Postexercise changes in myocellular lipid droplet characteristics of young lean individuals are affected by circulatory nonesterified fatty acids

Abstract

Intramyocellular lipid (IMCL) content is an energy source during acute exercise. Non-esterified fatty acid (NEFA) levels can compete with IMCL utilization during exercise. IMCL content is stored as lipid droplets (LDs) that vary in size, number, subcellular distribution and in coating with LD protein PLIN5. Little is known about how these factors are affected during exercise and recovery. Here, we aimed to investigate the effects of acute exercise with and without elevated NEFA levels on intramyocellular LD size and number, intracellular distribution and PLIN5 coating, using high-resolution confocal microscopy. In a cross-over study, 9 healthy lean young men performed a 2h moderate intensity cycling protocol in the fasted (high NEFA levels) and glucose-fed state (low NEFA levels). IMCL and LD parameters were measured at baseline, directly after exercise and 4h post-exercise. We found that total IMCL content was not changed directly after exercise (irrespectively of condition), but IMCL increased 4h post-exercise in the fasting condition, which was due to an increased number of LDs rather than changes in size. The effects were predominantly detected in type I muscle fibers and in LDs coated with PLIN5. Interestingly, subsarcolemmal, but not intermyofibrillar IMCL content, was decreased directly after exercise in the fasting condition and was replenished during the 4h recovery period. In conclusion, acute exercise affects IMCL storage during exercise and recovery, particularly in type I muscle fibers, in the subsarcolemmal region and in the presence of PLIN5. Moreover, the effects of exercise on IMCL content are affected by plasma NEFA levels.

Acute exercise increases the contact between lipid droplets and mitochondria independently of obesity and type 2 diabetes

“…A plausible explanation for this apparent discrepant finding may be methodological differences in assessing subcellular compartments. However, considering the present results reporting no effect after 1 h of exercise, utilization of LDs may require exercise stimuli of longer durations, as reported by others (Brechtel et al., 2001; Decombaz et al., 2001; De Bock et al., 2007; Devries et al., 2007; Stellingwerff et al., 2007; Jevons et al., 2020; Daemen et al., 2021; Fell et al., 2021).…”

“…Nevertheless, in a recent study (Daemen et al., 2021), 2 h of moderate‐intensity cycling reduced subsarcolemmal, but not intermyofibrillar, LDs in overnight‐fasted healthy untrained young men. Contrary to athletes, LD storage may be more abundant in those untrained individuals, thus favouring a utilization of subsarcolemmal LDs during exercise.…”

“…Healthy young lean untrained (Decombaz et al., 2001; Shepherd et al., 2012, 2013; Daemen et al., 2021), moderately active (White et al., 2003; De Bock et al., 2007; Devries et al., 2007; Egger et al., 2013; Bucher et al., 2014; Chee et al., 2016) and endurance‐trained athletes (Staron et al., 1989; Romijn et al., 1993; Krssak et al., 2000; Romijn et al., 2000; Brechtel et al., 2001; Decombaz et al., 2001; Schrauwen‐Hinderling, van Loon et al., 2003; van Loon et al., 2003; Zehnder et al., 2005; Stellingwerff et al., 2007; Vermathen et al., 2012; Koh et al., 2017; Bergman et al., 2018; Jevons et al., 2020; Fell et al., 2021), but not metabolically compromised (Chee et al., 2016; Bergman et al., 2018) or elderly lean individuals (Chee et al., 2016), reduce intramuscular LDs during acute exercise. Given the differences in methodology and exercise prescriptions in the previous studies, we confirm these results by demonstrating no net reduction in intramuscular LDs in middle‐aged patients with type 2 diabetes nor glucose‐tolerant lean and obese controls.…”

“…Studies have consistently reported decreased intramuscular lipids during an acute exercise bout in healthy young, lean untrained and physically trained individuals. This has been demonstrated using diverse methods, including transmission electron microscopy (TEM) (Staron et al., 1989; Devries et al., 2007; Chee et al., 2016; Koh et al., 2017), light microscopy (van Loon et al., 2003; De Bock et al., 2007; Stellingwerff et al., 2007; Shepherd et al., 2012, 2013; Jevons et al., 2020; Daemen et al., 2021; Fell et al., 2021), stable isotope tracers (Romijn et al., 1993; Romijn et al., 2000; Bergman et al., 2018) and 1 H‐magnetic resonance spectroscopy (Krssak et al., 2000; Brechtel et al., 2001; Decombaz et al., 2001; Schrauwen‐Hinderling, van Loon et al., 2003; White et al., 2003; Zehnder et al., 2005; De Bock et al., 2007; Vermathen et al., 2012; Egger et al., 2013; Bucher et al., 2014). However, metabolically compromised (i.e.…”