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Background: The relationship between exercise-induced intratendinous blood flow (IBF) and tendon pathology or training exposure is unclear.
Objective: This study investigates the acute effect of running exercise on sonographic detectable IBF in healthy and tendinopathic Achilles tendons (ATs) of runners and recreational participants.
Methods: 48 participants (43 ± 13 years, 176 ± 9 cm, 75 ± 11 kg) performed a standardized submaximal 30-min constant load treadmill run with Doppler ultrasound “Advanced dynamic flow” examinations before (Upre) and 5, 30, 60, and 120 min (U5-U120) afterward. Included were runners (>30 km/week) and recreational participants (<10 km/week) with healthy (Hrun, n = 10; Hrec, n = 15) or tendinopathic (Trun, n = 13; Trec, n = 10) ATs. IBF was assessed by counting number [n] of intratendinous vessels. IBF data are presented descriptively (%, median [minimum to maximum range] for baseline-IBF and IBF-difference post-exercise). Statistical differences for group and time point IBF and IBF changes were analyzed with Friedman and Kruskal-Wallis ANOVA (α = 0.05).
Results: At baseline, IBF was detected in 40% (3 [1–6]) of Hrun, in 53% (4 [1–5]) of Hrec, in 85% (3 [1–25]) of Trun, and 70% (10 [2–30]) of Trec. At U5 IBF responded to exercise in 30% (3 [−1–9]) of Hrun, in 53% (4 [−2–6]) of Hrec, in 70% (4 [−10–10]) of Trun, and in 80% (5 [1–10]) of Trec. While IBF in 80% of healthy responding ATs returned to baseline at U30, IBF remained elevated until U120 in 60% of tendinopathic ATs. Within groups, IBF changes from Upre-U120 were significant for Hrec (p < 0.01), Trun (p = 0.05), and Trec (p < 0.01). Between groups, IBF changes in consecutive examinations were not significantly different (p > 0.05) but IBF-level was significantly higher at all measurement time points in tendinopathic versus healthy ATs (p < 0.05).
Conclusion: Irrespective of training status and tendon pathology, running leads to an immediate increase of IBF in responding tendons. This increase occurs shortly in healthy and prolonged in tendinopathic ATs. Training exposure does not alter IBF occurrence, but IBF level is elevated in tendon pathology. While an immediate exercise-induced IBF increase is a physiological response, prolonged IBF is considered a pathological finding associated with Achilles tendinopathy.
Objective: This study investigated intraindividual differences of intratendinous blood flow (IBF) in response to running exercise in participants with Achilles tendinopathy.
Design: This is a cross-sectional study.
Setting: The study was conducted at the University Outpatient Clinic.
Participants: Sonographic detectable intratendinous blood flow was examined in symptomatic and contralateral asymptomatic Achilles tendons of 19 participants (42 ± 13 years, 178 ± 10 cm, 76 ± 12 kg, VISA-A 75 ± 16) with clinically diagnosed unilateral Achilles tendinopathy and sonographic evident tendinosis.
Intervention: IBF was assessed using Doppler ultrasound “Advanced Dynamic Flow” before (Upre) and 5, 30, 60, and 120 min (U5–U120) after a standardized submaximal constant load run.
Main Outcome Measure: IBF was quantified by counting the number (n) of vessels in each tendon.
Results: At Upre, IBF was higher in symptomatic compared with asymptomatic tendons [mean 6.3 (95% CI: 2.8–9.9) and 1.7 (0.4–2.9), p < 0.01]. Overall, 63% of symptomatic and 47% of asymptomatic Achilles tendons responded to exercise, whereas 16 and 11% showed persisting IBF and 21 and 42% remained avascular throughout the investigation. At U5, IBF increased in both symptomatic and asymptomatic tendons [difference to baseline: 2.4 (0.3–4.5) and 0.9 (0.5–1.4), p = 0.05]. At U30 to U120, IBF was still increased in symptomatic but not in asymptomatic tendons [mean difference to baseline: 1.9 (0.8–2.9) and 0.1 (-0.9 to 1.2), p < 0.01].
Conclusion: Irrespective of pathology, 47–63% of Achilles tendons responded to exercise with an immediate acute physiological IBF increase by an average of one to two vessels (“responders”). A higher amount of baseline IBF (approximately five vessels) and a prolonged exercise-induced IBF response found in symptomatic ATs indicate a pain-associated altered intratendinous “neovascularization.”
Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn’s post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.
Background: The relationship between exercise-induced intratendinous blood flow (IBF) and tendon pathology or training exposure is unclear.
Objective: This study investigates the acute effect of running exercise on sonographic detectable IBF in healthy and tendinopathic Achilles tendons (ATs) of runners and recreational participants.
Methods: 48 participants (43 ± 13 years, 176 ± 9 cm, 75 ± 11 kg) performed a standardized submaximal 30-min constant load treadmill run with Doppler ultrasound “Advanced dynamic flow” examinations before (Upre) and 5, 30, 60, and 120 min (U5-U120) afterward. Included were runners (>30 km/week) and recreational participants (<10 km/week) with healthy (Hrun, n = 10; Hrec, n = 15) or tendinopathic (Trun, n = 13; Trec, n = 10) ATs. IBF was assessed by counting number [n] of intratendinous vessels. IBF data are presented descriptively (%, median [minimum to maximum range] for baseline-IBF and IBF-difference post-exercise). Statistical differences for group and time point IBF and IBF changes were analyzed with Friedman and Kruskal-Wallis ANOVA (α = 0.05).
Results: At baseline, IBF was detected in 40% (3 [1–6]) of Hrun, in 53% (4 [1–5]) of Hrec, in 85% (3 [1–25]) of Trun, and 70% (10 [2–30]) of Trec. At U5 IBF responded to exercise in 30% (3 [−1–9]) of Hrun, in 53% (4 [−2–6]) of Hrec, in 70% (4 [−10–10]) of Trun, and in 80% (5 [1–10]) of Trec. While IBF in 80% of healthy responding ATs returned to baseline at U30, IBF remained elevated until U120 in 60% of tendinopathic ATs. Within groups, IBF changes from Upre-U120 were significant for Hrec (p < 0.01), Trun (p = 0.05), and Trec (p < 0.01). Between groups, IBF changes in consecutive examinations were not significantly different (p > 0.05) but IBF-level was significantly higher at all measurement time points in tendinopathic versus healthy ATs (p < 0.05).
Conclusion: Irrespective of training status and tendon pathology, running leads to an immediate increase of IBF in responding tendons. This increase occurs shortly in healthy and prolonged in tendinopathic ATs. Training exposure does not alter IBF occurrence, but IBF level is elevated in tendon pathology. While an immediate exercise-induced IBF increase is a physiological response, prolonged IBF is considered a pathological finding associated with Achilles tendinopathy.
Objective: To assess the reliability of measurements of paraspinal muscle transverse relaxation times (T2 times) between two observers and within one observer on different time points. <br /> Methods: 14 participants (9f/5m, 33 +/- 5 years, 176 +/- 10 cm, 73 +/- 12 kg) underwent 2 consecutive MRI scans (M1,M2) on the same day, followed by 1 MRI scan 13-14 days later (M3) in a mobile 1.5 Tesla MRI. T2 times were calculated in T-2 weighted turbo spin- echo-sequences at the spinal level of the third lumbar vertebrae (11 slices, 2 mm slice thickness, 1 mm interslice gap, echo times: 20, 40, 60, 80, 100 ms) for M. erector spinae (ES) and M. multifidius (MF). The following reliability parameter were calculated for the agreement of T2 times between two different investigators (OBS1 & OBS2) on the same MRI (inter rater reliability, IR) and by one investigator between different MRI of the same participant (intersession variability, IS): Test-Retest Variability (TRV, Differences/Mean*100); Coefficient of Variation (CV, Standard deviation/Mean*100); Bland-Altman Analysis (systematic bias = Mean of the Differences; Upper/Lower Limits of Agreement = Bias+/-1.96*SD); Intraclass Correlation Coefficient 3.1 (ICC) with absolute agreement, as well as its 95% confidence interval. <br /> Results: Mean TRV for IR was 2.6% for ES and 4.2% for MF. Mean TRV for IS was 3.5% (ES) and 5.1% (MF). Mean CV for IR was 1.9 (ES) and 3.0 (MF). Mean CV for IS was 2.5% (ES) and 3.6% (MF). A systematic bias of 1.3 ms (ES) and 2.1 ms (MF) were detected for IR and a systematic bias of 0.4 ms (ES) and 0.07 ms (MF) for IS. ICC for IR was 0.94 (ES) and 0.87 (MF). ICC for IS was 0.88 (ES) and 0.82 (MF). <br /> Conclusion: Reliable assessment of paraspinal muscle T2 time justifies its use for scientific purposes. The applied technique could be recommended to use for future studies that aim to assess changes of T2 times, e.g. after an intense bout of eccentric exercises.