Month: November 2018

Exercise and Longevity

There’s a couple of recent studies out that look at the effects of exercise using telomere length as a surrogate for longevity. Our telomeres shorten as we age.

The first study is (Beate Ø Osthus, Ida & Sgura, Antonella & Berardinelli, Francesco & Alsnes, Ingvild & Brønstad, Eivind & Rehn, Tommy & Kristian Støbakk, Per & Hatle, Håvard & Wisløff, Ulrik & Nauman, Javaid. (2012). Telomere Length and Long-Term Endurance Exercise: Does Exercise Training Affect Biological Age? A Pilot Study. PloS one. 7. e52769. 10.1371/journal.pone.0052769). The study:

Older endurance trained athletes had longer telomere length compared with older people with medium activity levels (T/S ratio 1.12±0.1 vs. 0.92±0.2, p = 0.04). Telomere length of young endurance trained athletes was not different than young non-athletes (1.47±0.2 vs. 1.33±0.1, p = 0.12).

A second study looked at the effects of the specific mode of exercise (Christian M Werner, Anne Hecksteden, Arne Morsch, Joachim Zundler, Melissa Wegmann, Jürgen Kratzsch, Joachim Thiery, Mathias Hohl, Jörg Thomas Bittenbring, Frank Neumann, Michael Böhm, Tim Meyer, Ulrich Laufs; Differential effects of endurance, interval, and resistance training on telomerase activity and telomere length in a randomized, controlled study , European Heart Journal, ehy585).

The results were interesting.

This randomized, controlled, and prospective training study shows that specific training protocols lead to differential effects on cellular aging. Aerobic endurance and high-intensive interval training, but not resistance training, increases telomerase activity and telomere length in blood mononuclear cells.

This study was fairly impressively powered with 124 subjects.

One hundred and twenty-four healthy previously inactive individuals completed the 6 months study. Participants were randomized to three different interventions or the control condition (no change in lifestyle): aerobic endurance training (AET, continuous running), high-intensive IT (4 × 4 method), or RT (circle training on 8 devices), each intervention consisting of three 45 min training sessions per week.

The specific results were statistically significant.

Telomerase activity in blood mononuclear cells was up-regulated by two- to three-fold in both endurance exercise groups (AET, IT), but not with RT. In parallel, lymphocyte, granulocyte, and leucocyte TL increased in the endurance-trained groups but not in the RT group. Magnet-activated cell sorting with telomerase repeat-ampliflication protocol (MACS-TRAP) assays revealed that a single bout of endurance training—but not RT—acutely increased telomerase activity in CD14+ and in CD34+ leucocytes.

Things to note is that this is an older (~49 years on average), untrained group of people who were at healthy BMI (~24).

Mechanism

The mechanism is interesting.

Exercise Intensity and Blood Sugar

I’ve come to the conclusion that for me as a diabetic intense exercise (at high heart rates) is not good for my blood sugar control. Here’s a study of Type 1 Diabetics which shows the increase in blood sugar from intense exercise (Vinutha S, Paul F, Raymond D, et al. Effect of exercise intensity and blood glucose level on glucose requirements to maintain stable glycaemia during exercise in individuals with type 1 diabetes. Int J Pediatr Endocrinol. 2015;2015(Suppl 1):O39). The study looked at:

Nine young adults with T1D underwent euglycaemic clamps, whereby stable blood glucose levels between 4.5 to 6mmol/L were maintained during the study at basal insulin levels. Participants performed up to 40 minutes of exercise at four different exercise intensities (35%, 50%, 65% and 80% VO2peak) on four separate days following a randomised counterbalanced design. In a subsequent experiment, eight participants underwent either a euglycaemic or hyperglycaemic (9.5 – 10.5mmol/L) clamp at basal insulin levels, during which they performed 40 minutes of exercise at 50% VO2peak, on two separate days. In both studies, glucose infusion rates (GIR) to maintain stable glycaemia were measured during exercise, constant deuterated glucose was infused to determine glucose kinetics and blood samples were collected for the analysis of glucoregulatory hormones.

The result was:

The average GIR to maintain euglycaemia during exercise was 2.0±0.9, 4.0±1.5, and 4.1±1.7g/h (mean±SEM) at 35%, 50% and 65% VO2peak, respectively. These GIRs were all significantly greater than that at 80% VO2peak where no glucose was required (p<0.05). Exercise at 80% VO2peak was associated with a significant rise in catecholamine levels and endogenous glucose production (p<0.05). The average GIR to maintain stable glycaemia during exercise performed during the second experiment at 50% VO2peak was similar at euglycaemia (4.9±2.1g/h) and hyperglycaemia (5.5±2.5g/h; p>0.05).