Sport is my super power

There is indeed evidence that hypertrophying muscles take up more glucose and that this improves glycaemic control and reduces white adipose tissue. Figure 2A shows the 18F-fluoro-2-deoxy-D-glucose positron emission tomography scan of a patient who had performed “strenuous upper limbs exercise [presumably resistance exercise] 24 h prior to the imaging”. The scan suggests that the pectoralis muscle of the patient takes up a high amount of glucose 1-day post-exercise [54]. The caveat, however, is that we are unable to say whether the taken-up glucose is channelled into anabolism or is simply used to resynthesise the glycogen that was used during exercise. In another study, a Copenhagen team asked healthy and type-2 diabetic volunteers to perform a 6-week, one-sided leg resistance training. After the training, they performed an isoglycaemic-hyperinsulinemic clamp procedure and found that the resistance-trained leg took up ≈ 25% (healthy) and ≈ 10% more glucose (type 2 diabetes, both p > 0.05) than the untrained leg [55]. Moreover, in mice, synergist ablation-induced soleus hypertrophy increased both glucose uptake and glycolytic flux in lean (especially at insulin concentrations < 5 nmol/L) and obese mice at all insulin concentrations when compared with the untreated control soleus [29]. Additionally, overloaded, hypertrophying mouse plantaris muscles take up ≈ 60% more glucose than control plantaris. In Slc2a4 (encoding the glucose transporter Glut4) knock-out mice, the difference is even greater, as the glucose uptake of the hypertrophying plantaris is similar to the wild-type hypertrophying plantaris but glucose uptake into the non-hypertrophying control plantaris is decreased [56]. Collectively, these studies suggest that resistance-trained and/or hypertrophying mouse and human muscles take up more glucose than untrained or non-hypertrophying muscles. But why? Is it just to replenish glycogen or is a fraction of the glucose channelled into anabolism?

An online survey was administered and disseminated via Google Forms from 17 May to 5 July 2020. The survey was shared via email and personal/group messaging applications (e.g., WhatsApp, Signal, and Telegram) and promoted on social media (e.g., Facebook, Twitter, and Instagram) through the professional networks of the research team (e.g., clubs, federations, and institutions). The English language “master” version of the survey was translated and administered in 34 further languages: Albanian, Arabic, Bangla, Chinese-simplified, Chinese-traditional, Croatian, Czech, Danish, Finnish, French, German, Greek, Hindi, Indonesian, Italian, Japanese, Korean, Malay, Nepalese, Norwegian, Persian, Polish, Portuguese, Punjabi, Romanian, Russian, Sinhala, Slovenian, Spanish, Swahili, Swedish, Thai, Turkish, and Vietnamese. The survey questions underwent translation and back-translation, performed by the research team (including at least one native speaker and one topic expert), including pilot completions of the survey by and feedback from native language speaking athletes, resulting in the finalized surveys for all languages.

Participants provided informed consent, and the study received ethical approvals from the University of Melbourne Human Research Ethics Committee (HREC; no. 2056955.1), Qatar University (QU-IRB 1346-EA/20), and the University of Cassino e Lazio Meridionale (10031) in the spirit of the Declaration of Helsinki. Data were collected and processed anonymously and according to the guidelines of the “General Data Protection Regulation” (gdpr-info.eu). Participation was voluntary, and all individuals were permitted to withdraw at any time before completion and submission of the survey. Participant eligibility criteria were as follows: (1) elite- or subelite athletes aged ≥ 18 years of either s*x with or without disability; (2) athletes experienced at least two consecutive weeks of lockdown (March–June 2020); (3) athletes had not missed training for ≤ 7 days because of illness/injury within the survey period; and (4) athletes experienced a “medium-to-high” lockdown severity. A medium–high lockdown severity was considered met when one or more of the following criteria were fulfilled: (1) movement was permitted only for essential supplies and groceries, (2) access to public exercise facilities was restricted (i.e., recreational areas such as parks or open spaces were closed or time/capacity limits were imposed), and (3) training facilities at institutions, clubs, colleges, etc. were closed. The a priori sample size estimation was 12,418 (see the supplementary material S1). In total, 13,772 entries were evident upon survey closure. After exclusions (n = 1246) for duplicates (n = 731), age limit violations (n = 410), and/or unmet lockdown severity criteria (n = 105) were completed, a final sample of data from 12,526 athletes (142 countries/territories across six continents) was used for subsequent statistical modeling. The sample represented 108 “team” and “individual” sports.

Whereas the negative effects of aging and smoking on pulmonary function are undisputed, the potential favorable effects of physical activity on the aging process of the otherwise healthy lung remain controversial. This question is of particular clinical relevance when reduced pulmonary function compromises aerobic exercise capacity (maximal oxygen consumption) and thus contributes to an increased risk of morbidity and mortality. Here, we discuss whether and when the aging-related decline in pulmonary function limits maximal oxygen consumption and whether, how, and to what extent regular physical activity can slow down this aging process and preserve pulmonary function and maximal oxygen consumption. Age-dependent effects of reduced pulmonary function (i.e., FEV1, the volume that has been exhaled after the first second of forced expiration) on maximal oxygen consumption have been observed in several cross-sectional and longitudinal studies. Complex interactions between aging-related cellular and molecular processes affecting the lung, and structural and functional deterioration of the cardiovascular and respiratory systems account for the concomitant decline in pulmonary function and maximal oxygen consumption. Consequently, if long-term regular physical activity mitigates some of the aging-related decline in pulmonary function (i.e., FEV1 decline), this could also prevent a steep fall in maximal oxygen consumption. In contrast to earlier research findings, recent large-scale longitudinal studies provide growing evidence for the beneficial effects of physical activity on FEV1. Although further confirmation of those effects is required, these findings provide powerful arguments to start and/or maintain regular physical activity.