Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Effects of hyperbaric oxygen on recovery from exercise-induced muscle damage in humans. Effects of hyperbaric oxygen on a human model of injury. Effect of hyperbaric oxygen therapy on exercise-induced muscle soreness. Hyperbaric oxygen therapy for acute ankle sprains. Effects of intermittent exposure to hyperbaric oxygen for the treatment of an acute soft tissue injury. Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness.
This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury.
                21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100-min exposure to 2.5 ATA and 100% oxygen with intermittent breathing of ambient air (30 min at 100% O2, 5 min at 20.93% O2). HBO treatments began either 2 (iHBO) or 24 h (dHBO) postexercise and were administered daily through day 4 postexercise. Forearm flexor cross-sectional area (CSA) and T2 relaxation time via magnetic resonance imaging (MRI) were assessed at baseline, 2, 7, and 15 d postinjury. Isometric strength and rating of perceived soreness of the forearm flexors were assessed at baseline, 1, 2, 3, 4, 7, and 15 d postinjury. Serum creatine kinase (CK) was assessed on day 0 and on days 1, 2, 7, and 15 postinjury.
                Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO, and dHBO, respectively. All groups showed significant increases in CSA in response to injury (21% at 2 d, 18% at 7 d) (P < 0.0001), but there were no significant differences between groups (P = 0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO, and dHBO, respectively. Significant increases in T2 relaxation time were observed for all groups (64% at 2 d, 66% at 7 d, and 28% at 15 d) (P < 0.0001), but there were no significant differences between groups (P = 0.692). Isometric strength (P < 0.0001), serum CK levels (P = 0.0007), and rating of perceived soreness (P < 0.0001) also indicated significant muscle injury for all groups, but there were no differences between groups (P = 0.459, P = 0.943, and P = 0.448, respectively).
                These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated. To determine whether hyperbaric oxygen (HBO) therapy could accelerate recovery from exercise-induced muscle damage in humans.
                Pretest-posttest design with random assignment to either a treatment (HBO) or placebo control (sham) group.
                University of Alberta and Misericordia Hospital, Edmonton.
                12 healthy male students (24.2 +/- 3.2 years) who were unaccustomed to strenuous eccentric exercise of the calf muscles.
                All subjects performed a strenuous eccentric exercise protocol designed to elicit muscle damage within the right gastrocnemius muscle. Subjects subsequently received either HBO (100% oxygen at 253 kPa [2.5 ATA] for 60 min; n = 6) or sham (atmospheric air at 132 kPa [1.3 ATA] for 60 min; n = 6) treatment conditions. The first treatment was administered 3-4 hours after damage, with a second and third at 24 and 48 hours after the first, respectively.
                Dependent variables included peak torque at 0.52 radians/s, peak isometric torque, and muscular endurance using isokinetic dynamometry; muscle cross-sectional area using magnetic resonance imaging; inorganic phosphate levels and T2 relaxation time using 31P and 1H magnetic resonance spectroscopy; pain sensation and unpleasantness using the Descriptor Differential Scale. These variables were assessed at baseline and until day 5 postdamage.
                There was little evidence of a difference in recovery rate between the HBO and sham groups. Faster recovery was observed in the HBO group only for isometric peak torque and pain sensation and unpleasantness.
                HBO cannot be recommended as an effective method of treatment of this form of muscle injury. To determine whether intermittent exposures to hyperbaric oxygen enhance recovery from delayed-onset muscle soreness of the quadriceps, we conducted a randomized, controlled, double-blinded, prospective study using 66 untrained men between the ages of 18 and 35 years. After the induction of muscle soreness, these subjects were treated in a hyperbaric chamber over a 5-day period in two phases, with four groups (control, hyperbaric oxygen treatment, delayed treatment, and sham treatment) in the first phase; and three groups (3 days of treatment, 5 days of treatment, and sham treatment) in the second phase. The hyperbaric exposures involved 100% oxygen for 1 hour per day at 2.0 atm. The sham treatments involved 21% oxygen for 1 hour per day at 1.2 atm. We monitored recovery using a leg dynamometer to test eccentric torque of the nondominant quadriceps muscle before and immediately after exercise and at 48 and 96 hours after exercise. Pain was tested daily using visual analog pain scales. In phase 1 a significant difference in recovery of eccentric torque was noted in the treatment group compared with the other groups. In phase 2, the recovery of eccentric torque for the 5-day treatment group was significantly greater than for the sham group from immediately after exercise to 96 hours after exercise. The pain data did not differ significantly in any comparison in either phase. The results suggest that treatment with hyperbaric oxygen may enhance recovery of eccentric torque of the quadriceps muscle from delayed-onset muscle soreness. The purpose of this study was to examine the effects of HBO2 therapy on exercise-induced muscle soreness. Subjects (n = 6 male and 10 female university student volunteers) were randomly divided into an experimental group that received HBO2 therapy and a control group that did not receive any treatments. HBO2 treatments consisted of 5 sessions of breathing 95% oxygen at 2.5 atm abs for 100 min. Temporary muscle soreness was created using a single-leg eccentric exercise task involving the quadriceps femoris. Over the next 14 days, measurements were obtained on muscle soreness, leg circumference, quadriceps peak torque, quadriceps average power, fatigue and plasma creatine kinase. After eccentric exercise, plasma creatine kinase (CK) levels and perceived muscle soreness were elevated but were not different between HBO2 and control groups. HBO2 therapy did not alter leg circumference, quadriceps peak torque, average power or fatigue compared to the control group. Faster recovery was observed in the HBO2 group on day 3 following the exercise protocol with perceived muscle soreness still elevated for the control group but not different from baseline for the HBO2 group. The data indicated that five HBO2 treatments did not speed recovery following eccentric exercise that induced temporary muscle soreness. We conducted a randomized double-blind study of 32 subject with acute ankle sprains to compare treatment with hyperbaric oxygen at 2 atmospheres absolute pressure (N = 16) (treatment group) with treatment with air at 1.1 atmosphere absolute pressure (N = 16) (control group) in a hyperbaric chamber. Each group received three treatments at their respective pressures: one for 90 minutes and two for 60 minutes each. Mean age, severity grade, and time to treatment (treatment group, 34.3 +/- 6.3 hours; control group, 32.6 +/- 4.6 hours) were similar in both groups. Joint function measured by a functional index improved from 0.40 +/- 0.2 to 6.3 +/- 0.4 with hyperbaric oxygen and from 0.8 +/- 0.3 to 5.3 +/- 0.6 with air. The change from initial to final evaluation was significantly greater in the treatment group. Foot and ankle volume by water displacement decreased from 1451 +/- 57 ml to 1425 +/- 63 ml with hyperbaric oxygen and from 1403 +/- 50 ml of 1371 +/- 45 ml with air (no difference was noted between hyperbaric oxygen treatment and air treatment using a two-day analysis of variance). Subjective pain index fell from 3.3 +/- 0.5 to 0.8 +/- 0.3 with hyperbaric oxygen and from 2.6 +/- 0.3 to 0.3 +/- 0.2 with air. No differences were noted in passive or active range of motion when comparing hyperbaric oxygen treatment with air treatment. Time to recovery was the same in both groups (treatment, 16.0 +/- 6.3 days; control, 15.4 +/- 2.8 days). Regression analysis to determine the influence of time to treatment, initial severity of injury, hyperbaric oxygen, and age showed no effect of hyperbaric oxygen treatment on time to recovery. To assess the hypothesis that subjects exposed to intermittent hyperbaric oxygen treatments would recover from signs and symptoms indicative of delayed-onset muscle soreness faster than subjects exposed to normoxic air.
                Randomized, double-blinded study with a 4-day treatment protocol.
                University-based sports medicine clinic.
                Sixteen sedentary female university students.
                All subjects performed 300 maximal voluntary eccentric contractions (30 sets of 10 repetitions per minute) of their nondominant leg (110 to 35 degrees of knee flexion) at a slow speed (30 degrees per second) on a dynamometer to elicit muscle damage and injury. Hyperbaric oxygen treatments consisted of 100% oxygen for 60 minutes at 2.0 atmospheres absolute (ATA), while the control group received 21% oxygen at 1.2 ATA for the same amount of time. Both groups received treatment immediately after the induction of delayed-onset muscle soreness and each day thereafter for a period of 4 days (day 1 postexercise through day 4 postexercise).
                Dependent variables (perceived muscle soreness, isokinetic strength, quadriceps circumference, creatine kinase, and malondialdehyde) were assessed at baseline (preexercise, day 0), 4 hours postexercise (day 1), 24 hours postexercise (day 2), 48 hours postexercise (day 3), and 72 hours postexercise (day 4). Magnetic resonance images (T2 relaxation time/short tip inversion recovery) were assessed at baseline (day 0), 24 hours postexercise (day 3), and 72 hours postexercise (day 5).
                Repeated-measures analysis of variance was performed on all of the dependent variables to assess differences between treatment and control groups. Analyses revealed no significant differences between groups for treatment effects for any of the dependent variables (pain, strength, quadriceps circumference, creatine kinase, malondialdehyde, or magnetic resonance images).
                The findings of this study suggest that hyperbaric oxygen therapy is not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated. This study investigated whether hyperbaric oxygen therapy (HBOT) improves recovery after exercise-induced muscle injury.
                Healthy male subjects (N = 24) were randomly assigned to either a placebo group or a HBOT group. Subjects were tested for maximal isometric strength (preexercise) of their right elbow flexors. Each subject then completed a high-force eccentric workout of the elbow flexor muscle group to induce delayed onset muscle soreness (DOMS). On the seven successive days after this workout, the subjects were exposed to a hyperbaric environment of 2.5 ATA for 60 min, inspiring either a normoxic mixture (P(I)O2 = 0.2 ATA; placebo group) or a hyperoxic gas mixture (P(I)O2 = 2.5 ATA; HBOT group). Before the eccentric workout and daily for the next 10 d, measurements were obtained regarding: maximal isometric muscle strength of the elbow flexor muscles, right upper arm circumferences, and rating of the perceived muscle soreness.
                Isometric strength decreased significantly from preexercise levels of 25.1 +/- 3.8 kp to postexercise levels of 12.0 +/- 4.6 kp, for the HBOT group, and from 24.6 +/- 3.4 kp to 12.5 +/- 3.7 kp, respectively, for the placebo group. Over the 10-d recovery period, there was no difference in the rate of recovery of muscle strength between the two groups. Perceived soreness peaked at about 48 h after exercise with no difference between groups. Also, the exercise-induced increases in arm circumference were similar in the two groups.
                These results indicate that HBOT is not an effective therapy for the treatment of DOMS.
There was insufficient evidence from comparisons tested within randomised controlled trials to establish the effects of HBOT on ankle sprain or acute knee ligament injury, or on experimentally induced DOMS. There was some evidence that HBOT may increase interim pain in DOMS. Any future use of HBOT for these injuries would need to have been preceded by carefully conducted randomised controlled trials which have demonstrated effectiveness.