Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage

2015 ◽  
Vol 216 ◽  
pp. 70-77 ◽  
Author(s):  
Christopher D. Black ◽  
Alexander R. Gonglach ◽  
Robert E. Hight ◽  
Jessica B. Renfroe
2003 ◽  
Vol 94 (1) ◽  
pp. 38-42 ◽  
Author(s):  
R. D. Telford ◽  
G. J. Sly ◽  
A. G. Hahn ◽  
R. B. Cunningham ◽  
C. Bryant ◽  
...  

There is a wide body of literature reporting red cell hemolysis as occurring after various forms of exercise. Whereas the trauma associated with footstrike is thought to be the major cause of hemolysis after running, its significance compared with hemolysis that results from other circulatory stresses on the red blood cell has not been thoroughly addressed. To investigate the significance of footstrike, we measured the degree of hemolysis after 1 h of running. To control for the potential effects of oxidative and circulatory stresses on the red blood cell, the same subjects cycled for 1 h at equivalent oxygen uptake. Our subjects were 10 male triathletes, who each completed two separate 1-h sessions of running and cycling at 75% peak oxygen uptake, which were performed in random order 1 wk apart. Plasma free hemoglobin and serum haptoglobin concentrations were measured as indicators of hemolysis. We also measured methemoglobin as a percentage of total hemoglobin immediately postexercise as an indicator of red cell oxidative stress. Plasma free hemoglobin increased after both running ( P < 0.01) and cycling ( P < 0.01), but the increase was fourfold greater after running ( P < 0.01). This was reflected by a significant fall in haptoglobin 1 h after the running trials, whereas no significant changes occurred after cycling at any sample point. Methemoglobin increased twofold after both running and cycling ( P < 0.01), with no significant differences between modes of exercise. The present data indicate that, whereas general circulatory trauma to the red blood cells associated with 1 h of exercise at 75% maximal oxygen uptake may result in some exercise-induced hemolysis, footstrike is the major contributor to hemolysis during running.


2017 ◽  
Vol 122 (3) ◽  
pp. 559-570 ◽  
Author(s):  
Jonathan M. Peake ◽  
Oliver Neubauer ◽  
Paul A. Della Gatta ◽  
Kazunori Nosaka

Unaccustomed exercise consisting of eccentric (i.e., lengthening) muscle contractions often results in muscle damage characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling, efflux of myocellular proteins). The time course of recovery following exercise-induced muscle damage depends on the extent of initial muscle damage, which in turn is influenced by the intensity and duration of exercise, joint angle/muscle length, and muscle groups used during exercise. The effects of these factors on muscle strength, soreness, and swelling are well characterized. By contrast, much less is known about how they affect intramuscular inflammation and molecular aspects of muscle adaptation/remodeling. Although inflammation has historically been viewed as detrimental for recovery from exercise, it is now generally accepted that inflammatory responses, if tightly regulated, are integral to muscle repair and regeneration. Animal studies have revealed that various cell types, including neutrophils, macrophages, mast cells, eosinophils, CD8 and T-regulatory lymphocytes, fibro-adipogenic progenitors, and pericytes help to facilitate muscle tissue regeneration. However, more research is required to determine whether these cells respond to exercise-induced muscle damage. A large body of research has investigated the efficacy of physicotherapeutic, pharmacological, and nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage, with mixed results. More research is needed to examine if/how these treatments influence inflammation and muscle remodeling during recovery from exercise.


2019 ◽  
Vol 51 (Supplement) ◽  
pp. 902
Author(s):  
Robert E. Hight ◽  
Darshit S. Patel ◽  
Jessica A. Peterson ◽  
Cameron Lohman ◽  
Jason A. Campbell ◽  
...  

2004 ◽  
Vol 97 (2) ◽  
pp. 579-584 ◽  
Author(s):  
Krista R. Howarth ◽  
Paul J. LeBlanc ◽  
George J. F. Heigenhauser ◽  
Martin J. Gibala

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 ± 1 yr) cycled at ∼80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 ± 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 ± 6 min). In addition to improved performance, training increased ( P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 ± 0.2 vs. 4.3 ± 0.2 mmol/kg dry wt ( P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 ± 0.2 vs. pretraining: 3.5 ± 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 ± 0.7 vs. pretraining: 7.7 ± 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 ± 0.2 vs. pretraining: 5.6 ± 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].


1998 ◽  
Vol 76 (5) ◽  
pp. 505-511 ◽  
Author(s):  
Bente Klarlund Pedersen ◽  
Kenneth Ostrowski ◽  
Thomas Rohde ◽  
Helle Bruunsgaard

Strenuous exercise is accompanied by an increase in circulating proinflammatory and inflammation responsive cytokines, having some similarities with the response to sepsis and trauma. The sequential release of tumour necrosis factor-alpha, interleukin (IL)1beta, IL-6, and IL-1 receptor antagonist (IL-1ra) in the blood is comparable to that observed in relation to bacterial diseases. Eccentric exercise is associated with an increase in serum IL-6 concentrations and is significantly correlated with the concentration of creatine kinase (CK) in the following days, whereas no changes are found after the concentric exercise; this demonstrates a close association between exercise-induced muscle damage and increased serum levels of IL-6. The time course of cytokine production, the close association with muscle damage, and the finding of mRNA-IL-6 in skeletal muscle biopsies after intense exercise all support the idea that during eccentric exercise myofibers are mechanically damaged and that this process stimulates the local production of inflammatory cytokines. It remains to be shown whether systemic endotoxemia during exercise is also a cause of elevated levels of cytokines in the plasma. The present review also discusses the possible roles of protein breakdown, delayed onset muscle soreness, and clinical implications of the acute-phase response following exercise.Key words: exercise, sport, trauma, sepsis, cytokines, interleukin, muscle.


Author(s):  
Marcelo G. Pompermayer ◽  
Régis Radaelli ◽  
Clarissa M. Brusco ◽  
Bruno M. Baroni ◽  
Eduardo L. Cadore ◽  
...  

1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.


Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2274 ◽  
Author(s):  
Leonardo C. R. Lima ◽  
Renan V. Barreto ◽  
Natália M. Bassan ◽  
Camila C. Greco ◽  
Benedito S. Denadai

This study examined the effects of anthocyanin-rich antioxidant juice (AJ) on the recovery of exercise-induced muscle damage (EIMD) and the running economy (RE) following downhill running (DHR). Thirty healthy young men were randomly divided into two blinded groups and consumed either AJ or placebo (PLA) for nine days (240 mL twice-a-day). On day 5, the participants from both groups ran downhill (−15%) for 30 min at 70% of their maximal oxygen uptake (VO2max) speeds. The changes in RE (oxygen uptake (VO2) and perceived effort (PE) during 5-min runs at 80%VO2max) and EIMD (isometric peak torque (IPT), muscle soreness (SOR) and serum creatine kinase activity (CK)) were compared over time and between the groups on the 4 days following DHR. VO2 and PE increased (p < 0.05) immediately following DHR for both groups and remained elevated for PLA until 48h post-DHR while fully recovering 24 h post-DHR for AJ. SOR was greater (p < 0.05) for PLA throughout the study. CK increased for both groups and was greater (p < 0.05) for PLA at 96 h post-DHR. IPT decreased for both groups but recovered faster for AJ (72 h) compared to PLA (no full recovery). AJ accelerated recovery of RE and EIMD and should be used in specific contexts, but not chronically.


Sports ◽  
2019 ◽  
Vol 7 (6) ◽  
pp. 132 ◽  
Author(s):  
John Fernandes ◽  
Kevin Lamb ◽  
Craig Twist

This study compared the time course of recovery after a squatting exercise in trained young (YG; n = 9; age 22.3 ± 1.7 years) and trained (MT; n = 9; 39.9 ± 6.2 years) and untrained (MU; n = 9; age 44.4 ± 6.3 years) middle-aged males. Before and at 24 and 72 h after 10 × 10 squats at 60% one-repetition maximum (1RM), participants provided measurements of perceived muscle soreness (VAS), creatine kinase (CK), maximal voluntary contraction (MVC), voluntary activation (VA), and resting doublet force of the knee extensors and squatting peak power at 20% and 80% 1RM. When compared to the YG males, the MT experienced likely and very likely moderate decrements in MVC, resting doublet force, and peak power at 20% and 80% 1RM accompanied by unclear differences in VAS, CK, and VA after the squatting exercise. MU males, compared to MT, experienced greater alterations in peak power at 20% and 80% 1RM and VAS. Alterations in CK, MVC, VA, and resting doublet force were unclear at all time-points between the middle-aged groups. Middle-aged males experienced greater symptoms of muscle damage and an impaired recovery profile than young resistance trained males. Moreover, regardless of resistance training experience, middle-aged males are subject to similar symptoms after muscle-damaging lower-body exercise.


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