Effects of high-intensity intermittent exercise on the contractile properties of human type I and type II skeletal muscle fibers.

In vitro studies have shown that alterations in redox state can cause a range of opposing effects on the properties of the contractile apparatus in skeletal muscle fibers. To test whether and how redox changes occurring in vivo affect the contractile properties, vastus lateralis muscle fibers from seven healthy young adults were examined at rest (PRE) and following (POST) high-intensity intermittent cycling exercise. Individual mechanically skinned muscle fibers were exposed to heavily buffered solutions at progressively higher free [Ca2+] to determine their force-Ca2+ relationship. Following acute exercise, Ca2+ sensitivity was significantly decreased in type I fibers (by 0.06 pCa unit) but not in type II fibers (0.01 pCa unit). Specific force decreased after the exercise in type II fibers (-18%) but was unchanged in type I fibers. Treatment with the reducing agent dithiothreitol (DTT) caused a small decrease in Ca2+-sensitivity in type II fibers at PRE (by ∼0.014 pCa units) and a significantly larger decrease at POST (∼0.035 pCa units), indicating that the exercise had increased S-glutathionylation of fast troponin I. DTT treatment also increased specific force (by ∼4%), but only at POST. In contrast, DTT treatment had no effect on either parameter in type I fibers at either PRE or POST. In type I fibers, the decreased Ca2+ sensitivity was not due to reversible oxidative changes and may have contributed to a decrease in power production during vigorous exercises. In type II fibers, exercise-induced redox changes help counter the decline in Ca2+-sensitivity while causing a small decline in maximum force.NEW & NOTEWORTHY This study identified important cellular changes occurring in human skeletal muscle fibers following high-intensity intermittent exercise: 1) a decrease in contractile apparatus Ca2+ sensitivity in type I but not type II fibers, 2) a decrease in specific force only in type II muscle fibers, and 3) a redox-dependent increase in Ca2+ sensitivity occurring only in type II fibers, which would help maintain muscle performance by countering the normal metabolite-induced decline in Ca2+ sensitivity.