Intermittent low dose carbon monoxide inhalation does not influence glucose regulation in overweight adults: a randomized controlled crossover trial.

NEW FINDINGS: What is the central question of this study? Low dose carbon monoxide (CO) inhalation plays a role in regulating proteins involved in glucose metabolism; does low dose CO improve glucose and insulin responses to an oral glucose tolerance test in overweight adults? What is the main finding and its importance? Five days of intermittent CO inhalation does not alter the glucose or insulin responses to ingestion of a glucose bolus in overweight adults. Low dose CO is utilized in various physiological assessment procedures; these findings allow researchers and clinicians to utilize these procedures without concern of altering glucose metabolism. ABSTRACT: Low dose carbon monoxide (CO) inhalation upregulates several proteins important for glucose metabolism. Such changes could be clinically significant and may be relevant to those who use CO as a research tool. We hypothesized that low dose CO inhalation would improve glucose and insulin responses to an oral glucose bolus in overweight humans. Eleven young adults (5 men, 6 women; body mass index: 25-35 kg m-2 ) were included in this randomized, placebo-controlled, single-blinded crossover study. Following screening, participants completed two 7-day protocols with a 4-week washout. Twenty-four hours prior to and following five consecutive days of either once daily CO (men: 1.2 ml (kg body mass)-1 ; women: 1.0 ml (kg body mass)-1 ) or placebo (room air) inhalation, participants underwent oral glucose tolerance tests (OGTT). For key outcome variables, there were no significant main effects or interactions across condition or time point (mean ± SD), including fasting glucose (mg dl-1 : pre-placebo: 85.2 ± 10.1; post-placebo: 82.9 ± 10.6; pre-CO: 83.6 ± 7.7; post-CO: 84.0 ± 9.0), 2 h post glucose (mg dl-1 : pre-placebo: 100.9 ± 20.0; post-placebo: 98.7 ± 13.1; pre-CO: 94.2 ± 23.2; post-CO: 94.4 ± 14.9), or the Matsuda index (pre-placebo: 16.1 ± 11.5; post-placebo: 20.3 ± 24.7; pre-CO: 15.6 ± 15.3; post-CO: 17.5 ± 16.8). In conclusion, 5 days of low dose CO administration did not influence glucose and insulin responses to an OGTT in overweight adults. Low dose CO inhalation is utilized in a variety of physiological assessment procedures; these findings allow researchers to utilize these procedures without concern of altering glucose metabolism.

Acute, Low-dose CO Inhalation does not Alter Energy Expenditure during Submaximal Exercise.

Carbon monoxide, a gas known most widely for its toxic effects at high doses, is receiving increased attention for its role as a physiological signaling molecule and potential therapeutic agent when administered in low doses. We sought to quantify any changes to oxygen consumption and energy expenditure during submaximal exercise after low-dose CO inhalation. 9 active individuals completed 4 graded submaximal exercise tests, with each test occurring during a separate visit. For their first exercise test, subjects inhaled CO or room air (1.2 mL·kg(-1) body mass) in a randomized, subject-blind fashion. A second test was repeated 24 h later when the inhaled gas should have cleared the system. Subjects repeated study procedures with the alternate dose after a washout period of at least 2 days. Low-dose CO administration did not affect oxygen consumption or energy expenditure during submaximal exercise immediately or 24 h following its administration. Increases in heart rate, blood [lactate], and perceived exertion were observed following acute CO inhalation but these effects were absent after 24 h. The results of this study suggest that low-dose CO administration does not influence the energetics of submaximal exercise, but it acutely increases the relative intensity associated with absolute workloads below the lactate threshold.

Estimating Energy Expenditure using Individualized, Power-Specific Gross Efficiencies.

Our purpose was to determine if using an individual's power-specific gross efficiency improves the accuracy of estimating energy expenditure from cycling power. 30 subjects performed a graded cycling test to develop 4 gross efficiencies: individual power-specific gross efficiencies, a group mean power-specific gross efficiency, individual fixed gross efficiencies, and a group mean fixed gross efficiency. Energy expenditure was estimated from power using these different gross efficiencies and compared to measured energy expenditure during moderate- and hard-intensity constant-power and 2 variable-power cycling bouts. Estimated energy expenditures using individual or group mean power-specific gross efficiencies were not different from measured energy expenditure across all cycling bouts (p>0.05). To examine the intra-individual variability of the estimates, absolute difference scores (absolute value of estimated minus measured energy expenditure) were compared, where values closer to zero represent more accurate individual estimates. The absolute difference score using individual power-specific gross efficiencies was significantly lower compared to the other gross efficiencies across all cycling bouts (p<0.01). Significant and strong correlations (r≥0.97, p<0.001) were found across all cycling bouts between estimated and measured energy expenditures using individual power-specific gross efficiencies. In conclusion, using an individual's power-specific gross efficiency significantly improves their energy expenditure estimate across different power outputs.

Ten Days of Intermittent, Low-dose Carbon Monoxide Inhalation does not Significantly Alter Hemoglobin Mass, Aerobic Performance Predictors, or Peak-power Exercise Tolerance.

Carbon monoxide (CO) rebreathing procedures are used to assess hemoglobin mass (Hbmass) but recent evidence suggests that CO is a signaling molecule that may alter physiological functions. We examined the effects of 10 days of intermittent, low-dose CO inhalation on Hbmass, aerobic performance predictors, and peak-power exercise tolerance. 18 recreationally-active men were randomized to either CO or placebo inhalation groups in a single-blind, pre-post parallel-groups trial. Primary outcomes were assessed before and after an intervention period during which subjects inhaled a bolus of 1.2 ml kg(-1) CO or placebo (room air) for 30 s, once per day on 10 days over a 12-day period. Cycling tests were performed >16 h following CO inhalation to exclude acute effects of CO exposure. CO inhalation elevated carboxyhemoglobin by 4.4±0.4% (mean±SD) following each exposure. Compared to placebo, chronic CO inhalation did not significantly alter Hbmass (p=0.99), peak oxygen uptake (p=0.59), peak power output (p=0.10), submaximal oxygen uptake (p=0.91), submaximal RER (p=0.22), lactate threshold (p=0.65), or peak-power exercise tolerance (p=0.60). In conclusion, our data support the ability to perform repeated measurements of Hbmass using CO rebreathing over a 12-day period without altering physiological responses.

Plasma matrix metalloproteinase-9 response to downhill running in humans.

Matrix metalloproteinase-9 is a proteolytic enzyme capable of degrading proteins of the muscle extracellular matrix. Systemic levels of MMP-9 or its inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1), have the potential to serve as blood markers of exercise-induced muscle damage. The purpose of this study was to determine if an eccentrically-dominated task, downhill running (DHR), produces changes in plasma MMP-9 or TIMP-1 and examine the relationship between MMP-9/TIMP-1 levels and indirect indicators of muscle damage. Subjects were sedentary (SED, n=12) or had a history of concentrically-biased training (CON, n=9). MMP-9 and TIMP-1 were measured before (Pre-Ex), immediately after (Post-Ex), and 1-, 2-, 4-, and 7-days post-DHR (-10°), and compared to discomfort ratings, creatine kinase activity and strength loss. At 1-day Post-Ex, discomfort increased (5.6 ± 7.8 to 45.5 ± 19.9 mm; 0-100 mm scale), strength decreased (-6.9 ± 1.6%) and CK increased (162.9 ± 177.2%). MMP-9 was modestly but significantly increased at Post-Ex in both CONC and SED (32.7 ± 33.6%) and at 4-days in SED (66.9 ± 88.1%), Individual responses were variable, however. There were no correlations between MMPs and discomfort ratings, plasma CK or strength. While plasma MMP-9 changes may be detectable in the systemic circulation after DHR, they are small and do not correspond to other markers of damage.

Exercise efficiency of low power output cycling.

Exercise efficiency at low power outputs, energetically comparable to daily living activities, can be influenced by homeostatic perturbations (e.g., weight gain/loss). However, an appropriate efficiency calculation for low power outputs used in these studies has not been determined. Fifteen active subjects (seven females, eight males) performed 14, 5-min cycling trials: two types of seated rest (cranks vertical and horizontal), passive (motor-driven) cycling, no-chain cycling, no-load cycling, cycling at low (10, 20, 30, 40 W), and moderate (50, 60, 80, 100, 120 W) power outputs. Mean delta efficiency was 57% for low power outputs compared to 41.3% for moderate power outputs. Means for gross (3.6%) and net (5.7%) efficiencies were low at the lowest power output. At low power outputs, delta and work efficiency values exceeded theoretical values. In conclusion, at low power outputs, none of the common exercise efficiency calculations gave values comparable to theoretical muscle efficiency. However, gross efficiency and the slope and intercept of the metabolic power vs mechanical power output regression provide insights that are still valuable when studying homeostatic perturbations.

Myosin heavy chains IIa and IId are functionally distinct in the mouse.

Myosin in adult murine skeletal muscle is composed primarily of three adult fast myosin heavy chain (MyHC) isoforms. These isoforms, MyHC-IIa, -IId, and -IIb, are >93% identical at the amino acid level and are broadly expressed in numerous muscles, and their genes are tightly linked. Mice with a null mutation in the MyHC-IId gene have phenotypes that include growth inhibition, muscle weakness, histological abnormalities, kyphosis (spinal curvature), and aberrant kinetics of muscle contraction and relaxation. Despite the lack of MyHC-IId, IId null mice have normal amounts of myosin in their muscles because of compensation by the MyHC-IIa gene. In each muscle examined from IId null mice, there was an increase in MyHC-IIa- containing fibers. MyHC-IIb content was unaffected in all muscles except the masseter, where its expression was extinguished in the IId null mice. Cross-sectional fiber areas, total muscle cross-sectional area, and total fiber number were affected in ways particular to each muscle. Developmental expression of adult MyHC genes remained unchanged in IId null mice. Despite this universal compensation of MyHC-IIa expression, IId null mice have severe phenotypes. We conclude that despite the similarity in sequence, MyHC-IIa and -IId have unique roles in the development and function of skeletal muscle.

A comparison of skeletal muscle morphology with training between young and old Fischer 344 rats.

Muscle mass, fiber area, total fiber number, fiber population and capillarity were assessed in 6- and 25-month-old animals trained by treadmill running at 75% mean maximal capacity for 10 weeks. Serial cross-sections were stained for ATPase activity to differentiate fiber types and expose capillaries. Aging and training effects were demonstrated in maximal running speed and endurance running time. Soleus muscle mass increased in the aged, however, soleus and EDL total fiber number were declining. When adjusted for muscle weight, a significant reduction existed in fiber number for the aged soleus. Fiber area increased in the old soleus compared to young. All changes in the EDL were specific to the deep region. While there was a tendency for the capillaries/fiber and fiber area to be higher with training in the Type I fibers of the soleus, it was only significant for the young animals. Thus, while the majority of variables that showed a training effect did so across both age groups, this was not the case for vascularity. Age-associated changes in muscle morphology appear to be both muscle and fiber specific.

Factors influencing excess postexercise oxygen consumption in trained and untrained women.

This study investigated the effects of blood lactate and norepinephrine levels and rectal temperature on excess postexercise oxygen consumption (EPOC) following two different exercise intensities. Six trained and seven untrained women each performed two exercise tests, short-term high-intensity exercise ([HI] approximately 80% maximum oxygen consumption [VO2max]) and long-term low-intensity exercise ([LOW] approximately 65% VO2max) until 300 kcal were expended. Rectal temperature, oxygen consumption (VO2), and lactate and norepinephrine levels were monitored at rest, during exercise, and for 60 minutes into recovery. Exercise times averaged 30.0 +/- 4.5 and 23.7 +/- 0.9 minutes in trained women and 45 +/- 3.6 and 30.0 +/- 0.4 minutes in untrained women for LOW and HI, respectively. Rectal temperature, VO2, and lactate and norepinephrine levels were significantly elevated (P < .05) during HI compared with LOW in both groups. VO2 was elevated throughout recovery following LOW and HI in untrained women only. Additionally, VO2 was elevated until minutes 50 and 40 following LOW and HI, respectively, in trained subjects. Rectal temperature returned to resting levels after 30 minutes of recovery following LOW, but remained significantly elevated throughout minute 50 of recovery following HI in trained women. However, values remained significantly elevated throughout recovery following both exercise bouts in untrained subjects. Norepinephrine levels remained elevated above resting levels throughout recovery following HI and until minute 50 following LOW in trained subjects, whereas levels remained elevated for 5 minutes following LOW and 50 minutes following HI in untrained subjects. Lactate levels remained elevated above baseline values throughout recovery following HI and LOW in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the oxygen drift in downhill vs. level running.

This investigation explored the recent theory that muscle damage causes the drift in oxygen consumption (VO2) during low-intensity downhill running. Seven subjects participated in a maximal VO2 (VO2max) test and three submaximal bouts [one level (Level) and two downhill runs (Down 1, Down 2) at 40% peak VO2]. Two downhill runs (30 min at -10% grade) were performed to vary the extent of muscle damage. Creatine kinase (CK) increased more after Down 1 (61%) than after Down 2 (11%), as did soreness ratings, indicating reduced muscle damage during Down 2. Significantly greater increases in VO2 over time were noted for Down 1 (15.6%) and Down 2 (14.7%) than for Level (1.2%). Heart rate increased 8 beats/min for Level but 29 and 25 beats/min for Down 1 and Down 2, respectively. Expired ventilation increased more for Down 1 (20.5%) and Down 2 (24%) than for Level (3.5%). Rectal temperature increased approximately 0.8 degree C for all bouts. Because the magnitude of the drift was similar in the two downhill bouts, the findings suggest that muscle damage does not cause the drift in VO2 during low-intensity downhill running.

Skeletal muscle adaptations in response to voluntary wheel running in myosin heavy chain null mice.

10.1152/ japplphysiol.00832.2001.-To examine the effects of gene inactivation on the plasticity of skeletal muscle, mice null for a specific myosin heavy chain (MHC) isoform were subjected to a voluntary wheel-running paradigm. Despite reduced running performance compared with nontransgenic C57BL/6 mice (NTG), both MHC IIb and MHC IId/x null animals exhibited increased muscle fiber size and muscle oxidative capacity with wheel running. In the MHC IIb null animals, there was no significant change in the percentage of muscle fibers expressing a particular MHC isoform with voluntary wheel running at any time point. In MHC IId/x null mice, wheel running produced a significant increase in the percentage of fibers expressing MHC IIa and MHC I and a significant decrease in the percentage of fibers expressing MHC IIb. Muscle pathology was not affected by wheel running for either MHC null strain. In summary, despite their phenotypes, MHC null mice do engage in voluntary wheel running. Although this wheel-running activity is lessened compared with NTG, there is evidence of distinct patterns of muscle adaptation in both null strains.

Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training.

Twelve male subjects with recreational resistance training backgrounds completed 12 wk of intensified resistance training (3 sessions/wk; 8 exercises/session; 3 sets/exercise; 10 repetitions maximum/set). All major muscle groups were trained, with four exercises emphasizing the forearm flexors. After training, strength (1-repetition maximum preacher curl) increased by 25% (P < 0.05). Magnetic resonance imaging scans revealed an increase in the biceps brachii muscle cross-sectional area (CSA) (from 11.8 +/- 2.7 to 13.3 +/- 2.6 cm2; n = 8; P < 0.05). Muscle biopsies of the biceps brachii revealed increases (P < 0.05) in fiber areas for type I (from 4,196 +/- 859 to 4,617 +/- 1,116 microns2; n = 11) and II fibers (from 6,378 +/- 1,552 to 7,474 +/- 2,017 microns2; n = 11). Fiber number estimated from the above measurements did not change after training (293.2 +/- 61.5 x 10(3) pretraining; 297.5 +/- 69.5 x 10(3) posttraining; n = 8). However, the magnitude of muscle fiber hypertrophy may influence this response because those subjects with less relative muscle fiber hypertrophy, but similar increases in muscle CSA, showed evidence of an increase in fiber number. Capillaries per fiber increased significantly (P < 0.05) for both type I (from 4.9 +/- 0.6 to 5.5 +/- 0.7; n = 10) and II fibers (from 5.1 +/- 0.8 to 6.2 +/- 0.7; n = 10). No changes occurred in capillaries per fiber area or muscle area. In conclusion, resistance training resulted in hypertrophy of the total muscle CSA and fiber areas with no change in estimated fiber number, whereas capillary changes were proportional to muscle fiber growth.

Delayed onset muscle soreness following repeated bouts of downhill running.

Perceived muscle soreness ratings, serum creatine kinase (CK) activity, and myoglobin levels were assessed in three groups of subjects following two 30-min exercise bouts of downhill running (-10 degrees slope). The two bouts were separated by 3, 6, and 9 wk for groups 1, 2, and 3, respectively. Criterion measures were obtained pre- and 6, 18, and 42 h postexercise. On bout 1 the three groups reported maximal soreness at 42 h postexercise. Also, relative increases in CK for groups 1, 2, and 3 were 340, 272, and 286%, respectively. Corresponding values for myoglobin were 432, 749, and 407%. When the same exercise was repeated, significantly less soreness was reported and smaller increases in CK and myoglobin were found for groups 1 and 2. For example, the percent CK increases on bout 2 for groups 1 and 2 were 63 and 62, respectively. Group 3 demonstrated no significant difference in soreness ratings, CK activities, or myoglobin levels between bouts 1 and 2. It was concluded that performance of a single exercise bout had a prophylactic effect on the generation of muscle soreness and serum protein responses that lasts up to 6 wk.

Cardiac and skeletal muscle adaptations to voluntary wheel running in the mouse.

In this paper, we describe the effects of voluntary cage wheel exercise on mouse cardiac and skeletal muscle. Inbred male C57/Bl6 mice (age 6-8 wk; n = 12) [corrected] ran an average of 4.3 h/24 h, for an average distance of 6.8 km/24 h, and at an average speed of 26.4 m/min. A significant increase in the ratio of heart mass to body mass (mg/g) was evident after 2 wk of voluntary exercise, and cardiac atrial natriuretic factor and brain natriuretic peptide mRNA levels were significantly increased in the ventricles after 4 wk of voluntary exercise. A significant increase in the percentage of fibers expressing myosin heavy chain (MHC) IIa was observed in both the gastrocnemius and the tibialis anterior (TA) by 2 wk, and a significant decrease in the percentage of fibers expressing IIb MHC was evident in both muscles after 4 wk of voluntary exercise. The TA muscle showed a greater increase in the percentage of IIa MHC-expressing fibers than did the gastrocnemius muscle (40 and 20%, respectively, compared with 10% for nonexercised). Finally, the number of oxidative fibers as revealed by NADH-tetrazolium reductase histochemical staining was increased in the TA but not the gastrocnemius after 4 wk of voluntary exercise. All results are relative to age-matched mice housed without access to running wheels. Together these data demonstrate that voluntary exercise in mice results in cardiac and skeletal muscle adaptations consistent with endurance exercise.

Walking and running energy expenditure estimated by Caltrac and indirect calorimetry.

The purpose of this study was to examine the accuracy of the Caltrac personal activity computer during walking and running. Ten women and 10 men walked at speeds of 2-5 mph and ran at speeds of 4-8 mph on a horizontal treadmill. Two Caltrac monitors were attached over opposite hips: one programed to give caloric expenditure and the other to give Caltrac counts. Oxygen uptake was measured simultaneously. Significant correlations were found during walking between Caltrac estimated and actual energy expenditure (r = 0.91) and between activity counts and net exercise VO2.kg-1 (r = 0.87). However, the Caltrac significantly overestimated energy cost during horizontal walking at speeds above 2 mph. Although there was a significant correlation between Caltrac estimated and actual energy expenditure during running (r = 0.71), the correlation between Caltrac counts and net exercise VO2.kg-1 was not significant (r = 0.29). There was no significant increase in Caltrac kcal or counts with increased running speed between 5 and 8 mph. It is concluded that the Caltrac is a valid indicator of physical activity during walking but does not adequately discriminate between running speeds of 5-8 mph.

Creatine kinase and muscle soreness after repeated isometric exercise.

This study examined adaptation to isometric exercise with regard to changes in serum creatine kinase (CK) activity and muscle soreness. Forty-five college-age males were placed into six groups, each performing two bouts of strenuous isometric exercise of the knee extensors. In experiment 1 (N = 27), after performing the first bout of exercise, groups A, B, and C performed the second bout 3, 6, and 9 wk later, respectively. In experiment 2 (N = 18), groups D, E, and F performed the second exercise bout 1, 2, and 3 wk after the first bout, respectively. In experiment 3, group D performed two additional exercise bouts; thus, this group performed a total of four bouts spaced 1 wk apart. Muscle soreness and CK were assessed prior to and 6, 18, and 24 (or 42) h following each exercise. In experiment 1, no significant difference in soreness or serum CK was found between bouts 1 and 2. In experiment 2, a significant decrease in the CK and soreness responses was found on bout 2 compared with bout 1 (P less than 0.05). In experiment 3, serum CK and soreness responses were highest following bout 1 while bouts 2, 3, and 4 were not significantly different from one another. Performance of this isometric exercise results in an adaptation that lasts approximately 3 wk, with the greatest adaptation occurring after one bout.

Alterations in oxygen consumption during and between bouts of level and downhill running.

Since the etiology of the drift in VO2 during downhill running is unclear, this study was designed to assess the contribution of heart rate (HR), ventilation (VE), blood lactate, rectal temperature (RT), muscle damage, and several variables that have not previously been included in VO2 drift research: muscle temperature (MT), and stride rate (SR) and length (SL), to the drift in VO2. Six subjects participated in a 45-min level run (LEVEL) and two 45-min downhill runs (DOWN1 and DOWN2) at 50% VO2max. Although VO2 increased significantly over time for all bouts, the magnitude [4.3% (LEVEL), 5.4% (DOWN1), and 8.1% (DOWN2)] did not differ between bouts (P > 0.05). VO2 was significantly lower during DOWN2 than during LEVEL and DOWN1 (P < 0.05). MT increased during the three bouts (P < 0.05) but the change over time was not different between bouts. SR and SL did not change over time within each bout nor between the two downhill runs. Muscle damage, as indicated by serum creatine kinase levels and perceived soreness, was less following LEVEL and DOWN2 than DOWN1 (P < 0.05). HR and RT increased over time (P < 0.05) but did not differ between bouts. VE and blood lactate did not differ over time or between bouts. VO2 drift during the three bouts paralleled changes in RT, MT, and HR but appears unrelated to muscle damage or biomechanical factors.

Submaximal exercise quantified as percent of normoxic and hyperoxic maximum oxygen uptakes.

Maximum oxygen uptake (VO2max) was measured in six college-aged males under normoxic (NVO2max) and hyperoxic (HVO2max; 70% oxygen) conditions. Subjects then randomly performed the following three 20-min submaximal exercise bouts: 75% normoxic VO2max under normoxia (NVO2N), 75% normoxic VO2max under hyperoxia (NVO2H), and 75% hyperoxic VO2max under hyperoxia (HVO2H). Metabolic parameters were obtained at 5-min intervals. Hyperoxia resulted in a 13% increase (P less than 0.01) in VO2max (NVO2max = 3.54 l X min-1 vs HVO2max = 4.00 l X min-1). Significant (P less than 0.05) decreases were observed in VE (ventilation) (13%), epinephrine (37%), norepinephrine (26%), and blood lactate (28%), with no change in oxygen uptake (VO2), carbon dioxide production (VCO2), or respiratory exchange ratio (R) during hyperoxia at the same absolute power output (NVO2N vs NVO2H). However, at the same relative power outputs (NVO2N vs HVO2H) no significant changes in VE, epinephrine, norepinephrine, or blood lactate were observed when hyperoxia and normoxia were compared.

The reproducibility of VO2max, ventilatory, and lactate thresholds in elderly women.

The reproducibility of VO2max, ventilatory, and lactate thresholds in elderly women. Med. Sci. Sports Exerc., Vol. 18, No. 4, pp. 425-430, 1986. This investigation examined the reproducibility of maximal (VO2max) and submaximal measures of fitness for elderly women. Eight subjects [age (yr): mean = 80.6 +/- 3.7; range = 73-86] volunteered to repeat three continuous, incremental maximal effort treadmill tests. Blood lactate determinations were made for each increment from blood samples taken from an indwelling venous catheter located in the back of the hand. Average VO2max values (ml X min-1 X kg X l-1) were 13.21 + 1.95 for test 1, 13.44 +/- 1.83 for test 2, and 13.62 + 2.95 for test 3. In all but one subject, a threshold was not definable by either ventilatory or lactate measurements. Maximal lactate values were low, with the average values for tests 1, 2, and 3 being 1.89, 1.46, and 1.86 mmol X l-1, respectively. The data demonstrates that VO2max is reproducible for older women and can, therefore, be used for fitness assessment and exercise prescription. The use of ventilatory or lactate thresholds as submaximal measures of fitness or as minimal intensities for exercise prescription was determined not to be applicable for women in the eighth and ninth decades of life.

Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy.

PURPOSE: This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury. METHODS: 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. RESULTS: 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). CONCLUSION: These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated.