No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Effect of consecutive exercise days of jogging or cycling on the resting metabolic rate and nitrogen balance
Abstract
The resting metabolic rate (RMR) following recovery from level jogging, which includes an eccentric component, was hypothesized to be greater and remain elevated longer than following concentric cycling due to repair of exercise-induced muscle damage. Nine males participated in both a jogging and cycling protocol. RMR measurements were determined by indirect calorimetry before and on the seven mornings following three consecutive days of 45-min exercise sessions performed at equal energy expenditures. Daily protein intake and urinary nitrogen (N) output were measured throughout both protocols. No differences were observed in the resting oxygen consumption, respiratory exchange ratio, or heart rate between baseline measurements and from any of the postexercise days following the third exercise bout. Urinary N and the estimated N balance during postexercise also did not change from baseline values over time or mode x time. However, the overall estimated N balance for the jogging protocol was less positive than for the cycling protocol (p < 0.05). Muscular soreness was greater (p < 0.05) and lasted longer from the jogging protocol. Although, muscle damage may have been more severe in the jogging protocol, RMR and N balance were not different between the two exercise modes.
... En la literatura científica se le ha dado considerable atención al miembro de la ecuación del balance energético correspondiente al gasto energético, especialmente a los factores que afectan la tasa metabólica basal (BMR) de la persona. Dado que la BMR representa el mayor porcentaje de el gasto energético diario de un individuo (~60-75% del gasto energético total), muchos investigadores se han interesado en identificar los tipos de intervenciones que pudieran potenciar el incremento en la BMR (26) y en la tasa metabólica de reposo (RMR) para facilitar la pérdida de peso (14). De manera característica, el ejercicio de resistencia ha sido utilizado para alterar la composición corporal, debido a que este tipo de ejercicio tiene la capacidad de incrementar el gasto energético y la utilización de grasas. ...
... Debido a que en los humanos, la urea es el principal producto metabólico que contiene nitrógeno derivado del catabolismo proteico, la degradación de la FFM produce una liberación de nitrógeno derivado del amoniaco que causa una elevación del nitrógeno de la urea urinaria (24). Aunque los niveles de nitrógeno de la urea urinaria no se incrementaron significativamente luego de días consecutivos de trote, Kolkhorst et al. (14) observaron un balance total de nitrógeno reducido luego de la realización de ejercicios, de lo cual se puede inferir que hubo una mayor degradación de FFM. En un estudio clínico llevado a cabo con pacientes que se recuperaban de una cirugía de baypass en las arterias coronarias, Shaw et al. (24) mostraron incrementos en nitrógeno de la urea urinaria que acompañaba a la perdida de FFM luego de los primeros días de reposo en cama. ...
RESUMEN Treinta hombres saludables, físicamente activos (20.1±1.6 años) fueron aleatoriamente asignados para participar durante 10 semanas en uno de los siguientes grupos de entrenamiento: entrenamiento de resistencia (ET; trote y/o carreras durante 3 días por semana); entrenamiento de la fuerza (RT; entrenamiento de pesas durante 3 días por semana); o entrenamiento combinado de fuerza y resistencia (CT). Antes y después del entrenamiento se determinó en cada sujeto la tasa metabólica basal (BMR), el porcentaje de grasa corporal (BF), la potencia aeróbica máxima, y una repetición máxima en press de banca y sentadilla. También se determinó la concentración de nitrógeno de la urea urinaria antes, durante y después del entrenamiento. La BMR se incrementó significativamente desde el pre-al post-entrenamiento en el grupo RT (7613±968 hasta 8090±951kJ/día) y en el grupo CT (7455±964 hasta 7,802±981kJ/día), pero no en el grupo ET (7231±554 hasta 7029±666kJ/día). El BF para el grupo CT (12.2±3.5 hasta 8.7±1.7%) se redujo significativamente en comparación con el grupo RT (15.4±2.7 hasta 14.0±2.7%) y el grupo ET (11.8±2.9 hasta 9.5±1.7%). La potencia aeróbica máxima se incrementó significativamente en el grupo ET (13%), pero no en el grupo RT (-0.2%) o en el grupo CT (7%), mientras que las mejoras en una repetición máxima en los ejercicios de press de banca y sentadilla fueron mayores en el grupo RT (24 y 23%, respectivamente), en comparación con el grupo CT (19 y 12%, respectivamente). La perdida de nitrógeno de la urea urinaria fue mayor en el grupo ET (14.6±0.9 g/24h) que en el grupo RT (11.7±1.0g/24h) y CT (11.5±1.0g/24h), al final de las 10 semanas de entrenamiento. Estos datos indican que, aunque el entrenamiento de la fuerza por si solo incrementa la BMR y la fuerza muscular, y que el entrenamiento de la resistencia por si solo incrementa la potencia aeróbica y reduce el BF, el entrenamiento combinado proporciona todos estos beneficios, pero con una menor magnitud que el RT y el ET por separado, luego de 10 semanas de entrenamiento.
... The energy expenditure side of the energy balance equation, especially those factors affecting a person's basal metabolic rate (BMR), has been given considerable attention in the literature. Given that BMR represents the largest percentage of an individual's daily energy expenditure (ϳ60-75% of total energy expenditure), many researchers have been interested in identifying interventions that may potentiate an increase in BMR (26) and resting metabolic rate (RMR) to facilitate weight loss (14). Typically, endurance exercise has been used for altering body composition because of its ability to increase energy expenditure and fat utilization. ...
... Because urea is the major nitrogen-containing metabolic product of protein catabolism in humans, as FFM is degraded there is a release of nitrogen-derived ammonia that causes urinary urea nitrogen to become elevated (24). Although urinary urea nitrogen levels did not significantly increase after consecutive days of jogging, Kolkhorst et al. (14) noted that overall nitrogen balance decreased after exercise, inferring a greater breakdown of FFM. In a clinical study of recovering coronary artery bypass graft surgery patients, Shaw et al. (24) showed increases in urinary urea nitrogen accompanying the loss of FFM after the initial days of bed rest. ...
Thirty physically active healthy men (20.1 +/- 1.6 yr) were randomly assigned to participate for 10 wk in one of the following training groups: endurance trained (ET; 3 days/wk jogging and/or running), resistance trained (RT; 3 days/wk resistance training), or combined endurance and resistance trained (CT). Before and after training, basal metabolic rate (BMR), percent body fat (BF), maximal aerobic power, and one-repetition maximum for bench press and parallel squat were determined for each subject. Urinary urea nitrogen was determined pre-, mid-, and posttraining. BMR increased significantly from pre- to posttraining for RT (7,613 +/- 968 to 8,090 +/- 951 kJ/day) and CT (7,455 +/- 964 to 7,802 +/- 981 kJ/day) but not for ET (7,231 +/- 554 to 7,029 +/- 666 kJ/day). BF for CT (12.2 +/- 3.5 to 8.7 +/- 1.7%) was significantly reduced compared with RT (15.4 +/- 2.7 to 14.0 +/- 2.7%) and ET (11.8 +/- 2.9 to 9.5 +/- 1.7%). Maximal aerobic power increased significantly for ET (13%) but not RT (-0.2%) or CT (7%), whereas the improvements in one-repetition maximum bench press and parallel squat were greater in RT (24 and 23%, respectively) compared with CT (19 and 12%, respectively). Urinary urea nitrogen loss was greater in ET (14.6 +/- 0.9 g/24 h) than in RT (11.7 +/- 1.0 g/24 h) and CT (11.5 +/- 1.0 g/24 h) at the end of 10 wk of training. These data indicate that, although RT alone will increase BMR and muscular strength, and ET alone will increase aerobic power and decrease BF, CT will provide all of these benefits but to a lesser magnitude than RT and ET after 10 wk of training.
... Additionally , although RT subjects had a similar time course in RMR elevation when compared with the UT subjects, we believe that their attenuated [CK] and RPMS response to the eccentric exercise suggested that there was a lesser degree of muscle damage thereby equating to a diminished elevation in postexercise RMR. Although our findings are not directly comparable to those of others (13,19,20,29) due to protocol differences (i.e., exercise mode, intensity, and duration), some comparisons are in order. Gillette et al. (13) and Melby et al. (20) reported a prolonged recovery RMR from resistance exercise; however , unlike the results in the present investigation, RMR remained elevated only up to 15 h. ...
... Consequently, this may have been reflected in the smaller elevation found in postexercise RMR. In summary, as evidenced by the present data and other researchers who have speculated from the results of their own studies (13,19,20,29), we believe that the events associated with muscle damage from leg presses that emphasized the eccentric movement partially contributed to the elevations found in postexercise RMR. Although the reasons for this observation are not completely understood and need considerably more invasive measurements, the events which led to differences in postexercise RMR for the UT and RT subjects seem to lend additional support to this theory. ...
The purpose of this investigation was to determine whether muscle damage caused from acute resistance exercise with an eccentric overload would influence resting metabolic rate (RMR) up to 72 h postexercise in resistance-trained (RT) and untrained (UT) subjects.
Nine RT and 9 UT male subjects (mean +/- SD; age = 20.7 +/- 2.1 yr; body mass = 79.0 +/- 1.4 kg; height = 178.4 +/- 3.1 cm; and body fat = 10.2 +/- 1.6%) were measured for RMR, creatine kinase concentration ([CK]), and rating of perceived muscle soreness (RPMS) on five consecutive mornings. To induce muscle damage, after the measurements on day 2, each subject performed leg presses that emphasized the eccentric movement for 8 sets at his six-repetition maximum (6-RM).
Compared with baseline, the RMR (kJ x d(-1) and kJ x kg FFM(-1) x h(-1) was significantly elevated for RT and UT at 24 h and 48 h postexercise. From 24 h to 48 h to 72 h postexercise, RMR significantly decreased within both groups. The UT group had a significantly higher RMR at 24 h (9,705.4 +/- 204.5 kJ x d(-1)) and 48 h postexercise (8,930.9 +/- 104.4 kJ x d(-1)) when compared with the RT group (9,209.3 +/- 535.3 and 8,601.7 + 353.7 kJ x d(-1)). Both [CK] and RPMS showed a similar time course.
There was a significantly higher [CK] for the UT group at 24 h postexercise (320.4 +/- 20.1 U x L(-1)) and for both [CK] and RPMS at 48 h (1,140.3 +/- 37.1 U x L(-1) and 4.4 +/- 0.5, respectively) and 72 h postexercise (675.9 +/- 41.7 U x L(-1) and 1.67 +/- 0.5, respectively) when compared with the RT group (24 h, 201.9 +/- 13.4 U x L(-1); 48 h, 845.4 +/- 30.7 U x L(-1) and 3.7 +/- 0.5: and 72 h postexercise, 420.2 +/- 70.2 U x L(-1) and 0.89 +/- 0.3). These data indicate that eccentrically induced muscle damage causes perturbations in RMR up to 48 h postexercise.
... This finding is in agreement with that of Hudson et al. (2020) who, albeit in a different sport, reported RMR andVO 2 to be significantly increased following a match in senior professional rugby union players. They proposed that the elevated RMR was a consequence of a raised energy requirement due to a combination of either prolonged excessive postexercise oxygen consumption (Kolkhorst et al., 1994) or a high eccentric-focused physical load (Hackney et al., 2008) inducing the degradation and resynthesis of damaged muscle fibers (Burt et al., 2014). This proposed mechanism aligns to the current study within soccer as research by Silva et al. (2013) suggests that muscle damage markers (creatine kinase) in professional soccer players are increased for up to 48 hr following a competitive match. ...
Resting metabolic rate (RMR) is an important component of total daily energy expenditure; however, it is currently not understood how it varies across a typical competitive match week in professional soccer players. For the first time, we aimed to assess RMR throughout an in-season competitive week in professional soccer players. Additionally, we aimed to assess energy and carbohydrate intake across the same week. Twenty-four professional soccer players from an English Premier League club (age: 18 ± 1.6 years) completed the study. RMR was assessed each morning of a typical competitive match week (match day [MD] −3, −2, −1, +1, +2, and + 3), and dietary intake (including MD) was assessed daily via the remote food photography method and 24-hr recall. Daily training load was quantified using Global Positioning System, daily muscle soreness ratings were recorded, and body composition was assessed via dual-energy X-ray absorptiometry. There was a significant ( p = .0004) increase in mean RMR of ∼261 kcal/day on MD + 1, compared with MD − 1. Additionally, volume of oxygen consumed significantly increased at MD + 1 ( p = .0002) versus MD − 1. There were no significant differences in daily energy or carbohydrate intake across the competitive week ( p > .05), with inadequate carbohydrate intakes on MD − 1 (∼3.9 g/kg body mass), MD (∼4.2 g/kg body mass), and MD + 1 (∼3.6 g/kg body mass) in relation to current recommendations. We report, for the first time, that RMR is significantly increased following a competitive match in professional soccer players. In addition, we confirm previous findings to reinforce that players exhibit inadequate nutrition periodization practices, which may impair physical performance and recovery.
... Moreover, Nieman et al. (2014) observed that after three days of intensified training, runners experienced a greater relative increase in proinflammatory cytokines than did cyclists. In addition, Kolkhorst, Londeree, and Thomas (1994) observed post-running muscular soreness was greater and lasted longer than following cycling. This intimates potential for a greater muscle damage following running compared to cycling, and therefore the possibility that ACT may improve running performance to a greater extent than cycling performance requires exploration. ...
Although considerable research concerning the efficacy of analgesics in sport exists, there is a paucity of data concerning effects of acute acetaminophen (ACT) ingestion on sprint interval running exercise. This investigation concerned the effect of acute ACT ingestion on eight 30 s maximal treadmill sprints on a non-motorized treadmill, interspersed with two-minute rests in males (N=8, age 26±3 years, body height 174±7 cm, body mass 71±8 kg) in a placebo-controlled, randomized crossover design. A time x condition repeated measures analysis of variance (ANOVA) determined ACT ingestion did not influence mean power output, peak power output, peak vertical ground reaction force, peak oxygen uptake, or total distance completed (p>.05). Perceived pain was reduced by 8-15% during the final three sprints following ACT ingestion (p<.05). Data presented here suggest ACT may reduce exercise-induced pain during the latter stages of sprint interval treadmill running, without influencing performance.
In the recovery period after strenuous exercise, there is increased O2 uptake, termed the excess postexercise O2 consumption (EPOC). One of the mechanisms suggested to explain EPOC is activation of the triglyceride/fatty acid (TG/FA) cycle by catecholamines. The purpose of this study was to determine the effect of selective beta1- and nonselective beta-adrenoceptor blockade on EPOC and the TG/FA cycle. Seven healthy young men each participated in three control and three exercise experiments in a randomized and balanced sequence. In the exercise experiments, subjects exercised for 90 minutes at 58% +/- 2% (mean +/- SD) of maximal O2 uptake on a cycle ergometer, followed by a 4.5-hour bedrest. The control experiments followed the same protocol, but without exercise. In one control and one exercise experiment, the selective beta1-adrenoceptor antagonist atenolol (0.062 mg.kg(-1) body weight) was administered intravenously immediately after the exercise (EXAT) and at the corresponding time in the rest-control experiment (REAT). In a second set of control and exercise experiments, the nonselective beta-adrenoceptor antagonist propranolol (0.15 mg.kg(-1) body weight) was administered (REPRO and EXPRO). In a third set of rest and exercise experiments, an injection of saline was given instead of beta-antagonist (RE and EX). TG/FA cycling was calculated by combining results obtained with a two-stage glycerol infusion and indirect calorimetry. O2 uptake was significantly increased above control levels throughout the recovery period after exercise with the nonselective beta-adrenoceptor antagonist, beta1-adrenoceptor antagonist, and saline. However, there was no difference between the time course or magnitude of EPOC in the three situations. After 4.5 hours of bedrest, the mean increase in O2 uptake was 8% to 9% in all three conditions. TG/FA cycling was increased after exercise, but no effects of beta-antagonists were observed. We conclude that EPOC and the rate of TG/FA cycling are not attenuated by selective beta1- or nonselective beta-adrenoceptor blockade after an acute prolonged exercise protocol.
After strenuous exercise there is a sustained increase in resting O2 consumption. The magnitude and duration of the excess post-exercise O2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that beta-adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through beta-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG-FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O2 uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post-exercise O2 uptake has been shown when beta-blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of beta-antagonist after exercise did not seem to change EPOC.
In the recovery period after exercise there is an increase in oxygen uptake termed the ‘excess post-exercise oxygen consumption’ (EPOC), consisting of a rapid and a prolonged component. While some studies have shown that EPOC may last for several hours after exercise, others have concluded that EPOC is transient and minimal. The conflicting results may be resolved if differences in exercise intensity and duration are considered, since this may affect the metabolic processes underlying EPOC. Accordingly, the absence of a sustained EPOC after exercise seems to be a consistent finding in studies with low exercise intensity and/or duration. The magnitude of EPOC after aerobic exercise clearly depends on both the duration and intensity of exercise. A curvilinear relationship between the magnitude of EPOC and the intensity of the exercise bout has been found, whereas the relationship between exercise duration and EPOC magnitude appears to be more linear, especially at higher intensities.
Differences in exercise mode may potentially contribute to the discrepant findings of EPOC magnitude and duration. Studies with sufficient exercise challenges are needed to determine whether various aerobic exercise modes affect EPOC differently. The relationships between the intensity and duration of resistance exercise and the magnitude and duration of EPOC have not been determined, but a more prolonged and substantial EPOC has been found after hardversus moderate-resistance exercise. Thus, the intensity of resistance exercise seems to be of importance for EPOC.
Lastly, training status and sex may also potentially influence EPOC magnitude, but this may be problematic to determine. Still, it appears that trained individuals have a more rapid return of post-exercise metabolism to resting levels after exercising at either the same relative or absolute work rate; however, studies after more strenuous exercise bouts are needed. It is not determined if there is a sex effect on EPOC.
Finally, while some of the mechanisms underlying the more rapid EPOC are well known (replenishment of oxygen stores, adenosine triphosphate/creatine phosphate resynthesis, lactate removal, and increased body temperature, circulation and ventilation), less is known about the mechanisms underlying the prolonged EPOC component. A sustained increased circulation, ventilation and body temperature may contribute, but the cost of this is low. An increased rate of triglyceride/fatty acid cycling and a shift from carbohydrate to fat as substrate source are of importance for the prolonged EPOC component after exhaustive aerobic exercise. Little is known about the mechanisms underlying EPOC after resistance exercise.
We investigated the effects of a single bout of aerobic and resistance exercise of similar relative intensity and duration on resting energy expenditure (REE) and substrate utilisation. Ten young healthy males volunteered [age 22 (1.8) years, weight 76 (7.9) kg, height 176 (4.1) cm, percentage body fat 10.5 (4.0)%; mean (SEM)]. They randomly underwent three conditions in which they either lifted weights for 60 min at 70-75% of 1-RM (WL), ran for 60 min at 70-75% of maximal oxygen intake (R) or did not exercise (C). REE and substrate utilisation, determined via respiratory exchange ratio ( R), were measured prior to exercise, and 10, 24, 48 and 72 h post-exercise. It was revealed that REE was significantly elevated ( P<0.05) 10 and 24 h after the end of WL [2,124 (78) and 2,081 (76) kcal, respectively] compared to pre-exercise [1,972 (82) kcal]. REE was also significantly increased ( P<0.05) 10 and 48 h after the completion of R [2,150 (73) and 1,995 (74) kcal, respectively] compared to pre-exercise data [1,862 (70) kcal]. R was lower 10 and 24 h following either WL or R [0.813 (0.043); 0.843 (0.040) and 0.818 (0.021); 0.832 (0.021), respectively] compared to baseline measurements [0.870 (0.025) and 0.876 (0.04), respectively]. Creatine kinase was significantly elevated ( P<0.05) 24 h after both WL and R, whereas delayed onset muscle soreness became significantly elevated ( P<0.05) 24 h after only WL. There were no significant changes for any treatment in thyroid hormones (T(3) and T(4)). These results suggest that a single bout of either WL or R exercise, characterised by the same relative intensity and duration, increase REE and fat oxidation for at least 24 h post-exercise.
ResearchGate has not been able to resolve any references for this publication.