¹) and vitamin E (11 ± 3 μmol l⁻¹) concentrations relative to baseline (P < 0.001) and the placebo group (P ≤ 0.02). Exercise reduced peak isometric torque (i.e. 9–19% relative to baseline; P ≤ 0.001), which persisted for the first 48 h of recovery with no difference between treatment groups. In contrast, changes in the urine concentration of F₂-isoprostanes responded differently to each treatment (P = 0.04), with a tendency for higher concentrations after 48 h of recovery in the supplemented group (6.2 ± 6.1 vs. 3.7 ± 3.4 ng ml⁻¹). Vitamin C & E supplementation also affected serum cortisol concentrations, with an attenuated increase from baseline to the peak values reached after 1 h of recovery compared with the placebo group (P = 0.02) and serum interleukin-6 concentrations were higher after 1 h of recovery in the antioxidant group (11.3 ± 3.4 pg ml⁻¹) than the placebo group (6.2 ± 3.8 pg ml⁻¹; P = 0.05). Combined vitamin C & E supplementation neither reduced markers of oxidative stress or inflammation nor did it facilitate recovery of muscle function after exercise-induced muscle damage.     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

Summary The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean ±SEM showed that the ANF plasma level decreased significantly (p<0.05) from 32.5±4 to 28±6 pg · ml⁻¹ after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60±13.6 pg · ml⁻¹ and 53±13 pg · ml⁻¹): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Angiotensin II induced reduction of peritubular capillary diameter in the rat kidney

Summary Large peritubular capillaries were infused consecutively (20 nl · min⁻¹) in random sequence with isotonic saline and angiotensin II (20–80 ng · ml⁻¹). The diameters of the infused capillaries were measured, without knowledge of the infusate used, from colour photographs of the infused area. Angiotensin II induced a significant (p<0.001) decrease in capillary diameter (Δ=−1.2±0.2 (SE) μm and Δ=−2.1±0.2 (SE) μm with 20 ng · ml⁻¹ and 80 ng · ml⁻¹ angiotensin II infusates, respectively). This decrease was shown to be independent of external tubular compression: separate experiments in which the surrounding tubules were collapsed by injection of oil blocks yielded similar results. The possibility that the observed reduction in diameter was caused by an angiotensin II induced change in capillary permeability to the staining solution was excluded, since the angiotensin II effect was unchanged when fluorescent dextran (mol. wt. 150000) was substituted for lissamin green. These experiments indicate that peritubular capillaries contract actively when infused with angiotensin II.     

The effects of whole body vibration and exercise on fibrinolysis in men

Whole body vibration (WBV) is a novel modality that has been demonstrated to enhance muscular and cardiovascular functions reported to increase fibrinolytic activity. The purpose of this study was to examine the fibrinolytic response to WBV and exercise in men. Twenty healthy males (23.8 ± 0.9 years, 25.6 ± 0.2 kg m⁻²) participated in the study. Each subject performed three trials in randomized order separated by 1 week: exercise (X), vibration (V) and vibration + exercise (VX). Exercise sessions consisted of 15 min of unloaded squatting at a rate of 20 per minute. Vibration sessions were conducted on a WBV platform vibrating for 15 min. Tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI-1) were assessed at baseline and immediately after each condition. The increase in tPA activity was significantly greater in VX (0.87 ± 0.35 to 3.21 ± 1.06 IU ml⁻¹) compared to X (0.71 ± 0.36 to 2.4 ± 1.13 IU ml⁻¹) or V (0.83 ± 0.25 to 1.00 ± 0.37 IU ml⁻¹) conditions, and greater in the X condition compared to the V condition. PAI-1 activity decreased significantly more in the VX (6.54 ± 5.53 to 4.89 ± 4.13 IU ml⁻¹) and X (9.76 ± 8.19 to 7.48 ± 7.11 IU ml⁻¹) conditions compared to the V (5.68 ± 3.53 to 5.84 ± 3.52 IU ml⁻¹) condition. WBV does not augment fibrinolytic activity in healthy men. However, WBV combined with squatting exercise increases fibrinolytic activity more than exercise alone.     

Involvement of muscarinic cholinergic and α2-adrenergic mechanisms in growth hormone secretion during exercise in humans

The purpose of this study was to examine the role of muscarinic cholinergic and α₂-adrenergic mechanisms in growth hormone (GH) secretion during exercise in humans. The GH responses induced during moderate-intensity exercise (using a cycle ergometer at 60% maximal oxygen uptake, V˙O_2max, for 30 min) without treatment (control) and after the administration of a muscarinic cholinergic antagonist (atropine 1 mg) or after an α₂-adrenergic antagonist (yohimbine 15 mg) were compared in seven healthy men. Although, serum GH concentration had increased significantly after exercise in the control experiment [mean peak GH concentration 52.64 (SEM 18.60) ng · ml⁻¹], the increase was suppressed by the administration of either atropine [mean peak GH concentration 8.64 (SEM 7.47)  ng · ml⁻¹] or yohimbine [mean peak GH concentration 17.50 (SEM 7.89) ng · ml⁻¹]. The area under the curve of serum GH concentration against time was significantly lower in the experiment using these drugs [with atropine, mean area 458 (SEM 409) ng · ml⁻¹ · min], with yohimbine mean area 946 (SEM 435) ng · ml⁻¹ · min] than in the control experiment [mean area 3135 (SEM 1098) ng · ml⁻¹ · min]. These results suggest that muscarinic cholinergic and α₂-adrenergic mechanisms are involved in GH secretion during exercise in humans. Accepted: 9 March 2000     

Optimal glycaemic control in unrestrained diabetic dogs using programmed compound squarewave insulin infusions

A glycaemic control identical with the normal has been achieved in unrestrained totally depancreatised dogs using a portable open-loop insulin delivery system. The device consisted of a battery power pack with a flow-rate controller, an insulin reservoir and a peristaltic pump from which pulses of insulin were delivered every 90 seconds into the inferior vena cava through an exteriorised indwelling catheter. Insulin was infused at the basal rate of 0.45±0.03 mUkg⁻¹ min⁻¹ (Mean±s.e.m.) in the postabsorptive state resulting in peripheral IRI and plasma glucose levels of 12±1 μU ml⁻¹ and 86±7 mg dl⁻¹. In the postprandial period the infusion rate was enhanced sevenfold to the rate of 3.16±0.21 mU kg⁻¹min⁻¹ for 7h and then reduced to 1.05±0.07 mU kg⁻¹ min⁻¹ for an additional 2.25 h. A weight-maintaining constant diet was provided and the resulting glycaemic profiles were similar to age, sex and weight-matched healthy controls. Fasting peripheral insulin levels in the infused diabetic dogs were not significantly different from non-diabetic controls (10±1μUml⁻¹). However, in the postprandial period of enhanced delivery, insulin levels in the diabetic dogs were 3.1 times higher than the controls. With the compound square waveforms of preprogrammed insulin infusion found appropriate in this study unaccountable low or high plasma glucose levels did not occur but hyperinsulinism accompanied the glycaemic normalisation following a mixed meal.     

Cardiorespiratory responses to fatiguing dynamic and isometric hand-grip exercise

In occupational work, continuous repetitive and isometric actions performed with the upper extremity primarily cause local muscle strain and musculoskeletal disorders. They may also have some adverse effects on the cardiorespiratory system, particularly, through the elevation of blood pressure. The aim of the present study was to compare peak cardiorespiratory responses to fatiguing dynamic and isometric hand-grip exercise. The subjects were 21 untrained healthy men aged 24–45 years. The dynamic hand-grip exercise (DHGE) was performed using the left hand-grip muscles at the 57 (SD 4)% level of each individual's maximal voluntary contraction (MVC) with a frequency of 51 (SD 4) grips · min^−l. The isometric hand-grip exercise (IHGE) was done using the right hand at 46 (SD 3)% of the MVC. The endurance time, ventilatory gas exchange, heart rate (HR) and blood pressure were mea- sured during both kinds of exercise. The mean endurance times for DHGE and IHGE were different, 170 (SD 62) and 99 (SD 27) s, respectively (P < 0.001). During DHGE the mean peak values of the breathing frequency [20 (SD 6) breaths · min⁻¹] and tidal volume [0.89 (SD 0.34) l] differed significantly (P < 0.01) from peak values obtained during IHGE [15 (SD 5) breaths · min⁻¹, and 1.14 (SD 0.32) l, respectively]. The corresponding peak oxygen consumptions, pulmonary ventilations, HR and systolic blood pressures did not differ, and were 0.51 (SD 0.06) and 0.46 (SD 0.11) l · min⁻¹, 17.1 (SD 3.0) and 16.7 (SD 4.7) l · min⁻¹, 103 (SD 18) and 102 (SD 17) beats · min⁻¹, and 156 (SD 17) and 161 (SD 17) mmHg, respectively. The endurance times of both DHGE and IHGE were short (<240 s). The results indicate that the peak responses for the ventilatory gas exchange, HR and blood pressure were similar during fatiguing DHGE and IHGE, whereas the breathing patterns differed significantly between the two types of exercise. The present findings emphasize the importance of following ergonomic design principles in occupational settings which aim to reduce the output of force, particularly in tasks requiring isometric and/or one-sided repetitive muscle actions. Accepted: 16 February 2000     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

Summary The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (T _db=33.4°C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% , with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml·kg BW⁻¹ of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol·l⁻¹ Na⁺, 3.2 mmol·l⁻¹ K⁺). Beverages were administered in double blind, counterbalanced order. Mean (±SE) times for the 1200 cycling task differed significantly: WP=13.62±0.33 min, *6%=13.03±0.24 min, 8%=13.30±0.25 min, 10%=13.57±0.22 min (*=different from WP and 10%,P<0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P<0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance. Compared to ingestion of a water placebo, consumption of beverages containing 6% to 10% sucrose resulted in similar physiologic and sensory response, while ingestion of the 6% sucrose beverage resulted in significantly improved end-exercise performance following only 60 min of intermittent cycling exercise.     

Dynamic model of the short-term regulation of arterial pressure in the cat

The purpose of this study was to characterise the dynamics of the short-term control of arterial pressure in the cat with the aid of a model consisting of a nonlinear negative-feedback control system. The arterial system was described by a three element windkessel model (peripheral resistance, R, aortic characteristic impedance, R_c, and total arterial compliance, C). The resistance regulation was represented by a second-order system with static gain G_R, a damping factor σ and an undamped natural frequency ω_n. The resistance gain, G_R, and the windkessel parameters were obtained from measurements of aortic and venous pressures and cardiac output in two steady states. The parameters σ and ω_n were estimated from mean pressure and mean flow during the transient from control to the new steady state. Pressure reductions averaged 10 per cent and resistance changes averaged 12 per cent. Average windkessel model parameters in the control condition were: C=(25·9±6·1) 10⁻⁶ g⁻¹ cm⁴ s², R_c=(2·51±0·53) 10³ g cm⁻⁴ s⁻¹, R=(40·9±9·8) 10³ g cm⁻⁴ s⁻¹. Average estimates of parameters of the resistance regulator were: G_R=(4·14±2·38) 10⁻³ min ml⁻¹, ω_n = 1·0 ± 1·0 rad s⁻¹, σ=0·41±0·19. A satisfactory fit was found between model predicted and measured pressure. The results suggest that the dynamic short-term control of pressure is underdamped and oscillatory. The amplitude of these oscillations is affected by arterial compliance, suggesting an interaction between the arterial system and short-term resistance regulation.     

Circulating reverse triiodothyronine in humans during exercise

Summary Circulating thyroxine (T₄), triiodothyronine (T₃) and reverse triiodothyronine (rT₃) as well as blood lactate and glucose concentrations were measured in a group of 12 trained volunteer subjects prior to and after swimming 0.18 or 0.9 km, to determine if increase in metabolic activity was accompanied by diversion of T₄ monodeiodination from the active (T₄ to T₃) to the inactive (T₄ to rT₃) pathway. The resting T₄, T₃, and rT₃ levels were 8.5 Μg·100 ml⁻¹, 108 ng·100 ml⁻¹, and 57 ng·100 ml⁻¹, respectively, whereas after 0.18 km of swimming the corresponding levels were 9.5 Μg·100 ml⁻¹, 135 ng. 100 ml⁻¹ and 70 ng·100 ml⁻¹. After 0.9 km of swimming, T₄, T₃, and rT₃ levels were 9.0 Μg·100 ml⁻¹, 126 ng·100 ml⁻¹, and 66 ng·100 ml⁻¹, respectively. The swimming was accompanied by hemoconcentration and increase in blood lactate but not in glucose concentrations. In two other investigations thyroid hormones were measured prior to and after 60 or 90 min of moderate exercise on a bicycle ergometer. This exercise had no effect on circulating thyroid hormone levels. Free thyroxine (FT₄) concentration and thyroxine binding globulin (TBG) capacity were unaltered after exercise. In conclusion, brief strenuous swimming or moderate bicycle exercise had minor or no effect on thyroid hormone concentrations when consideration was given to the attendant hemoconcentration. Even when exercise induced small T₃ and rT₃ changes were noted, they were in the same direction (increase) thus demonstrating a lack of diversion of peripheral T₄ monodeiodination. Investigations partially supported by NIH grant AG-01613 and the Narveen Medical Research Foundation, St. Louis, Missouri, USA     

Prefrontal cortex oxygenation and neuromuscular responses to exhaustive exercise

Near-infrared spectroscopy (NIRS) allows non-invasive monitoring of central and peripheral changes in oxygenation during exercise and may provide valuable insight into the factors affecting fatigue. This study aimed to explore the changes in oxygenation of prefrontal cortex and active muscle tissue as limiting factors of incremental exercise performance in trained cyclists. Thirteen trained healthy subjects (mean ± SE: age 24.9 ± 1.5 years, body mass 70.1 ± 1.2 kg, training 6.1 ± 0.9 h week⁻¹) performed a progressive maximal exercise to exhaustion on a cycling ergometer. Prefrontal cortex (Cox) and vastus lateralis muscle (Mox) oxygenation were measured simultaneously by NIRS throughout the exercise. Maximal voluntary isometric knee torques and quadriceps neuromuscular fatigue (M-wave properties and voluntary activation ratio) were evaluated before and after exercise. Maximal power output and oxygen consumption were 380.8 ± 7.9 W and 75.0 ± 2.2 ml min⁻¹ kg⁻¹, respectively. Mox decreased significantly throughout exercise while Cox increased in the first minutes of exercise but decreased markedly from the workload corresponding to the second ventilatory threshold up to exhaustion (P < 0.05). No significant difference was noted 6 min after maximal exercise in either the voluntary activation ratio or the M-wave properties. These findings are compatible with the notion that supraspinal modulation of motor output precedes exhaustion. An erratum to this article can be found at     

Increased glucagon secretion during hyperthermia in a sauna

Summary Plasma glucagon, adrenaline, noradrenaline, insulin and glucose concentrations were measured in 7 healthy young males during hyperthermia in a sauna bath: plasma glucagon levels increased from baseline values of 127.0±12.9 (SEM) pg · ml⁻¹ to a maximum of 173.6±16.1 (SEM) pg · ml⁻¹ at the 20th min of exposure. No change in plasma insulin and a slight increase in plasma glucose concentration were seen. Since a concomitant moderate increase in plasma catecholamine levels was also present, the adrenergic stimulus is believed to trigger glucagon release during hyperthermia. Diminished visceral blood flow, known to occur in sauna baths, may cause a decrease in the degradation of plasma glucagon and thus contribute to the elevated plasma glucagon levels.     

Muscle bio-energetics in acute glycolytic block: in vivo phosphorus-nuclear magnetic resonance study of iodo-acetate injected rats

Summary In vivo phosphorus nuclear magnetic resonance spectroscopy of muscle was performed at rest, during work and during postexercise recovery in rats injected with iodo-acetate (IA) (35–40 mg· kg⁻¹, intra-arterially), in order to follow bio-energetic changes in muscle with acute glycolytic block. Three animals with contracture had very low ratios of phosphocreatine: inorganic phosphate (PCr∶Pi) at rest (0.5–0.9). The PCr∶Pi were normal at rest (6.9±2.0,±2 SD) in all other rats. Exercise-induced continuous accumulation of phosphomonoesters (PME), the characteristic finding of glycolytic block, was observed. The end-exercise levels of PME correlated with the degree of block measured in vitro. During steady-state work, induced by nerve stimulation at four frequencies, PCr∶Pi values were significantly lower (p<0.02) than the control values at 0.25, 1.0 and 2.0 Hz. The ATP levels fell during exercise to reach 75%±7% of initial values. The recovery of PCr∶Pi from exercise and the disappearance of PME were slow. Two animals which survived the IA injection demonstrated much lower PME accumulation 18 h later. It is concluded that in acute muscle glycolytic block: (1) energy metabolism is impaired during exercise and also at rest, (2) accumulating PME can serve as an indicator of the degree of glycolytic block, (3) ATP levels fall during work, and (4) postexercise recovery is slow. The findings are compared with³¹P-NMR observations in chronic muscle glycolytic disorders.     

The influence of free fatty acids on glycogen recovery in rat heart after exercise

Summary Glycogen supercompensation is the term used to denote the abnormally high levels of glycogen found in the heart shortly after an exercise-induced reduction of the substrate. Using rats, we tested whether this condition was linked to the use of plasma free fatty acids (FFA), which normally rise with exercise. Before a 1-h swim, animals received an injection of either saline (S) or nicotinic acid (NA). The nicotinic acid treatment dramatically suppressed the rise in plasma FFA observed in the S-group. Exercise caused a significant but similar reduction (35–38%) of the myocardial glycogen content in both groups. After 1 h of recovery in the S-group, myocardial glycogen reached a value of 30.3±1.7 Μmol·g⁻¹ or 113% of that measured before the exercise began. In contrast, the value for hearts from the NA-group with reduced FFA levels was 24.0±1.9 Μmol·g⁻¹ or only 91% of that measured before exercise. After 2 h the values were 33.8±1.4 and 29.0±1.9 Μmol·g⁻¹ respectively. These data indicate that glycogen repletion in rat heart after exercise is related to the amount of FFA present in the plasma. We suggest that carbohydrate metabolism is diverted towards synthesis and storage as a result of the glycolytic inhibition exerted by the increased use of fat as an energy source as previously observed in hearts from fasted or diabetic animals. This work was supported by a grant from the Utah Heart Association and the Deseret Gym Corporation     

Beta-endorphin immunoreactivity during high-intensity exercise with and without opiate blockade

Nine highly fit men [mean (SE) maximum oxygen uptake, : 63.9 (1.7) ml·kg^–1·min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials to determine plasma β-endorphin immunoreactivity during intense exercise (80% ). A double-blind experimental design was used, and subjects performed the two exercise trials in counterbalanced order. Exercise trials were 30 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (1.2 mg; 3 cm³) and the other after receiving a placebo (0.9% NaCl saline; 3 cm³). Prior to each experimental trial, a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Thereafter, each subject received either a naloxone or placebo bolus injection. Blood samples were also collected after 10, 20 and 30 min of continuous exercise. β-Endorphin was higher (P<0.05) during exercise when compared to pre-exercise in both trials. However, no statistically significant difference was found (P>0.05) between exercise time points within either experimental trial. β-endorphin immunoreactivity was greater (P<0.05) in the naloxone than in the placebo trial during each exercise sampling time point [10 min: 63.7 (3.9) pg·ml^–1 vs 78.7 (3.8) pg·ml^–1; 20 min: 68.7 (4.1) pg·ml^–1 vs 83.8 (4.3) pg·ml^–1; 30 min: 71.0 (4.3) pg·ml^–1 vs 82.5 (3.2) pg·ml^–1]. These data suggest that intense exercise induces significant increases in β-endorphin that are maintained over time during steady-rate exercise. Exercise and naloxone had an interactive effect on β-endorphin release that warrants further investigation. Electronic Publication     

The effect of citrate loading on exercise performance,acid-base balance and metabolism

Summary Nine subjects ( 65±2 ml·kg⁻¹·min⁻¹, mean±SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g·kg⁻¹ body mass) or a sodium chloride placebo (P, 0.045 g·kg⁻¹ body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% , followed by exercise to exhaustion at 95% . Pre-exercise arterialized-venous [H⁺] was lower in C (36.2±0.5 nmol·l⁻¹; pH 7.44) than P (39.4±0.4 nmol·l⁻¹; pH 7.40); the plasma [H⁺] remained lower and [HCO ₃ ⁻ ] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% was similar in C (310±69 s) and P (313±74 s). Cardiorespiratory variables (ventilation, , , heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195±19 μmol·l⁻¹; P, 81±7 μmol·l⁻¹) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% . Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.