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Effects of intermittent hypoxia-hyperoxia on performance- and health-related outcomes in humans
(2022)
Background:
Intermittent hypoxia applied at rest or in combination with exercise promotes multiple beneficial adaptations with regard to performance and health in humans. It was hypothesized that replacing normoxia by moderate hyperoxia can increase the adaptive response to the intermittent hypoxic stimulus.
Objective:
Our objective was to systematically review the current state of the literature on the effects of chronic intermittent hypoxia-hyperoxia (IHH) on performance- and health-related outcomes in humans.
Methods:
PubMed, Web of Science (TM), Scopus, and Cochrane Library databases were searched in accordance with PRISMA guidelines (January 2000 to September 2021) using the following inclusion criteria: (1) original research articles involving humans, (2) investigation of the chronic effect of IHH, (3) inclusion of a control group being not exposed to IHH, and (4) articles published in peer-reviewed journals written in English.
Results:
Of 1085 articles initially found, eight studies were included. IHH was solely performed at rest in different populations including geriatric patients (n = 1), older patients with cardiovascular (n = 3) and metabolic disease (n = 2) or cognitive impairment (n = 1), and young athletes with overtraining syndrome (n = 1). The included studies confirmed the beneficial effects of chronic exposure to IHH, showing improvements in exercise tolerance, peak oxygen uptake, and global cognitive functions, as well as lowered blood glucose levels. A trend was discernible that chronic exposure to IHH can trigger a reduction in systolic and diastolic blood pressure. The evidence of whether IHH exerts beneficial effects on blood lipid levels and haematological parameters is currently inconclusive. A meta-analysis was not possible because the reviewed studies had a considerable heterogeneity concerning the investigated populations and outcome parameters.
Conclusion:
Based on the published literature, it can be suggested that chronic exposure to IHH might be a promising non-pharmacological intervention strategy for improving peak oxygen consumption, exercise tolerance, and cognitive performance as well as reducing blood glucose levels, and systolic and diastolic blood pressure in older patients with cardiovascular and metabolic diseases or cognitive impairment. However, further randomized controlled trials with adequate sample sizes are needed to confirm and extend the evidence. This systematic review was registered on the international prospective register of systematic reviews (PROSPERO-ID: CRD42021281248) (https://www.crd.york.ac.uk/prospero/).
Objective: To examine the effect of plyometric jump training on skeletal muscle hypertrophy in healthy individuals.
Methods: A systematic literature search was conducted in the databases PubMed, SPORTDiscus, Web of Science, and Cochrane Library up to September 2021.
Results: Fifteen studies met the inclusion criteria. The main overall finding (44 effect sizes across 15 clusters median = 2, range = 1–15 effects per cluster) indicated that plyometric jump training had small to moderate effects [standardised mean difference (SMD) = 0.47 (95% CIs = 0.23–0.71); p < 0.001] on skeletal muscle hypertrophy. Subgroup analyses for training experience revealed trivial to large effects in non-athletes [SMD = 0.55 (95% CIs = 0.18–0.93); p = 0.007] and trivial to moderate effects in athletes [SMD = 0.33 (95% CIs = 0.16–0.51); p = 0.001]. Regarding muscle groups, results showed moderate effects for the knee extensors [SMD = 0.72 (95% CIs = 0.66–0.78), p < 0.001] and equivocal effects for the plantar flexors [SMD = 0.65 (95% CIs = −0.25–1.55); p = 0.143]. As to the assessment methods of skeletal muscle hypertrophy, findings indicated trivial to small effects for prediction equations [SMD = 0.29 (95% CIs = 0.16–0.42); p < 0.001] and moderate-to-large effects for ultrasound imaging [SMD = 0.74 (95% CIs = 0.59–0.89); p < 0.001]. Meta-regression analysis indicated that the weekly session frequency moderates the effect of plyometric jump training on skeletal muscle hypertrophy, with a higher weekly session frequency inducing larger hypertrophic gains [β = 0.3233 (95% CIs = 0.2041–0.4425); p < 0.001]. We found no clear evidence that age, sex, total training period, single session duration, or the number of jumps per week moderate the effect of plyometric jump training on skeletal muscle hypertrophy [β = −0.0133 to 0.0433 (95% CIs = −0.0387 to 0.1215); p = 0.101–0.751].
Conclusion: Plyometric jump training can induce skeletal muscle hypertrophy, regardless of age and sex. There is evidence for relatively larger effects in non-athletes compared with athletes. Further, the weekly session frequency seems to moderate the effect of plyometric jump training on skeletal muscle hypertrophy, whereby more frequent weekly plyometric jump training sessions elicit larger hypertrophic adaptations.
Objective: To examine the effect of plyometric jump training on skeletal muscle hypertrophy in healthy individuals.
Methods: A systematic literature search was conducted in the databases PubMed, SPORTDiscus, Web of Science, and Cochrane Library up to September 2021.
Results: Fifteen studies met the inclusion criteria. The main overall finding (44 effect sizes across 15 clusters median = 2, range = 1–15 effects per cluster) indicated that plyometric jump training had small to moderate effects [standardised mean difference (SMD) = 0.47 (95% CIs = 0.23–0.71); p < 0.001] on skeletal muscle hypertrophy. Subgroup analyses for training experience revealed trivial to large effects in non-athletes [SMD = 0.55 (95% CIs = 0.18–0.93); p = 0.007] and trivial to moderate effects in athletes [SMD = 0.33 (95% CIs = 0.16–0.51); p = 0.001]. Regarding muscle groups, results showed moderate effects for the knee extensors [SMD = 0.72 (95% CIs = 0.66–0.78), p < 0.001] and equivocal effects for the plantar flexors [SMD = 0.65 (95% CIs = −0.25–1.55); p = 0.143]. As to the assessment methods of skeletal muscle hypertrophy, findings indicated trivial to small effects for prediction equations [SMD = 0.29 (95% CIs = 0.16–0.42); p < 0.001] and moderate-to-large effects for ultrasound imaging [SMD = 0.74 (95% CIs = 0.59–0.89); p < 0.001]. Meta-regression analysis indicated that the weekly session frequency moderates the effect of plyometric jump training on skeletal muscle hypertrophy, with a higher weekly session frequency inducing larger hypertrophic gains [β = 0.3233 (95% CIs = 0.2041–0.4425); p < 0.001]. We found no clear evidence that age, sex, total training period, single session duration, or the number of jumps per week moderate the effect of plyometric jump training on skeletal muscle hypertrophy [β = −0.0133 to 0.0433 (95% CIs = −0.0387 to 0.1215); p = 0.101–0.751].
Conclusion: Plyometric jump training can induce skeletal muscle hypertrophy, regardless of age and sex. There is evidence for relatively larger effects in non-athletes compared with athletes. Further, the weekly session frequency seems to moderate the effect of plyometric jump training on skeletal muscle hypertrophy, whereby more frequent weekly plyometric jump training sessions elicit larger hypertrophic adaptations.
Background and Objectives: Low back pain is a worldwide health problem. An early diagnosis is required to develop personalized treatment strategies. The Risk Stratification Index (RSI) was developed to serve the purpose. The aim of this pilot study is to cross-culturally translate the RSI to a French version (RSI-F) and evaluate the test-retest reliability of RSI-F using a French active population. Materials and Methods: The RSI was translated from German to French (RSI-F) based on the guidelines of cross-cultural adaptation of self-report measures. A total of 42 French recreational athletes (age 18–63 years) with non-specific low back pain were recruited and filled in the RSI-F twice. The test-retest reliability was examined using intraclass correlation coefficient (ICC1,2) and Pearson correlation coefficient. Results: Finally, 33 questionnaires were analyzed (14 males and 19 females, age 31 ± 10 years, 9.5 ± 3.2 h/week of training). The test-retest of RSI-F CPI and DISS were excellent (CPI: ICC1,2 = 0.989, p < 0.001; r = 0.989, p < 0.001; DISS: ICC1,2 = 0.991, p < 0.001; r = 0.991, p < 0.001), as well as Korff pain intensity (ICC1,2 = 0.995, p < 0.001; r = 0.995, p < 0.001) and disability (ICC1,2 = 0.998, p < 0.001; r = 0.998, p < 0.001). Conclusion: The RSI-F is linguistically accurate and reliable for use by a French-speaking active population with non-specific low back pain. The RSI-F is considered a tool to examine the evolution of psychosocial factors and therefore the risk of chronicity and the prognostic of pain. Further evaluations, such as internal, external validity, and responsiveness should be evaluated in a larger population.
Exercise is known for its beneficial effects on preventing cardiometabolic diseases (CMDs) in the general population. People living with the human immunodeficiency virus (PLWH) are prone to sedentarism, thus raising their already elevated risk of developing CMDs in comparison to individuals without HIV. The aim of this cross-sectional study was to determine if exercise is associated with reduced risk of self-reported CMDs in a German HIV-positive sample (n = 446). Participants completed a self-report survey to assess exercise levels, date of HIV diagnosis, CD4 cell count, antiretroviral therapy, and CMDs. Participants were classified into exercising or sedentary conditions. Generalized linear models with Poisson regression were conducted to assess the prevalence ratio (PR) of PLWH reporting a CMD. Exercising PLWH were less likely to report a heart arrhythmia for every increase in exercise duration (PR: 0.20: 95% CI: 0.10–0.62, p < 0.01) and diabetes mellitus for every increase in exercise session per week (PR: 0.40: 95% CI: 0.10–1, p < 0.01). Exercise frequency and duration are associated with a decreased risk of reporting arrhythmia and diabetes mellitus in PLWH. Further studies are needed to elucidate the mechanisms underlying exercise as a protective factor for CMDs in PLWH.
The effects of exercise interventions on unspecific chronic low back pain (CLBP) have been investigated in many studies, but the results are inconclusive regarding exercise types, efficiency, and sustainability. This may be because the influence of psychosocial factors on exercise induced adaptation regarding CLBP is neglected. Therefore, this study assessed psychosocial characteristics, which moderate and mediate the effects of sensorimotor exercise on LBP. A single-blind 3-arm multicenter randomized controlled trial was conducted for 12-weeks. Three exercise groups, sensorimotor exercise (SMT), sensorimotor and behavioral training (SMT-BT), and regular routines (CG) were randomly assigned to 662 volunteers. Primary outcomes (pain intensity and disability) and psychosocial characteristics were assessed at baseline (M1) and follow-up (3/6/12/24 weeks, M2-M5). Multiple regression models were used to analyze whether psychosocial characteristics are moderators of the relationship between exercise and pain, meaning that psychosocial factors and exercise interact. Causal mediation analysis were conducted to analyze, whether psychosocial characteristics mediate the exercise effect on pain. A total of 453 participants with intermittent pain (mean age = 39.5 ± 12.2 years, f = 62%) completed the training. It was shown, that depressive symptomatology (at M4, M5), vital exhaustion (at M4), and perceived social support (at M5) are significant moderators of the relationship between exercise and the reduction of pain intensity. Further depressive mood (at M4), social-satisfaction (at M4), and anxiety (at M5 SMT) significantly moderate the exercise effect on pain disability. The amount of moderation was of clinical relevance. In contrast, there were no psychosocial variables which mediated exercise effects on pain. In conclusion it was shown, that psychosocial variables can be moderators in the relationship between sensorimotor exercise induced adaptation on CLBP which may explain conflicting results in the past regarding the merit of exercise interventions in CLBP. Results suggest further an early identification of psychosocial risk factors by diagnostic tools, which may essential support the planning of personalized exercise therapy.
Level of Evidence: Level I.
Clinical Trial Registration: DRKS00004977, LOE: I, MiSpEx: grant-number: 080102A/11-14. https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00004977.
The effects of exercise interventions on unspecific chronic low back pain (CLBP) have been investigated in many studies, but the results are inconclusive regarding exercise types, efficiency, and sustainability. This may be because the influence of psychosocial factors on exercise induced adaptation regarding CLBP is neglected. Therefore, this study assessed psychosocial characteristics, which moderate and mediate the effects of sensorimotor exercise on LBP. A single-blind 3-arm multicenter randomized controlled trial was conducted for 12-weeks. Three exercise groups, sensorimotor exercise (SMT), sensorimotor and behavioral training (SMT-BT), and regular routines (CG) were randomly assigned to 662 volunteers. Primary outcomes (pain intensity and disability) and psychosocial characteristics were assessed at baseline (M1) and follow-up (3/6/12/24 weeks, M2-M5). Multiple regression models were used to analyze whether psychosocial characteristics are moderators of the relationship between exercise and pain, meaning that psychosocial factors and exercise interact. Causal mediation analysis were conducted to analyze, whether psychosocial characteristics mediate the exercise effect on pain. A total of 453 participants with intermittent pain (mean age = 39.5 ± 12.2 years, f = 62%) completed the training. It was shown, that depressive symptomatology (at M4, M5), vital exhaustion (at M4), and perceived social support (at M5) are significant moderators of the relationship between exercise and the reduction of pain intensity. Further depressive mood (at M4), social-satisfaction (at M4), and anxiety (at M5 SMT) significantly moderate the exercise effect on pain disability. The amount of moderation was of clinical relevance. In contrast, there were no psychosocial variables which mediated exercise effects on pain. In conclusion it was shown, that psychosocial variables can be moderators in the relationship between sensorimotor exercise induced adaptation on CLBP which may explain conflicting results in the past regarding the merit of exercise interventions in CLBP. Results suggest further an early identification of psychosocial risk factors by diagnostic tools, which may essential support the planning of personalized exercise therapy.
Level of Evidence: Level I.
Clinical Trial Registration: DRKS00004977, LOE: I, MiSpEx: grant-number: 080102A/11-14. https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00004977.
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.”
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.”
The aim was to analyze the risk of hip fracture in German primary care patients with dementia. This study included patients aged 65-90 from 1072 primary care practices who were first diagnosed with dementia between 2010 and 2013. Controls were matched (1:1) to cases for age, sex, and type of health insurance. The primary outcome was the diagnosis of hip fracture during the three-year follow-up period. A total of 53,156 dementia patients and 53,156 controls were included. A total of 5.3% of patients and 0.7% of controls displayed hip fracture after three years. Hip fracture occurred more frequently in dementia subjects living in nursing homes than in those living at home (9.2% versus 4.3%). Dementia, residence in nursing homes, and osteoporosis were risk factors for fracture development. Antidementia, antipsychotic, and antidepressant drugs generally had no significant impact on hip fracture risk when prescribed for less than six months. Dementia increased hip fracture risk in German primary care practices.