Time-course of changes in cardiac function during recovery after acute exercise

2007 ◽  
Vol 32 (6) ◽  
pp. 1164-1169 ◽  
Author(s):  
Karen Y. Wonders ◽  
David S. Hydock ◽  
Reid Hayward
Keyword(s):  
Lipid Peroxidation ◽  
Cardiac Function ◽  
Time Course ◽  
Acute Exercise ◽  
Exercise Bout ◽  
Left Ventricular ◽  
Antioxidant Potential ◽  
Exhaustive Exercise ◽  
Post Exercise ◽  
Single Bout

Exercise-induced cardiac dysfunction (EICD) has been observed immediately following exhaustive exercise in trained individuals, but limited and conflicting data are available regarding EICD in a previously untrained population days after an exhaustive exercise bout. The purpose of this study was to examine the effects of a single bout of acute exercise on cardiac function during the 72 h after exercise and identify potential contributing mechanisms. After completing an acute exercise bout on a motorized treadmill (25 m/min, 5% grade, 60 min), rats were sacrificed immediately, 24 h, 48 h, or 72 h after the exercise bout. At the scheduled time of sacrifice, hearts were isolated and perfused for determination of ex vivo cardiac function, and examined for malondialdehyde (MDA), a lipid peroxidation index, and antioxidant potential (AOP). During the 48 h post exercise, left ventricular developed pressure decreased by 30%, dP/dtmax declined by 37%, and dP/dtmin showed a 34% decrease (p < 0.05). By 72 h, cardiac function had returned to control levels. MDA was increased immediately after the exercise bout and at the 24 and 48 h intervals (p < 0.05). Conversely, AOP progressively decreased at the 24 and 48 h intervals. As with cardiac function, MDA and AOP had returned to control levels by 72 h post-exercise. These data indicate that a single bout of prolonged, moderately intense exercise performed by previously sedentary rats impaired cardiac function for up to 48 h. This decrement in cardiac function was associated with increased lipid peroxidation and decreased antioxidant potential.

scholarly journals Exercise shifts hypothetical food choices towards greater amounts and more immediate consumption

2020 ◽  
Author(s):  
Karsten Koehler ◽  
Safiya E Beckford ◽  
Elise Thayer ◽  
Alexandra R Martin ◽  
Julie B Boron ◽  
...  
Keyword(s):  
Food Intake ◽  
Aerobic Exercise ◽  
Acute Exercise ◽  
Food Preferences ◽  
Exercise Bout ◽  
Food Choices ◽  
Post Exercise ◽  
Single Bout ◽  
Electronic Questionnaires ◽  
The Impact

Although exercise modulates appetite regulation and food intake, it remains poorly understood how exercise impacts decision making about food. The purpose of the present study was to assess the impact of an acute exercise bout on hypothetical choices related to the amount and timing of food intake. Forty-one healthy participants (22.0 ± 2.6 years; 23.7 ± 2.5 kg/m2, 56% female) completed 45 minutes of aerobic exercise and a resting control condition in randomized order. Food amount preferences and intertemporal food preferences (preference for immediate vs. delayed consumption) were assessed using electronic questionnaires with visual food. Compared to rest, exercise resulted in a greater increase in the food amount selected, both immediately post exercise (+25.8 ± 11.0 vs. +7.8 ± 11.0 kcal/item, p = 0.02) and 30 min post exercise (+47.3 ± 12.4 vs. +21.3 ± 12.4 kcal/item, p = 0.005). Exercise further resulted in a greater increase in the preference for immediate consumption immediately post exercise (+0.23 ± 0.10 vs. +0.06 ± 0.10; p = 0.03) and 30 min post exercise (+0.30 ± 0.12 vs. +0.08 ± 0.12; p = 0.01). Our findings demonstrate that a single bout of aerobic exercise shifts hypothetical food choices towards greater amounts and more immediate consumption, highlighting the importance of the timing of food choices made in the exercise context.

Effect of a single bout of exercise and chronic exercise training on insulin sensitivity in racing sled dogs

2014 ◽  
Vol 10 (3) ◽  
pp. 167-172 ◽  
Author(s):  
S.E. Pratt-Phillips ◽  
R.J. Geor ◽  
M. Buser ◽  
A. Zirkle ◽  
A. Moore ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Exercise Bout ◽  
Post Exercise ◽  
Exercise Challenge ◽  
Sled Dogs ◽  
Significant Difference ◽  
Single Bout ◽  
Three Stages

Two experiments were designed to investigate the role of exercise on insulin sensitivity (IS) in Alaskan racing sled dogs. In both experiments, IS was quantified with an isoglycemic-hyperinsulinemic clamp (IHC), whereby IS was defined as the glucose infusion rate (GIR) divided by the mean insulin concentration during the clamp. In Experiment 1, IS was quantified in 12 racing sled dogs during three stages of exercise training: unexercised for 4 months over the summer (deconditioned), and after two and four months of exercise conditioning. At each stage IS was assessed in unexercised dogs (n=6) and 60 h following a standard exercise challenge (n=6) consisting of a 35.4 km run completed in 2.5 h. In Experiment 2, IS was assessed in deconditioned dogs (n=6) and in well-conditioned dogs that had either completed a 708 km race 5-days prior (n=3) or were unraced for the previous month (n=3). In Experiment 1, there were no significant differences (Pã0.05) in GIR or IS between the three levels of conditioning, nor were there any effects of the exercise bout 60 h prior to the IHC. In Experiment 2 there was no significant difference in IS between well-conditioned dogs and untrained dogs (Pã0.05). However, dogs that completed a 708 km race 5-days prior to the IHC had a significantly higher IS than dogs that were deconditioned and those that were conditioned but unraced. These results suggest that the workload of an exercise challenge is a factor in post-exercise changes in IS but that exercise conditioning has little impact on IS in Alaskan sled dogs.

scholarly journals Resistance training reduces the acute exercise-induced increase in muscle protein turnover

1999 ◽  
Vol 276 (1) ◽  
pp. E118-E124 ◽  
Author(s):  
S. M. Phillips ◽  
K. D. Tipton ◽  
A. A. Ferrando ◽  
R. R. Wolfe
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Acute Exercise ◽  
Muscle Protein ◽  
Exercise Bout ◽  
Muscle Contractions ◽  
Breakdown Rates ◽  
Single Bout ◽  
Fractional Synthesis ◽  
Exercise Induced

We examined the effect of resistance training on the response of mixed muscle protein fractional synthesis (FSR) and breakdown rates (FBR) by use of primed constant infusions of [2H5]phenylalanine and [15N]phenylalanine, respectively, to an isolated bout of pleiometric resistance exercise. Trained subjects, who were performing regular resistance exercise (trained, T; n = 6), were compared with sedentary, untrained controls (untrained, UT; n = 6). The exercise test consisted of 10 sets (8 repetitions per set) of single-leg knee flexion (i.e., pleiometric muscle contraction during lowering) at 120% of the subjects’ predetermined single-leg 1 repetition maximum. Subjects exercised one leg while their contralateral leg acted as a nonexercised (resting) control. Exercise resulted in an increase, above resting, in mixed muscle FSR in both groups (UT: rest, 0.036 ± 0.002; exercise, 0.0802 ± 0.01; T: rest, 0.045 ± 0.004; exercise, 0.067 ± 0.01; all values in %/h; P< 0.01). In addition, exercise resulted in an increase in mixed muscle FBR of 37 ± 5% (rest, 0.076 ± 0.005; exercise, 0.105 ± 0.01; all values in %/h; P < 0.01) in the UT group but did not significantly affect FBR in the T group. The resulting muscle net balance (FSR − FBR) was negative throughout the protocol ( P < 0.05) but was increased in the exercised leg in both groups ( P < 0.05). We conclude that pleiometric muscle contractions induce an increase in mixed muscle protein synthetic rate within 4 h of completion of an exercise bout but that resistance training attenuates this increase. A single bout of pleiometric muscle contractions also increased the FBR of mixed muscle protein in UT but not in T subjects.

Effects of a single bout of exercise on glucose effectiveness

1996 ◽  
Vol 80 (3) ◽  
pp. 754-759 ◽  
Author(s):  
Y. Higaki ◽  
T. Kagawa ◽  
J. Fujitani ◽  
A. Kiyonaga ◽  
M. Shindo ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Exercise Bout ◽  
Threshold Level ◽  
Tolerance Test ◽  
Cycle Ergometer ◽  
Intravenous Glucose Tolerance Test ◽  
Exhaustive Exercise ◽  
Intravenous Glucose ◽  
Glucose Effectiveness ◽  
Single Bout

The effects of a single bout of exercise on glucose effectiveness (SG) and insulin sensitivity (SI) in 22 sedentary subjects were estimated with a minimal model approach. The intravenous glucose tolerance test (IVGTT) was performed 1) 11 h after an exercise bout on a cycle ergometer at the lactate threshold level (mild exercise) for 60 min, 2) 11 h after an exercise bout at the 4 mM lactate level (hard exercise) for 36 +/- 1 min, 3) 11 h after an exhaustive-exercise bout (exhaustive exercise) for 96 +/- 7 min, or 4) without any prior exercise (control). Only the exhaustive exercise increased the glucose disappearance constant (2.69 +/- 0.28 vs. 2.05 +/- 0.13%/min; P < 0.05) and SI (15.0 +/- 2.0 vs. 10.3 +/- 0.9 x 10(-5) min/pM: P < 0.05) in comparison with the control condition. The SG and SG at zero insulin (GEZI) were not affected by any exercise condition. However, a marked individual difference in GEZI emerged after the exhaustive exercise and could be divided into two subgroups: one decreased in GEZI (0.014 +/- 0.001 vs. 0.007 +/- 0.001 min-1) and the other increased in GEZI (0.014 +/- 0.001 vs. 0.021 +/- 0.003 min-1). The former subgroup was accompanied by elevated levels of plasma creatine kinase (100 +/- 16 vs. 598 +/- 315 IU/l; P < 0.05) and myoglobin (Mb; 46 +/- 4 vs. 126 +/- 47 ng/ml; P < 0.05), whereas the latter subgroup showed no significant change in creatinine kinase (99 +/- 10 vs. 128 +/- 9 IU/l; P = 0.05) and Mb (50 +/- 7 vs. 51 +/- 4 ng/ml; P = 0.05). In both subgroups, SI was similarly increased after the exhaustive exercise. These results thus suggest that a single bout of exercise that results in muscle damage or changes in muscle permeability, as reflected in the increased creatine kinase and Mb levels, decreases GEZI, whereas exhaustive exercise without such alterations increases GEZI.

scholarly journals Gender differences in insulin action after a single bout of exercise

2004 ◽  
Vol 97 (3) ◽  
pp. 1013-1021 ◽  
Author(s):  
Leigh Perreault ◽  
Jennifer M. Lavely ◽  
Bryan C. Bergman ◽  
Tracy J. Horton
Keyword(s):  
Gender Differences ◽  
Insulin Action ◽  
Acute Exercise ◽  
Exercise Bout ◽  
Whole Body ◽  
Peripheral Tissues ◽  
Euglycemic Clamp ◽  
Hyperinsulinemic Euglycemic Clamp ◽  
Lower Glucose ◽  
Single Bout

Effects of a single exercise bout on insulin action were compared in men ( n = 10) and women ( n = 10). On an exercise day, subjects cycled for 90 min at 85% lactate threshold, whereas on a rest (control) day, they remained semirecumbent. The period of exercise, or rest, was followed by a 3-h hyperinsulinemic-euglycemic clamp (30 mU·m−2·min−1) and indirect calorimetry. Glucose kinetics were measured isotopically by using an infusion of [6,6-2H2]glucose. Glucose infusion rate (GIR) during the clamp on the rest day was not different between the genders. However, GIR on the exercise day was significantly lower in men compared with women ( P = 0.01). This was mainly due to a significantly lower glucose rate of disappearance in men compared with women ( P = 0.05), whereas no differences were observed in the endogenous glucose rate of appearance. Nonprotein respiratory quotient (NPRQ) increased significantly during the clamp from preclamp measurements in men and women on the rest day ( P < 0.01). Exercise abolished the increase in NPRQ seen during the clamp on the rest day and tended to decrease NPRQ in men. Our results indicate the following: 1) exercise abolishes the usual increase in NPRQ observed during a hyperinsulinemic-euglycemic clamp in both genders, 2) men exhibit relatively lower whole body insulin action in the 3–4 h after exercise compared with women, and 3) gender differences in insulin action may be explained by a lower glucose rate of disappearance in the men after acute exercise. Together, these data imply gender differences in insulin action postexercise exist in peripheral tissues and not in liver.

scholarly journals Consistency in compensatory eating responses following acute exercise in inactive, overweight and obese women

2015 ◽  
Vol 113 (7) ◽  
pp. 1170-1177 ◽  
Author(s):  
Jessica L. Unick ◽  
Kevin C. O'Leary ◽  
Leah Dorfman ◽  
J. Graham Thomas ◽  
Kelley Strohacker ◽  
...  
Keyword(s):  
Acute Exercise ◽  
Intraclass Correlation ◽  
Exercise Bout ◽  
Moderate Intensity ◽  
Exercise Session ◽  
Obese Women ◽  
Post Exercise ◽  
Overweight Women ◽  
Increase Energy Intake ◽  
The Difference

It is often assumed that some individuals reliably increase energy intake (EI) post-exercise (‘compensators’) and some do not (‘non-compensators’), leading researchers to examine the characteristics that distinguish these two groups. However, it is unclear whether EI post-exercise is stable over time. The present study examined whether compensatory eating responses to a single exercise bout are consistent within individuals across three pairs of trials. Physically inactive, overweight/obese women (n28, BMI 30·3 (sd2·9) kg/m2) participated in three pairs of testing sessions, with each pair consisting of an exercise (30 min of moderate-intensity walking) and resting testing day. EI was measured using a buffet meal 1 h post-exercise/rest. For each pair, the difference in EI (EIdiff= EIex− EIrest) was calculated, where EIexis the EI of the exercise session and EIrestis the EI of the resting session, and women were classified as a ‘compensator’ (EIex>EIrest) or ‘non-compensator’ (EIex≤ EIrest). The average EI on exercise days (3328·0 (sd1686·2) kJ) was similar to those on resting days (3269·4 (sd1582·4) kJ) (P= 0·67). Although EI was reliable within individuals across the three resting days (intraclass correlation coefficient (ICC) 0·75, 95 % CI 0·60, 0·87;P< 0·001) and three exercise days (ICC 0·83, 95 % CI 0·70, 0·91;P< 0·001), the ICC for EIdiffacross the three pairs of trials was low (ICC 0·20, 95 % CI − 0·02, 0·45;P= 0·04), suggesting that compensatory eating post-exercise is not a stable construct. Moreover, the classification of ‘compensators’/‘non-compensators’ was not reliable (κ =− 0·048;P= 0·66). The results were unaltered when ‘relative’ EI was used, which considers the energy expenditure of the exercise/resting sessions. Acute compensatory EI following an exercise bout is not reliable in overweight women. Seeking to understand what distinguishes ‘compensators’ from ‘non-compensators’ based on a single eating episode post-exercise is not justified.

scholarly journals Increased net muscle protein balance in response to simultaneous and separate ingestion of carbohydrate and essential amino acids following resistance exercise

2014 ◽  
Vol 39 (3) ◽  
pp. 329-339 ◽  
Author(s):  
Oliver C. Witard ◽  
Tara L. Cocke ◽  
Arny A. Ferrando ◽  
Robert R. Wolfe ◽  
Kevin D. Tipton
Keyword(s):  
Amino Acids ◽  
Resistance Exercise ◽  
Acute Exercise ◽  
Muscle Protein ◽  
Exercise Bout ◽  
Essential Amino Acids ◽  
Delayed Response ◽  
Protein Balance ◽  
Post Exercise ◽  
Exercise Muscle

Relative to essential amino acids (EAAs), carbohydrate (CHO) ingestion stimulates a delayed response of net muscle protein balance (NBAL). We investigated if staggered ingestion of CHO and EAA would superimpose the response of NBAL following resistance exercise, thus resulting in maximal anabolic stimulation. Eight recreationally trained subjects completed 2 trials: combined (COMB — drink 1, CHO+EAA; drink 2, placebo) and separated (SEP — drink 1, CHO; drink 2, EAA) post-exercise ingestion of CHO and EAA. Drink 1 was administered 1 h following an acute exercise bout and was followed 1 h later by drink 2. A primed, continuous infusion of l-[ring-13C6]-phenylalanine was combined with femoral arteriovenous sampling and muscle biopsies for the determination of muscle protein kinetics. Arterial amino acid concentrations increased following ingestion of EAA in both conditions. No difference between conditions was observed for phenylalanine delivery to the leg (COMB: 167 ± 23 μmol·min−1·(100 mL leg vol)−1 × 6 h; SEP: 167 ± 21 μmol·min−1·(100 mL leg vol)−1 × 6 h, P > 0.05). In the first hour following ingestion of the drink containing EAA, phenylalanine uptake was 50% greater for the SEP trial than the COMB trial. However, phenylalanine uptake was similar for COMB (110 ± 19 mg) and SEP (117 ± 24 mg) over the 6 h period. These data suggest that whereas separation of CHO and EAA ingestion following exercise may have a transient physiological impact on NBAL, this response is not reflected over a longer period. Thus, separation of CHO and EAA ingestion is unnecessary to optimize post-exercise muscle protein metabolism.

Rat skeletal muscle hexokinase II mRNA and activity are increased by a single bout of acute exercise

1994 ◽  
Vol 266 (2) ◽  
pp. E171-E178 ◽  
Author(s):  
R. M. O'Doherty ◽  
D. P. Bracy ◽  
H. Osawa ◽  
D. H. Wasserman ◽  
D. K. Granner
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Recovery Period ◽  
Exhaustive Exercise ◽  
Male Rats ◽  
Hexokinase Ii ◽  
Glut 4 ◽  
Heat Stable ◽  
Single Bout

This study addresses the potential role of skeletal muscle hexokinase (HK) II in the regulation of glucose uptake and metabolism in vivo. Male rats undertook a single bout of treadmill exercise and were then killed immediately or after a predetermined recovery period. Three muscles [soleus (Sol), gastrocnemius/plantaris (Gc), and white vastus] were excised, and HK II mRNA, GLUT-4 mRNA, total HK (HK I and HK II) and heat-stable HK (predominantly HK I) activities were assessed. Three hours after the cessation of a single bout of exhaustive exercise, HK II mRNA was significantly increased in all three muscles. Ninety or thirty minutes of exercise, with a 3-h recovery, increased Gc HK II mRNA to the same extent as exhaustive exercise, but 15 min of exercise had no effect. Gc HK II mRNA continued to increase up to 8 h after the cessation of 90 min of exercise but returned to basal by 24 h postexercise. In contrast to HK II mRNA, Gc GLUT-4 mRNA was unchanged at 0, 3, 8, and 24 h after the cessation of 90 min of exercise. Total HK activity was significantly increased in Sol and Gc, 8 and 24 h after the cessation of 90 min of exercise. Heat-stable HK activity was unchanged in all three muscles. The increase in total HK activity, inferred to be an increase of HK II, may be important in the persistence of the postexercise increase in insulin action.

scholarly journals Gas exchange, metabolite status and excess post-exercise oxygen consumption after repetitive bouts of exhaustive exercise in juvenile rainbow trout

1992 ◽  
Vol 167 (1) ◽  
pp. 155-169 ◽  
Author(s):  
M. Scarabello ◽  
G. J. Heigenhauser ◽  
C. M. Wood
Keyword(s):  
Oxygen Consumption ◽  
Rainbow Trout ◽  
Exercise Bout ◽  
Creatine Phosphate ◽  
Lactate Clearance ◽  
Exhaustive Exercise ◽  
Oxygen Debt ◽  
Whole Body ◽  
Post Exercise ◽  
Lactate Levels

Juvenile rainbow trout (approximately 6 g) were exercised to exhaustion in two 5 min bouts given 6 h apart. Resting levels of whole-body lactate and glycogen were restored prior to the second bout. The rate of O2 consumption increased about threefold 5 min after each bout of exercise, while recovery time decreased from 4 h after the first bout to 2–3 h after the second. The excess post-exercise oxygen consumption, i.e. ‘oxygen debt’, was significantly reduced by 40% after the second exercise bout, despite almost identical rates of lactate clearance and glycogen resynthesis. The rates of CO2 and ammonia excretion increased sixfold and threefold, and recovery times decreased from 4–6 h to 3 h and from 3 h to 1.5 h, respectively. After the first bout, whole-body lactate levels peaked at 5 min post-exercise at about 8.5 times pre-exercise levels. After the second bout, lactate levels peaked at 0 min post-exercise and fell more rapidly during recovery. Whole-body glycogen levels decreased by 70% and 80% and ATP levels decreased by 75% and 65% after the first and second bouts, respectively, while glucose levels increased about 1.5-fold immediately after both bouts. Creatine phosphate levels decreased by 70% and 80% after the first and second bouts, respectively. After 6 h of recovery, creatine phosphate levels were higher after the second bout than after the first. These findings suggest that exhaustive exercise may cause a ‘non-specific’ increase in metabolic rate not directly related to the processing of metabolites, which is reduced upon a subsequent exercise bout. This is in contrast with the classical ‘oxygen debt hypothesis’, which states that the oxygen debt and lactate clearance are linked. Furthermore, it appears that two sequential exercise bouts are sufficient to induce a ‘training effect’, i.e. improved rates of metabolic recovery.

Abstract 12547: Time-Course Influence of Brain Death on Cardiac Function and Its Impact on Posttransplant Graft Function

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Shiliang Li ◽  
Sevil Korkmaz ◽  
Sivakkanan Loganathan ◽  
Tamás Radovits ◽  
Peter Hegedüs ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Brain Death ◽  
Time Course ◽  
Ischemia Reperfusion ◽  
Balloon Catheter ◽  
Graft Function ◽  
Left Ventricular ◽  
Control Group ◽  
Sham Operation ◽  
Brain Dead

Introduction: Heart transplantation became the most effective treatment for end-stage heart failure. Donors after brain death are currently the only reliable source for cardiac transplants. However, hemodynamic instability and cardiac dysfunction have been demonstrated in brain-dead donors and this could therefore also affect posttransplant graft function. Hypothesis: Our aims were to evaluate in rats the time-course cardiac influence of brain death and we tested the hypothesis that brain death impairs graft left ventricular function. Methods: Lewis rats were either maintained brain death for 5h by inflation of a subdurally placed balloon catheter (n=7) or subjected to sham-operation (control group, n=9). We continuously assessed cardiac function during 5 h. Then, hearts were excised, stored in cold preservation solution for 1 h, and heterotopically transplanted. We evaluated graft function 1.5 h after transplantation. Results: Brain death was associated with decreased left ventricular contractility (ejection fraction: 37±6% vs. 57±5%; dP/dt max : 4770±197 mmHg/s vs. 7604 ±348 mmHg/s; dP/dt max -EDV: 60±7 mmHg/s vs. 74±2 mmHg/s; E max : 2.4±0.1 mmHg/μl vs. 4.4±0.3 mmHg/μl; PRSW: 47±9 mmHg vs. 78±3 mmHg; p<0.05) and relaxation (dP/dt min: -6638±722 mmHg/s vs. -11285±539 mmHg/s; Tau: 12.6±0.7 ms vs.10.5±0.4 ms; EDPVR: 0.33±0.14 mmHg/μl vs. 0.09±0.03 mmHg/μl, p<0.05) 45 min after its initiation and for the rest of 5 h compared to controls. Moreover, after transplantation, graft systolic and diastolic functions were impaired in the brain-dead group compared to controls (reflected by decreased left ventricular systolic and developed pressures, dP/dt max and dP/dt min , and prolonged Tau). Conclusions: In conclusion, we have a well detailed characterized in vivo rat model to examine the influence of brain death on ventricular dysfunction using a microconductance catheter technology via pressure-volume analysis. These results demonstrate that brain death increases the susceptibility of donor heart to ischemia/reperfusion injury after transplantation.

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