Erythrocyte ion regulation across inactive muscle during leg exercise

1992 ◽  
Vol 70 (12) ◽  
pp. 1625-1633 ◽  
Author(s):  
R. S. McKelvie ◽  
M. I. Lindinger ◽  
N. L. Jones ◽  
G. J. F. Heigenhauser

Ion concentration changes in whole blood, plasma, and erythrocytes across inactive muscle were examined in eight healthy males performing four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Blood was sampled from the arm brachial artery and deep antecubital vein during the intermittent exercise period and for 90 min of recovery. Arterial and venous erythrocyte lactate concentration ([Lac−]) increased from 0.3 ± 0.1 to 12.5 ± 1.3 (p < 0.01) and 1.1 ± 0.4 to 8.5 ± 1.5 mmol/L (p < 0.01), respectively, returning to control values during recovery. Arterial and venous plasma [Lac−] increased from 1.5 ± 0.2 to 27.7 ± 1.8 and from 1.3 ± 0.4 to 25.7 ± 3.5 mmol/L, respectively, and was greater than erythrocyte [Lac−] throughout exercise and recovery. Arterial and venous [K+] increased in erythrocytes from 119.5 ± 5.1 to 125.4 ± 4.6 (p < 0.01) and from 113.6 ± 1.7 to 120.6 ± 7.1 mmol/L, respectively, decreasing to control during recovery. In arterial and venous plasma, [K+] increased from 4.3 ± 0.1 to 6.1 ± 0.2 (p < 0.01) and from 4.5 ± 0.2 to 5.3 ± 0.2 mmol/L (p < 0.01), respectively, decreasing to control during recovery. The efflux of Lac− out of erythrocytes against an electrochemical concentration gradient suggests the presence of an active transport system. Efflux of K+ from erythrocytes as blood passes across inactive muscle affords an important adaptation to the K+ release from muscle activated in heavy exercise.Key words: isokinetic cycle ergometer, potassium, lactate, red cell volume, arteriovenous difference.

1988 ◽  
Vol 65 (5) ◽  
pp. 2080-2089 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
M. I. Lindinger ◽  
J. R. Sutton ◽  
N. L. Jones

To assess the importance of factors influencing the resolution of exercise-associated acidosis, measurements of acid-base variables were made in nine healthy subjects after 30 s of maximal exercise on an isokinetic cycle ergometer. Quadriceps muscle biopsies (n = 6) were taken at rest, immediately after exercise, and at 3.5 and 9.5 min of recovery; arterial and femoral venous blood were sampled (n = 3) over the same time. Intracellular and plasma inorganic strong ions were measured by neutron activation and ion-selective electrodes, respectively; lactate concentration ([La-]) was measured enzymatically, and plasma PCO2 and pH were measured by electrodes. Immediately after exercise, intracellular [La-] increased to 47 meq/l, almost fully accounting for a reduction in intracellular strong ion difference ([SID]) from 154 to 106 meq/l. At the same time, femoral venous PCO2 increased to 100 Torr and plasma [La-] to 9.7 meq/l; however, plasma [SID] did not change because of a concomitant increase in inorganic [SID] secondary to increases in [K+], [Na+], and [Ca2+]. During recovery, muscle [La-] fell to 26 meq/l by 9.5 min; [SID] remained low (101 and 114 meq/l at 3.5 and 9.5 min, respectively) due almost equally to the elevated [La-] (30 and 26 meq/l) and reductions in [K+] (from 142 meq/l at rest to 123 and 128 meq/l). Femoral venous PCO2 rose to 106 Torr at 0.5 min postexercise and fell to resting values at 9.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)


PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3769 ◽  
Author(s):  
Zübeyde Aslankeser ◽  
Şükrü Serdar Balcı

BackgroundIt has been believed that the contribution of fat oxidation to total energy expenditure is becoming negligible at higher exercise intensities (about 85% VO2max). The aim of the present study was to examine the changes in substrate oxidation during high-intensity interval exercise in young adult men.MethodsA total of 18 healthy well-trained (aged 19.60 ± 0.54 years, BMI = 22.19 ± 0.64 kg/m2,n = 10) and untrained (aged 20.25 ± 0.41 years, BMI = 22.78 ± 0.38 kg/m2,n = 8) young men volunteered to participate in this study. After an overnight fast, subjects were tested on a cycle ergometer and completed six 4-min bouts of cycling (at ∼80% VO2max) with 2 min of rests between intervals. Energy expenditure and the substrate oxidation rate were measured during the experiment by using indirect calorimetry. The blood lactate concentration was collected immediately after each interval workout.ResultsThe fat oxidation rate during each workout was significantly different between the untrained and the athlete groups (p < 0.05), and the carbohydrate (CHO) oxidation rate during the experiment was similar between groups (p > 0.05). Moreover, lactate concentration significantly increased in the untrained group (p < 0.05), whereas it did not significantly change in the athlete group during the workouts (p > 0.05). Fat contribution to energy expenditure was significantly higher in the athlete group (∼25%) than in the untrained group (∼2%).ConclusionsThe present study indicates that 17 times more fat oxidation was measured in the athlete group compared to the untrained group. However, the athletes had the same CHO oxidation rate as the recreationally active subjects during high-intensity intermittent exercise. Higher fat oxidation rate despite the same CHO oxidation rate may be related to higher performance in the trained group.


1997 ◽  
Vol 45 (3) ◽  
pp. 165-182 ◽  
Author(s):  
Hiroaki Minoura ◽  
Yasunobu Iwasaka

2011 ◽  
Vol 138 (1) ◽  
pp. 95-116 ◽  
Author(s):  
James A. Fraser ◽  
Christopher L.-H. Huang ◽  
Thomas H. Pedersen

Activation of skeletal muscle fibers requires rapid sarcolemmal action potential (AP) conduction to ensure uniform excitation along the fiber length, as well as successful tubular excitation to initiate excitation–contraction coupling. In our companion paper in this issue, Pedersen et al. (2011. J. Gen. Physiol. doi:10.1085/jgp.201010510) quantify, for subthreshold stimuli, the influence upon both surface conduction velocity and tubular (t)-system excitation of the large changes in resting membrane conductance (GM) that occur during repetitive AP firing. The present work extends the analysis by developing a multi-compartment modification of the charge–difference model of Fraser and Huang to provide a quantitative description of the conduction velocity of actively propagated APs; the influence of voltage-gated ion channels within the t-system; the influence of t-system APs on ionic homeostasis within the t-system; the influence of t-system ion concentration changes on membrane potentials; and the influence of Phase I and Phase II GM changes on these relationships. Passive conduction properties of the novel model agreed with established linear circuit analysis and previous experimental results, while key simulations of AP firing were tested against focused experimental microelectrode measurements of membrane potential. This study thereby first quantified the effects of the t-system luminal resistance and voltage-gated Na+ channel density on surface AP propagation and the resultant electrical response of the t-system. Second, it demonstrated the influence of GM changes during repetitive AP firing upon surface and t-system excitability. Third, it showed that significant K+ accumulation occurs within the t-system during repetitive AP firing and produces a baseline depolarization of the surface membrane potential. Finally, it indicated that GM changes during repetitive AP firing significantly influence both t-system K+ accumulation and its influence on the resting membrane potential. Thus, the present study emerges with a quantitative description of the changes in membrane potential, excitability, and t-system ionic homeostasis that occur during repetitive AP firing in skeletal muscle.


1993 ◽  
Vol 74 (1) ◽  
pp. 435-443 ◽  
Author(s):  
P. G. Catcheside ◽  
G. C. Scroop

Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P < 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.


1996 ◽  
Vol 76 (2) ◽  
pp. 1015-1024 ◽  
Author(s):  
I. L. Kopysova ◽  
S. M. Korogod ◽  
J. Durand ◽  
S. Tyc-Dumont

1. In vivo experiments have shown that extracellular microelectrophoretic application of N-methyl-D-aspartate (NMDA) induced oscillatory plateau potentials with bursts of action potentials in rat abducens motoneurons. The period of these slow NMDA oscillations could be altered by single trigeminal non-NMDA excitatory input delivered at low frequency during the NMDA oscillations. 2. A resetting of the oscillations was observed depending on the phase of slow oscillatory cycle during which the trigeminal excitation occurred. 3. We investigated local mechanisms responsible for the phase-dependent modifications of NMDA oscillations, including contributions of voltage and concentration transients, in the mathematical model of the isopotential membrane compartment equipped with voltage-gated Na+, K+, and Ca2+ channels, with Ca2+-dependent K+ channels, and with ligand-gated NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor channels. The faithful model was constructed with the use of models described earlier, which were modified by increasing time constants of kinetic variables of all voltage-gated conductances and by including coupled dynamics of voltages and ion concentrations. The changes in ion concentrations were produced near the membrane by transmembrane currents and removal mechanisms (pumps, diffusion). 4. This work focuses on local arrangement of voltage- and ligand-gated conductances and on local ion concentration changes in two separate pools: the postsynaptic pool of AMPA receptors and the extrasynaptic pool. In terms of the electrotonic and diffusional length constants, these pools were electrotonically close but diffusionally remote. 5. It was found that the effect of resetting can be produced by a local interaction between plateau and spike-generating conductances and glutamate receptors. 6. In vivo phase-dependent interactions between NMDA oscillations and AMPA synaptic input were reproduced by the local model only when changes in intracellular sodium and extracellular potassium concentrations were taken into account and the mechanisms of ion removal from postsynaptic pools had slower kinetics than the fast pump system operating in the extracellular pool. 7. Postsynaptic changes in ion concentrations of Na+ and K+ in intra- and extracellular layers near the membrane shift of Nernst equilibrium potentials for these ions depending on the phase of activation of synaptic input. Thus Na+ and k+ components of all transmembrane currents involved in the pattern generation are differently affected by synaptic action during the oscillations. We conclude that slow postsynaptic changes in ion concentrations near the membrane play a key role in the resetting of the NMDA oscillations.


1992 ◽  
Vol 262 (5) ◽  
pp. R852-R859 ◽  
Author(s):  
R. B. Weinstein ◽  
R. J. Full

Most animals move intermittently, yet many proposed performance limitations of terrestrial locomotion are based on steady-state measurements and assumptions. We examined the effect of work-rest transitions by exercising the ghost crab, Ocypode quadrata (28.1 +/- 8.1 g), intermittently on a treadmill at 0.30 m/s, a supramaximal speed [i.e., greater than the speed that elicits the maximal rate of oxygen consumption (VO2)]. Duration of the exercise and pause periods, ratio of exercise to pause, and speed during the exercise period were varied to determine the effect on performance. Crabs fatigued after 7.5 min of continuous running, a distance capacity (i.e., total distance traveled before fatigue) of 135 m. When the task was done intermittently with 2-min exercise and 2-min pause periods, the crabs fatigued after 87 min (a total distance of 787 m), representing an 5.8-fold increase in distance capacity compared with continuous exercise at the same absolute speed (0.30 m/s) and a 2.2-fold increase in distance capacity compared with continuous exercise at the same average speed (0.15 m/s). Pause periods less than 30 s did not result in greater distance capacity compared with continuous exercise at the same average speed. Longer (3-5 min) and shorter exercise periods (less than or equal to 30 s) decreased distance capacity. Leg muscle lactate increased 10-fold to 15 mumol/g leg during intermittent exercise. However, significant amounts of lactate were cleared from the leg during the brief pause periods.(ABSTRACT TRUNCATED AT 250 WORDS)


1980 ◽  
Vol 49 (4) ◽  
pp. 722-728 ◽  
Author(s):  
G. A. Gaesser ◽  
G. A. Brooks

Patterns of postexercise glycogen repletion in heart, skeletal muscle, and liver in the absence of exogenously supplied substrates during the first 4 h of recovery were assessed. Female Wistar rats were run to exhaustion using continuous (1.0 mph, 15% grade) and intermittent (alternate 1-min intervals at 0.5 and 1.5 mph, 15% grade) exercise protocols. Rats at exhaustion were characterized by marked depletion of glycogen in heart (55%), skeletal muscle (94%), and liver (97%). Blood glucose levels at exhaustion (1.33 mumol/g) were only 37% of preexercise levels. There were no significant differences between continuous and intermittent exercise groups for any of the tissue glycogen or blood glucose values. Cardiac muscle was the only tissue capable of complete restoration of glycogen levels while relying exclusively upon endogenous substrates. Concentrations of endogenous substrates present at the end of exercise were insufficient to support restoration of blood glucose levels to preexercise values nor support glycogen repletion in skeletal muscle and liver during the initial 4-h food-restricted postexercise period. With subsequent feeding, skeletal muscle demonstrated a glycogen supercompensation effect at 24 h (181.1 and 191.8% of preexercise levels for continuous and intermittent exercise, respectively). Lactate concentration in all tissues at the point exhaustion (1.5--2.5 times resting levels) were only moderately elevated and returned to preexercise levels within 15 min. It was concluded that lactate removal after exercise contributed only minimally to the repletion of muscle glycogen.


1993 ◽  
Vol 74 (3) ◽  
pp. 1248-1255 ◽  
Author(s):  
S. Oyono-Enguelle ◽  
A. Heitz ◽  
J. Marbach ◽  
C. Ott ◽  
A. Pape ◽  
...  

Arterial and femoral venous lactate concentrations were measured before, during, and after short intermittent exercise (55 (55118% of maximal O2 consumption) in thermoneutral (N, 25 degrees C, 10.5 Torr) and hot (H, 45 degrees C, 17.5 Torr) conditions. The thermal load induced significantly higher heart rate and rectal temperature in H relative to N. All the arterial lactate (La) recovery curves were fitted to an equation containing two exponential time functions of the form La(t) = La(0) + A1a(1 - e-gamma 1at) + A2a(1 - e-gamma 2at) where the velocity constants gamma 1a and gamma 2a are the body's overall ability to exchange and remove lactate after exercise, respectively, and t is time. There was no significant difference in these constants, regardless of thermal conditions. The arterial lactate concentration at the end of exercise, the peak lactate concentration during recovery, the amplitudes A1a and A2a of the biexponential function, and the arteriofemoral venous lactate concentration difference during recovery were not significantly different in H relative to N. However, measured and computed arterial lactate concentrations during recovery, especially at the end of the tests, were higher in H (P < 0.04). The more elevated lactate concentrations in H at rest at the end of recovery denote a higher basal lactate production, and they were not due to muscle hypoxia.


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