Effects of deep heat as a preventative mechanism on delayed onset muscle soreness

The effects of increased muscle temperature via continuous ultrasound prior to a maximal bout of eccentric exercise were investigated on the symptoms of delayed onset muscle soreness (DOMS) of the elbow flexors. Perceived muscle soreness, upper arm circumferences, range of motion (ROM), and isometric and isokinetic strength were measured over 7 days on 14 college-aged men (n = 6) and women (n = 8). Ten minutes of continuous ultrasound (ULT) or sham-ultrasound (CON) were administered. Muscle temperature was measured in the biceps brachii of both arms. Muscle temperature increased by 1.79 degrees +/- 0.49 degrees C (mean +/- SD) in the experimental arm of the ULT group. Muscle soreness was induced by a single bout of 50 maximal eccentric contractions. The ULT group did not differ significantly (p < 0.05) from the CON group with respect to perceived muscle soreness, upper arm circumference, ROM, and isometric and isokinetic strength. In conclusion, increased muscle temperature failed to provide significant prophylactic effects on the symptoms of DOMS.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40 min of bench stepping (knee high step; 15 steps · min⁻¹). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150 W, with increments of 50 W every 2 min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P < 0.05). Endurance time and peak V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P < 0.05) during cycling after eccentric exercise compared with the control condition. Peak blood lactate concentration, observed at 2 min post-exercise was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The higher blood lactate concentration during cycling exercise after prior eccentric exercise may be attributable to an increased rate of glycogenolysis possibly arising from an increased recruitment of Type II muscle fibres. It follows that determination of lactate thresholds for the purpose of fitness assessment in subjects experiencing DOMS is not appropriate. Accepted: 27 September 1997     

Treatment and prevention of delayed onset muscle soreness

Eccentric exercise continues to receive attention as a productive means of exercise. Coupled with this has been the heightened study of the damage that occurs in early stages of exposure to eccentric exercise. This is commonly referred to as delayed onset muscle soreness (DOMS). To date, a sound and consistent treatment for DOMS has not been established. Although multiple practices exist for the treatment of DOMS, few have scientific support. Suggested treatments for DOMS are numerous and include pharmaceuticals, herbal remedies, stretching, massage, nutritional supplements, and many more. DOMS is particularly prevalent in resistance training; hence, this article may be of particular interest to the coach, trainer, or physical therapist to aid in selection of efficient treatments. First, we briefly review eccentric exercise and its characteristics and then proceed to a scientific and systematic overview and evaluation of treatments for DOMS. We have classified treatments into 3 sections, namely, pharmacological, conventional rehabilitation approaches, and a third section that collectively evaluates multiple additional practiced treatments. Literature that addresses most directly the question regarding the effectiveness of a particular treatment has been selected. The reader will note that selected treatments such as anti-inflammatory drugs and antioxidants appear to have a potential in the treatment of DOMS. Other conventional approaches, such as massage, ultrasound, and stretching appear less promising.     

Eccentric contractions leading to DOMS do not cause loss of desmin nor fibre necrosis in human muscle

High force eccentric muscle contractions can result in delayed onset muscle soreness (DOMS), prolonged loss of muscle strength, decreased range of motion, muscle swelling and an increase of muscle proteins in the blood. At the ultrastructural level Z-line streaming and myofibrillar disruptions have been taken as evidence for muscle damage. In animal models of eccentric exercise-induced injury, disruption of the cytoskeleton and the sarcolemma of muscle fibres occurs within the first hour after the exercise, since a rapid loss of staining of desmin, a cytoskeletal protein, and the presence of fibronectin, a plasma and extracellular protein, are observed within the muscle fibres. In the present study, biopsies from subjects who had performed different eccentric exercises and had developed DOMS were examined. Our aim was to determine whether eccentric exercise leading to DOMS causes sarcolemmal disruption and loss of desmin in humans. Our study shows that even though the subjects had DOMS, muscle fibres had neither lost staining for desmin nor contained plasma fibronectin. This study therefore does not support previous conclusions that there is muscle fibre degeneration and necrosis in human skeletal muscle after eccentric exercise leading to DOMS. Our data are in agreement with the recent findings that there is no inflammatory response in skeletal muscle following eccentric exercise in humans. In combination, these findings should stimulate the search for other mechanisms explaining the functional and structural alterations in human skeletal muscle after eccentric exercise.     

Rofecoxib and tramadol do not attenuate delayed-onset muscle soreness or ischaemic pain in human volunteers

We assessed the effect of rofecoxib, a cyclo-oxygenase-2 inhibitor, and tramadol, a centrally acting analgesic, on both delayed-onset muscle soreness (DOMS) and experimentally induced ischaemic pain. We induced DOMS in 10 male and 5 female healthy volunteers by downhill running for 30 min at a 12% decline and a speed of 9 km x h(-1). We also induced ischaemic pain by finger movements with an arterial tourniquet around the arm. In a randomized, double-blind crossover format, we administered rofecoxib (50 mg, daily), tramadol (50 mg, 3 times per day), and a placebo (orally for 3 days), starting immediately after exercise. A 100 mm visual analogue scale (VAS) and McGill pain questionnaire were used to describe muscle soreness and ischaemic forearm pain 24 h after the exercise. The pressure pain threshold (PPT) in the thigh and ischaemic pain tolerance in the forearm were measured before exercise and 24 and 72 h after exercise. PPT decreased 24 h after exercise, compared with pre-exercise values (ANOVA, p < 0.05), but neither drug had any significant effect on the PPT. Neither rofecoxib nor tramadol had any effect on time of ischaemia tolerated or amount of finger activity during ischaemia. The VAS and pain-rating index, for both muscle soreness and experimental ischaemic pain, were not affected significantly by either drug. Both DOMS and ischaemic pain share peripheral and central mechanisms, yet neither are attenuated by rofecoxib or tramadol.     

The Effects of Estrogen on Indices of Skeletal Muscle Tissue Damage after Eccentric Exercise in Postmenopausal Women

This study examined if estrogen (E) usage (in the form of hormone replacement therapy (HRT)) has a protective effect on skeletal muscle damage in postmenopausal women. Nine postmenopausal women (age 55.2 ± 9.9 [mean ± SD]) performed two exercise sessions at 70% of their maximal heart rate on HRT (E-HI) and without HRT (E-LO; following a 28–45 day HRT washout). All subjects followed a condition order of E-HI and then E-LO with at least 42 days between exercise sessions. Serum creatine kinase (CK), perceived delayed onset muscle soreness (DOMS), and maximal quadriceps isometric force (MIF) were determined before exercise and 24, 48, and 72 h after exercise. E-HI and E-LO conditions produced a rise in CK (p < 0.001) after exercise, but CK after E-HI was greater than in E-LO (p < 0.001) at 24 and 48 h. DOMS was significantly elevated at 24, 48, and 72 h after each exercise session (p < 0.05). The greatest peak DOMS score occurred during the E-HI condition. MIF was similarly reduced after each exercise session (p < 0.05). These results suggest that elevated E does not offer a protective effect to skeletal muscle; however, design limitations (i.e., condition order) confound the present data. Interestingly, an association between peak CK during the E-LO condition and the number of washout days (r = +0.707, p < 0.05) between conditions existed. This suggests that a longer washout period may be necessary to elucidate the actual effects of E on skeletal muscle. These findings suggest that more work on this topic, correcting for the present design limitations, is warranted.     

Effects of branched-chain amino acid supplement on knee peak torque and indicators of muscle damage following isokinetic exercise-induced delayed onset muscle soreness

[Purpose] This study aimed to investigate the effects of branched-chain amino acid (BCAA) supplement on delayed onset muscle soreness (DOMS) by analyzing the maximum muscle strength and indicators of muscle damage.[Methods] Twelve men with majors in physical education were assigned to the BCAA group and placebo group in a double-blinded design, and repeated measurements were conducted. DOMS was induced with an isokinetic exercise. Following BCAA administration, the changes in the knee extension peak torque, flexion peak torque, aspartate aminotransferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) concentrations were analyzed. The maximum knee muscle strength was measured at the baseline (pre-D0) following BCAA administration for 5 days before exercise (-D5, -4D, -3D, -2D, -1D). In contrast, the post-treatment measurements (D3) were recorded after BCAA administration for 3 days (post-D0, D1, D2). Blood samples were obtained before (pre-D0), immediately after (post-D0), 24 h (D1), 48 h (D2), and 72 h (D3) after the exercise to analyze the indicators of muscle strength. BCAA was administered twice daily for 8 days (5 days and 3 days before inducing DOMS and during the experimental period, respectively).[Results] There was no difference in the flexion peak torque between the groups. However, the BCAA group showed a significantly higher extension peak torque at D3 (second isokinetic exercise), compared to the placebo group (p<.05). There was no difference in AST changes between the groups. Nonetheless, the CK and LDH were significantly reduced in the BCAA group, compared to the placebo group. There was no correlation between the extension peak torque and flexion peak torque. However, the CK and LDH increased proportionately in DOMS. Moreover, their concentrations significantly increased with a decreasing peak torque (p<.01).[Conclusion] An exercise-induced DOMS results in a decrease in the peak torque and a proportional increase in the CK and LDH concentrations. Moreover, the administration of BCAA inhibits the reduction of the extension peak torque and elevation of CK and LDH concentrations. Therefore, BCAA might be administered as a supplement to maintain the muscle strength and prevent muscle damage during vigorous exercises that may induce DOMS in sports settings.     

Dissociated time course of recovery between genders after resistance exercise

Comparisons between men and women of time course responses of strength, delayed-onset muscle soreness (DOMS), and muscle swelling after a resistance training session are still controversial. Therefore, this study examined gender differences in strength loss, muscle thickness (MT), and DOMS between young men and women. Thirty apparently healthy, untrained volunteers (14 women and 16 men) participated in the study protocol. The resistance exercise session consisted of 8 sets at 10 repetition maximum load of the elbow flexor muscles of their dominant arm. Maximum isokinetic peak torque (PT), MT, and DOMS were recorded at baseline (TB), immediately after exercise (T0), and at 1 (T1), 2 (T2), 3 (T3), and 4 (T4) days after exercise. Baseline strength was expressed as 100%. There were no significant differences between the sexes for relative PT loss immediately after exercise (T0 = 74.31 ± 8.26% for men and 76.00 ± 6.31% for women). Also, PT was still significantly less than baseline from T1 to T4 for both genders. In contrast, recovery from PT was longer in women when compared with that in men. Muscle thickness responded similarly to PT in both genders. However, there was no significant difference between genders for DOMS at any time point. The time point that showed the greatest degree of mean soreness was T2 (4.94 ± 2.38 mm for men and 4.45 ± 2.07 mm for women). Our data suggest that after resistance exercise, women and men experience similar immediate strength loss; however they have dissimilar strength recovery across 4 days of recovery. Likewise, both genders experience a different time course of MT response after a traditional resistance exercise protocol. In contrast, men and women develop and dissipate muscle soreness in a similar manner.     

Influence of estrogen on markers of muscle tissue damage following eccentric exercise.

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill running bout at approximately 60% VO2max. The OC completed the exercise during the mid-luteal phase (day 22.9 +/- 1.5; high estrogen) while the EU did their exercise in the mid-follicular phase (day 9.6 +/- 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed pre-exercise, immediately post-, 24, 48 and 72 h post-exercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p < 0.001), and the interaction of group x time was significantly different (p < 0.01). The OC group had lower CK at 72 h post-exercise than did the EU group. Pre-exercise estrogen levels correlated with the overall mean CK (r = -0.43, p < 0.05) and 72 h (r = -0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p < 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear but may be related to the anti-oxidant characteristics and membrane stability properties associated with estrogen and its derivatives.     

The effects of estrogen on indices of skeletal muscle tissue damage after eccentric exercise in postmenopausal women

This study examined if estrogen (E) usage (in the form of hormone replacement therapy [HRT]) has a protective effect on skeletal muscle damage in postmenopausal women. Nine postmenopausal women (age 55.2 +/- 9.9 [mean +/- SD]) performed two exercise sessions at 70% of their maximal heart rate on HRT (E-HI) and without HRT (E-LO; following a 28-45 day HRT washout). All subjects followed a condition order of E-HI then E-LO with at least 42 days between exercise sessions. Serum creatine kinase (CK), perceived delayed onset muscle soreness (DOMS), and maximal quadriceps isometric force (MIF) were taken pre-exercise, 24, 48 and 72-hr post exercise. E-HI and E-LO conditions produced a rise in CK (p < 0.001) after exercise; but CK after E-HI was greater than in E-LO (p < 0.001) at 24 hours and at 48 hours. DOMS was significantly elevated at 24, 48, and 72-hr post each exercise session (p < 0.05). The greatest peak DOMS score occurred during the E-HI condition. MIF was similarly reduced after each exercise session (p < 0.05). These results suggest elevated E does not offer a protective effect to skeletal muscle; however, design limitations (i.e., condition order) confound the present data. Interestingly, an association between peak-CK during the E-LO condition and the number of washout days (r = +0.707, p < 0.05) between conditions existed. This suggests a longer washout period may be necessary to elucidate the actual E effects on skeletal muscle. These findings suggest that more work correcting for the present design limitations is warranted on this topic.     

Influence of Estrogen on Markers of Muscle Tissue Damage Following Eccentric Exercise

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill run at 60% VO_2max. The OC completed the exercise during the midluteal phase (day 22.9 ± 1.5; high estrogen) while the EU did their exercise in the midfollicular phase (day 9.6 ± 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed preexercise, immediately postexcercise, 24, 48, and 72 h postexercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p< 0.001), and the interaction of group x time was significantly different (p< 0.01). The OC group had lower CK at 72 h postexercise than did the EU group. Preexercise estrogen levels correlated with the overall mean CK (r= –0.43. p< 0.05) and 72 h (r= –0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p< 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear, but it may be related to the antioxidant characteristics and membrane stability properties associated with estrogen and its derivatives.     

Piroxicam fails to reduce myocellular enzyme leakage and delayed onset muscle soreness induced by isokinetic eccentric exercise

To test the hypothesis that delayed onset muscular soreness (DOMS) following intense eccentric muscle contraction could be due to increased production of prostaglandin E(2) (PGE(2)), ten healthy male subjects were studied. Using a double-blind randomized crossover design, each subject performed two isokinetic tests separated by a period of at least 6 weeks: once with placebo, and once with piroxicam (Feldene((R))). They were given one capsule containing either placebo or piroxicam (20 mg) per day for 6 days with initial doses given starting 3 days prior to isokinetic testing. Exercise consisted of eight stages of five maximal contractions of the knee extensor and flexor muscle groups of both legs separated by 1 min rest phases, on a Kin Trex device at 60( degrees )/s angular velocity. The subjective presence and intensity of DOMS were evaluated using a visual analogue scale immediately after, and 24 and 48 h after each test. The mean plasma concentration of PGE(2) measured at rest and after exercise was significantly lower in the group treated with piroxicam (p < 0.05). However, statistical analysis (two-way ANOVA test) revealed that exercise did not cause any significant change of mean plasma PGE(2) over time in either of the two groups. Eccentric work was followed by severe muscle pain in extensor and flexor muscle groups. Maximal soreness was noted 48 h postexercise. Serum creatine kinase activity and the serum concentration of myoglobin increased significantly, and reached peak values 48 h after exercise in both experimental conditions (p < 0.001). By paired t-test, it appeared that there were no significant differences in the serum levels of these two markers of muscle damage between the two groups at any time point. We conclude that: (1) oral administration of piroxicam fails to reduce muscle damage and DOMS caused by strenuous eccentric exercise; and (2) the hypothetical role of increased PGE(2) production in eccentric exercise-induced muscle damage, DOMS, and reduced isokinetic performance is not substantiated by the present results.     

Re-Evaluation of Sarcolemma Injury and Muscle Swelling in Human Skeletal Muscles after Eccentric Exercise

The results regarding the effects of unaccustomed eccentric exercise on muscle tissue are often conflicting and the aetiology of delayed onset muscle soreness (DOMS) induced by eccentric exercise is still unclear. This study aimed to re-evaluate the paradigm of muscular alterations with regard to muscle sarcolemma integrity and fibre swelling in human muscles after voluntary eccentric exercise leading to DOMS. Ten young males performed eccentric exercise by downstairs running. Biopsies from the soleus muscle were obtained from 6 non-exercising controls, 4 exercised subjects within 1 hour and 6 exercised subjects at 2–3 days and 7–8 days after the exercise. Muscle fibre sarcolemma integrity, infiltration of inflammatory cells and changes in fibre size and fibre phenotype composition as well as capillary supply were examined with specific antibodies using enzyme histochemistry and immunohistochemistry. Although all exercised subjects experienced DOMS which peaked between 1.5 to 2.5 days post exercise, no significant sarcolemma injury or inflammation was detected in any post exercise group. The results do not support the prevailing hypothesis that eccentric exercise causes an initial sarcolemma injury which leads to subsequent inflammation after eccentric exercise. The fibre size was 24% larger at 7–8 days than at 2–3 days post exercise (p<0.05). In contrast, the value of capillary number per fibre area tended to decrease from 2–3 days to 7–8 days post exercise (lower in 5 of the 6 subjects at 7–8 days than at 2–3 days; p<0.05). Thus, the increased fibre size at 7–8 days post exercise was interpreted to reflect fibre swelling. Because the fibre swelling did not appear at the time that DOMS peaked (between 1.5 to 2.5 days post exercise), we concluded that fibre swelling in the soleus muscle is not directly associated with the symptom of DOMS.     

Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study

The myofibrillar and cytoskeletal alterations observed in delayed onset muscle soreness (DOMS) caused by eccentric exercise are generally considered to represent damage. By contrast our recent immunohistochemical studies suggested that the alterations reflect myofibrillar remodeling (Yu and Thornell 2002; Yu et al. 2003). In the present study the same human muscle biopsies were further analyzed with transmission electron microscopy and immunoelectron microscopy. We show that the ultrastructural hallmarks of DOMS, Z-disc streaming, Z-disc smearing, and Z-disc disruption were present in the biopsies and were significantly more frequent in biopsies taken 2–3 days and 7–8 days after exercise than in those from controls and 1 h after exercise. Four main types of changes were observed: amorphous widened Z-discs, amorphous sarcomeres, double Z-discs, and supernumerary sarcomeres. We confirm by immunoelectron microscopy that the main Z-disc protein alpha-actinin is not present in Z-disc alterations or in the links of electron-dense material between Z-discs in longitudinal register. These alterations were related to an increase of F-actin and desmin, where F-actin was present within the strands of amorphous material. Desmin, on the other hand, was seen in less dense regions of the alterations. Our results strongly support that the myofibrillar and cytoskeletal alterations, considered to be the hallmarks of DOMS, reflect an adaptive remodeling of the myofibrils.     

Resting energy expenditure and delayed-onset muscle soreness after full-body resistance training with an eccentric concentration

The purpose of this investigation was to determine the effect of an acute bout of high-volume, full-body resistance training with an eccentric concentration on resting energy expenditure (REE) and indicators of delayed-onset muscle soreness (DOMS). Eight resistance trained (RT) and eight untrained (UT) participants (mean: age = 23.5 years; height = 180.76 cm; weight = 87.58 kg; body fat = 19.34%; lean mass = 68.71 kg) were measured on four consecutive mornings for REE and indicators of DOMS: creatine kinase (CK) and rating of perceived muscle soreness (RPMS). Delayed-onset muscle soreness was induced by performing eight exercises, eight sets, and six repetitions using a 1-second concentric and 3-second eccentric muscle action duration. A two-factor repeated-measures analysis of variance revealed that REE was significantly (p < 0.05) elevated at 24, 48, and 72 hours post compared with baseline measures for both UT and RT groups. Ratings of perceived muscle soreness were significantly elevated within groups for UT and RT at 24 and 48 hours post and for UT only at 72 hours post compared with baseline (p < 0.05). Nonparametric analyses revealed that CK was significantly increased at 24 hours post for both UT and RT and at 48 and 72 hours post for UT only compared with baseline (p < 0.05). Resting energy expenditure and indicators of DOMS were higher in UT compared with RT on all measures, but no significant differences were determined. The main finding of this investigation is that full-body resistance training with an eccentric concentration significantly increased REE up to 72 hours postexercise in UT and RT participants.     

Effects of delayed onset muscle soreness on selected physiological responses to submaximal running

This study examined the effects of delayed-onset muscle soreness (DOMS) on selected physiological responses to submaximal exercise. Seven male and four female subjects (Ss) aged 21-37 years completed two submaximal running sessions at an individualized pace corresponding to a blood lactate concentration (bLa) of approximately 2.5 mmol x L(-1). Following the first session (T1), Ss performed a series of lower extremity resistance exercises designed to induce DOMS. Subjects were then retested (T2) 24-30 hours later, during which time all Ss experienced DOMS. Oxygen uptake, heart rate (HR), respiratory exchange ratio, rating of perceived exertion (RPE), and bLa were measured every 6 minutes. Significant trial effects (p < 0.05) were observed for HR and RPE. HR was significantly higher during T1 at minutes 6 and 12 (p < 0.05), and RPE values were significantly higher at T2 during all recording periods (p < 0.05). Results from this study suggest that DOMS does not affect submaximal oxygen uptake. However, DOMS does appear to affect one's perception of effort.     

Effect of downhill running on motoneuron pool excitability.

The purpose of this study was to compare alterations in motoneuron pool excitability after eccentric-biased (ECC-B) downhill running exercise with non-biased (NO-B) level running exercise. Six male subjects (25-34 yr) participated in the study, which included ECC-B exercise (-10% grade) and NO-B exercise (0% grade) at 50% of maximal O2 uptake for 20 min. The control trial consisted of 20 min of quiet rest with all subjects participating in all conditions (repeated measures). Motoneuron pool excitability was measured by the Hoffman reflex (H-wave), which was expressed as a ratio (H/M ratio) of the maximal electrically stimulated muscle action potential (M-wave). NO-B exercise resulted in a 9.3 +/- 2.7% (SE) reduction in the H/M ratio. ECC-B exercise resulted in a 24.6 +/- 5.7% reduction in the ratio (P less than 0.05 for both). The two exercise treatment conditions were also significantly different from one another (P less than 0.05). Twenty-four-hour postexercise H/M ratios were similar to baseline (P greater than 0.05). Postexercise subjective muscle soreness assessment (DOMS) produced significant increases in DOMS of 36 and 166% immediately and 24 h after exercise, respectively, for the ECC-B trial only (P less than 0.001). The data show that ECC-B exercise results in greater postexercise H/M ratio reductions than NO-B exercise and that H/M ratio changes post-ECC-B exercise are not solely associated with DOMS.     

Nitric oxide: Is it the cause of muscle soreness?

Skeletal muscle hosts all of the isoforms of nitric oxide synthase (NOS). It is well documented that nitric oxide (NO) regulates force generation and satellite cell activation, and therefore, damage repair of skeletal muscle. NO can also activate nociceptors of C-fibers, thereby causing the sensation of pain. Although delayed-onset of muscle soreness (DOMS) is associated with decreased maximal force generation, pain sensation and sarcomere damage, there is a paucity of research linking NO and DOMS. The present mini-review attempts to elucidate the possible relationship between NO and DOMS, based upon current literature.