1190 Training & Testing

Authors

N. D. M. Jenkins, T. J. Housh, D. A. Traylor, K. C. Cochrane, H. C. Bergstrom, R. W. Lewis, R. J. Schmidt, G. O. Johnson, J. T. Cramer

Affiliation

Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, United States

Key words

Abstract

▶ delayed onset muscle ● ▶ ● ▶ ● ▶ ● ▶ ●

soreness recovery muscle strength rapid torque-time curve rate of force development



This study examined the time courses of recovery for isometric peak torque and rate of torque development (RTD) after eccentric-induced muscle damage. 18 men completed 6 sets of 10 maximal eccentric isokinetic muscle actions at 30 ° · s − 1. Peak torque, peak RTD and RTD at 10 (RTD10), 50 (RTD50), 100 (RTD100) and 200 ms (RTD200), serum creatine kinase and lactate dehydrogenase were measured before (PRE), immediately after (POST), 24, 48 and 72 h after eccentric exercise. Creatine kinase and lactate dehydrogenase increased from 139 to 6 457 and

Introduction



accepted after revision April 08, 2014 Bibliography DOI http://dx.doi.org/ 10.1055/s-0034-1375696 Published online: September 26, 2014 Int J Sports Med 2014; 35: 1190–1195 © Georg Thieme Verlag KG Stuttgart · New York ISSN 0172-4622 Correspondence Joel T. Cramer Nutrition and Health Sciences University of Nebraska-Lincoln 211 Ruth Leverton Hall Lincoln United States 68583 Tel.: + 1/402/4727 533 Fax: + 1/402/4720 522 [email protected]

Historically, decreases in maximal voluntary strength have been used to study and describe the time course of recovery from eccentricinduced muscle damage [6, 12, 13, 18, 19, 21]. In fact, Warren et al. [33] identified maximal voluntary isometric peak torque (PT) as the single best non-invasive indicator of eccentric-induced muscle damage. It has been hypothesized that the decreases in PT following eccentric exercise are related to structural mechanisms, such as a disorganization and misalignment of the sarcomere [5, 16, 24], loss in sarcolemmal integrity [22], and disruption of the excitation-contraction coupling processes [27]. Neural deficits may also contribute to losses in strength after unaccustomed eccentric exercise, such as decreased voluntary activation [26, 28] and reductions in electromyographic (EMG) amplitude [7]. Consequently, Beck et al. [6] suggested that a single indicator of muscle function, such as PT, may not adequately describe all of the structural and neural mechanisms that underlie eccentric-induced muscle soreness.

from 116 to 199 IU · L − 1 from PRE to 72 h, respectively. Peak torque and all RTDs decreased at POST. Peak torque and RTD200 remained lower than PRE through 72 h. Peak RTD remained lower than PRE through 48 h, but was not different from PRE at 72 h. RTD10 and RTD100 were lower than PRE through 24 h, but were not different from PRE at 48 and 72 h. RTD50 decreased at POST, but was not different from PRE at 24 h. Early phase RTDs recovered more quickly than PT and RTD200. Early phase RTDs may reflect neural mechanisms underlying eccentric-induced force decrements, while late RTDs may describe the same physiological mechanisms as PT.

The RTD is defined as “…the ability to rapidly develop muscular force” (pg. 46; [4]), but it is most commonly measured during the first 250 ms after the onset of torque production during a rapid or explosive isometric joint moment. The RTD is thought to reflect motor unit firing rate as a motor control summation strategy during the rapid initiation of a maximal voluntary isometric muscle action [2, 3]. Buller and Lewis [10] examined the effects of increasing stimulation frequencies on the rate of isometric tension development and peak tension with in-situ preparations of cat flexor hallucis longis and flexor digitorum longus muscles. Large increases in the rate of isometric tension development were observed [10] despite no further increases in peak tension when the stimulation frequencies were increased beyond what was necessary to achieve peak tension. More recently, Van Cutsem et al. [32] found that 12 weeks of resistance training resulted in an 82 % increase in peak RTD, which the authors explained by the 70–102 % increases in motor unit firing rates and the 5–32 % increases in doublet discharges measured with intramuscular EMG during the onset of ballistic

Jenkins NDM et al. Recovery of PT and Rate of Torque Development … Int J Sports Med 2014; 35: 1190–1195

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The Rate of Torque Development: A Unique, Noninvasive Indicator of Eccentric-induced Muscle Damage?

Training & Testing 1191

VISIT 1 PRE 1. Blood Draw 2. Maximal Voluntary Isometric Muscle Action

POST 20 min: ECCENTRIC EXERCISE PROTOCOL

1. Maximal Voluntary Isometric Muscle Action 2. Blood Draw

Materials and Methods



Participants 18 men (mean ± standard deviation (SD) age = 22.2 ± 3.0 years; height = 182.9 ± 6.0 cm; mass = 80.5 ± 15.9 kg) volunteered to participate in this study, which complied with the ethical standards of the International Journal of Sports Medicine [17] and was approved by the university Institutional Review Board for the protection of human subjects. Prior to testing, all participants signed an informed consent form, completed a health history questionnaire, and all subjects were free from any current or ongoing neuromuscular diseases or musculoskeletal injuries involving the wrist, elbow, or shoulder joints. In addition, the subjects (a) had not participated in any upper-body resistance training during the 6 months prior to enrollment, (b) had not used creatine in the previous 9 weeks prior to enrollment, and (c) did not have any acute infections that may have caused inflammation.

Experimental design This study consisted of 4 laboratory visits, each separated by 24 h ( ± 2 h). Prior to each visit, the subjects reported to the University Health Center for a fasting blood sample. During visit 1, subjects were familiarized with the testing procedures by completing a warm-up of 5 submaximal isometric muscle actions. Following the familiarization and warm-up, the subjects performed two 6-s maximal voluntary isometric muscle actions (MVICs) of the forearm flexors separated by 2 min of rest. Following the MVICs, subjects completed an eccentric exercise protocol that consisted of 6 sets of 10 maximal eccentric isokinetic muscle actions of the forearm flexors at 30 ° · s − 1. One min of rest was given between each set. Strong verbal encouragement was provided throughout the protocol to ensure that a maximal effort was given during each muscle action. Following the eccentric protocol, a 2-min rest was allowed. Subjects then performed 2 post-exercise MVICs separated by 2 min of rest, followed by a post-exercise blood draw. During visits 2, 3, and 4, subjects completed a warm-up of 5 submaximal isometric muscle actions before performing two 6-s MVICs of the forearm flexors separated by 2-min of rest. The blood samples and MVIC testing was performed 5 times during visits 1–4: before (PRE), immediately after (POST), and 24, 48 and 72 h after the eccentric exercise ▶ Fig. 1). (●

VISIT 2

VISIT 3

VISIT 4

24H

48 H

72 H

1. Blood Draw 24 ±2 h (REST)

ine the time courses of recovery for isometric PT and RTD at peak, 10, 50, 100 and 200 ms for up to 72 h after eccentricinduced muscle damage in the forearm flexors. We hypothesized that the RTD would be a sensitive, non-invasive indicator of muscle damage that may provide unique information from PT after eccentric-induced muscle damage.

2. Maximal Voluntary Isometric Muscle Action

1. Blood Draw 24 ±2h (REST)

2. Maximal Voluntary Isometric Muscle Action

1. Blood Draw 24 ±2 h (REST)

Fig. 1 Schematic of the testing schedule for visits 1–4. Testing was performed before (PRE), immediately after (POST), and 24, 48 and 72 h after the eccentric exercise.

2. Maximal Voluntary Isometric Muscle Action

Jenkins NDM et al. Recovery of PT and Rate of Torque Development … Int J Sports Med 2014; 35: 1190–1195

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voluntary isometric muscle actions. While Aagaard et al. [3] has since demonstrated increases in RTD after 14 weeks of resistance training and hypothesized that increases in EMG amplitude and rate of EMG rise reflected increases in motor unit firing rate that caused the increases in RTD, firing rate was not directly measured. Therefore, RTD may reflect motor unit firing rate during initial rapid increases in maximal isometric torque production and, consequently, may provide information regarding the neural component of strength loss after unaccustomed eccentric exercise. The RTD is often calculated during specific time intervals, including 30, 50, 100 and 200 ms from the onset of torque production [3]. Aagaard et al. [3] demonstrated concurrent increases in EMG amplitude, rate of EMG rise and RTD during the early phases of maximal voluntary isometric muscle actions (0–30, 0–50, and 0–100 ms) after a resistance training program. In contrast, Anderson and Aagaard [4] reported that PT accounted for 80 % of the variance in RTD calculated in later time intervals of 150–250 ms from the onset of torque, while it only explained 18–30 % of the variance in RTD calculated in earlier time intervals (0–50 ms). Despite the widespread use [2, 3, 23, 30, 31] of these specific time intervals originally described by Aagaard and colleagues [3], no clear evidence or rationale has been provided to justify them. In fact, the high correlation between PT and RTD during later phases (150–250 ms) has questioned whether later phase RTD variables provide unique information beyond what is provided by PT. By studying the time course of recovery for RTD calculated during these time intervals (0–10, 0–50, 0–100, 0–200 ms), in addition to peak RTD and PT, this study may provide evidence regarding whether these RTD time intervals contribute unique information to the explanation of recovery from a damaging bout of eccentric exercise. Studies [6, 13, 29] have reported serum concentrations of enzymes, such as creatine kinase (CK) and lactate dehydrogenase (LDH), to characterize and monitor eccentric-induced muscle damage. Unaccustomed eccentric muscle actions cause structural damage to the muscle cell [25], resulting in leakage of intracellular enzymes into the interstitial fluid, uptake into the lymphatic system and subsequent release into the circulation [9]. CK is responsible for the exchange of high-energy phosphates between phosphocreatine and adenosine diphosphate, while LDH catalyzes the conversions between lactate and pyruvate. Both enzymes are found in high concentrations within the muscle cell. Thus, the humoral appearance of these 2 enzymes has been used as invasive markers of muscle damage [9]. Consequently, serum CK and LDH were measured in the present study to validate the existence and magnitude of muscle damage. There are no previous studies, to our knowledge, that have examined the time courses of recovery for PT and RTD during isometric muscle actions across a period of 72 h following eccentric exercise. Therefore, the purpose of this study was to exam-

1192 Training & Testing

Subjects were placed in supine position on an upper body exercise-testing bench with a strap placed around their waists to ▶ Fig. 2). The isometric and prevent excessive movement (● eccentric muscle actions were performed with a neutral hand position, and torque was recorded with a calibrated isokinetic dynamometer (Cybex 6000, CYBEX Division, LUMEX Inc., Ronkonkoma, NY). Prior to the MVIC and eccentric muscle actions, the limb was weighed and gravity-corrected using HUMAC software (HUMAC2009, CSMi, Stoughton, MA). During the MVICs, the joint angle between the arm and forearm was set at 115 ° (65 ° from full extension), while the angle between the arm and trunk was set at 45 ° (45 ° of abduction). In order to remove any free play from the dynamometer lever arm, the investigator placed a minimal baseline pressure on the lever arm prior to the initiation of the MVICs. Careful instruction was given to each subject to ensure that they contracted as “hard and fast” as possible. The range of motion utilized for the eccentric muscle actions was set from 115 ° (starting point of forearm flexion resulted in 65 ° between the arm and forearm) to 0 ° of forearm flexion (full extension).

Blood-sampling procedures Serum concentrations of creatine kinase (CK) and lactate dehydrogenase (LDH) were measured from 7.5-ml blood samples taken from the median cubital vein of the arm contralateral to that used for MVIC testing and eccentric exercise. A trained phlebotomist performed all blood draws. The samples were collected

Fig. 2 An example of subject positioning during a maximal voluntary isometric muscle action.

into silicon dioxide dry-coated tubes and centrifuged for 10 min at 3 000 r · min − 1 to separate the serum. The separated samples were frozen and shipped on dry ice to a third party laboratory for CK and LDH analyses (ARUP Laboratories, Salt Lake City, Utah).

Signal processing The torque signals during the MVICs were sampled from the isokinetic dynamometer at 1000 Hz, stored on a personal computer (Dell OptiPlex, GX270, Dell Inc., Round Rock, TX, USA), and processed off-line with custom software (Labview 11.0, National Instruments, Austin, TX, USA). The torque signals were low-pass filtered with a 15 Hz cutoff (zero phase shift 4th-order Butterworth filter), and all subsequent analyses were completed on the filtered signals. Peak torque (PT) was calculated as the highest 500 ms average torque value obtained during the plateau of each MVIC. The MVIC that resulted in the highest PT during each visit was used for analysis. The peak rate of torque development (RTD) was calculated as the peak of the first derivative of the torque signal (Nm · s − 1) occurring between the onset of torque and peak torque. The onset of torque was determined by the software when the torque signal crossed the value equal to 3 standard deviations above the baseline. In addition to the peak RTD, RTD was calculated as the average of the first 10 (RTD10), 50 (RTD50), 100 (RTD100) and 200 (RTD200) ms of the torque signal derivative following the onset of torque.

Statistical analyses Means and standard deviations were calculated for each of the ▶ Table 1). 8 separate one-way repeated dependent variables (● measures analyses of variance (ANOVA) (PRE vs. POST vs. 24 h vs. 48 h vs. 72 h) were used to analyze the raw values for PT, peak RTD, RTD10, RTD50, RTD100, RTD200, CK and LDH, and Bonferroni-corrected dependent samples t-tests were used for followup analyses. In addition, peak torque and the RTD variables were normalized for each subject by expressing the POST, 24, 48 and 72 h values as a percentage of the respective PRE value. A twoway repeated measures ANOVA (variable [PT, peak RTD, RTD10, RTD50, RTD100, and RTD200] × time [POST, 24, 48, and 72 h]) was used to analyze the normalized PT and RTDs. When appropriate, follow-up analyses included one-way ANOVAs and Bonferroni-corrected dependent samples t-tests. IBM SPSS version 21 (IBM, Inc., Chicago, IL) was used for all statistical analyses. A type I error rate of 5 % was considered statistically significant for the ANOVAs, while the type I error rate was appropriately adjusted for the Bonferroni-corrected post-hoc dependent-samples t-tests.

Table 1 Means ( ± standard errors) for absolute PT, peak RTD, RTD10, RTD50, RTD100, RTD200, CK and LDH at PRE, POST, 24, 48 and 72 h. PRE PT (Nm) peak RTD (Nm · s − 1) RTD10 (Nm · s − 1) RTD50 (Nm · s − 1) RTD100 (Nm · s − 1) RTD200 (Nm · s − 1) CK (IU · L − 1) LDH (IU · L − 1)

69.8 ( ± 3.3) * † ‡ # 694.3 ( ± 55.1) * † ‡ # 37.0 ( ± 7.4) * † 189.4 ( ± 31.8) * 350.4 ( ± 29.8) * † 246.0 ( ± 15.9) * † ‡ # 139.0 ( ± 41.1) 115.6 ( ± 6.9)

POST 36.3 ( ± 2.3) a b c 310.4 ( ± 37.3) a b c 13.1 ( ± 2.6) c 71.7 ( ± 14.3) a b c 163.3 ( ± 23.1) a c 119.3 ( ± 14.0) a c 142.4 ( ± 43.1) 119.2 ( ± 6.6)

24 h 47.0 ( ± 4.5) 472.6 ( ± 53.3) e 18.47 ( ± 2.9) 141.3 ( ± 24.9) 245.4 ( ± 30.2) 159.2 ( ± 16.9) 1 392.7 ( ± 977.1) 123.4 ( ± 10.5)

48 h 47.8 ( ± 4.7) 497.9 ( ± 59.2) f 27.5 ( ± 6.1) 168.2 ( ± 34.0) f 273.9 ( ± 38.7) 162.5 ( ± 18.0) 3 972.4 ( ± 2 293.5) 194.3 ( ± 53.7)

72 h 49.7 ( ± 4.3) 573.4 ( ± 57.8) 32.3 ( ± 6.8) 194.6 ( ± 33.4) 285.9 ( ± 36.2) 172.0 ( ± 17.34) 6 456.9 ( ± 3 009.7) g 198.8 ( ± 46.2) g

*PRE > POST, (p ≤ 0.05); † PRE > 24 h, (p ≤ 0.05); ‡ PRE > 48 h, (p ≤ 0.05); # PRE > 72 h, (p ≤ 0.05); a

POST < 24 h, (p ≤ 0.05); b POST < 48 h, (p ≤ 0.05); c POST < 72 h, (p ≤ 0.05); d 24 h < 48 h, (p ≤ 0.05); e 24 h < 72 h, (p ≤ 0.05); f 48 h < 72 h, (p ≤ 0.05); g One-way ANOVA indicated

increases from PRE to 72 h (p ≤ 0.05)

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Testing procedures

Results



Serum CK and LDH ▶ Table 1 shows the means and standard errors for CK and LDH ● at PRE, POST, 24, 48 and 72 h. The one-way repeated measures ANOVAs indicated that CK (p < 0.01) and LDH (p < 0.05) increased from PRE to 72 h. However, the Bonferroni-corrected post-hoc t-tests revealed no significant differences (p > 0.05) among PRE, POST, 24, 48 or 72 h for either CK or LDH.

Absolute PT and RTD ▶ Table 1 shows the means and standard errors for PT, peak RTD, ● RTD10, RTD50, RTD100 and RTD200 at PRE, POST, 24, 48 and 72 h. Significant main effects were present for each ANOVA (p < 0.001). For PT, PRE was greater than (p < 0.01) POST, 24, 48 and 72 h, and POST was less than (p ≤ 0.05) 24, 48 and 72 h. For peak RTD, PRE was greater than (p ≤ 0.05) POST, 24, 48 and 72 h; POST was less than (p ≤ 0.05) 24, 48 and 72 h; and 24 and 48 h were less than (p < 0.01) 72 h. For RTD10, PRE was greater than (p ≤ 0.05) POST and 24 h, and POST was less than (p < 0.05) 72 h. For RTD50, PRE was greater than (p < 0.001) POST, and POST was less than (p < 0.05) 24, 48 and 72 h, and 48 h was less than (p < 0.01) 72 h. For RTD100, PRE was greater than (p ≤ 0.001) POST and 24 h, and POST was less than (p ≤ 0.05) 24 and 72 h. For RTD200, PRE was greater than (p ≤ 0.001) POST, 24, 48 and 72 h, and POST was less (p < 0.05) than 24 and 72 h.

Normalized PT and RTD ▶ Fig. 3 displays the normalized PT, peak RTD, RTD10, RTD50, ●

Percentage of Baseline

RTD100, and RTD200 at PRE, POST, 24, 48 and 72 h. There was a two-way interaction for variable × time (p = 0.001). Normalized PT, peak RTD, RTD10, RTD50, RTD100 and RTD200 decreased from PRE to POST (p ≤ 0.05). For normalized PT, PRE was greater than (p ≤ 0.001) 24, 48 and 72 h, and POST was less than (p ≤ 0.05) 24, 48 and 72 h. For normalized peak RTD, PRE was greater than

140 130 120 110 100 90 80 70 60 50 40

C

RTD50 B

D

RTD10

RTD100 peak RTD PT RTD200

A

PRE

POST

24 Time

48

72

Fig. 3 The means ( ± standard errors) for normalized peak torque (PT), peak rate of torque development (peak RTD) and RTD at 10 (RTD10), 50 (RTD50), 100 (RTD100), and 200 (RTD200) ms after the onset of torque normalized as percentages of their respective baseline values (PRE) at PRE, POST, 24, 48 and 72 h after the eccentric exercise. *PRE > POST, (p ≤ 0.05); † PRE > 24 h, (p ≤ 0.05); ‡ PRE > 48 h, (p ≤ 0.05); # PRE > 72 h, (p ≤ 0.05); a POST < 24 h, (p ≤ 0.05); b POST < 48 h, (p ≤ 0.05); c POST < 72 h, (p ≤ 0.05); d 24 h < 48 h, (p ≤ 0.05); e 24 h < 72 h, (p ≤ 0.05); f 48 h < 72 h, (p ≤ 0.05); A peak RTD, RTD10, and RTD50 were less than PT (p ≤ 0.05); B RTD50 > RTD100 and RTD100 > RTD200 (p ≤ 0.05); C RTD50 > RTD100, RTD200, and PT (p ≤ 0.05); D RTD10 > RTD200 and PT and peak RTD > PT (p ≤ 0.05).

(p ≤ 0.01) 24 and 48 h, POST was less than (p ≤ 0.001) 24, 48, and 72 h, and 24 and 48 h were less than (p ≤ 0.01) 72 h. For normalized RTD10, PRE was greater than (p ≤ 0.05) 24 h, and POST was less than (p ≤ 0.05) 48 and 72 h. For normalized RTD50, POST was less than (p < 0.05) 48 and 72 h. For normalized RTD100, PRE was greater than (p = 0.001) 24 h, and POST was less than (p ≤ 0.05) 24, 48 and 72 h. For normalized RTD200, PRE was greater than (p < 0.001) 24, 48 and 72 h, and POST was less than (p < 0.05) 24 h. Post-hoc dependent samples t-tests revealed that normalized PT was greater than peak RTD, RTD10 and RTD50 at POST (p ≤ 0.05); however, normalized PT was less than (p ≤ 0.05), peak RTD, RTD10 and RTD50 at 72 h. RTD50 was greater than RTD100 (p ≤ 0.05) and RTD100 was greater than RTD200 (p = 0.04) at 48 h. RTD10 was greater than RTD200 (p ≤ 0.01), and RTD50 was greater than RTD100 (p = 0.02), RTD200 (p = 0.02) and PT (p = 0.02) at 72 h.

Discussion



The primary findings of the present study were that early phase RTDs decreased to a greater extent and recovered more quickly than PT and late phase RTD within 72 h after eccentric-induced muscle damage. Specifically, eccentric-induced muscle damage caused greater relative decreases in peak RTD, RTD10, and RTD50 (56–62 % decrease) than PT (47 % decrease) from PRE to POST. PT recovered to 67 % of baseline at 24 h, but remained at 69–72 % from 48 to 72 h. In contrast, RTD10 and RTD50 recovered to 62–82 % at 24 h, 81–88 % at 48 h and 97–117 % at 72 h. Peak RTD and RTD100 recovered to 67–68 % at 24 h, 72–78 % at 48 h and 84 % at 72 h. Previous data from our lab [20] has shown that peak RTD occurs at < 100 ms after the onset of contraction and thus would be expected to behave similarly to RTD100, which was supported by these data. All of the RTD variables ▶ Fig. 3). In recovered completely by 72 h except for RTD200 (● fact, RTD200 responded similarly to PT, recovering to 63 % at 24 h, while remaining at 65–69 % from 48 to 72 h. Our findings suggested, therefore, that unlike PT and RTD200, early phase RTDs may be unique non-invasive markers of muscle damage that are capable of fully recovering within a 72 h period. It has been suggested that isometric PT may be the best noninvasive indicator of muscle damage following eccentric exercise [14, 33]. Decreases in PT observed after eccentric-induced muscle damage have been attributed to structural and neural mechanisms [8, 11, 33]. For example, structural damage has been hypothesized to limit torque production by (a) disorganization of myofilaments, (b) loss of sarcomere integrity [15, 25], and (c) disruption of the excitation-contraction coupling process [27]. In contrast, Beck et al. [7] reported a 23 % reduction in normalized EMG amplitude and suggested that subjects were unable to maximally activate their biceps brachii immediately following eccentric exercise. Prasartwuth et al. [26] and Behrens et al. [8] also found reductions in voluntary activation after eccentricinduced muscle damage that recovered prior to PT and peak twitch torque. Thus, the recovery of PT following eccentricinduced muscle damage may be influenced, in part, by an inability to fully activate muscles, particularly during the early phases of recovery. Incidentally, RTD may also reflect neural adaptations [1], and specifically, RTD is thought to be influenced by the discharge rate of motor units at the onset of contraction [3, 20, 32]. For example, Aagaard et al. [3] demonstrated parallel

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Training & Testing 1193

1194 Training & Testing

Acknowledgements



This study was funded by a grant from Rock Creek Pharmaceuticals, Inc.

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Jenkins NDM et al. Recovery of PT and Rate of Torque Development … Int J Sports Med 2014; 35: 1190–1195

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increases in EMG amplitude, rate of EMG rise, and RTD during the initial phases of contraction (0–30, 0–50, and 0–100 ms) after resistance training. Therefore, the quicker recovery of RTD compared to PT in the present study, in conjunction with previous studies [3, 7, 8, 26, 32], suggested that RTD may also be a sensitive indicator of muscle damage and may reflect the neural mechanisms responsible for the loss of force observed after eccentric-induced muscle damage. Andersen and Aagaard [4] demonstrated that RTD calculated from 150–250 ms predicted 72–81 % of the variance in PT, which implied that these variables are physiologically similar. In the present investigation, peak RTD, RTD10 and RTD50 decreased to a greater extent than PT from PRE to POST. RTD10 and RTD50 recovered by 48 h and RTD100, and peak RTD recovered by 72 h, while PT and RTD200 did not recover. These findings indicated that RTD calculated in the early phase of torque development provided unique information about the time course of recovery from eccentric-induced muscle damage. The late phase RTD (RTD200) in the present study responded similarly to PT, which supported the finding of Andersen and Aagaard [4] that late phase RTDs may provide the same information as PT. Therefore, future studies may focus on early phase RTDs and PT, rather than late phase RTDs, when characterizing the time course of recovery from eccentric-induced muscle damage. In the present study, serum CK and LDH increased from PRE to 72 h. The increase in CK of 139 IU · L − 1 to 6 457 IU · L − 1 from PRE to 72 h was comparable to the increases of 150 to 225 IU · L − 1 to 4 500 to 8 500 IU · L − 1 from PRE to 72 h observed in previous investigations that used similar muscle damage protocols [6, 13, 29]. The increases in LDH of 116 IU · L − 1 to 199 IU · L − 1 from PRE to 72 h in the present study were also comparable to the LDH increases of 155 to 280 IU · L − 1 to 100 to 250 IU · L − 1 from baseline to 72 h observed by Rawson et al. [29] and Cooke et al. [13], respectively. Although there were no histological measurements of muscle damage, these data supported the consistency of muscle damage between the present study and previous studies using similar eccentric damage protocols [6, 13, 29]. The results of the present study suggested that RTD recovers quicker than PT after eccentric-induced muscle damage. Our study provided a 72 h time course of recovery for PT, RTD, CK, and LDH, which included POST and 72 h data, and included the measurement of RTD during widely used time intervals [2, 3, 23, 30, 31]. RTDs calculated in the first 100 ms may be considered sensitive indicators of muscle damage, provide unique information in addition to PT, and may reflect the neural component of eccentric-induced strength loss. However, the late phase RTD (RTD200) in the present study responded similarly to PT, supporting the finding of Andersen and Aagaard [4] that late phase RTDs may provide the same information as PT. Therefore, future studies may focus on early phase RTDs and PT, rather than late phase RTDs, when characterizing the time course of recovery from eccentric-induced muscle damage. Finally, future studies are needed to verify the hypothesis that early phase RTDs may reflect the neural component of eccentric-induced strength loss.

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31 Thompson BJ, Ryan ED, Sobolewski EJ, Smith DB, Conchola EC, Akehi K, Buckminster T. Can maximal and rapid isometric torque characteristics predict playing level in division I American collegiate football players? J Strength Cond Res 2013; 27: 655–661 32 Van Cutsem M, Duchateau J, Hainaut K. Changes in single motor unit behaviour contribute to the increase in contraction speed after dynamic training in humans. J Physiol 1998; 513 (pt 1): 295–305 33 Warren GL, Lowe DA, Armstrong RB. Measurement tools used in the study of eccentric contraction-induced injury. Sports Med 1999; 27: 43–59

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26 Prasartwuth O, Taylor JL, Gandevia SC. Maximal force, voluntary activation and muscle soreness after eccentric damage to human elbow flexor muscles. J Physiol 2005; 567 (pt 1): 337–348 27 Proske U, Morgan DL. Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications. J Physiol 2001; 537 (pt 2): 333–345 28 Racinais S, Bringard A, Puchaux K, Noakes TD, Perrey S. Modulation in voluntary neural drive in relation to muscle soreness. Eur J Appl Physiol 2008; 102: 439–446 29 Rawson ES, Gunn B, Clarkson PM. The effects of creatine supplementation on exercise-induced muscle damage. J Strength Cond Res 2001; 15: 178–184 30 Thompson BJ, Ryan ED, Sobolewski EJ, Conchola EC, Cramer JT. Age related differences in maximal and rapid torque characteristics of the leg extensors and flexors in young, middle-aged and old men. Exp Gerontol 2013; 48: 277–282

Jenkins NDM et al. Recovery of PT and Rate of Torque Development … Int J Sports Med 2014; 35: 1190–1195

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The rate of torque development: a unique, non-invasive indicator of eccentric-induced muscle damage?

This study examined the time courses of recovery for isometric peak torque and rate of torque development (RTD) after eccentric-induced muscle damage...
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