Background Management of Long COVID (LC) is hugely challenging for clinicians. This pilot study evaluated a breathing retraining and singing programme (SingStrong for LC) to address common LC symptoms. The study hypothesized that this intervention would improve symptoms impacting disordered breathing and participant wellbeing. Methods The 10-week, bi-weekly online programme was comprised of a 45-min class of mindfulness, breathing retraining, vocal exercises, and singing. Sessions were recorded for non-attenders and conducted by a trained vocal coach experienced in respiratory cohorts. Persons with a confirmed COVID-19 diagnosis and persisting symptoms were invited to participate. Demographic and COVID-19 data were collected, and the DePaul Symptom Questionnaire Short Form (DSQ- SF) and COVID-19 Yorkshire Rehab Screen questionnaires were administered. Post-intervention focus groups were also conducted. Results Of 27 ( F = 23(85%)) participants recruited, data from 21 who completed at least 10 (50%) classes were analysed. Participants showed significant pre–post-intervention improvements in all breathlessness symptoms (at rest: P < 0.001; dressing: P = 0.01; stairs: P < 0.001), fatigue ( P = 0.03), usual activities ( P = 0.04), pain/disability ( P = 0.03), voice quality ( P = 0.01), and communication/cognition ( P = 0.04). Pre–post number of instances meeting DSQ-SF criteria for myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) decreased by a net of nine cases (14.3%). No association between COVID-19 hospitalisation status and diagnosis of ME/CFS was identified. Qualitative feedback from eight participants was overwhelmingly positive with all reporting improvements in breathing and general well-being. Conclusion The SingStrong programme shows promise as a viable treatment option for LC sufferers. Future studies are required to further investigate the efficacy of this intervention.
Cardiac mitochondrial dysfunction contributes to obesity-associated heart disease. Maternal and postnatal diet plays an important role in cardiac function, yet the impacts of a mismatch between prenatal and postweaning diet on cardiometabolic function are not well understood. We tested the hypothesis that switching to a standard chow diet after weaning would attenuate systemic metabolic disorders and cardiac and mitochondrial dysfunction associated with maternal and postnatal high-fat/high-sucrose (HFHS) diet in mice. Six-month-old male CD1 offspring from dams fed a HFHS diet and weaned to the same HFHS diet (HH) or switched to a standard chow diet (HC) were compared to offspring from dams fed a low-fat/low-sucrose diet and maintained on the same diet (LL). HC did not decrease body weight (BW) but normalized glucose tolerance, plasma cholesterol, LDL, and insulin levels compared to the HH. Systolic function indicated by the percent fractional shortening was not altered by diet. In freshly isolated cardiac mitochondria, maximal oxidative phosphorylation-linked respiratory capacity and coupling efficiency were significantly higher in the HC in the presence of fatty acid substrate compared to LL and HH, with modification of genes associated with metabolism and mitochondrial function. Switching to a standard chow diet at weaning can attenuate the deleterious effects of long-term HFHS in adult male mouse offspring.
A wealth of studies have shown that an adverse intrauterine and perinatal environment is a strong predictor for cardiometabolic diseases in offspring. Conversely, maternal exercise before and during pregnancy has been shown to diminish the risk of offspring developing metabolic disorders later in life. A few promising human and animal studies demonstrated that adult‐onset exercise in offspring can overcome the detrimental effects on offspring health associated with maternal obesity. However, it is unknown whether exercise initiated by adult offspring can mitigate the negative cardiometabolic health induced by maternal obesity. Female CD‐1 mice were fed either a high‐fat, high‐sucrose diet (HFHS) or a refined low‐fat, low‐sucrose diet (LFLS) for eight weeks before pregnancy and gestation, and during lactation. All dams were sedentary throughout the study. At 21 days, female offspring were weaned onto their maternal diet. At 15 weeks, offspring were randomly divided into exercise and sedentary groups which yielded 4 groups: LLS, LLE, HHS, and HHE (first letter denotes maternal diet, second letter offspring diet, and third letter indicates sedentary (S) and exercised group in offspring(E)). For exercise groups, mice had unrestricted exercise wheel access for 10 weeks. Glucose tolerance test (GTT) was performed at 25 weeks and tissues were collected to evaluate cardiac mitochondrial respiratory function at 26 weeks. Maternal diet did not affect body weight (BW) at weaning. Diet did not affect the daily average distance or hours run. BW was significantly higher in the HHS compared to other groups, but exercise did not alter final body weight. This was also true for fat mass. Exercise induced cardiac hypertrophy in mice fed LL, but not in HH mice. Surprisingly, mice in HHE had impaired glucose tolerance compared to other groups. However, no difference was found between LLE and LLS for GTT. In freshly isolated cardiac mitochondria, HHS significantly lowered the coupling efficiency of carbohydrate (pyruvate) and fatty acid (palmitoylcarnitine) oxidation compared to LLS. Exercise training prevented these effects in the HH mice, but had no exercise effect on OXPHOS coupling with either substrate in LL mice. These results demonstrate that adult‐onset exercise can prevent the deleterious effects of maternal obesity on cardiac mitochondrial function in offspring, but may alter glucose handling by mechanisms that merit further investigation.
Mitochondrial dysfunction has been suggested to be linked to disuse-induced muscle atrophy. A previous study demonstrated that acupuncture can attenuate muscle atrophy, but whether acupuncture treatment impacts muscle mitochondrial function is unknown. PURPOSE: To test the hypothesis that acupuncture would modulate mitochondrial respiratory function in soleus muscles from the casted models. METHODS: Female Sprague Dawley rats were randomly divided into 3 groups: 1) Control (CON), 2) Casting (CT), 3) Acupuncture treatment in the casted hind paw (AC) (n=8 each). The plaster casting material was wrapped from the trunk to the middle of one hind paw. Acupuncture was applied by needling ST36 and GB34 (acupoints) for 15 minutes, 3 times/week for 14 days. Soleus muscles were dissected in ice-cold BIOPS and teased fiber bundles. Mitochondrial respiratory function was measured in saponin-permeabilized fiber bundles (2-2.5mg) under a variety of substrate conditions. Group differences were compared using one-way ANOVA followed by Fisher's Least Significant Difference (LSD) post hoc test. RESULTS: AC attenuated muscle atrophy induced by casting in soleus (70. 99 ± 2.09 in CT vs. 85.90 ± 4.93 in AC, p<0.05). In the presence of fatty acid substrate (palmitoylcarnitine + malate), CT decreased the complex I and II supported maximal oxidative phosphorylation (OXPHOS) compared to the CON. AC significantly decreased respiratory leak, and increased OXPHOS coupling control compared to the CT. In the absence of fatty acids, AC significantly decreased respiratory leak, and complex I and II supported maximal oxidative phosphorylation (OXPHOS) compared to the CON, but no differences were observed between the CT and the AC across all respiratory states. CONCLUSION: AC attenuates muscle atrophy induced by casting and may improve the efficiency of energy production from fatty acids in oxidative muscle fibers.
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