Inflammation is notorious health villain. New research shows that simple strategies after a workout can help to reap benefits of it - build muscle, boost immunity, and fight stress.

Researchers have recently discovered that inflammation can actually make us healthier. It has powerful healing effects and is a critical component of the immune system. It is necessary to generate muscle and heal from injuries.

Whenever you train, you’re creating mini-traumas in your muscles. That triggers inflammation, which prompts the release of chemicals and hormones to repair the affected tissue and leads to stronger muscle fibers. Bones also benefit. The load placed on your bones during strength training creates tiny divots in their weak areas, and inflammation kicks off a process that fills in those spots with new, stronger bone. Inflammation is also crucial to recovering from an injury. After an injury white blood cells move to the injury site. They assess the damage and fire up clusters of molecules known as inflammasomes, which activate small proteins that make the injury site turn red and swell. These inflammatory symptoms draw immune cells to the area to begin the healing process.

Each workout, tweak how long you do your speed intervals.

Researchers from McMaster University in Canada, who have spent the past decade tinkering with the timing of HIIT sessions to measure their potency, recently found that one minute of intense work - three 20-second all-out sprints alternated with two-minute recoveries - is as effective as 45 minutes of steady cardio in boosting your cardiovascular fitness. So have they finally found the HIIT recipe that delivers the biggest body payoff in record time? “There actually isn't a single best way to do intervals,” says lead study author Martin Gibala, Ph.D. “The variety is infinite with these routines, and that's empowering.“ His suggestion: Switch up the duration of your sprints from one workout to the next to throw your body a different challenge each time.

Reference:

Gillen JB, Martin BJ, MacInnis MJ, Skelly LE, Tarnopolsky MA, Gibala MJ (2016) "Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment." PLoS ONE 11(4): e0154075.

DNA breaks activate the DNA damage response and, if left unrepaired, trigger cellular senescence. Telomeres are specialized nucleoprotein structures that protect chromosome ends from persistent DNA damage response activation. Whether protection can be enhanced to counteract the age-dependent decline in telomere integrity is a challenging question. Telomeric repeat–containing RNA (TERRA), which is transcribed from telomeres, emerged as important player in telomere integrity. However, how human telomere transcription is regulated is still largely unknown. Identified nuclear respiratory factor 1 and peroxisome proliferator–activated receptor γ coactivator 1α as regulators of human telomere transcription. In agreement with an upstream regulation of these factors by adenosine 5′-monophosphate (AMP)–activated protein kinase (AMPK), pharmacological activation of AMPK in cancer cell lines or in normal nonproliferating myotubes up-regulated TERRA, thereby linking metabolism to telomere fitness. Cycling endurance exercise, which is associated with AMPK activation, increased TERRA levels in skeletal muscle biopsies obtained from 10 healthy young volunteers. The data support the idea that exercise may protect against aging.

Reference:

Aurélie Diman, Joanna Boros, Florian Poulain et al. "Nuclear respiratory factor 1 and endurance exercise promote human telomere transcription", Science Advances 27 Jul 2016: Vol. 2, no. 7, e1600031

Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Reviewed findings suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.

Reference:

Ying Wang, Siegfried Hekimi "Mitochondrial dysfunction and longevity in animals: Untangling the knot", Science 04 Dec 2015: Vol. 350, Issue 6265, pp. 1204-1207