Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

2000 ◽  
Vol 98 (1) ◽  
pp. 39 ◽  
Author(s):  
D. ROBERTS ◽  
D. J. SMITH ◽  
S. DONNELLY ◽  
S. SIMARD
Keyword(s):  
Plasma Volume ◽  
Volume Contraction ◽  
Healthy Humans ◽  
Erythropoietin Production ◽  
Exercise Induced

Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

1999 ◽  
Vol 98 (1) ◽  
pp. 39-45 ◽  
Author(s):  
D. ROBERTS ◽  
D. J. SMITH ◽  
S. DONNELLY ◽  
S. SIMARD
Keyword(s):  
Plasma Volume ◽  
Significant Rise ◽  
Normobaric Hypoxia ◽  
Hypoxic Exposure ◽  
Volume Depletion ◽  
Volume Contraction ◽  
Healthy Humans ◽  
Exercise Induced ◽  
Power Outputs ◽  
Response To Exercise

This study examined exercise-induced hypoxaemia (EIH) and plasma volume contraction as modulators of serum erythropoietin (Epo) production. Five athletes cycled for 3 min at supra-maximal power outputs, at each of two different elevations (1000 m and 2100 m). Five subjects were exposed to normobaric hypoxia (FIO2 = 0.159), seven subjects underwent plasmapheresis to reduce plasma volume and eight subjects were time controls for Epo levels. Oxyhaemoglobin saturation was significantly reduced during exercise and during normobaric hypoxia. The time period of haemoglobin oxygen saturation < 91% was 24±29 s (mean±S.D., n = 5) for exercise at 1000 m, 136±77 s (mean±S.D., n = 5) for exercise at 2100 m and 178±255 s (mean±S.D., n = 5) with resting hypoxic exposure. However, significantly increased serum Epo levels were observed only following exercise (24±3%; mean±S.D., n = 5 at 1000 m and 36±5%; mean±S.D., n = 5 at 2100 m). Volume contraction also resulted in increased serum Epo (35±6%; mean±S.D., n = 7) in spite of a significant rise in haematocrit of 2.2%. Despite similar degrees of arterial desaturation, only the hypoxaemia induced by exercise was associated with an increase in serum Epo. This finding indicates that other factors, in addition to hypoxaemia, are important in modulating the production of Epo in response to exercise. Volume depletion in the absence of exercise resulted in increases in Epo levels that were comparable with those observed in response to exercise. The paradoxical responses of the increased haematocrit and the increase in Epo in subjects undergoing plasmapheresis suggests that plasma volume may also modulate the production of Epo.

scholarly journals UCC118 supplementation reduces exercise‐induced gastrointestinal permeability and remodels the gut microbiome in healthy humans

2019 ◽  
Vol 7 (22) ◽  
Author(s):  
Christopher L. Axelrod ◽  
Connery J. Brennan ◽  
Gail Cresci ◽  
Deborah Paul ◽  
Michaela Hull ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Healthy Humans ◽  
Exercise Induced ◽  
Gastrointestinal Permeability

Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Light Chain ◽  
Human Skeletal Muscle ◽  
Transgenic Animal ◽  
Dependent Manner ◽  
Healthy Humans ◽  
Transgenic Animal Models ◽  
Exercise Induced

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.

scholarly journals Hormonal Responses after Exercise-induced Muscle Damage in Healthy Humans

2018 ◽  
Vol 50 (5S) ◽  
pp. 744 ◽  
Author(s):  
Anastassios Philippou ◽  
Roxane Tenta ◽  
Maria Maridaki ◽  
Michael Koutsilieris
Keyword(s):  
Muscle Damage ◽  
Hormonal Responses ◽  
Healthy Humans ◽  
Exercise Induced

Pregnancy-induced changes in the maximal physiological responses during swimming

1991 ◽  
Vol 71 (4) ◽  
pp. 1454-1459 ◽  
Author(s):  
R. G. McMurray ◽  
A. C. Hackney ◽  
V. L. Katz ◽  
M. Gall ◽  
W. J. Watson
Keyword(s):  
Pregnant Women ◽  
Plasma Volume ◽  
Physiological Responses ◽  
Cycle Ergometry ◽  
O2 Uptake ◽  
Heart Rates ◽  
Capillary Dynamics ◽  
Exercise Induced ◽  
Induced Changes

The effect of pregnancy on peak O2 uptake (VO2 peak) during tethered swimming was evaluated in 10 women during their 25th and 35th wk of pregnancy, as well as 9–11 wk postpartum. The swim results were compared with cycle ergometry results obtained at similar times. The results indicated that exercise-induced maximal heart rates remained the same and were similar for the swim and cycle trials, approximately 184 +/- 4 beats/min. Cycling VO2 peak was not affected by pregnancy, averaging 1.94 +/- 0.11 l/min. Postpartum swim VO2 peak was similar to the cycle results; however, during pregnancy it was significantly lower than cycling VO2 peak (P less than 0.05; postpartum, 1.78 +/- 0.14 l/min; 25th wk, 1.64 +/- 0.12; 35th wk, 1.48 +/- 0.11). Hemoglobin concentrations and hematocrits were lower during pregnancy; however, changes in plasma volume (based on hematocrit and hemoglobin) were found to be significantly greater during cycling than during swimming and also greater during pregnancy for both modes of exercise. It was concluded that, unlike cycling, the VO2 peak of pregnant women during swimming is reduced. This reduction in VO2 peak was associated with a decreased peak ventilation (r = 0.864) but was not correlated to exercise-induced hemoconcentration (r = -0.29). Furthermore, pregnancy results in a greater-than-normal exercise-induced hemoconcentration, which may be related to pregnancy-induced changes in capillary dynamics.

Importance of chloride for the correction of chronic metabolic alkalosis in the rat

1987 ◽  
Vol 253 (5) ◽  
pp. F1031-F1039 ◽  
Author(s):  
B. M. Wall ◽  
G. V. Byrum ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Plasma Volume ◽  
Metabolic Alkalosis ◽  
Choline Chloride ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Volume Contraction ◽  
Chloride Depletion ◽  
Sprague Dawley Rats ◽  
Sodium And Potassium

To determine whether chloride repletion without sodium could correct chronic chloride depletion metabolic alkalosis (CDA) in Sprague-Dawley rats without volume expansion and without increasing glomerular filtration rate (GFR), CDA was generated by peritoneal dialysis (PD) against 0.15 M NaHCO3 and maintained for 7-10 days by a chloride-restricted diet supplemented with sodium and potassium salts. Control animals were dialyzed against Ringer bicarbonate. The maintenance period of chronic CDA, compared with control, was characterized by hypokalemic metabolic alkalosis (serum TCO2 31.9 +/- 0.6 vs. 23.1 +/- 0.5 meq/l, P less than 0.05), volume contraction (plasma volume 3.76 +/- 0.08 vs. 4.19 +/- 0.22 ml/100 g body wt, P less than 0.05), decreased GFR (838 +/- 84 vs. 1045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), increased plasma renin activity (PRA) (63 +/- 13 vs. 12 +/- 3 ng.ml-1.h-1, P less than 0.05), but unchanged plasma aldosterone concentrations (PAC) (4.1 +/- 1.0 vs. 3.4 +/- 1.6 ng/dl, P = NS). Complete correction of chronic CDA was accomplished by 24 h of ingestion of choline chloride drink, and despite negative sodium balance, neutral potassium balance, continued bicarbonate ingestion, and persistent volume contraction (plasma volume 3.76 +/- 0.08 vs. 3.73 +/- 0.12 ml/100 g body wt pre- and postcorrection, P = NS), GFR remained decreased (659 +/- 87 vs. 1,045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), PRA decreased (63 +/- 13 vs. 33 +/- 5 ng.ml-1.h-1, P less than 0.05), but PAC did not change (4.1 +/- 1.0 vs. 6.1 +/- 1.6 ng/dl, P = NS) after correction of CDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of thermal and exercise factors in the mechanism of hypervolemia

1980 ◽  
Vol 48 (4) ◽  
pp. 657-664 ◽  
Author(s):  
V. A. Convertino ◽  
J. E. Greenleaf ◽  
E. M. Bernauer
Keyword(s):  
Exercise Training ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Rectal Temperature ◽  
Heat Exposure ◽  
Bicycle Ergometer ◽  
Thermal Factor ◽  
Albumin Content ◽  
Exercise Induced

Our purpose was to determine whether the chronic increase in plasma volume (PV), resulting from heat exposure (HE) and exercise training (ET), was due only to elevated rectal temperature (Tre) or whether there were additional nonthermal factors related to the exercise. Eight men were divided into two groups. The HE group sat for 2 h/day (Tdb = 42 degrees C, 93% rh) for 8 consecutive days; Tre was raised by 1.72 +/- 0.04 degrees C to 38.5 degrees C each day. The ET group rode a bicycle ergometer for 2 h/day for 8 days (Tdb = 25 degrees C, 60% rh) at a load (60-65 Vo2max) that gave the same area under their Tre curve. PV increased by 177 ml (4.9%, P less than 0.05) in the HE group and by 427 ml (12.0%, P less than 0.05) in the ET group. This exercise-induced hypervolemia was associated with thermal factor(s) that contributed 40% and nonthermal factors that accounted for the remaining 60%. Some nonthermal, exercise-induced factors were twofold greater increases in plasma osmotic and vasopressin levels during exercise, and a fivefold increase in resting plasma protein (albumin) content.

Mechanism for the posture-specific plasma volume increase after a single intense exercise protocol

1999 ◽  
Vol 86 (3) ◽  
pp. 867-873 ◽  
Author(s):  
Kei Nagashima ◽  
Gary W. Mack ◽  
Andrew Haskell ◽  
Takeshi Nishiyasu ◽  
Ethan R. Nadel
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Urine Volume ◽  
Peak Oxygen Consumption ◽  
Plasma Volume Expansion ◽  
Plasma Albumin ◽  
Postural Changes ◽  
Albumin Content ◽  
Exercise Induced

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 ± 0.8 ml/kg in Up but decreased 2.1 ± 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 ± 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup ( P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.

Post-exercise Protein And Carbohydrate Ingestion Enhances Exercise-induced Increase In Plasma Volume And Albumin Content

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 491
Author(s):  
Kazunobu Okazaki ◽  
Ryosuke Takeda ◽  
Akina Suzuki ◽  
Daiki Imai ◽  
Takashi Kawabata ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Carbohydrate Ingestion ◽  
Post Exercise ◽  
Albumin Content ◽  
Exercise Induced

scholarly journals Electrolyte and Plasma Responses After Pickle Juice, Mustard, and Deionized Water Ingestion in Dehydrated Humans

2014 ◽  
Vol 49 (3) ◽  
pp. 360-367 ◽  
Author(s):  
Kevin C. Miller
Keyword(s):  
Plasma Volume ◽  
Plasma Osmolality ◽  
Plasma Potassium ◽  
Large Mass ◽  
Deionized Water ◽  
Plasma Sodium ◽  
Similar Amount ◽  
Water Ingestion ◽  
Exercise Induced ◽  
Conventional Unit

Context: Some athletes ingest pickle juice (PJ) or mustard to treat exercise-associated muscle cramps (EAMCs). Clinicians warn against this because they are concerned it will exacerbate exercise-induced hypertonicity or cause hyperkalemia. Few researchers have examined plasma responses after PJ or mustard ingestion in dehydrated, exercised individuals. Objective: To determine if ingesting PJ, mustard, or deionized water (DIW) while hypohydrated affects plasma sodium (Na+) concentration ([Na+]p), plasma potassium (K+) concentration ([K+]p), plasma osmolality (OSMp), or percentage changes in plasma volume or Na+ content. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: A total of 9 physically active, nonacclimated individuals (age = 25 ± 2 years, height = 175.5 ± 9.0 cm, mass = 78.6 ± 13.8 kg). Intervention(s): Participants exercised vigorously for 2 hours (temperature = 37°C ± 1°C, relative humidity = 24% ± 4%). After a 30-minute rest, a baseline blood sample was collected, and they ingested 1 mL/kg body mass of PJ or DIW. For the mustard trial, participants ingested a mass of mustard containing a similar amount of Na+ as for the PJ trial. Postingestion blood samples were collected at 5, 15, 30, and 60 minutes. Main Outcome Measure(s): The dependent variables were [Na+]p, [K+]p, OSMp, and percentage change in plasma Na+ content and plasma volume. Results: Participants became 2.9% ± 0.6% hypohydrated and lost 96.8 ± 27.1 mmol (conventional unit = 96.8 ± 27.1 mEq) of Na+, 8.4 ± 2 mmol (conventional unit = 8.4 ± 2 mEq) of K+, and 2.03 ± 0.44 L of fluid due to exercise-induced sweating. They ingested approximately 79 mL of PJ or DIW or 135.24 ± 22.8 g of mustard. Despite ingesting approximately 1.5 g of Na+ in the PJ and mustard trials, no changes occurred within 60 minutes postingestion for [Na+]p, [K+]p, OSMp, or percentage changes in plasma volume or Na+ content (P &gt; .05). Conclusions: Ingesting a small bolus of PJ or large mass of mustard after dehydration did not exacerbate exercise-induced hypertonicity or cause hyperkalemia. Consuming small volumes of PJ or mustard did not fully replenish electrolytes and fluid losses. Additional research on plasma responses pre-ingestion and postingestion to these treatments in individuals experiencing acute EAMCs is needed.

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